Women and Exercise - Physiology and Sports Medicine

Medical Conditions Arising during Sports 277 the use of procedures between women and cancer among college alumni. J Natl Cancer men hospitalized for coronary heart disease. Inst 83:1324,1991. N Engl J Med 325:221,1991. 26. Dupont WD, and Page DL:Menopausal estro- 12. Gordon T: Cardiovascular risk factors in gen replacement and breast cancer. Arch In- women. Pract Cardiol5:137,1974. tern Med 151:67, 1991. 13. Wood PD, Stepanick ML, Williams PT, et al: 27. WyndhamCH, Morrison JF, and WilliamsCG: The effects on plasma lipoproteins of a pru- Heat reactions of male and female Cauca- dent weight-reducing diet, with or without sians. J Appl Physiol 20:357,1965. exercise, in overweight men and women. N 28. Wells CL: Sexual differences in heat stress re- Engl J Med 325:461,1991. sponse. Phys Sportsmed 5(9):78,1977. 14. Somers VK, Conway J, Johnston J, et al: Ef- 29. Drinkwater BL, Kupprat JC, Denton JE, et al: fects of endurance trainingon baroreflex sen- Heat tolerance of female distance runners. sitivity and blood pressure in borderline hy- Ann NY Acad Sci 301:777,1977. pertension. Lancet 337:1363, 1991. 30. Statement of the American College of Sports 15. Helmrich SP, Ragland DR, Leung RW, et al: Medicine: Prevention of heat injuries during Physical activity and reduced occurrence of distance running. J Sports Med 9(7):105, non-insulin-dependent diabetes mellitus. N 1976. Engl J Med 325:147,1991. 31. Sutton JR: Heatstroke from running. JAMA 16. Marcus BH, Albrecht AE, Niaura RS, et al: 243:1896,1980. Usefulness of physical exercise for maintain- 32. Koppes GM, Daly JJ, ColtmanCA,et al: Exer- ing smoking cessation in women. Am J Car- tion-induced rhabdomyolysis with acute diol 68:406,1991. renal failure and disseminated intravascular 17. Chen Y, Home SL, Dosman JA: Increased sus- coagulation in sickle cell trait. Am J Med ceptibility to lung dysfunction in female 63:313,1977. smokers. Am Rev Respir Dis143:1224,1991. 33. Stewart PJ, and Posen GA: Case report: Acute 18. Williamson DF, Madans J, Anda RF, et al: renal failure following a marathon. Phys Smoking cessation and severity of weight Sportsmed 8(4):61, 1980. gain in a national cohort. N Engl J Med 34. Scott DE,and Pritchard JA: Iron deficiencyin 324:739, 1991. healthy young college women. JAMA 199:147, 19. Moffatt RJ, and Owens SG: Cessation from 1967. cigarette smoking: Changes in body weight, 35. Steenkamp I, Fuller C, Graves J, et al: Mara- body composition, resting metabolism, and thon running fails to influence RBC survival energy consumption. Metabolism 40:465, rates in iron-repleted women. Phys 1991. Sportsmed 14(5):89, 1986. 20. Daughton DM, Heatley SA, Prendergast JJ, et 36. McMahon LJ, Ryan MJ, Larson D,et al: Occult al: Effect of transdermal nicotine delivery as gastrointestinal blood loss in marathon run- an adjunct to low-intervention smoking ces- ners. Ann Intern Med 100:846,1984. sation therapy: A randomized, placebo-con- 37. Martin DE, Vroon DH, May DF, et al: Physio- trolled, double-blindstudy. Arch InternMed logical changes in elite male distance run- 151:749,1991. ners training for Olympic competition. Phys 21. Hurt RD, Lauger GG, Offord KP, et al: Nico- Sportsmed 14(1):152,1986. tine-replacement therapy with use of a trans- 38. Priebe WM,and Priebe J: Runners' diarrhea dermal nicotine patch: A randomized double- (RD): Prevalence and clinical symptomatol- blind placebo-controlled trial. Mayo Clin ogy. Am J Gastroenterol 79:827, 1984. Proc 65:1529, 1990. 39. Siegel AJ, Silverman LM, and Lopez RE:Cre- 22. Egeland GM, Kuller LH, Matthews RA, et al: atine kinase elevations in marathon runners, Hormone replacement therapy and lipopro- relationship to training and competition. tein changes duringearly menopause. Obstet Yale J Biol Med 53:275, 1980. Gynecol 76:776, 1990. 40. Poortsmans JR: Exercise and renal function. 23. Sullivan JM, Vander Zwaag R, Hughes JP, et Sports Med 1:125,1984. al: Estrogen replacement and coronary ar- 41. McFadden ER, and Ingram RH:Exercise-in- tery disease: Effect on survival in postmeno- duced asthma. Seminars in Medicine of the pausal women. Arch Intern Med 150:2557, Beth Israel Hospital, Boston 301:763,1979. 1990. 42. Sheffer AL, and Austen KF: New exercise-in- 24. Glazer G:Atherogenic effects of anabolic ste- duced anaphylactic syndrome identified. roids on serum lipid levels—a literature re- Mod Med 1:96,1981. view. Arch Intern Med 151:1925,1991. 43. Siegel AJ: Exercise induced anaphylaxis. 25. Lee IM, Paffenbarger RS, Hsieh C, et al: Phys- Phys Sportsmed 8(1):55, 1980. ical activity and risk of developing colorectal 44. Gardner KD Jr: Athletic pseudonephritis al-

278 Special Issues and Concerns teration of urine sediment by athletic com- 49. Siegel AJ, Silverman LM, and Holman BL:El- petition. JAMA 161:613,1956. evated creatine kinase MB isoenzyme levels 45. Siegel AJ, Hennekens CH, Solomon HS, et al: in marathon runners. JAMA 246:1049,1981. Exercise-related hematuria findings in a group of marathon runners. JAMA 241:391, 50. Siegel AJ, Silverman LM, and Evans WJ: Ele- 1979. vated skeletal muscle creatine kinase MBiso- 46. BlacklockNS:Bladder trauma in the long dis- enzyme levels in marathon runners. JAMA tance runner. 10,000 metres hematuria. Br J 250:2835,1983. Urol 49:129, 1977. 47. Apple FS, and Rogers MA: Serum and muscle 51. Evans WJ, and Meredith CN:Exercise and nu- alanine aminotransferase activities in mara- trition in the elderly. In Munro HM and Dan- thon runners. JAMA 252:626, 1984. ford DE (eds): Nutrition, Aging, and the El- 48. Leslie BR, and Sanders NW:Runner's hemo- derly. Plenum, New York, p 89. lysis and pigment gallstones. N Engl J Med 313:1230,1985. 52. Camacho TC, Roberts RE, Lazarus NB, et al: Physical activity and depression: Evidence from the Alameda County Study. Am J Epi- demiol 134:220,1991. APPENDIX 15-1 Sport Candidate's Questionnaire Name Age Date of birth School Athlete's address Grade Sex Parent's name &address Regular physician Tel. No. Tel. No. Tel. No. Medical History Yes No Past or Present Please Circle Item(s) in ( ) 1. Discuss with a doctor a (health problem, injury, diet)? 2. Discuss with a doctor (emotional problem, stress management)? 3. Any close family member with (diabetes, migraines, asthma, heart trouble, high blood pressure)? 4. Any family member who died suddenly under age 50, excluding accidents? 5. Any (illnesses lasting more than 1 wk, chronic or recurrent illness)? 6. Any (hospitalizations or surgery)? 7. Any (injuries or illnesses) requiring treatment by a doctor? 8. Any allergies (hay fever, hives, asthma, bee sting, or drug allergies)? 9. Any medications taken regularly or within last 6 mo? 10. Any neck injury? 11. Any (concussions, skull fracture, loss of memory or consciousness, convulsions or epilepsy, headaches)? 12. Any (eyeglasses, contact lenses, decreased vision, oir temporary loss of vision)? 13. Any (hearing loss, perforated eardrum, recurrent ear infections)? 14. Any (broken nose, nosebleeds, dentures, braces, bridges, tooth caps)? 15 Have you ever fainted during exercise?

APPENDIX 15-1 Sport Candidate's Questionnaire—Continued Medical History Yes No Past or Present Please Circle ltem(s) in ( ) 16. Any (heart trouble, murmur,arrhythmias, chest pain, high 17. blood pressure)? 18. Doyou (smoke, drink alcohol, take drugs)? 19. Any (pneumonia, tuberculosis, chronic cough)? Any loss of, or serious injury to (eye, testicle, kidney, 20. lung)? 21. Girls,any menstrual problems? Age at first menstrual 22. period Any (hernias, kidney problems, ulcer, heartburn, bowel 23. problems, hepatitis)? 24. Any (diabetes, thyroid disorders, anemia, abnormal 25. bleeding)? 26. Any knee injury (sprain, fracture, dislocation, surgery, 27. chronic pain)? Any ankle injury (sprain, fracture, dislocation, surgery, 28. 29. chronic pain)? 30. Any bone (fracture, infection, deformity)? Any (injuries, sprains, dislocations, surgery) in (shoulder, 31. Date of last tetanus booster wrist, finger, or any other joint)? Any skin disorders (recurrent rash, fungal infection, boils, athlete's foot)? Any injury not mentioned? Any (heat exhaustion, heat stroke)? Any reasons why you were unable to participate in the past or should not be able to in the future? Explain Any QuestionsAnswered With \"Yes\" Below (please be as specific as possible: dates, treating physician, list medications, residual problems, etc.) Signature of student athlete Date Signature of parent or physician Date Source: From Gregg JR, and Spindler KP:Screening school-age athletes. Drug Therapy, September 1985, p 75, with permission. 279

Appendix 15-2 Physical Examination Form Name Age Date of birth School Grade Height (in) Weight (Ib) Pulse BP (sitting, right arm) Vision (acuity) R —/— L —/ Check one: — normal without glasses — normal with glasses — abnormal without glasses — abnormal with glasses OK Circle in ( ) if Abnormality Presentor Normal Comments Initials 1. Condition Absent 2. 3. Dental (dental prosthesis, severe caries) 4. Skin, scalp, lymphatics (active infection, acne, 5. rashes, adenopathy) 6. Eyes/fundi (vision-color, depth, peripheral; 7. pupils, extraocular movements, fundi) 8. Ears, nose, throat (hearing, tympanic 9. membranes, nasal septum, tonsils, throat) 10. Neck (soft tissue) (adenopathy, thyroid, 11. carotid pulses) 12. Cardiovascular (PMI,pulses [femoral- branchial], rhythm, murmurs) 13. Chest and lung (breath sounds, shape, excursion) 14. Abdomen (hepatosplenomegaly, masses, costovertebral angle tenderness) 15. Genitalia-hernia(scrotal contents, inguinal region) Sexual maturity (Tanner staging) Neurologic(sensation, deep-tendon reflexes, mental status) Orthopedic (all for active range of motion and strength besides information in parentheses) a. Cervical spine/back (scoliosis) b. Shoulders (symmetry) c. Arm/elbow/wrist/hand d. Hip/foot (passive range of motion hip, foot stance with weight bearing) e. Knee (ligamentous stability) f. Ankle (ligamentous stability) g. Flexibility h. % Body fat (specify method) Laboratory tests Hg g/dl Hct % Transferrin saturation % Urinalysis Other Review by team physician a. No athletic participation b. Limited participation, e.g., c. Clearance withheld until: d. Full unlimitedparticipation Comment/Advice: 16. Team physician's signature Date Source: From Gregg JR, and Spindler KP: Screening school-age athletes. Drug Therapy, September 1985, p 77, with permission.

Appendix 15-3 Disqualifying Conditions (Indicated by an X) for Sports Participation, by Type of Sport Condition Collision* Contactt Noncontact Others§ General X XX X Acute infection (respiratory, genitourinary, X X X infectious mononucleosis, hepatitis, active rheumatic fever, active X XX || tuberculosis) X XX X Obvious physical immaturity i n comparison with other competitors in || || || group X XX Hemorrhagic disease (hemophilia, purpura, other serious bleeding tendencies) Diabetes, inadequately controlled Diabetes controlled Jaundice Ears X X Absence or loss of function of one eye Respiratory System X XX X X XX X Tuberculosis (active o r symptomatic) Severe pulmonary insufficiency Cardiovascular System Mitral stenosis, aortic stenosis, aortic X XX X insufficiency, coarctation of aorta, X ¶ cyanotic heart disease, recent carditisof any cause Hypertension, organic XXX Previous heart surgery for congenital or ¶ ¶ ¶ acquired heart disease Liver XX Enlargement *Football, rugby, hockey, lacrosse, etc. †Baseball, soccer, basketball, wrestling, etc. Cross-country, track, tennis, crew, swimming, etc. §Bowling, golf, archery, field events, etc. ||No exclusions necessary. ¶Each patient should be judged individually in conjunction with cardiologist and surgeon. Source: From Blum RW: Preparticipation evaluation of the adolescent athlete. Postgrad Med 78:2,52- 55, 1985, with permission. 281

16CHAPTER Cardiovascular Issues PAMELA S. DOUGLAS, M.D. AEROBIC CAPACITY EXERCISE LIMITATIONS IN HEART DISEASE CARDIAC FUNCTION IN RESPONSE TO EXERCISE Mitral Valve Prolapse EXERCISE Anorexia Nervosa ELECTROCARDIOGRAPHIC TESTING Sudden Death Other Forms of Heart Disease As participation in both competitive and noncompetitive sports increases, the numbers of female athletes, of athletes with known forms of heart disease, and of older athletes more likely to have occult heart disease, also increases. In gen- eral, the cardiovascular responses to exercise are similar in both sexes, both in healthy individualsand in those with heart disease. However, physiologic and pathologic differences do exist between the sexes and are important in the eval- uation and treatment of the exercising woman. Exercise of any type or intensity requires increased oxygen delivery towork- ing tissue. This is accomplished through peripheral mechanisms, whichinclude the differential perfusion of vascular beds and increased oxygen extraction by muscle, and through central or cardiac mechanisms, chiefly an increase in car- diac output. Thus, maximal exercise, or maximal oxygen uptake, is determined by maximal increases in the peripheral arteriovenous O2 difference, and by car- diac output and its components, stroke volume and heart rate. AEROBIC CAPACITY In the average sedentary woman, maximum aerobic workload is 15% to30% lower than in the average sedentary man,1,2 even when corrected for body size. This may be due to a number of factors. Women normally possess a lower total oxygen-carrying capacity of blood, owing to lower blood volume,fewer red blood cells, and lower hemoglobin content. Women also have smaller hearts, even when corrected for body size, with smaller stroke volumes and thereforehigher heart rates for a given cardiac output or oxygen uptake. Finally, womengenerally possess a higher percentage of adipose tissue and a lower percentage of working 282

Cardiovascular Issues 283 muscle than do men.These differences com- have been defined as those able to increase bine to produce, on average, a lower maxi- their ejection fraction by at least five per- mal level of work or aerobic capacity in centage points during exercise.7 Persons women. with a lesser increase, or even a decrease, are felt to have a component of myocardial In part, these \"physiologic\" differences dysfunction, or at the least, impaired car- may also be explained by considering that, diac reserve. Higginbotham and associates8 on the average, men are more active than studied healthy, sedentary adults and found women and therefore maintain a more that the generally accepted \"normal\" in- trained state, particularly as women tend to crease in left ventricular ejection fraction become relatively more sedentary after pu- during exercise occurred only in men and berty. Several factors support this hypothe- not in women. Of the 16 women studied, sis. Training programs produce similar in- only 7 increased their ejection fraction by creases in aerobic capacity in both sexes, five points or more (compared with 14 of 15 even when older individuals are exam- men), and the average ejection fraction was ined.2-4 Maximal oxygen uptake in individ- unchanged (63% at rest compared with64% ual highly trained female athletes can ap- at peak exercise). In contrast, the average proach and equal that of similarly trained ejection fraction in men increased from 62% males.5 Finally, there is little difference in to 77%(Fig. 16-1). exercise capacity between boys and girls under the age of 12.1 In addition, the mechanisms used to in- crease cardiac output during exercise ap- Regardless of cause, recognition of the peared different in men than in women. In lower maximal aerobic capacity and higher men, end-diastolic left ventricular size did heart rates during submaximal exercise in not change, whereas end-systolic size de- women as compared with men is essential to creased, leading to increases in stroke vol- the accurate interpretation of exercise re- ume and ejection fraction. In contrast, sults in women. Sex-specificstandards have women achieved a similarincrease in stroke been developed for maximal aerobic capac- volume by increasing end-diastolic size ity, as well as nomograms for the calcula- while end-systolic size remained un- tion, in women, of maximal capacity from changed. Thus, women appeared to dilate submaximal heart rate and oxygen uptake their left ventricles, or increase preload, values. Exerciseperformance in womencan- whereas men increased ventricular short- not be adequately evaluated without refer- ening. The physiologicbasis for these differ- ence to such standards. ent mechanisms of achieving the same end—increasing cardiac output and there- CARDIAC FUNCTION IN fore oxygen supply to muscle—is unknown, RESPONSE TO EXERCISE as is its significance for preserved health or training. In addition to differences in aerobic ca- pacity, the normal cardiac response to ex- These findings have importantclinical im- ercise in women may be different than in plications. If good health is defined by the men.6 The most widely used diagnostic test healthy male pattern of response, the re- for the evaluation of left ventricular function mainder of the population, or women who during exercise is the gated blood pool scan. normally respond differently, may be falsely This test involves the use of radiolabeled diagnosed as unwell. Since exercise gated red blood cells (using technetium)to deter- blood pool scanning is commonly used to mine ejection fraction, or the percentage of measure the cardiac functional response to blood within the left ventricular chamber exercise and is recommended as a diagnos- that is ejected with each heart beat, at rest tic test for the evaluation of a variety of car- and at maximal exercise. Normalindividuals diac complaints, the problem is potentially a large one. At special risk for misdiagnosis

