nerve, and a loose connective tissue layer called outer layers of the root sheath arc similar to the pia epineurium. cells of the spinal cord, and the cells in the distal part are more similar to the arachnoid cells of the \"\"Vhen the ncnlC root approaches the interverte- spinal dura. The inner layers of the rOOl sheath are bral foramen. the root sleeve gradually encloses the comprised of cells that show similarities to the cells nerve tissue more lighLly. The subarachnoid space of the perineurium of peripheral nerves. An in- and the amount of cerebrospinal fluid surrounding lerrupted basement membrane encloses these each nen'c root pair will thus become gradually re- cells separately. The inner layers of the root sheath duced in the caudal direction. Compression injury constitute a diffusion barrier bet\\veen the cl1do~ of a nerve root may induce an increase in the per- neurium of the nerve roots and the cerebrospinal meability of the endoneurial capillaries. resulting in fluid, This barrier is considered to be relatively edema formation (Olmarker et aI., 1989b; Rydevik & weak and may only prevent the passage or macro- Lundborg, 1977), This can lead to an increase of the molecules. imraneural fluid and subsequent impairment of the nutritional transport to the nerve (Myers & Powell. The spinal dura encloses the nerve roots and the 1981; Myers, 1998), Such a mechanism might be cerebrospinal fluid, When the two layers of the cra- particularly important at locations where the nerve nial dura enter the spinal canal. the outcr layer roots are tightly enclosed by connective tissue. Thus blends with the periosteum of the pan of the lami- there is a more pronounced risk for an \"entrapment nae of the cervical vertebrae facing the spinal canal. syndrornc\" within the nerve roots at the intcrvene- The inner layers join the arachnoid and become the bral foramen than more central in the cauda equina spinal dura. [n contrast to the rooL sheath, the (Rydevik et aI., 1984), The dorsal root ganglion, with spinal dura is an effective difTusion barrier: The bar- its content of sensory nCt've cell bodies, tighlly en- rier properties are located in a connective tissue closed by meninges, might be panicularly suscepti- sheath between the dura and the arachnoid called ble to edema formation. the neurotheliunl. Sirnilar to the inner layer or the root sheath, this ncurothclium resembles the MICROSCOPIC ANATOMY OF SPINAL NERVE perineurium of the pel'iphcral nen'es. It is suggested ROOTS thal these t\\VO layers in facl form the perincuriulll when the nerve rooL is transformed to a peripheral There are two microscopically different rc.:::gions of nerve upon leaving the spinal. the ncnlC roots. Closest to the spinal cord is a cen- tral glial segment comprised of glial cells and there- THE MICROVASCULAR SYSTEM OF SPINAL fore resembles the microscopic organization of cen- NERVE ROOTS tral nervous structures at the spinal cord or the brain. This glial segment is transferred to a nonglial Information about the vascular anatomy of the segment in a \"dome-shaped\" junction a few mil- nerve roots has mainly been derived from studies limeters from the spinal cord. This nonglial segment on the vascularization of the spinal corel. Therefore. is organized in the same manner as the en- the nomenclature of the various vessels has been doneurium of the peripheral nerves, that is, with somewhat confusing. A SLlllllTIat·y of the existing Schwann cells instead of glia cells. However, some knowledge on nerve root vasculature will be pre- small islets of glia cells also are found in this other- senteel below, wise \"peripherally\" organized endoncurium. The segnlental arteries generally divide into three MEMBRANOUS COVERINGS OF SPINAL NERVE branches when approaching the intervertebral fora- ROOTS men: (1) an anterior branch that supplies the poste- rior abdominal wall and lumbar plexus. (2) a poste- The axons in the endoneurium are separated from rior branch that supplies the paraspinal muscles the cerebrospinal fluid by a thin layer of connective and facet joints, and (3) an intermediate branch that tissue called the root sheath, This root sheath is the supplies the contents of the spinal canal. A branch structural analogue to the pia mater that covers the of the intermediate branch joins the nCI\"ve root at spinal cord. There are usually 2 to 5 cellular layers the level of the dorsal root ganglion, There are usu- in the root sheath, but as many as 12 layers have ally three branches from this vessel: one La the ven- been identified, The cells of the proximal part of the tcal root, one to the dorsal root, and one to the vasa corona of the spinal corel.