284 Special Issues and Concerns Figure 16-1. Ejection fraction responses during exercise in which the workloadwas increased every 3 minutes. Progressive individual data are shown for women (top left) and men (bottom left). Mean submaximal and maximal group data are plotted on the right as mean data ± standard deviation for normal female (F) and male (M) volunteers. Significant intergroup differences are shown for the slope of the response, as well as for data from subjects at rest and during maximal exercise. (From Higginbotham et al.,8 with permission.) as having impaired cardiac function is the Blood pressure is little changed in the nor- healthy woman, whether sedentary or ac- mal person following either isotonic or iso- tive, undergoing evaluation of cardiac func- metric exercise training. There is some evi- tion. In a similar manner, a woman with mild dence that both systolic and diastolic known cardiac disease may be classified as pressures may be reduced by training in in- having more severe impairment than is ac- dividuals with hypertension; however, tually the case, owing to use of the male re- these effects are small and not known to dif- sponse as a normal reference standard. fer between the sexes.9 In contrast to aerobic capacity and the The hearts of both men and women ap- functional response to exercise, other as- pear to adapt similarly to exercise training.1,2 pects of cardiac-related exercise physiology This has been documented in studies of appear to show few differences between women pursuing typically female-domi- men and women. Aging affects aerobic ca- nated sports such as field hockey and pacity of healthy individuals of both sexes dance,10,11 as well as those pursuingjogging, similarly, causing a decline in maximaloxy- swimming, and triathlon trainings.12-14 gen uptake. This results from a decrease in Weight training or isometric exercise ap- both the maximal achievable heart rate and pears to produce cardiovascular effects sim- the mechanical performance of the myocar- ilar to those of aerobic, dynamic exercise.15 dium, as well as limitations in the function- A detailed discussion of the structural car- ing of other organ systems (Fig. 16-2). diac changes associated with dynamic and

Cardiovascular Issues 285 Age (years) Age (years) Figure 16-2. Derived values for observed and maximal cardiovascular variables in 104normal, healthy women. (A) Observed age- and weight-adjusted value of maximal oxygen uptake(Vo2max). The regression line is shown and the normal range indicated by +2 standard deviations (SD). The standard deviation for oxygen uptake is 3.59 m L - k g - 1 - m i n - 1 ) . (B) Estimated age-adjusted valuesof maximal cardiac output are Qmax. The standard deviation for cardiac output is 1.35 L - m i n - 1 . (C) Observed age-adjusted values of maximal heart rate (HRmax). The standard deviation for heart rate is 14 beats per minute. (D) Estimatedage-adjusted values of maximalstroke volume (SV). The stan- dard deviation for stroke volume is 8 mL. (From Hossack et al.,6 with permission.) resistive exercise training is beyond the both sexes develop cardiac arrhythmias scope of this chapter and has been well re- with training, probably because of altera- viewed.14 At present, no differences between tions of vagal tone and catecholamine me- the sexes have been found in the extent or tabolism. Although sinus bradycardia is incidence of cardiac adaptations to exercise. most common, low-grade atrioventricular block, premature atrial or ventricular con- Female athletes develop clinical findings tractions, and repolarization abnormalities of left ventricular hypertrophy, includingan are also seen.14 Highly trained aerobic ath- enlarged heart on chest radiograph, in- letes also demonstrate a greater prevalence creased left and right ventricular cavity of multivalvular regurgitation.17 sizes and wall thicknesses on echocardiog- raphy, and increased voltage on ECG, Since many of these adaptive changes reflecting an increased myocardial mass.16 may also signify the presence of true heart Following weight training, the cardiac disease, it is important to recognize that for chambers tend to remain normal-sized and women, as well as men, physical training the walls become hypertrophied. Athletes of may lead to physiologic structural and elec-

286 Special Issues and Concerns Figure 16-3. The marked differ- ence in the incidence offalse-posi- tive test results between men and women is statistically significant (p < 0.001, regardless of coronary anatomy). Hatched bars indicate the percentage of positive exercise test results associated with normal coronary arteries or less than50% stenosis (false-positive results). Open bars indicate the percentage of positive tests associated with 75% or greater coronary stenosis (true-positive results). Overall, 60 of 77 subjects (78%) had both pos- itive exercise tests and significant coronary disease. In men, 55 of 62 (89%) had true-positive test re- sults, whereas only 5 of 15 women (33%) did. This difference is statis- tically significant (p < 0.001). (From Sketch et al.,18 with permis- sion.) trical changes in a healthy heart that must ference. The most important of these is the not be confused with similar findings in car- age-related difference in the prevalence of diac disease states. heart disease between men and women. In general, the effect of disease prevalence in EXERCISE the population studied has a great impact ELECTROCARDIOGRAPHIC upon the accuracy and usefulness of any TESTING given diagnostic test. This is termed Bayes' theorem and is highly applicable to the com- The most common form of heart disease parability of exercise testing results in men in the United States today is coronary ath- and women.20 Because coronary disease is erosclerosis. Coronary stenoses limit the relatively less likely in a younger middle- delivery of adequate amounts of oxygen to aged woman,any given positive test result is the heart, a problem often not noted until more likely to be a false rather than a true oxygen demands are increased by exercise. result. Thus, the diagnostic utility of exer- Thus, monitoring of electrocardiographic cise testing for coronary artery disease in recordings capable of detecting cardiac women is lower than for men. To elimi- ischemia during a controlled exercise pro- nate the Bayesian factor, Barolsky and co- tocol is the most widely used diagnostic pro- workers21 studied the utility of exercise test- cedure for the detection of coronary dis- ing in groups of men and women with similar ease. In men, regardless of symptoms, such disease prevalences. This markedly im- exercise testing is an excellent screening proved the validity of test results, although test, with few false-positive results. In con- women still had a higher incidence of false- trast, in women, the incidence offalse-posi- positive test results. tive test results (appearance of electro- cardiographic changes characteristic of Another reason for the high rate of false- myocardial ischemia leading to a diagnosis positive test results is the higher incidence of coronary disease in its absence) is quite in women of other characteristics that are high, perhaps as high as two thirds of all associated with nondiagnostic results.22,23 positive tests (Fig. 16-3).18,19 These characteristics include atypical chest pain, resting electrocardiographic abnor- Several factors partially explain this dif- malities including nonspecific ST- and T- wave changes, and ingestion of medications

Cardiovascular Issues 287 such as digoxin and anxiolytics. Since these EXERCISE LIMITATIONS IN characteristics appear more commonly in HEART DISEASE women than in men, test results are more frequently confounding in women. The effects of exercise in those with heart disease appear to be similar in both men and Several alternative strategies have been women. However, since little attention has proposed to render exercise testing more been focused on the potential differences useful in women. These include more strin- between men and women, it is possible that gent use of probability analysis,24 alternate such differences do exist but have been or additional electrocardiographic lead overlooked. It is known that women in gen- placement,25 consideration of R-wave ampli- eral have a worse prognosis following myo- tude as well as ST-segment changes,26 and cardial infarction29 and a higher mortality use of thallium-201 myocardial scintigraphy and lower immediate success rate following with exercise testing.19,27The addition of iso- coronary artery bypass grafting30 than men tope imaging does markedly improve the have. Whether this dichotomy extends to specificity of exercise testing; however, the other forms of therapy, such as exercise false-positive rate is still higher for women training, is unknown. A low level of physical than for men. In part, this may be due to at- fitness, as measured by treadmill testing, is tenuation of tracer signal resulting from a powerful risk factor for coronary heart dis- overlying breast tissue.27,28 In addition, thal- ease and cardiac death in women, as it is in lium scanning is costly, time consuming, men.31 Longitudinal studies of exercise in- and requires radiation exposure and the tervention have shown some benefit incar- availability of special equipmentand trained diac risk factors such as lipid profiles, blood personnel. pressure, obesity, and diabetes mellitus, al- though the effect is generally smaller in The different sensitivity and specificity of women than in men.32 exercise testing in women has important clinical implications. In diagnostic exercise In men, the use of exercise in the treat- testing performed to define and classify pre- ment of known coronary heart disease, or existing complaints, women with chest pain for rehabilitation following myocardial in- due to noncardiac causes are far more likely farction or revascularization surgery, is of to be wrongly diagnosed as having coronary established value in hastening recovery and disease than anemia. This is obviously an improving the quality of life in the short undesirable event and,in addition to caus- term; longer-term benefitssuch as reduction ing a great deal of patient anxiety, may lead of recurrence or improved long-term sur- to taking unnecessary medications and/or vival are more difficult to prove. Rehabilita- undergoing additional testing, which is tive programs for those with nonischemic more expensive and may endanger health. heart disease are more controversial. How- In contrast, a negative test result is a good ever, the effectiveness of exercise regimens indication of the absence of heart disease. in the primary and secondary treatment of Exercise testing performed to ensure that a any form of heart disease has not been ex- training program may be undertaken safely amined in adequate numbers of women; is at even greater risk of producing a false their effectiveness can only be extrapolated suspicion of cardiac disease. The high false- from studies performed in men. Possible positive rate of exercise testing in women sex-related differences have not been ex- makes it a very poor screening test forcar- plored. diovascular disease in women, regardless of symptoms. Unfortunately, no better alter- Mitral Valve Prolapse native screening or diagnostic test exists for women, nor is the remarkably low predic- In contrast to most forms of either con- tive accuracy of exercise testing in women genital or acquired heart disease, mitral fully understood.

288 Special Issues and Concerns valve prolapse occurs with greater fre- be kept in mind, however, that the natural quency in women than in men. For this rea- history of the disorder is not well known and son, information regarding cardiac function its clinical significance remains somewhat and exercise in this disease process may be controversial. The American College ofCar- more likely to represent the female than the diology has recommended that a small sub- male circumstance. Mitral valve prolapse is set of patients with mitral valve prolapse a generally benign syndrome characterized limit competitive participation tolow-inten- by a broad variety of cardiac findings, which sity sports such as bowlingand golf.37 These may include some or all of the following: patients include those with a history of syn- midsystolic, nonejection click; late systolic cope, a family history of sudden death due to murmur; echocardiographic or cineangio- mitral valve prolapse, chest pain worsened graphic evidence of systolic billowing of the by exercise, repetitive ventricular ectopy or mitral valve leaflets into the left atrium; sustained supraventricular tachycardia (es- thickened mitral valve; atypical chest pain; pecially if worsened by exercise), moderate palpitations; dizziness; abnormal electro- or severe mitral regurgitation, and dilata- cardiogram; atrial or ventricular arrhyth- tion of the ascending aorta (associated with mia; systemic emboli; mitral regurgitation; Marfan's syndrome). It was recommended Marfan's syndrome; syncope; and sudden that no restrictions be placed on those with death.33 any or all other manifestationsof the mitral valve prolapse syndrome. The question of myocardial involvement in mitral valve prolapse has been raised by Anorexia Nervosa documentation of left ventricular segmental Another disorder primarily afflicting contraction abnormalities, and by its asso- ciation with chest pain and ventricular ar- women and thought to affect cardiac perfor- rhythmias. This has led to the examination mance is anorexia nervosa, which is dis- of global function using rest and exercise cussed in Chapter 17. Previous studies of ejection fractions as measured by gated starvation have demonstrated decreased blood pool scanning.34-36 As might be ex- heart size, blood pressure, and heart rate, pected, owing to the preponderance of which may not be reversible with refeeding. women with the disease, patients with mi- A recent study38 has shown that cardiac tral valve prolapse have an \"abnormal\" fail- function is preserved and that the observed ure to increase ejection fraction in response changes in cardiac architecture, load, and to exercise. This has been taken to besug- function are appropriate responses to de- gestive of a \"cardiomyopathic process\"34 creased blood pressure. These parameters, and renders difficult the accurate diagnosis as well as exercise performance, return to of the etiology of chest pain (ischemicver- normal with weight gain. Thus, the observed sus nonischemic).3536 However, as noted cardiac abnormalities should not in them- previously, normal healthy females also selves represent limitationsto exercise. may fail to increase their ejection fraction with exercise; therefore, it is difficult to label Sudden Death the behavior of those with mitral valve pro- The risk factors predisposing to unex- lapse as indicative of myocardial pathology. pected sudden death in women and the In the overwhelming majority of cases, prevalence of coronary artery disease in mitral valve prolapse is a benign, isolated such patients are somewhat different from auscultatory or echocardiographic finding those in men.39 Data from the Framingham that has no known influence on exercise per- Heart Study showed that age and, margin- formance or the advisability of pursuing ally, cholesterol were risk factors in both competitive or recreational sports. This sexes. In addition, hematocrit, vital capac- view is supported by the rarity ofcomplica- tions documented during exercise. It must

Cardiovascular Issues 289 ity, and glucose were significantly related to ferences in disease processes, other than the incidence of sudden death in women those discussed previously, that would sug- only. In men, additional risk factors for sud- gest different exercise limitations in men den death were those associated with coro- and women. The reader is referred to the nary disease, including systolic blood Task Force on Cardiovascular Abnormali- pressure, obesity, smoking, and electrocar- ties in the Athlete and its recommendations diographic evidence of left ventricular hy- regarding eligibility for competition.40 This pertrophy. conference, which was sponsored by the American College of Cardiology and by the Although the significance of these find- National Heart, Lung and Blood Institute, ings for the exercising woman isunknown, compiled an up-to-date, comprehensive several other forms of heart disease are summary of both resistive and dynamic ex- clearly associated with sudden death during ercise limitations in all forms of congenital exercise. As far as is known,relative risks for and acquired heart disease. It must be men and women relate to the prevalence of stressed that any person with known orsus- these cardiac illnesses; the consequences or pected heart disease, regardless of sex, severity of each disease process do not dif- should undergo a full cardiovascular evalu- fer in men and women, and female patients ation before undertaking exercise training should observe the same restrictions. or sports competition. These recommenda- tions apply equally to male and femaleath- Chief among cardiac diseases causing letes. sudden death in young people during exer- cise is hypertrophic cardiomyopathy. This SUMMARY disease is idiopathic, genetically transmit- ted, and characterized by a thickened left In conclusion, although many aspects of ventricle with normal chamber size. Be- the female cardiac response to exercise ap- cause cardiac adaptation to exercise may pear similar to the male response, many produce a similar picture, differentiating be- other aspects have not been fully examined tween physiologic and pathologic hypertro- with respect to differences between the phy may be difficult and may depend on sexes. In areas that have been studied, a identification of other pathologic features number of important differences exist. Be- such as asymmetric septal hypertrophy and cause many of these differences must be systolic anterior motion of the mitral valve. kept in mind for the correct interpretation of Any athlete suspected of having this disor- diagnostic cardiac exercise testing per- der should be fully evaluated by a cardio- formed in women, an appreciation of the vascular specialist. The American College of normal female response is vital. These dif- Cardiology recommends that patients with ferences are just as important to keep in this disease should never participate in mind in examining the female athlete as they high-intensity competitive sports, regard- are in examining the sedentary woman. less of disease severity.37 Those with marked Much research remains to be done before a hypertrophy, significant left ventricular out- complete examination can be made of all the flow tract obstruction, arrhythmias, or a unique aspects of cardiovascular problems family history of sudden death or syncope in the exercising woman. should not participate in any form of athletic endeavors. REFERENCES 1. Astrand I: Aerobic work capacity in men and Other Forms of Heart Disease women with special reference to age. Acta Consideration of the exercise limitations Physiol Scand 49:169, 1960. imposed by each form of heart disease is be- yond the scope of this review. In addition, there is no evidence available to indicate dif-

290 Special Issues and Concerns 2. Astrand PO:Human physical fitness with spe- Prevalence of multivalvular regurgitation in cial reference to sex and age. Physiol Rev athletes. Am J Cardiol 64:209,1989. 36:307, 1956. 18. Sketch MH, Mohiuddin SM, Lynch JD, et al: Significant sex differences in the correlation 3. Adams GM, and de Vries HA: Physiologic ef- of electrocardiographic exercise testing and fects of an exercise training regimen upon coronary arteriograms. Am J Cardiol 36:169, women aged 52 to 79. J Gerontol 28:50, 1973. 1975. 19. McCarthy D: Stress electrocardiography in 4. Wessel JA, Small DA,Van Huss WD,et al: Age women. Int J Cardiol 5:727, 1984. and physiological responses to exercise in 20. Patterson RE, Eng C, and Horowitz SF: Prac- women 20-69 years of age. J Gerontol 23:269, tical diagnosis of coronary artery disease: A 1968. Bayes' theorem nomogram to correlate clin- ical data with noninvasive exercise tests.Am 5. O'Toole ML, Hiller WDB, Douglas PS, et al: J Cardiol 53:252, 1984. Cardiovascular responses to prolonged cy- 21. Barolsky SM, Gilbert CA, Faruqui A, et al: Dif- cling and running. Med Sci Sports Exerc ferences in electrocardiographic response to 17:219,1985. exercise in women and men: A non-Bayesian factor. Circulation60:1021,1979. 6. Hossack KF, Kusumi F, and Bruce RA: Ap- 22. Linhart JW, Laws JG, and Satinsky JD: Maxi- proximate normal standards of maximal car- mum treadmill exercise electrocardiography diac output during upright exercise in in female patients. Circulation50:1173,1974. women. Am J Cardiol 47:1080,1981. 23. Detry JMR,Kapita BM, Cosyns J, et al: Diag- nostic value of history and maximal exercise 7. Borer JS, Bacharach SL,Green MV, et al: Real- electrocardiography in men and women sus- time radionuclide cineangiography in the pected of coronary heart disease. Circulation non-invasive evaluation of global and re- 56:756,1977. gional left ventricular function at rest and 24. Melin JA, Wins W, Vanbutsele RJ, et al:Alter- during exercise in patients with coronary ar- native diagnostic strategies for coronary ar- tery disease. N Engl J Med 296:839, 1977. tery disease in women: Demonstration of the usefulness and efficiency of probability anal- 8. HigginbothamMB, Morris KG,Coleman E, et ysis. Circulation 71:535,1985. al: Sex-related differences in the normal car- 25. Guiteras P, ChaitmanBR,Waters DD,et al: Di- diac response to upright exercise. Circula- agnostic accuracy of exercise ECGlead sys- tion 70:357,1984. tems in clinical subsets of women. Circula- tion 65:1465, 1982. 9. Seals DR, and Hagberg JM: The effect of ex- 26. Ilsley C, Canepa-Anson R, Westgate C, et al: ercise training on human hypertension: Are- Influence of R wave analysis upon diagnostic view. Med Sci Sports Exerc 16:207,1984. accuracy of exercise testing in women. Br Heart J 48:161, 1982. 10. Cohen JL, Gupta PK, Lichstein E, et al: The 27. Friedman TD, Greene AC,IskandrianAS,et al: heart of a dancer: Noninvasive cardiac eval- Exercise thallium-201 myocardial scintigra- uation of professional ballet dancers. Am J phy in women: Correlation with coronary ar- Cardiol 45:959, 1980. teriography. Am J Cardiol 49:1632,1982. 28. Stolzenberg J, and Kaminsky J: Overlying 11. Zeldis SM, Morganroth J, and Rubier S: Car- breast as cause of false-positive thallium diac hypertrophy in response to dynamic scans. Clin Nucl Med 3:229, 1978. conditioning in female athletes. J Appl Phys- 29. Puletti M, Sunseri L, Curione M, et al: Acute iol 44:849, 1978. myocardial infarction: Sex-related differ- ences in prognosis. Am Heart J 108:63, 1984. 12. Douglas PS, O'Toole ML, Hiller WDB,et al: 30. Fisher LD, Kennedy JW, Davis KB, et al: As- Left ventricular structure and function by sociation of sex, physical size, and operative echocardiography in ultraendurance ath- mortality after coronary artery bypass in the letes. Am J Cardiol 58:805, 1986. coronary artery surgery study (CASS). Thorac Cardiovasc Surg 84:334, 1982. 13. Douglas PS, Hiller WDB,O'Toole ML, et al: 31. Blair SN, Kohl HW, Paffenbarger RS, et al: Left ventricular structure and function in ul- Physical fitness and all-cause mortality: A traendurance athletes. Med Sci Sports Exerc prospective study of healthy men and 17:203, 1985. women. JAMA 262:2395,1989. 32. Lokey EA, and Tran ZV: Effects of exercise 14. Huston TP, Puffer JC, and Rodney WM: The athletic heart syndrome. N Engl J Med 313:24, 1985. 15. Stone MH, and Wilson GD: Resistive training and selected effects. In Goldberg L, and Elliot DL (eds): The Medical Clinics of North Amer- ica. WBSaunders, Philadelphia, 1985. 16. Douglas PS, O'Toole ML, Hiller DB,et al: Elec- trocardiographic diagnosis of exercise-in- duced left ventricular hypertrophy. Am Heart J 116:784, 1988. 17. Douglas PS, Berman GO, O'Toole ML, et al:

Cardiovascular Issues 291 training on serum lipid and lipoprotein con- thy, other myopericardial diseases and mi- centrations in women: A meta-analysis. Int J tral valve prolapse. J Am Coll Cardiol 6:1215, Sports Med 10:424, 1989. 1985. 33. Jeresaty RM:Mitral valve prolapse-click syn- 38. St. John Sutton MG, Plappert T, Crosby L, et drome. Prog Cardiovasc Dis 15:623, 1973. al: Effects of reduced left ventricular mass on 34. Gottdiener JS, Borer JS, Bacharach SL, et al: chamber architecture, load, and function: A Left ventricular function in mitral valve pro- study of anorexia nervosa. Circulation lapse: Assessment with radionuclide cinean- 72(S):991,1985. giography. Am J Cardiol47:7,1981. 39. SchatzkinA, Cupples LA,Heeren T, et al: The 35. Newman GE,Gibbons RJ, and Jones RH: Car- epidemiology of sudden unexpected death: diac function during rest and exercise in pa- Risk factors for men and women in the Fra- tients with mitral valve prolapse. Am J Car- mingham Heart Study. Am Heart J 107:1300, diol 47:14,1981. 1984. 36. Ahmad M, and Haibach H: Left ventricular 40. Mitchell JH, Maron BJ, and Epstein SE: 16th function in patients with mitral valve pro- Bethesda Conference: Cardiovascular abnor- lapse: A radionuclide evaluation. Clin Nucl malities in the athlete: recommendations re- Med 7:562,1982. garding eligibility for competition. J Am Coll 37. Maron EJ, Gaffney FA, Jeresaty RM, et al: Cardiol 6:1186,1985. Task force III: Hypertrophic cardiomyopa-

17CHAPTER Eating Disorders JACK L. KATZ,M.D. EPIDEMIOLOGY DIAGNOSIS, COURSE, AND PROGNOSIS OF THE EATING SETTING AND ONSET DISORDERS Anorexia Nervosa Bulimia Nervosa CO-MORBIDITY THEORIES OF ETIOLOGY CLINICAL PICTURE Anorexia Nervosa TREATMENT Bulimia Nervosa EXERCISE AND EATING BIOLOGY OF EATING DISORDERS DISORDERS Physical Sequelae Laboratory Findings EATING DISORDERS AND OTHER Endocrine Abnormalities.- SPECIAL SUBCULTURES Hypothalamic Implications Two striking developments in recent decades have made the topic of eating disorders germane to any scientific work on women and exercise. The first is the enormous increase in dedicated athletic participation by women. What tradi- tionally had been almost exclusively the domain of men has now become a flour- ishing and important aspect of living for a substantial numberof women in indus- trialized societies. The second is the dramatic rise in the incidence of eating disorders, specifically anorexia nervosa (AN) and bulimia nervosa (BN). As these syndromes are primarilydisorders of women (90%to 95% of all cases), and as issues related to weight, food intake, and physical activity are central both to eating disorders and to athletics, it is not surprising that the topic of eating dis- orders is relevant to this book's mission of examining the physiologic, medical, and psychologic ramifications of exercise in women. While this chapter will review in detail the nature, theories of etiology, and approaches to treatment of the eating disorders, it will also seek to address those concerns that are particularly related to exercise. For example, 1 Is sustained, strenuous exercising, especially by women,a risk factor for the development of an eating disorder? 2 Are women with a vulnerabilityto eating disorders drawn to serious athletic activity as a way of dealing with thatvulnerability? 292

Eating Disorders 293 3 Do anorexia nervosa and intense ath- nonindustrialized societies, they have a par- letic involvement share common ticular affinity for females growing up in in- underlying psychologic themes and dustrialized cultures. Earlier writings sug- conflicts? gested that white, upper-middle-class girls were at particular risk, but more recent re- 4 What are the physical risks to the exer- ports suggest that minority groups are now cising woman with a known eating also vulnerable.6 Rather than socioeco- disorder? nomic background being the critical vari- able, achievement orientation of the fami- EPIDEMIOLOGY lies may be the more relevant common denominator. As indicated earlier, since the 1960s, there has been a remarkable increase in the inci- SETTING AND ONSET dence of the eating disorders that goes be- yond heightened diagnostic acuity.1 Surveys Anorexia Nervosa of the lifetime prevalence of AN in women Although there are perhaps \"typical\" cir- have generally yielded a figure of about 1%,1,2 while representative figures for BN fall cumstances associated with the onset of AN, around 4%.3 Thus, perhaps almost 5% of it must be emphasized that a substantial mi- women in industrializedsocieties can be ex- nority of patients present histories that can pected to develop an eating disorder at deviate conspicuously from the usualste- some time duringtheir life. reotypic scenario. Clearly, these are not trivial figures, and Classically, the impendinganorectic indi- they have prompted various speculations vidual is in her teens, most likely approach- about the sources of this alarming increase ing either 14or 18years of age (i.e., about to in frequency. The most common proposals make a significant transition in her school- are that the media's emphasis on thinness ing). She has seemingly been a well-func- as a culturallydesirable physical character- tioning girl, who indeed is often described istic has prompted more widespread dieting by her parents as having been \"perfect ... than ever before, and that the increasingly never a problem.\" She is highly conscien- complex and demanding roles of women in tious about her schoolwork, appears to have our society have created particular stress friends, and is usually well organized. But and conflict for them around issues of iden- beneath this veneer of health, there is often tity and control, which are being played out found a girl with low self-esteem, one who is by excessive attention to appearance.4 How- compulsive in her style, works excessively ever, we should also note that, perhaps be- conscientiously to maintainher grades (i.e., cause of better nutrition or subtle evolu- is an \"overachiever\"), and is overly depen- tionary trends, female adolescents are ex- dent in her relationships. She is also, more periencing menarche and puberty earlier often than not, slightly overweight, has a than ever before. Thus, they are encounter- \"sweet tooth,\" and has grown up in a family ing biologicand psychosocial stresses at an that is weight conscious or diet conscious earlier age than previously. If today's par- (e.g., because someone is diabetic). ents are also more self-absorbed than were those of prior generations, their children's Usually, but not always, a psychosocial earlier exposure to these stresses is being stressor can be identified which correlates met by less, rather than more, nurturance chronologically with the onset ofcon- and support, and food may then take on par- sciously initiated dieting (although the con- ticular symbolic importance.5 nection between the dieting and the stressor may not be consciously made by the individ- Finally, although AN and BN can occur in ual). Common triggering events are a loss males and can also occur in persons living in (e.g., parental death or divorce), a blow to

294 Special Issues and Concerns self-esteem (e.g., a failed first heterosexual The possible role of intense athletic activ- relationship), or a separation (e.g., a vaca- ity (e.g., long-distance running) in the tion abroad, beginning college). Of course, pathogenesis of anorexia nervosa will be some of these circumstances are intrinsic to discussed in a later section. adolescence and, while indeed stressful, are hardly uniqueto the life histories of anorec- Bulimia Nervosa tic girls. The setting, precipitating events, and Like most American female adolescents onset for AN have been described with and adults who are embarking on a diet, the rather impressive agreement, including the person at risk for AN makes the conscious acknowledgment of exceptions to the usual decision to reduce or even virtually elimi- pathogenetic formulations, but BN remains nate fats and carbohydrates. What makes a somewhat more difficult disorder to eluci- her different from her peers, though, is the date. intensity of her drive to lose weight, her stoic pleasure in enduring hunger pains, and However, we have come to recognize at her increasing preoccupation with achiev- least two forms of bulimia nervosa, which ing thinness at the expense of all other literally means \"nervous ox-hunger.\" In goals. one, what starts out as fairly typical AN evolves into BN over a course of time, typi- Initially, there is a sense of exhilaration,a cally 1 to 2 years. Thus, after weight has \"high,\" which may be consequent to a newly been driven down, and in the presence of found sense of mastery or to the accolades ongoing rigid and severe dieting, the ano- she begins to receive from peers and adults rectic individual may one day, to her shock for her willpowerand her improving figure. and horror, suddenly embark on an uncon- But it is also conceivable that this phenom- trollable binge. Not infrequently, two cir- enon is mediated by a rise in the body's en- cumstances coincide to facilitate the ap- dorphin level. Such a rise has been shown to pearance of the binge: an upsetting occur, at least initially, in conjunction with experience producinga dysphoric state (de- two aspects of the unfolding AN: decreased pression, anger, or anxiety) and the avail- food intake7 and increased physical activ- ability in abundance of \"forbidden\" foods ity.8 It has even been speculated that an un- (typically carbohydrates). The vulnerability conscious attempt to recapture this initial, to the binge may be further enhanced if the possibly endorphin-mediated, high drives food is available in private (e.g., in one's the anorectic into her ever-downward spi- own apartment or after everyone else has re- ral. tired for the evening). After the binge, there is considerable disgust, shame, and guilt, However, as indicated at the outset of this followed by firm resolve not only never to section, exceptions to this textbook picture permit this to happen again but also to diet abound. Not all future sufferers of AN are even more rigorously to compensate for the bright overachievers with compulsive weight presumably gained from the binge. styles, and not all begin their dieting in as- However, with increasing frequency, the sociation with a psychosocial stressor. binges recur, until ultimately the binging Some may actually follow the lead of a girl- may become a more conspicuous part of the friend in embarking on a diet; others may clinical picture than the dieting. have initially lost weight as a consequence of a bona fide medical illness (most com- In the other form, the individual becomes monly, perhaps, infectious mononucleosis); a bingerwithout havingever passed through still others begin to lose weight because of a the emaciated, officially diagnosed phase of real loss of appetite associated with a state AN. However, the initial circumstances and of depression; and not all anorectic women the emotional states are probably the same are initially overweight or come from in both forms. Although nonanorectic bu- weight- or food-preoccupied families.

Eating Disorders 295 limic women may have never been substan- among western female adolescents has gone tially underweight, most, if not all, have beyond the bounds of \"normal.\" The pres- been chronic dieters whose weights have ence of the features that follow will help an- fluctuated frequently and substantially. swer that question, but early prediction of Thus, chronic dieting with unstable weight which dieting adolescent will go on to de- appears to be a risk factor for BN in non- velop an actual eating disorder is a perplex- anorectic persons as well. ing challenge for even the most expert in the field. CLINICAL FEATURE While the etiology of the eating disorders Substantial Weight Loss. With progres- sion of the dieting, this is the symptom that remains controversial, as we shall discuss in typically calls attention to the illness. The a later section, the phenomenology of AN Diagnostic and Statistical Manual of Mental and BN has been impressively delineated Disorders, third edition revised (DSM-III- over the past two decades, and a rich, co- R),9 specifies a weight loss to at least 15% herent, and reliable clinical picture of these below expected body weight (includingpro- syndromes is now available. Both eating dis- jected weight for a still-growing adolescent), orders can be regarded as syndromes char- but the diagnosis of AN should be madewith acterized by an admixture of psychologic, the full clinical picture in view, rather than behavioral, and biologic disturbances. solely via mechanical .reliance on a desig- nated percentage of weight loss.10 Anorexia Nervosa Morbid Concern with Losing Control Core Features over Eating and Becoming Fat. A fear of loss of control is central to the psychology Self-imposed, Rigidly Enforced Dietary of AN. It is concretized around the dual con- Restriction. Classically, this is viewed as cern that food intake and weight will be- being at the heart of AN. Thus, in the face of come uncontrollable. Thus, the anorectic growing hunger and progressive weight woman believes that she cannot be \"thin loss, the anorectic individual consciously enough,\" much less \"too thin,\" because and deliberately elects to pursue a sustained there is always the lurking threat that some- course of restricted food intake. As previ- day the floodgates will open and her insatia- ously noted, carbohydrates and fats are in- ble appetite will spring forth to produce not creasingly avoided; while protein is \"per- only a gain in weight but a body of \"humon- mitted,\" many anorectics go on to become gous\" dimensions. exclusive vegetarians. Rituals in the prepa- ration and consumption of food are also Obsessional Preoccupation with Food. characteristic. Obviously, such dieting must Given the fear of loss of control over eating be differentiated from true anorexia, that is, and weight, it is not surprising that the an- real loss of appetite, which can occur with orectic's central preoccupation is with food. certain medical illnesses or affective disor- One might, however, view this repetitive, ders. However, as noted earlier, some pa- morbid dwelling on past, present, and future tients actually give a history of having lost diet in either biologic terms (i.e., as a reflec- weight in conjunction with medical illness tion of starvation's physiologic effects on or depression, only to have the process cat- central nervous system function and conse- apult them into consciously pursued dieting quently on appetite and related cognition) with weight loss and, ultimately, full-blown or psychodynamicterms (i.e., as a reflection AN. One dilemma for parents, of course, is to of an unconscious conflicted wish or im- know when the dieting that is ubiquitous pulse that underliesthe conscious preoccu- pation). In either case, the important fact is that, increasingly, the anorectic individual devotes her time to fantasies and plans about buying, cooking, and eating various

296 Special Issues and Concerns foods; this obsession progressively im- companies the excessive dieting. While pinges on all other aspects of her existence. many anorectic women were physically ac- tive people prior to the onset of their eating Distorted Body Image. Facilitating the disorder, their exercising takes on an in- descent into AN is the impaired capacity of creasingly frenetic quality as the syndrome its victims to gauge accurately their physical unfolds.13 Like the dieting, the physical ac- dimensions. While normal female adoles- tivity (most commonly running, calisthen- cents generally see themselves as somewhat ics, swimming) becomes ritualized and larger than they really are (and perhaps this rigid. When starvation begins to be serious, is one reason for the vulnerability of females the hyperactivity will usually give way to for developing eating disorders), anorectic weakness and lethargy, indicating the need patients markedlyoverestimate their bodily for urgent medical care; however, the ex- dimensions—as established by objective treme denial characteristic of these patients studies with distorting lenses, calipers, and may permit exercising to continue, some- so on.11 Clinically, the 70-lb anorectic adult times even in the face of advanced emacia- will continue to talk about the need to lose tion. some poundage here or there, despite her obvious emaciation. Paradoxically, this ten- Insomnia. Although often overlooked in dency appears to intensify with progression the early literature on AN, difficulty in both of the emaciation,thereby further confound- falling asleep and sleeping soundly is a com- ing attempts at treatment. mon complaint.14 It is not clear whether this symptom is a consequence of malnourish- Amenorrhea. Close to 100% of women ment, anxiety, mood disturbance, excessive who meet the above criteria will experience exercise, or some other aspect of the syn- a loss of menses (or not achieve menarche if drome, but it is sufficiently distressing so the illness begins prepubertally and goes that many anorectic patients will find them- untreated). DSM-III-R specifies that at least selves becoming increasinglydependent on three menstrual cycles (exclusive of hor- sedatives, particularly benzodiazepines, to mone administration) should be missed for attain satisfactory sleep. amenorrhea to be diagnosed in a previously regularly menstruating female. Obviously, Cold Intolerance. Conceivablyas a result there is no analogous feature in men (al- of diminished adipose tissue peripherally though sperm count does drop signifi- and more likely as a consequence of starva- cantly). Interestingly, not only does amen- tion's effect on hypothalamicallymediated orrhea usually occur relatively early in the thermoregulation centrally, AN commonly course of AN, but, in approximately 25% to elicits significant cold intolerance. This 35% of anorectic women, it actually appears symptom, compounded by the psychologic to occur prior to any significant weight loss defense of denial,accounts for the dress typ- (although usually after dieting has begun). ical of anorectic women, namely, multiple Furthermore, menses may take many layers of sweaters or sweatshirts, which months to resume after weight restoration; both keep them warm and hide their ema- AN has also developed in women after stop- ciation. ping oral contraceptives. It is because of aberrations such as these in hypothalamic- Use of Emetics, Cathartics, Diuretics, pituitary-ovarian axis function that endocri- and Other Chemical Agents. In addition to nologists have had a long-standing interest their excessive restriction of food intake, in AN.12 many anorectic women will employ various external agents to prevent weight gain. Common Features Thus, some will induce vomiting (particu- larly the bulimic subgroup) by mechanical High Level of Physical Activity. A dra- means (inserting a finger, toothbrush han- matic and highly prevalent symptom is the dle, or appliance cord into the throat to trig- striking level of physical activity that ac- ger the gag reflex) or chemical means (usu- ally with syrup of ipecac). Some will use

Eating Disorders 297 enemas or laxatives to \"clean out\" their gas- sional attention, at some point in their life trointestinal system (leading to chronic perhaps fully half of all patients with eating constipation eventually). And still others disorders manifest episodes of depressive will illicitly take diuretics to minimize the symptomatology that meet the criteria for a contribution of body fluids to their weight, formal diagnosis of affective disorder.17 thyroid hormone to increase metabolic rate, Thus, they may feel dejected, guilty, pessi- or amphetamines to suppress appetite.15 mistic, and hopeless; sleep poorly; have dif- ficulty concentrating; and even entertain Ritualistic Involvement with Food-Re- suicidal thoughts. Whether such states are a lated Activities. Paradoxically, the very ob- consequence of starvation,18 reflect a genu- ject that is dreaded, namely food, is often ine co-morbid affective disorder, are part of central not only to the anorectic individual's the affective lability characteristic of a bor- thoughts but also to her behavior. Thus, derline personality disorder, or are simply those with AN appear to derive vicarious reactive to the disruptions in normal living (and probably sadistic) pleasure from and interpersonal relations invariably pro- watching others eat what they have cooked duced by an eating disorder remains a con- or baked for them. They are often involved troversial issue.17 Vegetative signs (e.g., ap- in preparing exotic dishes and commonly petite loss and weight decline, insomnia, display various rituals when they eat. decreased libido, constipation) are particu- Women with both ANand BNfrequently also larly difficult to assess in the presence of an hoard and steal food, and a substantial num- eating disorder; moreover anhedonia, loss ber of patients with eating disorders actu- of reactivity to the environment, motor re- ally work as waitresses. tardation, and diurnal mood variation (i.e., the classic features of melancholia) are Difficulty in Recognizing Satiation. De- characteristically not evident. spite its formal name, and contrary to some of the earlier writings, AN is not a \"nervous Obsessional Features. Between 25% and loss of appetite\" and its victims do experi- 50% of all anorectic patients manifest behav- ence hunger pains (at least before the dis- ioral and cognitive patterns typical of obses- ease has entered the chronic phase). How- sive-compulsive disorder.19 Thus, eating ever, they are subject to real difficulty in and exercise rituals, compulsive hand wash- experiencing (or, more likely, interpreting) ing or checking, obsessive ruminations, ex- sensations of satiation. They will often com- cessive perfectionism, and so forth, are plain of being unable to know whether they common. Most of these individuals give his- are full or still hungry after eating a meal. tories of similar tendencies prior to the onset of the eating disorder, but it should Drug Abuse. About one quarter of all eat- also be noted that starvation studies in nor- ing-disorder patients (almost all of whom mal volunteers have established that obses- are anorectic-bulimic or just bulimic) give sive-compulsive, as well as affective, distur- prior or concurrent histories of drug abuse, bances can be a common consequence of typically with sedatives and/or with stimu- starvation.18 lants (which, of course, may also serve as anorexogenics). Cocaine use is common, Bulimia IMervosa but heroin use is rare. These patients, who As described earlier, BNwill evolve either frequently also carry a diagnosis of \"border- line personality,\" appear vulnerable to drug in the context of established ANor indepen- abuse by virtue of their emotional lability, dently of it, but typically in one who has fre- impulsive tendencies, and general anxiety, quently dieted and experienced weight fluc- as well as their specific panic over possibly tuations. Characteristically,the binge takes losing control of theirweight.16 place in private, usually during the evening hours, and involves the consumption of Depressive Symptomatology. Although huge quantities of food (often thousands of it is the symptomatology surrounding food, eating, and weightthat usuallybrings the in- dividual with an eating disorder to profes-

298 Special Issues and Concerns calories in the same sitting). The binge BIOLOGY OF EATING foods are commonly those that are most as- DISORDERS siduously avoided during the rest of the bu- limic's day, namely carbohydrate-rich While the psychologic and behavioral fea- items, but virtuallyany morsel of food in the tures of the eating disorders obviously pro- house is a potential target of the binge. Typ- duce a dramatic clinical picture, it is com- ically, the binge terminates in self-induced monly the ensuing impaired physiology that vomiting. Although most bulimic women brings the afflicted individual to medical at- vomit, however, not all do, and vomiting tention. The biology of AN is essentially the should not be considered a prerequisite for biology of starvation, whereas the biology of the diagnosis of BN. Some individuals sim- bulimia is principally a reflection of the ply exhaust themselves from the binge and physiologic derangements produced by eventually settle into a troubled sleep; oth- chronic vomiting and/or laxative/diuretic ers will try to compensate by using laxatives abuse, as well as by the violent swings in or enemas, as well as by dieting excessively food consumption. between binges. Physical Sequelae The binge, which may occur anywhere The physical consequences of the eating from several times per 24-hour period to several times per month (at least twice per disorders are summarized in Table 17-1. It week for at least 3 months, according to should be noted that the not uncommon DSM-III-R9), elicits enormous personal combination of AN and BN in the same in- shame. Not only are patients disgusted with dividual creates the possibility of findings themselves, but they are also initially un- from both disorders being present simulta- willing to discuss their symptoms with any- neously in that person. Moreover, even in one else. (This may account for the paucity the normal-weight bulimic woman, the fre- of references to bulimia in the literature quent interbingedieting and postbinge vom- until the past two decades, when it began to iting can produce physical effects similar to \"come out of the closet.\") More importantly, those seen in the pure restricting anorectic each binge triggers off an ever-greater re- woman; for example, while osteoporosis is solve to diet, and this only intensifies the well known to occur in women with AN, it fast-feast cycle. As with the anorectic pa- has now also been documented in women tient's eating, the bulimic patient's binge can become ritualized. Thus, the time, set- Table 17-1. POTENTIAL PHYSICAL ting, and type of food become increasingly FINDINGS IN EATINGDISORDERS important and fixed. However, in those bu- Anorexia Nervosa limic persons who vomit, the vomiting can Emaciation take on its own significance, eliciting rein- Dry skin forcement from the physical relief it pro- Lanugo (fine downy hair) vides for the abdominal discomfort, emo- Loss of scalp hair and brittle nails tional relief for the concern and guilt about Cold extremities with impaired temperature regulation having consumed so many calories, and per- Hypotension haps psychologic relief via symbolic reso- Bradycardia lution of unconscious conflicts about such Cardiac rhythm disturbances matters as sex, pregnancy, and relationship Edema with parents. As DSM-III-R notes,9 a persis- Bulimia Nervosa tent overconcern with body shape and Tooth decay weight is not confined to restricting (i.e., Salivary gland enlargement nonbulimic) anorectic women but is also Calluses on hands characteristic of normal-weight bulimic Facial and other petechial hemorrhages women. Cardiac rhythm disturbances

Eating Disorders 299 with BN,20 reflecting both decreased estro- Table 17-2. POTENTIAL RADIOLOGIC, gen and increased cortisol production.21 ELECTROCARDIOGRAM, AND ELECTROENCEPHALOGRAM FINDINGS IN The degree of emaciation in AN will obvi- EATING DISORDERS ously depend on the net caloric balance be- Anorexia Nervosa and BulimiaNervosa tween the limited food intake and the typi- Osteoporosis on x-ray cally excessive exercise expenditure; in BN, Diminished gastric emptyingon fluoroscopy weight will reflect the balance among bing- Cerebral atrophy and ventricular enlargement on CAT ing, vomiting, possible cathartic use, possi- ble substance and medication abuse, possi- scan or MRI ble excessive exercising, interbinge dieting, Conduction, wave, and rhythm changes on and so on, so that the individual might be below, at, or above ideal body weight. The electrocardiogram possibility of deception about weight by pa- Nonspecific spike abnormalities on tients with AN (whether by outright lying, adding weights to one's body or clothing, or electroencephalogram fillingoneself up with water) should always be borne in mind by the examining physi- in both anorectic and bulimic women, and cian. are discernible with special procedures (Table 17-2). For instance, cerebral atrophy The diminished sympathetic tone conse- and ventricular enlargement in the brain quent to starvation in AN is associated with have been reported in patients with either bradycardia and lowered blood pressure. AN23 or BN,24 and presumably are conse- But what has also become evident is that quent to malnutrition and reversible. De- more serious cardiac complications of star- layed gastric emptying can also occur in vation—such as rhythm disturbances, mi- both groups, possibly consequent to such tral valve prolapse, and congestive heart gastric insults as inadequate bulk intake, re- failure—are not rare.22 The perils of contin- peated vomiting, or bizarre diets. Electro- ued intensive exercise as AN progresses are lyte imbalance from vomiting, particularly evident in light of these potential cardiac hypokalemia, can produce significant, even problems. fatal, abnormalities in cardiac function, and thus an electrocardiogram should be ob- The salivary gland enlargement seen with tained for all vomiters; moreover, the fre- binging and vomiting,while of a benign na- quently abused emetic, syrup of ipecac, can ture (sialoadenosis), can combine with the produce a serious cardiomyopathy.25 Fi- not infrequently seen edema in eating dis- nally, about 25% of all eating-disorder pa- orders to reinforce the patient's conviction tients demonstrate nonspecific abnormali- that she is fat and must thus further intensify ties on electroencephalography, usually her dieting efforts. The tooth decay in BN is unilateral or bilateral spikes in the tempo- a direct consequence of gastric juices bath- ral-occipital region;the basis for thisfinding ing tooth enamel during repeated vomiting, is not known, but such EEG abnormalities while calluses on the hands are produced by are what prompted one of the earliest phar- the patient repeatedly sticking her fingers macotherapy trials in this field, using phe- down her throat to elicit the gag reflex. Pe- nytoin.26 techial hemorrhages can occur in the face, cornea, or soft palate following an extreme Laboratory Findings episode of binging and vomiting. The typical laboratory abnormalities in Radiologic, ECG, and EEG AN and BNare presented in Table 17-3. (En- Abnormalities docrine abnormalities are treated sepa- rately.) In addition to osteoporosis, several other physical and physiologic changes can occur A moderate anemia is not unusual in AN. Hematocrit values under 35%and hemoglo-

300 Special Issues and Concerns Table 17-3. POTENTIAL LABORATORY of bulimic women, despite their adequate FINDINGS IN EATING DISORDERS net caloric state. Anorexia Nervosa Vomiting is particularly pernicious be- Anemia and leukopenia cause of its possible effects on electrolyte Partial diabetes insipidus balance. The low potassium level and meta- Glucose tolerance abnormalities bolic alkalosis it produces can lead to car- Abnormal liver function tests diac arrhythmias and even to cardiac arrest Elevated serum cholesterol, carotene, and uric acid and death. Vomiting may also lead to dehy- dration, which can then confuse the inter- levels pretation of electrolyte values by producing Depressed serum or urinary zinc, magnesium, and spuriously high figures. copper levels Other laboratory abnormalities in AN can include an elevated level of plasma caro- Bulimia Nervosa tene, in part due to the high carrot consump- Evidence of dehydration (e.g., elevated BUN) tion characteristic of anorectic patients (be- Hypokalemia, hypochloremia, and metabolic alkalosis cause of the low calorie value of carrots) but possibly also related to low thyroid (partic- (but possible metabolic acidosis in laxative abuse) ularly T3) values; hypoproteinemia and liver Elevated serum amylase enzyme abnormalities in severe and chronic Glucose tolerance abnormalities cases (although characteristically uncom- mon in earlier cases); and hypercholester- bin levels under 11.0 g/dL are common, and olemia, perhaps also secondary to low T3 a panleukopenia also is not rare. The excre- values. The serum uric acid level may rise, tion of large amounts of dilute urine, reflect- and the serum or urinary zinc, magnesium, ing partial diabetes insipidus, can appear if and copper levels can decline. starvation becomes severe and chronic enough to affect hypothalamic function, Moderately elevated serum amylase lev- renal function, or both. Diabetes mellitus- els occur in at least 25% of bulimic patients like changes in glucose tolerance test results consequent to excessive salivary gland ac- will also begin to appear with long-term tivity in response to the frequent binging. avoidance of carbohydrates: fasting blood Fractionating the serum amylase, however, sugar falls to relatively low levels (less than will prevent overlooking a pancreatitis, 70 mg/100 mL), an excessive and sustained which can also occur in BNand may be the rise is noted after glucose load (greater than source of the elevation.29 180 mg/100 mL), and a \"rebound\" hypogly- cemia (less than 50 mg/100 mL) may appear Endocrine Abnormalities: as a delayed but excessive insulin outpour- Hypothalamic Implications ing then occurs. Patients will often claim that their \"problem\" is \"hypoglycemia,\" Because of the consistent and often early while physicians may actually propose the occurrence of amenorrhea in patients with presence of diabetes, but these glucose ab- AN, the endocrinologyof AN has undergone normalities are the consequence, not the substantial investigation. As shown in Table cause, of the chronic starvation and erratic 17-4, the characteristic endocrine abnor- carbohydrate consumption. Interestingly, malities have now been well delineated. despite being at seemingly normalweight, When taken as a group, these findings bulimic individuals can also have a low strongly suggest that hypothalamic function serum glucose level27 and can show a lower- is impaired in those with AN.30,31 This possi- than-expected rise on intravenous glucose bility is further reinforced by the previously challenge (which paradoxically can set off noted abnormalities in temperature regula- subjective cravings for carbohydrates).28 tion and urine concentrating ability com- These findings presumably reflect the monly seen with AN. highly chaotic, nonnutritional dietary intake

Eating Disorders 301 Table 17-4. POTENTIAL ENDOCRINE titive behavior, thus creating a vicious FINDINGS IN ANOREXIA NERVOSA circle.32 Hypothalamic-Pituitary-Gonadal Axis Abnormalities While these endocrine aberrancies have • Depressed plasma and urinary concentrationsof been well documented in most women with AN, hypothalamic-pituitary-gonadal/adre- gonadotropins (LH and FSH) in the face of nal abnormalities are also not infrequently depressed concentrations of estrogens and present in women with BN.33 Such findings androgens again serve to remind us that bulimic • Immature circadian LH secretory pattern women of totally normal weight do not eat • Absence of monthlycycling in LH secretion normally and are often malnourished de- • Deficient LH\"feedback\" response to administered spite their seemingly normal appearance. clomiphene citrate or ethinyl estradiol • Usually deficient LHresponse to administered DIAGNOSIS, COURSE, AND releasing hormone (LHRH), although correctable by PROGNOSIS OF THE EATING daily \"priming\" with LHRH. DISORDERS Hypothalamic-Pituitary-Adrenal AxisAbnormalities In its typical presentation, and given the • Elevated concentrations of plasma andurinary considerably enhanced sophistication in re- cent years of both professionals and lay per- cortisol (but usually with maintenance ofnormal sons in this area, the diagnosis of AN will circadian rhythm) pose little problem. Although several medi- • Diminished cortisol suppression by dexamethasone cal and psychiatric conditions are also as- administration sociated with weight loss (Table 17-5), the • Elevated cortisol production rate (despite the anorectic patient's characteristic adoles- elevated plasma level of cortisol) cent age, otherwise good physical health, and obvious pleasure in her increasingly Growth Hormone (GH) Abnormalities skeletonlike appearance should elicit little • High-normal or slightly elevated concentrations of diagnostic confusion. Problems can arise from the following confounding sources: de- plasma GH ception about true weight or other symp- • Impaired GHresponse to induced hyperglycemia and hypoglycemia,L-DOPA, and TRH Hypothalamic-Pituitary- Thyroid AxisAbnormalities • Low normal concentration of plasma T4and distinctly low T3 • Low or low normal concentration of plasma TSH (despite low T3 and possibly low T4 levels) • Normal (or delayed but correctable with priming) TSH response to administeredTRH We assume that this hypothalamic dys- Table 17-5. DIFFERENTIAL DIAGNOSIS function is a consequence of the starvation FOR ANOREXIANERVOSA and extreme weight loss in patients withAN. However, other variables conceivably play a Psychiatric Conditions role, such as the bizarre dietary intake (i.e., • Depression malnutrition as distinct from calorie insuffi- • Mania ciency), psychologic factors (such as anxi- • Schizophrenia (paranoid) ety or depression), impaired sleep-wake patterns, and even excessive exercise. Al- Medical Conditions though there is no firm evidence that the hy- • Malignancy pothalamic dysfunction precedes AN, it is • Hypothalamic tumor conceivable that AN can adversely affect hy- • Diabetes, hyperthyroidism,other endocrinopathies pothalamic function and thereby second- • Infectiousdiseases (infectious mononucleosis, arily impair hypothalamic control of appe- tuberculosis, etc.) • Gastrointestinal disorders (malabsorption syndromes, regionalenteritis, ulcerative colitis, etc.) • Chronicalcoholism or other substance abuse

302 Special Issues and Concerns toms by the patient, later age of onset (an in- family therapy,35 but most workers in the creasing number of cases now appear to be field report less successful results.11,34,36 A starting in the third, fourth, and even fifth consensus might be that about 40% of all decades of life), or the simultaneous pres- treated eating-disordered patients recover, ence of some other weight-losing condition about 30% show moderate but not definitive to which the physician totally attributes the improvement, and about 30%run a chroni- emaciation (e.g., substance abuse). Clearly, cally debilitating course (in which group alertness to these possibilities is indicated will be found the 5% to 10%who die of the when a person is suspected of having an eat- illness). Clearly, the eating disorders should ing disorder but does not quite fit the typical not be considered benign conditions. mold. Bulimia nervosa, of course, might be missed because of the usuallynormal weight CO-MORBIDITY of its sufferers, but, unlike women withAN, One of the more important developments women with BN who consult a physician usually do so of their own accord and are of the past decade of clinical research in the thus more committed to discussing their dif- eating disorders has been the documenta- ficulties honestly. tion that there is substantial psychiatric co- morbidity with AN and BN. Whether these One of the extraordinary aspects of the conditions are antecedents, concomitants, eating disorders is that the outcome is so or consequences of the eating disorders, or variable and unpredictable. At one end of whether they share similar etiologic or pre- the spectrum, probably a significant number disposing factors, is not clear, but it is now of teenage girls \"flirt\" with AN, someper- well established that at least four areas of haps even crossing over the border, only to psychopathology occur in eating disorder respond to their parents' or physician's patients with an incidence beyond what guidance or to their own good sense, and re- chance alone would predict. The areas are turn to more normal eating and weight. At depressive disorders, anxiety (including ob- the other end are the 5% to 10% of patients sessive-compulsive) disorders, substance who will die of direct complications of their abuse, and personality (particularly border- eating disorder. The causes of death are car- line) disorders. While the incidence of the diovascular collapse or cardiac arrest (par- co-morbidity will vary with the category of ticularly due to electrolyte imbalance from psychopathology, the type of eating disor- vomiting or cardiac toxicity from abuse of der (ANversus BN), and the setting in which syrup of ipecac), overwhelming sepsis (due incidence is being determined (inpatient to compromised immune function second- versus outpatient versus community sur- ary to starvation), or suicide. vey), it is probably safe to say that up to 75% of all eating-disorder patients will manifest Between these extremes, various courses at least one of these areas of co-morbid- and outcomes are possible: a single full- ity.19,37 blown episode, recurringdiscrete episides, or chronic disorder. The appearance of bu- The presence of such co-morbidity has limia in AN is usually regarded as a particu- several ramifications. First, it is incumbent larly ominous prognostic sign because of its upon the treating physician to be alert to the known likelihoodto become associated with presence of these other conditions. Second, chronicity, although, paradoxically, it may it is likely that a concomitant psychiatric somewhat alleviate the emaciation prob- disorder will have an adverse influence on lem.34 Moreover, as we shall discuss farther the course of the eating disorder. Finally, on, the frequent presence of co-morbid con- the diagnosed presence of a co-morbid con- ditions can further complicate the course dition means that the treatment plan will and prognosis of both AN and BN. have to be comprehensive enough to in- Minuchin and co-workers have claimed a better than 85% cure rate with their form of

Eating Disorders 303 elude provision for both the eating disorder of mastery and effectiveness but also helps and the co-morbid disorder(s).38 to define her as someone special; that is, her unique appearance shores up her precari- THEORIES OF ETIOLOGY ous self-image and meager sense of identity. The wide range of symptoms and signs Because this scenario is played out in the found in the eating disorders has elicited an context of the adolescent's family, however, equally broad array of proposals to \"ex- subsequent investigators, such as Palazzoli41 plain\" them. Yet, as our experience and so- and Minuchin and co-workers,35 have em- phistication with these syndromes have in- phasized the importance of understanding creased, we are becoming more cautious and treating the family as a system. Thus, about accepting simple etiologic formula- AN not only has significance for the diag- tions. nosed anorectic patient, but also reflects pathologic roles and relationships in the Perhaps the first significant contribution family. Minuchin's group identified four spe- historically to our understanding of eating- cific characteristics of such families: their disordered individuals, particularly those members are excessively enmeshed in each with restricting AN, was made by Hilde other's affairs, severely mutually overpro- Bruch,39 who moved away from a symbolic- tective, rigid in their style of relating to each libidinal-conflictual framework—for exam- other and to the outer world, and unable to ple, seeing AN as a defense against an un- achieve appropriate resolution and closure derlying wish for oral impregnation— on family conflicts. In this framework, AN toward more of an ego psychology frame- represents an attempt on one level to work. For Bruch,40 AN came to represent a achieve at least some \"space\" and auton- desperate attempt by the vulnerable adoles- omy within the family unit, while ensuring cent to achieve a sense of identity and mas- on another level that threats to the homeo- tery independent from that of her overbear- stasis of the family constellation—for ex- ing and intrusive parents (particularly ample, by the designated patient's trulyma- mother). She speculated that the mother's turing and moving out on her own—are insensitivity to physiologic and emotional thwarted. cues provided by the infant resulted in the developing child's experiencing deficien- Still other themes have been emphasized cies and confusion in identifying affective by various writers: the need to keep the and visceral experiences and thus in gaining body in a state of biologic immaturity to a reliable sense of self. This would lead to a avoid confronting sexual impulses and het- basic sense of ineffectiveness, perplexity erosexual relationships;42 the response to a over bodily sensations, and disturbances in cultural milieu that promises women happi- body image. In the context of the develop- ness and success if thinness can be at- mental transition of puberty and adoles- tained;4 and the symbolic attempt to rid the cence—producing such stresses as bodily self of the bad mother—withwhom the an- changes, separation, heterosexual encoun- orectic woman identifies her body—by lit- ters, increased independence and respon- erally starving it.41 (The bulimicwoman, on sibility, and scholastic demands—the an- the other hand, might be attempting to re- orexia-vulnerable person, who senses a gain mother by excessive eating or even by family need for high achievement but who regurgitating back the lost object.43) has little confidence in her capacity to be successful, presumably turns increasingly Unfortunately, all of these formulations, toward her own body as the one area in her whether intrapsychic, interpersonal, famil- life that she might truly control. Moreover, ial, or sociocultural, are based on observa- her thinness not only re-establishes a sense tions made after the fact. Thus, inferences are offered about premorbid characteristics not only after AN has been diagnosed but also commonly after it has been present for

304 Special Issues and Concerns months or years. The impact of such a per- Table 17-6. RISK FACTORS FOR THE nicious condition on self-esteem, family dy- DEVELOPMENT OF ANOREXIA NERVOSA namics, and perception of the environment Cultural Risk Factors cannot be readily determined; predispos- • Westernized andcontemporary culture ing, precipitating, and perpetuating ele- ments tend to become confused. Moreover, -Equates thinness with both beauty and happiness many of the common conflicts described -Emphasizes attention to self and body (e.g., conflicts over separation, indepen- -Demands varied, and at times conflicting, roles of dence, and sexuality) are characteristic of women normal adolescence as well, and the more • Capable of readily disseminatingcultural values and pathologic features of self and family (e.g., styles through visual media (e.g., movies, television, feelings of emptiness and enmeshment) are magazines) common to other pathologic, but non- • Has subcultures that particularlyemphasize weight eating-disordered, conditions such as \"bor- control (e.g., ballet, modeling, certain sports) derline\" and \"psychosomatic\" disorders. • Other? Family Risk Factors For all these reasons, workers in the field • Achievement-oriented have begun to move toward a \"risk-factor\" • Intrusive, enmeshing, overprotective, rigid, unable model for the eating disorders.44,45 Rather to resolve conflicts than postulating a specific etiology, we have • Frugal with support, nurturance,encouragement come to recognize that a variety of factors— • Overinvested in food, diet, weight, appearance, or cultural, familial, and individual—increase physical fitness one's vulnerability to developing an eating • Known to have members with a formal history of disorder (Table 17-6). As the number and eating disorder or affective disorder intensity of these risk factors increase, the • Other? vulnerability does as well. However, clearly Individual Risk Factors not all persons with eating disorders need • Female have exactly the same risk factors, and some • Adolescent persons with some risk factors might never • Slightlyoverweight develop a manifest eating disorder; protec- • Subject to feelings of ineffectiveness and low self- tive individual and family characteristics, esteem individual biologic differences, and seren- • Subject to conflicts and doubts about sense of dipity in life events could serve to modify personal identityand autonomy onset, course, and outcome. • Subject to bodily perceptual disturbances (e.g., distorted body image, uncertain feelings of satiation Moreover, the sustaining effects of star- after meals) vation and malnutrition in patients withAN • Subject to overgeneralization and other cognitive should not be overlooked.32 As dieting be- distortions comes prolonged, its impact on digestive ca- • Subject to an obsessional style and conflicts about pacity and function, endorphin levels, hy- control pothalamic function, cognitive capacity, • History of childhood sexual abuse affective state, body image, menstrual regu- • Other? larity, response of peers, and so forth, may actually serve to reinforce further food BN. While only a minorityof bulimic women avoidance, thereby creating an increasingly have a prior history of formally diagnosed self-perpetuating, treatment-resistant situa- AN, the overwhelming majority are chronic tion. or intermittent dieters whose weight fre- quently fluctuates substantially.3,46 On the Finally, whereas most of the focus in the biologic side, the loss of substantial weight eating-disorder literature has been on the (even if not to emaciated levels—e.g., an etiology and pathogenesis of AN, we are now obese individualwho diets to reach merely also beginning to understand more ade- normal weight47), in the face of ongoing, se- quately the nature of the vulnerability for verely restricted dietary intake, intensifies

Eating Disorders 305 the drive to eat. On the psychologic side, therapist must be prepared to deal with ed- this drive will most likely be responded to in ucational issues (e.g., about food, calories, excessive fashion (i.e., by binging)when the dieting), cognitive issues such as styles of individual is also characterized by so-called thinking (e.g., all or none,overgeneralizing, borderline features (impulsivity,emotional personalizing), and psychodynamic issues instability, an all-or-nothing orientation to (e.g., ambivalence toward parents, compet- life, feelings of inner emptiness, and so on). itiveness with siblings, fantasies about one's Thus, it is the mesh between biologic and body). Furthermore, the therapist must be psychologic vulnerabilities that \"loads the supportive, reliable, and respectful, and dice\" for the emergence of BN. must be prepared to address concrete is- sues concerning weight, while not permit- TREATMENT ting this to become the exclusive focus of therapy. While the numberof controlled studies on the efficacy of various treatment approaches The critical place of the family as the bat- to the eating disorders still remains rela- tleground upon which an eating disorder tively small, there has been a significant in- evolves suggests that family therapy is at crease over the past two decades in such least as important as individual therapy, studies, as well as in empirical clinical ex- particularly in younger patients living with perience in the management of AN and their families.35,41 Family therapy will em- BN 34,46,48 No sure.fire treatment for either phasize the workings of the family unit as a condition has been found, but certain guide- system and its need to be more flexible and lines have begun to emerge. less intrusive in response to perturbations produced by any of its members. Ideally, Perhaps the most important principles in this will complement concurrent individual the treatment of the eating disorders are (1) therapy. the earlier the intervention, the greater is the likelihood of response; (2) the treat- Group therapy for the treatment of BN has ment approach should be tailored to the elicited considerable interest in recent phase, severity, and setting of the disorder, years.46 Whereas nonbulimic anorectic and also to the uniquecharacteristics of the women tend to say little in groups and ac- individual patient; (3) multimodal treatment tually can become competitive with each is more likely to be effective than unimodal other over success in losing weight, bu- treatment; and (4) open-mindedness and limic women tend to be more open about flexibility on the part of the therapist or their feelings in a group and also to bene- treating team are crucial. fit from being confronted about their secre- tive gorging and purging behaviors. Whereas young adolescents who have just Moreover, most therapy groups also begun to diet excessively may respond to a incorporate cognitive-psychoeducational- good \"educational\" talk from a trusted pe- behavioral elements, often in the context of diatrician, individuals with more estab- a time-limited course of treatment, which lished cases of AN will require, at the very can be effective in dealing with and aborting least, individual psychotherapy with a pro- eating and thinking patterns that tend to fessional who has had experience working perpetuate the starve-binge cycle. with eating-disordered patients. The ther- apy will typically focus progressively on While the aforementioned approaches are concerns about control, self-esteem, and germane to the patient with relatively early sense of identity; on recognizing and ac- AN or BN, as well as to the chronic but rel- cepting bodily feelings and emotional atively stable patient, the importance of hos- states, and on facing the anxieties inherent pital treatment for the acutely starving ano- in becoming an independent adult. The rectic individual or the severely bulimic person in electrolyte imbalance—orboth, when they have lost control of their day-to-

3O6 Special Issues and Concerns day life to the eating disorder—should not unit activities, the most potent reinforcer— be minimized.Because restricting anorectic and one with obvious relevance to this patients can lose weight precipitously, med- book— may well involve access to exercise. ical involvement should be a principal part The importance of exercise in the mental of both the initial evaluation and subsequent economy of most anorectic individuals has outpatient treatment. Not only is the extent been demonstrated by Blinder, Freeman, of weight loss important, but the rate must and Stunkard.49 Using a behavioral paradigm also be considered. Some chronic patients in which access to exercise was contingent may be able to sustain a weight at 35% below on sufficient daily weight gain, they docu- their ideal after many years of AN, whereas mented that significant and rapid improve- a patient who has dropped to 25% below ment in weight could be attained during hos- ideal in just a few months may represent an pitalization. acute medical emergency. Clearly weight, electrolytes, blood chemistries, cardiac Whether on an inpatient or outpatient function, pulse, and blood pressure must be basis, medication has also begun to be part carefully examined to make a judgment of the therapeutic armamentarium. While about the need for hospital admission, but the earlier literature mainlyemphasized the compulsive exercise, food-related rituals, or use of chlorpromazine (Thorazine) in the numerous daily binges that interfere with acutely agitated, excessively exercising an- the patient's functioning or interpersonal orectic inpatient, the more recent emphasis relations are also indications for hospital- has been on the use of antidepressants, par- ization. ticularly the monoamine oxidase inhibitors (MAOIs); the tricyclic antidepressants; and The inpatient setting ideally would be a the serotonergic agent fluoxetine (Prozac), unit specifically geared for eating disorders. for the treatment of BN.50 The rationale for If necessary, however, a general medical or their use has been the seeming overlap in psychiatric floor can provide several impor- clinical, familial, and laboratory features in tant aspects of treatment. In addition to on- bulimia and affective disorders, but this ex- going physiologic monitoring and support- planation remains controversial. Neverthe- ive nursing, a hospital permits electrolyte less, while controlled studies do suggest a correction with intravenous fluids, external statistically significant reduction in fre- restraints on binging and vomiting, appli- quency of binges when these drugs are taken cation of a comprehensive behavior modifi- at therapeutic doses, a positive response is cation regimen to encourage weight gain, far from universal, and relapse both on and use of medications as indicated, and, in rare off medication is not uncommon.51 More- life-and-death circumstances, hyperalimen- over, side effects are poorly tolerated, and tation (total parenteral nutrition) through bulimic patients who may binge on tyra- an indwellingcatheter in a subclavian vein. mine-containing foods are obviously not If the patient not only is severely emaciated candidates for treatment with an MAOI. As but also categorically refuses to eat, feed- noted earlier, the not-infrequent combina- ings through a nasogastric tube also become tion of EEG abnormalities and eating disor- an option. ders has spurred interest in the application of anticonvulsants for binging, and both A behavior modification approach as- phenytoin (Dilantin) and carbamazepine sumes that the aberrant eating pattern, (Tegretol) have been reported as helpful; whatever its original determinants, has be- however, controlled studies on efficacy have come a \"habit\" by the time that hospitaliza- not been impressive.51 Finally, lithium has tion becomes necessary. Thus, it might best also been reported to be beneficial in BN,51a be undone, like most habits, by the institu- but again without the benefit of controlled tion of an appropriate schedule of positive studies. and negative reinforcers.Although common contingencies might include, for example, The only pharmacologic agent that has loss of visiting privileges or access to off- been shown to produce even a slight statis-

Eating Disorders 307 tical advantage in treating restricting AN is these issues has increased considerably cyproheptadine (Periactin), an antihista- over the past decade. For example, serious mine.52 While the efficacy of this drug is long-distance running triggering the emer- hardly profound, it is worthy of mention for gence of classic AN has been described,53 two reasons. First, its sedating effect can be but this appeared to represent the precipi- helpful in dealing with the insomnia char- tation of an eating disorder in persons who acteristic of AN.Second, its antiserotonergic already had a strong predisposition for its properties seem to stimulate appetite, while development. fluoxetine, fenfluramine, and other seroto- nergic agents appear to damp down bulimic Indeed, with so many people running and behavior.52a exercising, we would be faced with an epi- demic of AN or BN if such activities could ac- It must,of course, be noted that the eating tually \"cause\" an eating disorder. Neverthe- disorders become chronic conditions for less, the appearance of progressive weight many, if not most, of those afflicted with loss, amenorrhea, and increasing preoccu- them. The therapist must often be prepared pation with calorie intake in a female athlete to engage in long-term treatment, to use should alert the team physician or trainer to multiple modalities (including hospitaliza- the possibility that the ordinarily high level tion when indicated), and to be willing to of physical activity may be evolving into a settle for goals that emphasize minimizing manifest eating disorder. Possible biologic morbidity rather than achieving full cure. In- and psychologic mechanisms mediating deed, those patients and therapists who this phenomenon have been proposed.53 seek quick remedies are likely to meet only with frustration. The relationship between chronic exten- sive exercise and anorexia nervosa remains EXERCISE AND EATING controversial. Eisler and Le Grange54 have DISORDERS proposed four different models: (1) these are distinct phenomena which superficially As indicated in the introduction to this resemble each other because the use of ex- chapter, the inclusion of substantial mate- cessive exercise to work off calories is char- rial on the eating disorders in a text devoted acteristic of AN, and athletes need to control to women and exercise was prompted by weight to ensure maximum performance; several important concerns. Can vigorous (2) these are overlapping phenomena, with exercise or athletic competition \"cause,\" in- each increasing the risk for developing the crease the risk for developing, or precipitate other; (3) both phenomena are related in an eating disorder? Do people with a predis- some fashion to a third variable (e.g., obses- position for an eating disorder commonly sive-compulsive tendencies or affective dis- gravitate toward sports? Might physical ac- order), and thus occur together with more tivity in some fashion actually protect than chance frequency; (4) these are essen- against the emergence of an eating disor- tially variants of each other, with sexual, fa- der? Why is exercise so important to most milial, developmental, and cultural factors persons who are anorectic? What impact accounting for why one or the other expres- does continuingto exercise have on the an- sion of the underlying basic vulnerability orectic patient's attempt to regain weight becomes manifest in a given individual. with treatment? These and other questions are being asked with increasing frequency Clearly, the last of these models is the because of the growing number of women most interesting and also the most provoc- who are active athletically and the growing ative. Impetus for it came from a report by number of women who develop AN or BN. Yates and colleagues that appeared in the New England Journal of Medicine?55 These au- While definitive answers to these ques- thors reported that psychologic interviews tions are not available, our understanding of of male obligatory runners (men who ran a minimum of 50 miles per week) revealed so- cioeconomic and personality characteris-

3O8 Special Issues and Concerns tics strikingly similar to those reported in sures and demands of the sport but should anorectic women. They speculated that not be confused with the deep premorbid obligatory running in men and AN in women psychopathology of those with bona fide both represent unconscious attempts to es- AN.58 tablish a more definitive sense of identity and effectiveness. Cultural values simply Several more recent studies also raise make it easier, they proposed, for men to use questions about any underlying, fundamen- running and women, dieting. Moreover, tal (as opposed to a preciptating or perpet- they suggested that members of either sex uating) relationship between extensive ex- who use running to solve problems of iden- ercise (or competitive sports) and eating tity and effectiveness will be subject to de- disorders. Owens and Slade,59 for example, pression and manifest eating disturbances gave a questionnaire to 35 female marathon when they cannot run (for example, if they runners and found that, while their scores have been injured); this possibility is con- on the \"Perfectionism\" scale resembled sistent with case reports.53 those of anorectic patients, their \"Dissatis- faction\" scores were similar to those of nor- In a recent book,56 Yates has amplified mal control women and significantly lower these views. She proposes that at least some than those of anorectic patients. Richertand cases of eating disorders and some casesof Hummers60 found no correlation between compulsive exercising do not necessarily scores on the Eating Attitudes Test and have their roots in psychopathology. hours devoted weekly to a variety of physi- Rather, they represent a striving for excel- cal activities (e.g., swimming, bicycling), al- lence, whether by dieting or exercising vig- though, interestingly, hours spent jogging orously, but that, as the balance between ca- per week did show a significant correlation loric intake and expenditure begins to with EAT scores, perhaps lendingsome sup- diminish, the ensuing physiologic depriva- port to the thesis that runners represent a tion elicits biologic mechanisms that serve unique group among exercisers. On the to perpetuate the process. For example, other hand, Warren and co-workers,61 look- acute exercise transiently damps down ap- ing at a variety of physical, behavioral, and petite, while loss of weight may produce de- attitudinal measures in a group of college creased gastric capacity and feeling full athletes versus nonathletes, found no differ- quickly after relatively little intake; as ap- ences in varsity cross-country runners (un- petite then progressively builds and be- like Richert and Hummers) or in a variety of comes intense, the fear of utterly losing con- other varsity athletes, but did find signifi- trol becomes so anxiety-provoking that the cantly more pathologic scores in varsity exercising and dieting are further intensi- gymnasts. fied by the performance/appearance-ori- ented individual. Pathologic runners also That athletics might actuallybe protective seem to have, in Dr. Yates' view, the same against the emergence of an eating disorder ambivalent feeling toward their body as AN remains a possibility. For example, a study patients, being prepared to inflict pain on it of college women engaged in intramural in order to conform to some preconceived sports between 1977 and 1982, when the in- ideal. cidence of AN was clearly increasing, found no evidence of low weight for height among Nevertheless, the view that running is an the study subjects.62 While women not vul- analogue of AN has been questioned byBlu- nerable to AN might be attracted to college menthal and co-workers.57 Using more pre- intramural sports, or eating disorders might cisely defined and quantitative psychologic be common among such women but be hid- assessment scales, they could not replicate den by concomitant BN which maintains the qualitative impressions of Yates and as- weight at a generally normal level, it is also sociates. Moreover, it has been argued that conceivable that athletics contain physio- the weight loss and food aversions common logic or psychologic elements that are, in to many serious athletes reflect the pres- some manner, protective against the devel-

Eating Disorders 309 opment of AN. Further support for such a arrhythmias, loss of physical strength, de- thesis might be seen in a study of both ab- hydration, and electrolyte imbalance that normal eating attitudes and manifest AN in characterizes these syndromes. a large number of long-distance female run- ners.63 While 14% revealed aberrant atti- Once involved with athletic activity, some tudes on the Eating Attitudes Test and the persons who are vulnerable to, but not yet Eating Disorders Inventory, only 2.4% actu- manifesting, an eating disorder mayactually ally gave clinical evidence of having or pos- discover a relatively healthy solution to sibly having had AN. some of their psychologic conflicts. On the other hand, other such individuals may find But are persons who are prone to eating that the coincidental importance of weight disorders perhaps strongly \"pulled\" toward for performance, the inevitable competitive exercise and athletics? In addition to the defeats, the pressure to perform progres- previously mentioned report of relatively sively more successfully, the disruption of high percentages of female long-distance training schedules by injuries, the obstacles runners with elevated scores on eating atti- to regular eating patterns periodically posed tude screening tests, it is well knownthat an- by the demands of the sport, the common orectic individuals are typically excessively discussions among athletes about weight active physically during the disorder's acute and diet, and the impact of exercise on phase. Numeroushours are devoted daily to appetite64 and on the body's endorphin calisthenics, running, swimming, or other system8,65 only serve to intensify their pre- athletic activities; typically the exercising disposition. increasingly takes on a frenetic quality.This high level of physical activity might be seen Finally, for those individuals who are se- as merely the expected manifestationof the rious athletes and have developed AN, there conscious desire to work off as many calo- are certain special considerations. Osteo- ries as possible each day as part of the ob- porosis clearly puts the vigorous exerciser sessional drive to attain supreme thinness. at risk for pathologic fractures, while the However, at least one report suggests that progressive emaciation will at some point anorectic women are more active than their compromise the quality of athletic perfor- peers prior to the overt onset of the disor- mance (as must the growing preoccupation der, and that they continue to remain phys- with calories and weight). Obviously, bu- ically active even after apparent recovery limic athletes are faced with particular car- from AN.13Furthermore, as noted earlier, diovascular peril, as they add dehydration the importance of physical activity for ano- and electrolyte imbalance from perspiring rectic individuals is evident in the effective- to that from vomiting. And the maintenance ness of inpatient behavior modification pro- of a high level of physical activity can sig- grams that use access to physical activity as nificantly compromise the effectiveness a reinforcer for weight gain.49 of therapeutic weight-regaining regimens, even in a hospital setting.66 Presumably the truth rests somewhere in the middle of this debate. Those with con- EATING DISORDERS AND flicts over control and self-identity may seek OTHER SPECIAL SUBCULTURES solutions in exercise and sports competi- tion, in dietary control, or possibly in both. The importance of the mesh between en- Statistically, though, this group must cer- vironmental demands and individual vul- tainly represent a very small percentage of nerabilities is perhaps best demonstrated the vast numbers, male and female, who en- by the high prevalence of eating disorders gage in athletic activities. And among those among women in certain other subcul- who have manifest eating disorders, only a tures.67,68 These subcultures—suchas ballet, small percentage are likely to be involved in acting, and modeling—are characterized by serious, competitive sports, given the vul- an explicit emphasis on the desirability of nerability to pathologic fractures, cardiac

310 Special Issues and Concerns thinness. Thus, it is not surprising that many concerns, while still limited,suggests that a ballerinas, actresses, and models are under- high level of physical exercise becomes a weight; yet, not all or even most have eating risk factor for the development of an eating disorders. disorder only when it occurs in an individ- ual who has other predisposing risk factors, There is evidence that sociocultural back- such as conflicts or doubts about sense of ground can exert either a protective or a identity, self-esteem, and self-control. Ex- risk-enhancing influence even within such treme physical activity can also be a symp- narrow subcultures. Thus, Hamiltonand co- tom of an already-emerging state of AN, but workers,69 in a study of ballerinas in nine re- then the activity tends to be frenetic and the gional and national dance companies, found mental component involves the conscious mean weight for the entire group to be 12% desire to \"burn off\" calories, rather than a below ideal; however, no black American desire to experience the sheer fun of exer- dancers reported having AN or BN, while cise or the gratification inherent in success- 15%of the white American dancers admitted ful physical competition. It is conceivable to having AN and 19% acknowledged the that, for some athletes, female or male, ex- presence of BN.The anorectic ballerinas not treme exercise can be a way of defending only were thinner than their non-anorectic against certain conscious or unconscious ballerina peers but also manifested gener- conflicts, just as excessive dieting—or ex- ally greater psychopathology and were cessive stamp collecting, gambling, or more likely to be dancers with the most drinking—might. For most women who now competitive companies. exercise regularly, however, particularly those whose exercise is not part of a subcul- Finally, there is evidence that the pres- ture that explicitly attaches great status to ence of amenorrhea in ballerinas is medi- thinness (such as ballet or modeling), the ated not by their extensive physical activity risk of developing an eating disorder does but by their inadequate nutritionalintake.70 not appear to be enhanced, while the bene- This may well have implications for the fits of exercise to mental and physical well- amenorrhea common to other strenuous ex- being are undoubtedly substantial. ercisers, such as long-distance runners. REFERENCES Hence, we again note a complex interaction of multiple variables, perhaps what we should expect in any exploration of human psychobiology. SUMMARY 1. Lucas AR, Beard CM, O'FallonWM, and Kur- The eating disorders and participation in land LT: 50 year trends in the incidence of anorexia nervosa in Rochester, Minn: A serious exercise have both become strik- population-based study. Am J Psychiatry ingly more common among women over the 148:917,1991. past two to three decades. Since both areas are characterized by concerns about weight, 2. Crisp AH, Palmer RL, and Kalucy RA: How diet, and activity level, it is not surprising common is anorexia nervosa? A prevalence that questions about a possible relationship study. Br J Psychiatry 140:564,1983. between them have also begun to emerge. Because AN and BN are not benign disor- 3. Kendler KS, MacLean C, Neale M, et al: The ders, having behavioral, cognitive, emo- genetic epidemiology of bulimia nervosa. tional, and biologic consequences that can Am J Psychiatry 148:1627, 1991. readily become debilitating and chronic, such concerns are hardly academic. 4. Schwartz DM, Thompson MG,and Johnson CL: Anorexia nervosa and bulimia:The so- The available evidence relevant to these ciocultural context. Int J Eating Disorders 1(4):20, 1982. 5. Levenkron S: Treating and OvercomingAn- orexia Nervosa. Charles Scribner's Sons, New York, 1982. 6. Smith JE, and Krejei J: Minorities join the majority: Eating disturbances among His-

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312 Special Issues and Concerns orexia nervosa: Psychosomatic entity. Psy- ning—An analogue of anorexia? N Engl J chosom Med 2:3,1940. Med 308:251,1983. 40. Bruch H: Eating Disorders: Obesity, An- 56. Yates A: Compulsive Exercise and the Eat- orexia Nervosa, and the Person Within. ing Disorders: Toward an Integrated Theory Basic Books, New York, 1973. of Activity. Brunner/Mazel, New York, 1991. 41. Palazzoli MS: Anorexia nervosa. In Arieti S 57. BlumenthalJA, O'Toole L, and Chang JL: Is (ed): The World Biennial of Psychiatry and running an analogue of anorexia nervosa? Psychotherapy, Vol 1. Basic Books, New An empirical study of obligatory running York/London, 1970, p 197. and anorexia nervosa. JAMA 252:520,1984. 42. Abraham S, and Beaumont PJV:Varietiesof 58. Smith NJ: Excessive weight loss and food psychosexual experience in patients with aversion in athletes simulating anorexia anorexia nervosa. Int J Eating Disorders nervosa. Pediatrics 66:139,1980. 1(3):10, 1982. 59. Owens RB, and Slade PD: Running and an- 43. Shulman D: A multitiered view of bulimia. orexia nervosa: An empirical study. Int J Int J Eating Disorders 10:333,1991. Eating Disorders 6:771, 1987. 44. Johnson C,Lewis C,and Hagman J: The syn- 60. Richert AJ, and Hummers JA: Patterns of drome of bulimia—Review and synthesis. physical activity in college students at pos- Psychiatr Clin N America 7:247,1984. sible risk for eating disorder. Int J Eating 45. Katz JL: Some reflections on the nature of Disorders 5:757,1986. the eating disorders: On the need for humil- 61. Warren BJ, Stanton AL, and Blessing DL: ity. Int J Eating Disorders 4:617,1985. Disordered eating patterns in competitive 46. Johnson C, and Connors ME: The Etiology female athletes. Int J Eating Disorders 9:565, and Treatment of Bulimia Nervosa. Basic 1990. Books, New York, 1987. 62. Crago M, Yates A, Beutler LE, and Ari- 47. Marcus MD, Wing RR, and Lamparski DM: ymendi TG: Height-weight ratios among fe- Binge eating and dietary restraint in obese male athletes: Are collegiate athletics the patients. Addictive Behav 10:163, 1985. precursors to an anorexic syndrome? Int J 48. Garner DM, and Garfinkel PE (eds): Hand- Eating Disorders 4(1):79, 1985. book of Psychotherapy for Anorexia Ner- 63. Weight LM, and Noakes TD: Is running an vosa and Bulimia. Guilford Press, New York/ analogue of anorexia? A survey of the inci- London, 1985. dence of eating disorders in female distance 49. Blinder EJ, Freeman DMA, and Stunkard AJ: runners. Med Sci Sports Exerc 19:213, 1987. Behavior therapy of anorexia nervosa: Ef- 64. Epling WJ, Pierce WD,and Stefan L:A theory fectiveness of activity as a reinforcer of of activity-based anorexia. Int J EatingDis- weight gain. Am J Psychiatry 126:1093,1970. orders 3(1):27,1983. 50. Walsh BT: Psychopharmacologic treatment 65. Colt EWD, Wardlaw SL, and Frantz AG: The of bulimia nervosa. J Clin Psychiatry effect of running on plasma B-endorphin. 52(Suppl):34, 1991. Life Sci 28:1637, 1981. 51. Mitchell PB: The pharmacological manage- 66. Kaye WH, GwirtsmanHE, Obarzanck E, and ment of bulimia nervosa: A critical review. George DT: Relative importance of calorie Int J Eating Disorders 7(1):29, 1988. intake needed to gain weight and level of 51a. Hsu LKG: Treatment of bulimia with lithium. physical activity in anorexia nervosa. Am J Am J Psychiatry 141:1260,1984. Clin Nutr 47:989,1988. 52. Halmi KA, Eckert E, LaDu TJ, and Cohen J: 67. Druss RG, and Silverman JA: Body image Anorexia nervosa—Treatment efficacy of and perfectionism of ballerinas: Compari- cyproheptadine and amitriptyline. Arch son and contrast with anorexia nervosa. Gen Psychiatry 43:177,1986. Gen Hosp Psychiatry 1:115,1979. 52a. Goldbloom DS: Serotonin in eating disor- 68. Garner DM, and Garfinkel PE: Sociocultural ders. In Garfinkel PE, and Garner DM (eds): factors in the development of anorexia ner- The Role of Drug Treatments for Eating Dis- vosa. Psychol Med 10:647, 1980. orders. Brunner/Mazel,New York, 1987, p 69. Hamilton LH, Brooks-Gunn J, and Warren 124. MP: Sociocultural influences on eating dis- 53. Katz JL: Long distance running, anorexia orders in professional female ballet danc- nervosa, and bulimia: A report of two cases. ers. Int J Eating Disorders 4:465, 1985. Compr Psychiatry 27:74, 1986. 70. Hamilton LH, Brooks-Gunn J, and Warren 54. Eisler I, and Le Grange D: Excessive exer- MP: Nutritionalintake of female dancers: A cise and anorexia nervosa. Int J Eating Dis- reflection of eating problems. Int J Eating orders 9:377,1990. Disorders 5:925, 1986. 55. Yates A, Leehey K, and Shisslak CM:Run-

AAPPENDIX Exercise Following Injury, Surgery, or Infection I. Exercise Following Breast Trauma or Surgery CHRISTINE HAYCOCK, M.D. MINOR TRAUMA Patients who have minor abrasions or contusions do not require any time away from their athletic endeavors. Wearinga good supportive bra to minimize breast motion will suffice to keep them comfortable, along with a simple anal- gesic such as ibuprofen or aspirin. MINOR SURGERY Following minor surgery, such as a breast biopsy or excision of a small cyst, some limitationof upper arm use, especially throwingor lifting, is indicated for at least 3 to 5 days to allow good cosmetic wound healing. This is in addition to good breast support and analgesics. If the excision has been deep or extensive, requiringa drain for more than 24 hours, then 5 to 7 days of limited upper arm use may be indicated. This is an individual decision that must be made by the operating surgeon. If infection is present due to an infected hematoma, or develops postoper- atively, then upper arm motion must be restricted until all evidence of infection is gone. MASTECTOMY Programs such as \"Reach to Recovery,\" sponsored by the AmericanCancer Society, have shown the usefulness of exercise in the rehabilitation of the post- mastectomy patient. Fortunately, since radical mastectomies are now performed rarely, most patients do regain their full preoperative range of motion and strength in the ipsilateral arm. 313

314 Appendix A The athlete would be encouraged to begin arm raising at about 4 to 5 days after mastectomy and gradually to increase the motion daily. This routine is true as a matter of fact for all such patients to prevent formation of scar tissue that would limit future motion. However, in an athlete, at about the 2-week point, I would encourage the use of weights, beginning with a pound and gradually increasing, to build back upper arm strength. Squeezinga ball or other device for this purpose is also indicated. A good supervised physical therapy regimen is strongly advocated. There may be other limitations required for the mastectomy patient if she requires radiation therapy or chemotherapy. These would have to be individ- ually determined, as no set rule is feasible. It would depend on such factors as the amount of radiation given, the duration of the treatment, and the effect on her skin. Certainly,mild exercise would probably be permissible. REDUCTION OR AUGMENTATION MAMMOPLASTY Patients who have reduction mammoplasty would be limited in the same manner as mastectomy patients. Exercise would be limited until healing issuf- ficient such that no drainage or raw areas exist; then the same regimen outlined for mastectomy patients could be followed. Rehabilitation of the athlete following augmentation mammoplasty should include careful supervision by the plastic surgeon and a physical therapist, for physical and legal reasons. The type and size of the prosthesis used would play a role, especially if a silicone implantwas used, since the rupture of such a device may have serious medicalimplications.

Exercise Following Injury, Surgery, or Infection 315 II. Exercise Following Obstetric/Gynecologic Surgery MONA SHANGOLD, M.D. When to resume one's exercise program after obstetric or gynecologic sur- gery is best depicted in the accompanying table. EARLIEST TIME TO RESUME EXERCISE POSTOPERATIVELY Aerobic Exercise Nonwater Sports Water Sports Weight Training Procedure Light Intense Light Intense Light Submaximal D and C; first- Same or next Same or next When bleeding When bleeding Same day Same day trimester day day has ceased has ceased abortion Same day Same day 2 days 2 days When bleeding When bleeding Vaginal delivery; has ceased has ceased 1-2 days 1-2 days second- 1-2 days 1-2 days 21 days 21 days trimester 21 days 21 days 1-2 days 1-2 days 7 days 21 days abortion 7 days 21 days 21 days 21 days 21 days 21 days Diagnostic laparoscopy Operative laparoscopy Cesarean delivery; other laparotomy III. Exercise Following Common Orthopedic Injuries and Operative Procedures LETHA Y. GRIFFIN,M.D., Ph.D. ANKLE SPRAIN The proper time to return to activity following an ankle sprain depends on the severity of the injury. The level of severity is defined by a grading system: grade I refers to pain at the site of ligamentous injury but no laxity; grade II is pain at the site of ligamentous injury with mild laxity; and grade IIIdescribes pain at the site of ligamentous injury with significant laxity. With grade I ankle sprains it may take from several days to several weeks for the patient to return to activity, whereas with grade IIIankle sprains it will take

316 Appendix A a minimum of several weeks and may take up to several months. In grade I liga- mentous injuries about the ankle, initial protection, ice, compression, andele- vation are followed by rapid rehabilitation, stressing increasing range ofmotion and strength, along with return of proprioceptive feedbackfrom the ankle.Range of motion is achieved by having the athlete do figure-of-eights and circles with her foot. Rubber tubing can be used as a resistive device for gaining strength in dorsiflexion and plantarflexion and inversion-eversion. Gains in proprioceptive feedback can often be maximized by having the ath- lete stand on the affected extremity with her eyes closed and relearn how to bal- ance. Also helpful in this regard is a tilt board, a flat board attached to a half circle of wood, on which the athlete tries to balance her weight with the good foot planted on the ground and only partial weight on the injured side, which is on the tilt board. She then gradually increases her weight on the injured side until she has good balance and can stand independently on it. When the athlete has full range of motion and 90% strength and can hop independently on her extrem- ity without pain, she can return to pivotal sports. The rehabilitation programs for grade II and grade HI sprains about the ankle are similar. However, the period of immobilization and protection is longer, to allow for initial healing. ARTHROMENISCECTOMY Following an arthromeniscectomy, the athlete is encouraged to ice and ele- vate her extremity for the first 48 hours. This initial period of rest, compression, elevation, and icing helps prevent swelling and, hence, minimizes the time off from sport following this procedure. If after 48 hours the athlete has minimal to no swellingand good range of motion, she can begin strengtheningexercises, as well as functional strengthening activities such as biking and swimming (pro- vided sutures are removed), and within several weeks she can begin running. Pivotal activities are usually not allowed for 3 to 4 weeks, until the new meniscal rim has remodeled. PATELLA-STABILIZATION PROCEDURES Soft Tissue Releases Following a soft tissue release for patella stabilization (typically a medial reefing or tightening of the medial muscles, as well as a release of the lateralmus- cles), the athlete's affected limb is initially protected, iced, and elevated for 5 to 7 days. This allows the initial inflammation to diminish. Isometric exercises for the quadriceps, especially the vastus medialis, are encouraged during this period of time. A muscle stimulationunit to maintainthe oxidative enzyme con- tents of the involved muscle cells may be beneficial. Quadriceps-setting exercises and short arc extension exercises aretypically begun from 5 days to 2 weeks postoperatively. Biking, swimming, and walking can be begun as soon as the athlete has achieved control of her extremity and has a functional range of motion. Biking is often very useful in increasing range of motion, and therefore is to be encouraged. Return to pivotal sports may not be possible for up to 3 to 6 months, depending on the stability of the repair.

Exercise Following Injury, Surgery, or Infection 317 Bony Realignment Procedure for Patella Dislocation Following a bony realignment of the patella, the timing for initiating range of motion and strengthening exercises is dependent upon the bony fixation device used (e.g., screws, staples, and so on). The period of immobilization var- ies and should be dictated by the orthopedist. LUMBAR DISKECTOMY Immediately following diskectomy, the athlete is encouraged to begin walk- ing in her hospital room, progressing within 7 to 10 days to walking about the home and outside the home, going gradually from 10-minute walks to 30- to 45- minute walks, at an increasing pace. Sutures are removed in 10to 14days. If there is not marked swellingor spasm in the paravertebral muscles, the athlete is also encouraged to begin swimming at 2 to 3 weeks following surgery. Swimming, like running, develops abdominaland paravertebral muscle strength and is therefore to be encouraged. Pivotal sports are generally permitted within 3 to 4 months, as soon as the athlete has good muscle strength and no pain with activities of daily living.Gen- eral consensus is lackingon whether an athlete should be permitted to return to contact sports following diskectomy. Although many athletes have returned to long-distance running following diskectomy, one should encourage the athlete to choose a sport that does not require such impact loadingon the lumbarspine. BUNIONECTOMY Bunionectomy is not a \"simple\" procedure. It frequently necessitates bony realignment of the first metatarsal. Aspecial shoe with a nonflexible wooden sole may be needed to protect the osteotomy while walking. Ambulation can begin soon after the procedure, as long as protection is provided by such an appliance. When early bony union is seen and pain and swelling have subsided, the hard-soled shoe may be replaced by a comfortable shoe with a nonelevated heel. Within 3 to 4 weeks, the athlete will probably be allowed to return to swimming and biking, as well as to weight-training routines, as long as they do not involve rising up on the toes or impact loadingon the feet. Impact-loading activities such as running, soccer, tennis, and so forth should not be permitted until swellingis completely resolved, range of motion of the metatarsophalangeal joint of the great toe is restored, and good bony union is present at the osteotomy site,which may be any time from 3 to 6 months. REMOVAL OF MORTON'S NEUROMA The term \"Morton's neuroma\" refers to painful scarring about the interme- tatarsal nerve in the foot. If the neuroma is unresponsive to nonoperative meth- ods such as metatarsal pads, shoe modification, injection of steroids, and local anesthesia, then surgical excision can be accomplished.

318 Appendix A Following this procedure, the athlete is instructed to keep the foot elevated for several days to diminish swelling.Within 3 to 4 days, she can be performing normal, routine activities. However,if foot swelling occurs when she attempts to do so, further elevation is necessary. Generally, swelling has resolved by the sec- ond or third week. If the athlete is pain-free, swimming and biking are then per- mitted. It may be 3 to 6 weeks before the athlete can resume running and pivotal activities without discomfort. IV. Exercise Following an Infection GABE MIRKIN, M.D. It is probably all right to exercise during a systemic infection, provided that the athlete is afebrile and does not have myalgia before exercising. These same criteria should be used to determine when to return to exercising after recover- ing from an infection. However, each case should be decided on its own merits, rather than by general rules. Exercising with a fever increases cardiac output far beyond exercising with a normal body temperature. The heart must pump extra blood to skin to prevent heat build-up, in addition to its usual tasks of supplying oxygen and nutrients to exercising muscle. Some viruses that infect the respiratory tract can also infect the myocardium.1 The combinationof increased workload and viral myocarditis can result in a fatalarrhythmia.2 When skeletal muscles are infected by respiratory viruses, they usually hurt during exercise. Exercising when muscles hurt markedly increases susceptibility to injury. Infected muscles have reduced strength3 and endurance4 and decreased levels of necessary enzymes such as glyceraldehyde 3-phosphate dehydrogenase.5 REFERENCES 4. Arnold DL: Excessive intracellular acidosis of 1. Burch JA:Viral diseases of the heart. Acta Car- skeletal muscle on exercise in a patient with post-viral exhaustion syndrome. Lancet diol 1:5, 1979. 1:1367,1984. 2. Roberts JA: Viral illnesses and sports perfor- 5. Astrom E: Effect of viral and mycoplasma in- mance. Sports Med 3:296,1986. fections on ultrastructure and enzyme activi- 3. Friman G: Effect of acute infectious disease on ties in human skeletal muscle. Acta Pathol Mi- crobiol Immunol Scand 84:113, 1976. isometric muscle strength. Scand J Clin Lab In- vest 37:303, 1977.

Index Page numbers followed by F indicate figures; page numbers followed by T indicate tables Abdominal surgery, exercise after, 315t Amateur Athletic Union, 73 Abortion, 230-231, 315t Amenorrhea Abruptio placenta, 182 Acclimatization, lack of, 135, 265 anorexia nervosa and,296 Accommodating resistance exercise, 67 bone mass and, 97-98 Achilles tendinitis, 253-254 defined, 152-153 Acidosis, 74 diagnostic evaluation, 165t, 165-166 ACTH, 149, 159, 161 hypoestrogenic, 155, 163-165 Action stage in exercise adoption, 43 incidence of, athletes and, 156 Active tissue, defined, 4 prevalence of,153f Activity. See Physical activity primary, 130, 137, 168-169, 169t Actresses, eating disorders in, 309-310 treatment, 166-168, 167t, 168t Adenocarcinoma, 162, 168 American Cancer Society, 313 Adherence rates, 39-43, 44t American College of Cardiology, 288, 289 Adolescence. See also Eating disorder(s) American College of Obstetricians and Gynecologists, fitness, 31 180 growth spurt, 142 American College of Sports Medicine (ACSM), 10, 14, rnenarche, 142-143 physical activity, 41t, 143-146 15, 73 physiological aspects, 141-142 Amino acids, 103, 105 training, growth/maturation and, 146-150 Adolescent plateau, performance and, 145-146 branched-chain, 105, 114 Aerobic capacity. See also Functional capacity Anaerobic glycolysis, 79 gender and, 18, 282-283 Anaerobic metabolism, 106 maximal, prepubescence, 131 Anaerobic power and endurance, 131-132 oxygen uptake and, 12, 13 Anaerobic threshold, 13-14 Aerobic exercise, 15f,15-16 Anaphylaxis, exercise-induced, 272-273 Aerobic power, 198-202 Androgen, 165 adolescence, 144-145 Android pelvis, Q angle and, 237f prepubescence, 131 Anemia, 116-117, 163, 267-269,269t Affective disorder(s), 297 Anhedonia, 297 Age. See also Adolescence; Menopause; Ankle impingement, 250, 250f Ankle sprain, exercise after, 315-316 Prepubescence Anorexia nervosa fitness and, 5, 17, 41t physiologic response to exercise, 130t bone mass, 164, 193 strength development and, 69-70 clinical features, 30, 295-297 Alarm reaction of stress adaptation, 82 co-morbidity, 302-303 Albuterol, 272t course, 301-302 Alcohol intake,181 diagnosis, 301-302 Allergic reactions, 270, 272 differential diagnosis, 301t Alprazolam, 228 endocrine abnormalities, 300-301, 301t Altitude, exercise and,264 epidemiology, 293 etiology, theories of, 303-305 exercise and, 288, 307-309 incidence, 292-293, 309-310 319

32O Index Anorexia nervosa Continued BMR (basal metabolic rate), 204 laboratory findings, 299-300, 300t Body composition physical findings, 298t, 298-299 prognosis, 301-302 adolescence, 142, 146-147 radiographic/EEG/ECG findings, 299,299t endurance trainingand, 79-80, 80t risk factors for, 304t evaluation of, 9 setting/onset, 293-294 exercise and weight control, 37 thermoregulation and, 135 gender and, 18 treatment, 305-307 menarcheand, 136 Body fat Anovulation euestrogenic, 155 abdominal, 196, 206 Anthropometric measurements, 9 age, exercise and, 205-206 Antihistamines, 272 athletes, elite and, 80t Anxiety body composition and, 4 estrogen production, 156 disorders, 302 evaluation of, 9 reduction of, exercise and, 6, 8, 38, 157,207 menarche and, 136,149 Anxiolytics, 287 physiological aspects, 80 Aortic stenosis, 130 Body image Apolipoprotein, 165, 197 distorted, 296 Appetite, 36-37 improvement of, 6, 8, 38 Arrhythmias, cardiac, 130, 285, 318 Body mass index (BMI) Arsenic, 118 measurement of, 29 Arthralgia, 206 nomogram for, 29f Arthromeniscectomy, 316 risk classification algorithm, 30f Arthroscopic examination,knee joint,243 Body size, of adolescence, 142 Ascorbic acid, 115 Bone Aspiration of fluid, knee joint,241 cortical, 90, 90f, 189, 191, 193 Aspirin, 226t,246 formation, 189-196, 194f, 194t Asthma, 130, 270-272,272t hypertrophy, 93-94, 96 Astrand, Per-Olaf, 75 mineral content (BMC), 89,95f Astrand-Rhyming Nomogram, 12 physiologic aspects, 89-90 Atherogenic disease, menopause and, 196-202 trabecular, 91, 91f, 189, 190f, 191, 193 Athletes. See also Diet;Training Bone density, loss of. See also Osteoporosis endurance, body composition and,80t age and, 89, 90f, 192 minimum VO2 max values, 76 amenorrhea and, 162-164, 168 vitamin needs, 115 athletic amenorrhea and, 97-98 Athletic pseudosyndromes, 273-275 exercise, benefits of, 93-94, 96 ATPase activity, 74, 76, 78, 174-175 inactivity and, 93-96 B vitamins, 114-115 Bone meal, pollution of, 118 Back exercises and posture, 195 \"Bonking,\" 107 Back pain, low, 256-257 Bony realignmentfor patella dislocation,317 Ballet dancing Borderline personality, 297, 302 adolescence, 147, 148 Braces, patella stabilizing, 245, 245f, 248 eating disorders, 309-310 Brain endurance,107 prepubescence, 136 Bra, 217-219, 220 scoliosis, incidence of, 164 Breast cancer, riskof Basal metabolic rate (BMR), 204 hormone therapy, 205, 264 Base cycles (workouts), 84 luteal phase deficiency, 162,163 Bayes' theorem, 286 Breast(s) Bedrest, effects of, 94-95 augmentation, 219-220, 314 Bee-sting sensitivity, 273 biopsy, 313 Behavior Survey and Behavioral Risk Factor cysts, 220 fibrocystic, 220-221 Surveillance System (BRFSS), 28 lactation, 220 Bench-stepping, energy requirements, 12t nipple injury, 219 Benzodiazepines, 296 pregnancy, 220 B-endorphins, 149 premenstrual changes, 220-221 Bicycling. SeeCycling reduction, 219-220, 314 Biliary tract, 274 support of, 217-219, 218f, 220 Binge eating, 30, 294,297 surgery/trauma, exercise after, 313-314 Bioelectric impedance measurements, 9 trauma, 219 Birth control pills. See Oral contraceptives Bromocriptine, 228 Bleeding, break-through, 224, 225 Bronchospasm, 270 Blood doping, 75, 77 Bulimia nervosa Blood pressure clinical features, 30, 297-298 co-morbidity, 302-303 exercise and, 7, 38, 284 course, 301-302 obesity and, 29

Index 321 diagnosis, 302 Carnitine palmitoyl transferase, 82 endocrine abnormalities, 300-301, 301t Carnitine supplementation, 107-108 epidemiology, 293 Catecholamines, 108, 177 etiology, theories of, 303-305 Catecholestrogens, 157, 159 exercise and, 307-309 Cathartics, abuse of, 296-297 forms of, 294-295 Center for Climacteric Studies, 193, 197, 199 incidence, 292-293, 309-310 Cerebral palsy, 130 laboratory findings, 299-300, 300t Cerebrovascular accidents, 8, 38 physical findings, 298t, 298-299 Cesarean delivery, 315t potassium deficiency with, 119 Chest pain, 275 prognosis, 301-302 Child(ren). See also Prepubescence radiographic/EEG/ECG findings, 299, 299t treatment, 305-307 fitness, 31 illness and exercise, 129-130 Bunionectomy, exercise after, 317 physical activity,42f Bunions, 257-258, 258f, 317 Chlorpromazine, 306 Caffeine, 108 CHOICES (NIHprogram), 261 Calcium Cholesterol age and menopause, relationship to, 197t dietary intake, 117-118, 118t, 194-195 cardiovascular disease, risk factor of, 7, 38, 196 homeostasis, serum, 89-90, 90t, 112,113 obesity and, 29 loss, excess protein intake and, 114 Chylomicron particles, 105 pregnancy and, 183 Cigarette smoking. See Smoking supplementation, 8, 91-93, 118t Civil Rights Act (1972), Title IX, 73, 147 transport mechanism(s), 74,76 Clayton, Derek, 76 Calcium carbonate, 92 Climacteric, defined, 187-188, 188f Calcium citrate malate, 92 Climate. See Cold-weather exercise; Hot-weather Caloric needs physical activity and, 35t, 157 exercise pregnancy,182-183 Clomiphene citrate, 166 Cancer. See also Breast cancer, colon cancer Clothing, athletic, 266, 266t obesity and, 29 Cocaine, 297 risk and exercise, 264 Coeducational contact/collision sports, 137 Carbamazepine, 306 Cognitive behavioral therapy, 41-42 Carbohydrate(s) Cold injury to nipples, 219 composition of, 103,104f Cold intolerance, 296 dietary intake,113 Cold-weather exercise, 134-135, 264 energy per gram, 78 Collagen, 206 loading, 108 Collision sports, coeducational, 137 maximal body storage capacity, 106t Colon cancer, 264 metabolism, 174-175, 204-205 Condoms, 225 overload, 83 Contact sports Carbon dioxide, 14 Carbonated drinks, 113 breast augmentation and, 220 Cardiac output coeducational participation, 137 exercise and, 283 low back pain and, 257 oxygen uptake, 74-75, 81 Contemplation stage in exercise adoption, 42 pregnancy, 173, 174, 176 Contraception, 166, 223-226, 226t. See alsoOral Cardio-respiratory fitness. See also Functional contraceptives, names of individual devices. capacity Copper, serum level, 119 fitness, as component of, 4-5 Coronary artery disease menopause and, 196, 198-202 Cardiovascular disease. See also Coronary artery congenital anomalies, 18 prevention by exercise, 6-7, 7t, 263-264 disease risk factors of, 196 exercise limitationsin, 287-289 screening for, in women, 286 exercise training and, 6-8, 263-264 Corpus luteum, 154, 158 findings with eating disorders, 299 Corticosteroids, 119, 271, 272t menopause and, 196-202 Corticotropin-releasing hormone (CRH), 161 obesity and, 29 Cortisol, 149, 161, 175 pseudomyocarditis, 274-275 Creatine kinase, 274-275 risk factors for,206 Cromolyn sodium, 272,272t Cardiovascular fitness, development of, 14-15 Cross-country skiing Cardiovascular system body composition, 80 aerobic capacity, 282-283 endurance performance, 77 exercise ECGtesting, 286-287 Cromsisn-ismecutmionVaOl 2mmoamx evnatluoefsi,n7e6rtia (CSMI), 193 limitations on, exercise, 287-289 Cross training,20 response to, exercise, 283-286, 285f Cyanocobalamin, 115 Cycle ergometry energy requirements, l1t

322 Index Cycle ergometry Continued Eating. See Diet;Nutrition oxygen uptake, 12 Eating Attitudes Test (EAT), 159, 308 peak muscle power tests, 132 Eating disorder(s). See also Anorexia nervosa; Bulimia Cycling anaerobic examples of, 132 nervosa endurance performance, 77 biology of, 298-299 endurance performance, gender and, 80,82 clinical features, 295-298 maximal oxygen uptake and, 75 co-morbidity, 302-303 menstrual disorders, 152-153 course of, 301-302 muscle glycogen depletion, 106-107 diagnosis, 301-302 osteoporosis and, 195 endocrine abnormalities, 300-301 Cyproheptadine, 307 epidemiology, 294 Cystic fibrosis, 130, 135 etiology, theories of, 303-305 Cystocele, 230 exercise and, 307-309 Cysts, breast, 220,313 laboratory findings, 299-300, 300t Cytochrome oxidase activity, 77 menstrual disorders and, 167-168 Danazol, 227,228 overview, 292-293 Dean, Penny, 106 physical findings in, 298t Death, causes of prognosis, 301-302 eating disorders, 302 radiographic/ECG/EEG findings, 299t sudden cardiac, 18-19, 263, 288-289 setting/onset, 293-295 Dehydration, 111-113, 114, 265-267 special subcultures and, 309-310 Depletion training, 107, 108 treatment, 305-307 Depression, mental, 207, 294, 297, 302 Eccentric training, 65-67 DES exposure, 182 ECG. see Electrocardiography. Dexamethasone suppression, 159 EEG. see Electroencephalography. Diabetes insipidus, 135 Efficiency, performance, 78-79 Diabetes mellitus Ejection fraction, 283, 284f exercise, children and, 130 Electrocardiography (ECG) exercise, menopause and, 196,206 eating disorders, findings with, 299t exercise and, 8, 38 exercise testing, 286f, 286-287 thermoregulation and, 135 Electroencephalography (EEG) Diaphragm contraceptive, 223, 225 eating disorders, findings with, 299t Diarrhea, 119, 135, 269 Electrogoniometers, 9 Diet. See alsoNutrition Emetics, 296-297 athletics and, 119-120, 266t Endometrial hyperplasia, 162, 166, 168 menstrual disorders and, 157-159, 167-168 Endometriosis, 227 pregnancy and, 181, 182-183 Endometrium, 154 Dieting, yo-yo, 36 Endurance, defined, 106-107 Digitalis, 74 Endurance development Digoxin, 287 body composition, 79-80 Dilantin, 306 gender and, 80-82, 81t Dilatation and curettage (D and C), 230 maximal oxygen consumption, 74-77 exercise after, 315t mitochondrial density, 77-78 Disaccharides, 103,104f performance, 73, 78-79 Dislocation, patella, 242-245,317 training, priciples of, 84t Disqualifying conditions training for, 82-85 medical illness, 275-276, 281, 287-289 Endurance game activities, 14-15 Disseminated intravascular coagulation, 267, 269 Energy expenditure Distance covered, tests of, 13 exercise and, 34-36, 35t Diuretics MET equivalents, l0t, l1t abuse of, 30, 296-297 oxygen uptake and, 9-10 potassium, serum levels and, 119 Energy storage, 105-106 sodium, serum levels and, 118 Enzyme abnormalities, 274 Dolomite, pollution of, 118 Epilepsy, 130 Dopamine, 273 Epinephrine, 177, 207,272, 273 Drinking. See Hydration,Exercisedrinks Erythrocythemia, 75 Drug abuse, 297 Estradiol Dynamic flexibility, 9 adolescence, training and, 149 Dynamic loading, bone hypertrophy and, 93-94 menopause and, 188 Dynamic strength, defined, 61 menstrual disorders and, 156, 159, 166 Dysmenorrhea, 226-227 transdermal, 166 Dyspnea, 8, 275 Estrogen fat tissue and, 156 oral contraceptives, in, 224 physiologic effect, 154

Index 323 Estrogen therapy development contraindications, 167t components of, 4-5, 14-16 dosages, 264 economic aspects, 19 osteoporosis, 8, 96 factors affecting, 17-19 Estrone, 148 Ethinyl estradiol, 166, 224 evaluation of, 8-14 Exceed (solution), 111 maintenance, activity level and, 16-17 Exercise. See also Competition; Training;Weight Flexibility as component of fitness, 4 control and exercise evaluation of, 9 cardiac function and, 283-286, 285f Flexion, of back, 195 medical contraindications to, 275-276 Fluids. SeeHydration metabolic response, 174-175 Fluoxetine, 306, 307 physiologic response, 173-174 FNB (Food Nutrition Board), 115 well-being and, 206-208 Folacin, 115 Exercise, short-term Folic acid, 119 physiologic aspects in prepubescence, 130t, 131t, Follicle-stimulating hormone (FSH), 154, 188 Follicular phase, 154, 160f 130-132 Food. See also Diet; Nutrition Exercise drinks, 112,267 intake, competition and, 108-111, 109t, 110t, 113 Exercise ECG tests, false positive, 286f, 286-287 Food Nutrition Board (FNB), 115 Exercise-induced asthma (EIA), 270-272 Foot strike, patella pain and, 236 Exercise overuse (abuse), 47t, 47-48 Fracture(s) Exercise program(s) chondral, 243 endurance training and, 83 avoiding threshold mentality,43-44 hip, 188-189 components of, 14-15 stress, 83, 164, 255, 256-257 economic aspects, 19 Framingham Heart Study, 263, 288 physiologic effects, adult women, 55t-56t, 57t-59t Frank-Starling principle, 74 samples, 23-26 Free fatty acids, 176, 182 social aspects, 43 Free weights, 9 stages of change in, 42-43 Fructose, 103, 113 Exertion. See Exercise Fruit juices, 112 Exhaustion FSH (Follicle-stimulating hormone), 154, 188 acute/chronic, symptoms of, 83 Functional capacity heat, 135, 268t anaerobic threshold, 13-14 stage of stress adaptation, 82 measurement, 10-13 Extension terminology, 9-10 of back, 195 Galactose, 103 short arc exercises, knee, 244f, 244-245, 248 Gallbladder disease, 29 Fast-twitch fibers (FT), 70, 75, 77, 81, 82 GAS (General adaptation syndrome), 82 Fat. See also Bodyfat. Gated blood pool scan, 283, 288 dietary, 36-37, 78, 107 Gender maximal body storage capacity, 106t aerobic power and, 18 metabolism, 106 cardiovascular status and,284 utilizing in place of glycogen, 107-108 endurance performance and, 80-82, 81t Fat fold measurements, 9 energy storage, 106 Fat-free mass (FFM), 142,146 fitness and, 17-18, 40 Fatigue, causes of, 119 physiologic response, acute exercise, 131t, 131-132 Fatty acids, 105, 105t thermoregulation and, 135 Febrile illness, 276,318 weight perception and, 28, 30 Fenfluramine, 307 General adaptation syndrome (GAS), 82 Ferritin, serum levels of, 116, 117 Gilbert's disease, 274 Ferrous sulfate, 267 Girl(s). See Prepubescence Fertility, 229 Glucagon, 175 Fetal heart rate, 178-179, 180-182 Glucose metabolism, 103, 106, 113 Fetus, maternal exercise and, 178f,178-182, 179f Glycerol, 105, 105t Fibrocystic breasts, 220 Glycogen Fick equation, 173 endurance and, 78, 79, 83, 106-107 Fitness. See also Exercise; Training fat storage and, 103-104 adolescence, 31, 143-146 utilization of, 107-108 benefits of Glycolysis, 13 Gonadotropic hormones, 148-149, 159 healthy individuals,5-6 Gonadotropin-releasing hormone (GnRH), 154 medical illness, 6-8, 37-38, 46 children, 31 defined, 3

324 Index Gonadotropin-releasing hormone (GnRH)analog, 227 Hypertension Goniometer, 9 coronary artery disease, risk factor for, 196, 264 Grade walking,energy requirements, lot exercise training and, 7-8 Gravity, osteogenesis and, 191-192 Growth Hyperthermia, 112, 135, 264 Hypertrophic cardiomyopathy, 18 prepubescence, training and, 135-137 Hypoglycemia, 107, 109, 268t, 300 spurt, adolescence, 142-143, 146, 149 Hypohydration, in children 135 Growth hormone, 175, 202, 301t Hypokalemia, 112, 119, 119t, 299 Gymnastics, 136, 147 Hyponatremia, 112, 118, 265 Gynecoid pelvis, Q angle and, 237f Hypotension, 273 Gynecologic concerns Hypothalamic-pituitary-ovarianaxis, 148-149, 193, contraception, 223-226 dysmenorrhea, 226-227 229, 301t endometriosis, 227 Hypothermia, 135, 268t fertility, 229 Hypothyroidism, 165 menstrual cycle and performance, 231-232 Hypovolemia, 270 postoperative recovery, 230-231 Hypovolemic collapse, 268t premenstrual syndrome, 227-229 Hypoxemia, 74 stress urinary incontinence, 229-230 Ibuprofen, 226t Gynecologic surgery, exercise after, 315t Immobilization and bone loss, 93, 95 Hamstring stretch, 248f Impingement syndromes, 249-253 Health clubs, 19 Inactivity. See also Sedentary lifestyle Healthy individuals benefits of fitness, 5-6 obesity and, 31,206 exercise guidelines, 14 skeletal effects, 94-96 Heart defects, congenital, 18,130 Incompetent cervix, 182 Heart disease. See Cardiovascular disease Incontinence, stress urinary, 229-230 Heart rate, 74,284 Infection, exercise after, 318 fetal, 178-179, 180-182 Inhibition test, 239, 241f target, 15, 15f Injury(ies). See also Orthopedic concerns Heat, see also Thermoregulation breast, 219, 313-314 cramp(s), 111-112, 268t joint, 180 exhaustion, 135, 268t muscle, 274 injuries, treatment of, 268t musculoskeletal, 19 stress, 264-267, 269-270 overuse, 19, 85, 137 stroke, 114, 135, 267,268t sports associated with, 235t Hemarthrosis, 241, 243 types, 19, 234 Hematuria, 273 Inotropic agents, 74 Hemoglobin, 81-82 Insomnia, 207,296 Hepatic necrosis, 267 Insulin High-density lipoproteins (HDL), 7, 196-198 metabolic effects, 175, 204-205 Hip fractures, statistics, 188-189 pregnancy and, 176 \"Hitting the wall,\" 82, 106-107 Insulin-dependent diabetes mellitus, 8 Hives, exercise induced, 272, 273 Interval training, 19-20, 83, 84 Hormonal responses to exercise Intrauterine devices (IUDs),225 adolescence, 148-149 Iron menstruation and, 159-162 deficiency, 163, 267-269 pregnancy and, 176-177 dietary intake, 116 Hormone replacement therapy, 194f, 194t pregnancy and, 183 Hot flushes, 188, 205 Isokinetic Hot tubs, 266 machines, peak muscle power tests, 132 Hydration strength, defined, 9, 61 fluid intake and, 111-113, 266t training, 67 heat stress and, 265-267 Isoleucine, 105, 114 Hydrogen ions, buffering, 14 Isometric Hydrostatic weighing, 9 exercise, 284 Hymenoptera, 273 strength, defined, 61 Hyperandrogenism, 165 strength, maximal, 8-9 Hypercapnia, 74 training, 63-65 Hypercholesterolemia, 263-264 Isotonic Hyperinsulinemia, 109, 196 strength, defined, 61 Hypernatremia, 112 strength, maximal, 9 Hyperprolactinemia, 165 training, 61-62, 64-65 IUDs (intrauterine devices), 225

Index 325 Jenny Craig Foundation, 27 Jogging. See also Running Mastectomy, 313-314 Maturation, sexual, 135-137, 147-149 middle-aged women and injury, 206 MAX (solution), 111 Joint(s) Maximal oxygen uptake. See Oxygen uptake, maximal Maxim(aVlov2olmunaxta)ry contraction (MVC), 60-61, 69 injury, 180 Mechanical bone loading, 93-94, 95f range of motion, 4, 9 Medical illness Judo, 135 kcal, equivalents, 9,10 arising during sports Kegel exercise(s), 230 anaphylaxis, 272-273 Ketaprofen, 226t asthma, 270-272 Kinanthropometrists, 129 heart disease, 263-264 Kristiansen, Ingrid,103 heat stress, 264-267 Labor, premature, 181, 182 hematologic effects, 267-268 Lactate, 13 pseudosyndromes in athletes, 273-274 \"Lactate breaking point,\" 13, 14 \"runner's diarrhea,\" 269 Lactate inflection point, 83 urinary tract, effects on, 269-270 Lactation, exercise and, 220 urticaria, 273 Lactic acid clearance capacity, 76, 77, 82 differential diagnosis, abnormal test results, 270t production, 14, 78 disqualifying conditions, 275-276, 281, 287-289 Lactose, 103 exercise, benefits of, 6-8, 18-19, 37-38 Laparoscopy, exercise after, 231, 315t screening athletes for,275, 278-279, 280 Laparotomy, exercise after, 315t Medroxyprogesterone acetate, 166, 205 Laxatives, abuse of, 30 Mefenamic acid, 226t LBM (Lean body mass), 9, 37 Megestrol acetate, 205 Lead pollution, 118 Melatonin, 159 Lean body mass (LBM), 9, 37 Menarche Left ventricular function, 283 delayed, 136-137, 147, 148-149 Left ventricular hypertrophy, 285 onset, 142-143 Leucine, 105, 114 Menopause Leuprolide acetate, 227 atherogenic disease and, 196-202, 197t Licorice, 119 bone mass, 96 Lipase, 105 calcium supplementation, 92-93 Lipid profiles, 7 cardiorespiratory fitness and, 196-202 Lipids, 196-198 defined, 187-188, 188f Lipoprotein lipase (LPL) levels , 205 exercise, fat tissue and, 205-206 Lipoproteins, 7, 196-198 exercise, osteoarthrosis and, 206 Lithium, 306 exercise, well-being and, 206-208 Load cycles (workouts), 84 muscle tissue, strength and, 202-205 Longevity and fitness, 5 osteoporosis, bone health and, 189-196, 194f, Low back pain, 256-257 Low-density lipoproteins (LDL), 196-198 194t Lumbar diskectomy, 317 overview, 187-189 Lupron, 227,228 vasomotor symptoms, 205 Luteal phase, 154, 160f Menstrual disorder(s). See also Amenorrhea; Luteal phase deficiency physiologic aspects, 155, 156, 162 Oligomenorrhea treatment, 166 consequences of, 162-165 Luteinizing hormone (LH) diagnostic evaluation of, 165-166 menstrual disorders and, 161-162, 162f, 163f dysmenorrhea, 226-227 physiologic aspects, 154 premenstrual syndrome, 116, 118, 227-229 MacArthur Foundation Fellowship,27 prevalence of, 152-154, 153f Magnesium levels, 113 treatment, 166-168 Maintenance stage in exercise adoption, 43 types, 154-155 Maltodextrin glucose polymer solutions, 111 Menstruation Mammography, 220-221 cycle changes with exercise/training, 156-159 Mannose, 103 effect on performance, 231-232 Marfan's syndrome, 18 endurance training and, 82 Margaria step-running test, 132 hormonal changes with exercise/training, 158f, 159- 162 iron deficiency and, 267 physiology of, 154,155f Mercury pollution, 118 Metabolic equivalent (MET), 10, 10t, 11t, 15 Metabolic rate, 36, 174-175 METs (Metabolic equivalents), 10 Midluteal phase,160f

326 Index Minerals energy storage, 105-106 major/trace, 116t, 116-119 essential nutrients, 103-105 pregnancy and, 183 glycogen utilization,decreasing, 107-108 minerals, 116-119 Minority populations, 39 overview, 102-103 Mitochondria protein requirements, 113-114 vitamins, 114-116 fat content, 107-108 Oakland (CA) Growth Study, 143 oxygen extraction by, 75 Obesity Mitochondrial density demographics of, 39 endurance capacity and, 77-78 exercise programs for, 8, 44t over-distance training,83 inactivity and, 130,206 Mitral valve prolapse, 18, 287-288 nature/severity of, 28-31 Modeling, eating disorders with, 309-310 thermoregulation and, 135 Monoamine oxidase inhibitors (MAOIs), 306 Obligatory runners, 307-308 Monoglycerides, 105 Obstetric surgery, exercise after, 315t Monosaccharides, 103, 104f Oligomenorrhea Mood-elevating effect of exercise, 207 anovulatory, 162-163 Morton's neuroma, 258-259, 317-318 athletics and, 152-153, 156 Motor performance, adolescence, 144 bone loss and, 98 Mullerian agenesis, 168 diagnostic evaluation, 165t, 165-166 Muscle treatment, 166t, 166-168, 168t contraction, bone mass and, 93-94 O1,r2a5l-c(OonHtr)2acveitpatmiviensD, 89 hyperplasia of fibers, 68 biphasic, 224 hypertrophy, 68-69 bone density and, 117 injury, 274 iron needs and, 116 mass, 142 low-dose, 224,231 tissue loss, 202-205 menstrual disorders and, 164, 166-167 Muscle endurance mineral needs and, 119 defined,4 physiologic aspects, 224-225 evaluation of, 8-9 vitamin needs and, 115 nutrition and, 106 Orthopedic concerns Muscle strength Achilles tendinitis, 253-254 adolescence, 143-144 bunions, 257-258 defined, 4 exercise after, 315-318 evaluation of, 8-9 impingement syndromes, 249-253 menopause and, 202-205 low back pain, 256-257 prepubescence, 131-132 Morton's neuroma, 258-259 Muscular dystrophy, 130 overview, 234-235 Myocardial contractility, 74 patella dislocation, 242-245 Myocardial infarction, 38, 196, 263 patella pain, 235-242, 249 Myoglobinuria, 269, 270 patella plica,249 Nafarelin acetate, 227 patella subluxation, 245-247 Naloxone, 149 patellofemoral stress syndrome, 247-249 Naproxen, 226t shin splints, 254-255 National Academy of Science, 115 sports and related injuries, 235t National Health Examination Survey, 143 stress fractures, 255 National Heart, Lung and Blood Institute, 289 Orthostatic hypotension, 196 National Institute on Aging, 187 Osgood-Schlatter's disease, 241, 241f National Institutes of Health,261 Osteoarthritis, 29, 206 National Research Council, 115 Osteoblastic activity, 93-94 Nautilus Sports/Medical Industries, Inc.,187 Osteogenesis, 189-196 Neuroendocrine response to exercise, 175 Osteoporosis Niacin, 115, 119 causes, 89 Nichols, Cynthia, 106 eating disorders and, 298-299 Nipple injury, 219 economic aspects, 90-91 Non-insulin dependent diabetes mellitus, 29 exercise and, 8, 195-196 Norepinephrine, 175, 177, 181, 207 incidence, 90-91 Norplant, 225-226 trabecular bone, 190f Nutrients, essential, 103t, 103-105 Ovarian failure, 164, 165 Nutrition Ovarian follicle, 154 athletes, diet and, 119-120 Ovarian hormones, 148-149 competition, diet and, 108-111, 113 Over-distance training, 83 competition, fluid intake and, 111-113 eating before exercise, 110 endurance, 106-107, 108