The branches to the vasa corona of lhe spinal corel, called medullal)' arteries, arc inconsistcnt. 7 to 8 remain or the 128 from the cmbryologi- period of life, and each supplies more than one segment or the spinal core!. The main medullary in the thoracic region of the spine was dis- covered by Adamkiewicz in 1881 and still bears his name. The medullary arteries run parallel to the ~~-nt:rve roots (Fig. 5-6). In humans, there are no con- :7:. nections between these vessels and the vascular net M work of the nerve roOlS. Because the medullmy feeder artcrics only occasionally supply lhe nerve roots with blood, they have been referred to as the extrinsic vascular system of the cauda equina. The vasculature of thc nerve roots is formed by Schematic presentation of some anatomical features of t branches from the intermediate branch of the seg- intrinsic arteries of the spinal nerve roots. The arterioles mental arlclY distally and by branches from lhe within the cauda equina may be referred to either the e vasa corona of the spinal cord proximally. As op- trinsic (1) or the intrinsic (2) vascular system. From the su posed to the medullat)' arteries, this vascular net- perficial intrinsic arterioles are branches that continue al work has been named the intrinsic vascular system most at right angles down between the fascicles. These of the cauda equina. The dislal branch to the dorsal vessels often run in a spiraling course, thus forming vasc !I root first forms lhc ganglionic plexus within the dor- lar \"coils\" (3). When reaching a specific fascicle they sal root ganglion. The vessels run within the outcr branch in a T-like manner, with one branch running cra- layers of the root sheath, called cpi-pial tissuc. As nially and one caudally, forming interfascicular arterioles there are vesscls coming from both distal and prox- (2b). From these interfascicular arterioles are small imal directions, the ncr've roots are supplied by two branches that enter the fascicles, where they supply the separate vascular systems. The two syslems anasto- endoneurial capillary networks (2c). Arterioles of the ex- mose at approximalely two thirds of the nerve rool trinsic vascular system run outside the spinal dura (4) and lenglh from the spinal corel. This location demon- have no connections with the intrinsic system by local va strates i:\\ region of a less-developed vascular nClwork cular branches. The superiicial intrinsic arterioles (2a) are and has been suggested lo be a panicularly vulner- located within the root sheath (5). Reproduced with permi able site of lhe nerve rools. sion from Olmarker. K. (1991J. Spinal nerve rooe compression. Acuee compression of the cauda equina seudied in pigs. Acta The arterics of the intrinsic system send branches Qnhop Scand, 52. Supp1242. down to the decper parts of thc nerve tissue in a T- like manner. To compensate for elongation of the nerve roots, the m·teries are coiled both longitudi- nally and in thc steep running branches bClwccn the different fascicles (Fig. 5-6). Unlike peripheral nerves, the vcnules do not course togethcr with the Biomechanical Behavior of arteries in the nerve roots but instead usually have a spiraling course in the deeper pans of the nerve. Peripheral Nerves There is a barrier of the endoneurial capillaries in periphcral nerves called the blooel-nerve barrier, External trauma to the extremities and nerve e which is similar to the blood-brain barrier of lhe trapment may produce mechanical deformation central nervous system (Lundborg, 1975; Rydevik & the peripheral nerves that resulls in the deterior Lundborg. 1977). The presence of a corresponding tion of nerve Function. If the mechanical trauma e barrier in netlle roots has been queslioned. If pre- ceeds a certain degree, the nerves' buill-in mech sem, a blood-nerve barrier in nerve rOOlS does not nisms of prolcction may not be sufficient, resulli seem to be as well developed as in endoneuria I cap- in changes in nerve sLructure and function. Co illaries of peripheral nerve, which implies that . mon modes of nerve injlll)' are stretching and co edema may be formed more easily in nen.,'c roots pression. which may be. inflicted, respectively, lhan in peripheral nelves (Rydevik el aI., 1984). rapid eXlension and crushing.
STRETCHING (TENSILE) INJURIES OF ties, and the nerve behaves 1110re !ike a plastic m PERIPHERAL NERVES terial (I.e., its response to the release of loads is i complete recovery). Nerves arc strong structures with considerable ten- sile strength. The maximal load that call be SlIS- Although variations exist in the tensile streng tained b~/ the median and ulnar nerves is in the of various nerves, the maximal elongation at t rangc of 70 to 220 newtons (N) and 60 to 150 N, rc- elastic limit is approximately 20(~fi, and comple spectively. These f-igurcs afC of academic interest structural failure seen1S to occur at a maximu only because severe intraneural tissue damage is elongation of approximately 25 to 30(k;. These v produced b:v tension long before a nerve breaks. ues are for normal nerves; injury to a nell/e may duce changes in its mechanical properties, name A discussion of the elasticity and biomcchanical increased stiffness and decreased elasticit\\'. properties of nerves is complicated by the fact that nerves are not homogeneous isotropic I11aterials but, Stretching, or tensile, injuries of peripher instead, composite structures, \\vith each tissue com- nerves are usually' associated with severe acciden ponent having its O\\VI1 biomechanical properties. such as when high-energ.\\' tension is applied to t The connective tissues of the epineurium and per- brachial plexus in association with a birth~relat ineurium arc primarily longitudinal structures. injur.\\'. as a result of high-speed vehicular co!lisio or after a fall from a height. Such plexus injuri \\,Vhen tension is applied to a nen'e, initial elon- may result in partial or total functional loss of som gation of the nerve under a ver.v small load is fol- or all of the nerves in the upper extremity, and t lowed by! an interval in \\vhich stress and elongation consequent functional deficits represent a conside show a linear relationship characteristic of an elas- able disability in terms of sensory and motor lo tic material (Fig. 5-7). As the limit of the linear re~ The outcorne depends on which tissue componen gion is approached, the nerve fibers start to rupture of the nerves are damaged as well as on the exte inside the endoneurial tubes and inside the intact of the tissue injury'. Of clinical importance is the o perineurium. The perineurial sheaths rupture at ap- servation that there can be considerable structur proximately 25 to 30i?-c elongation (ultimate strain) damage (perineurial sheath injuries) induced above in vivo length (Rydevik et aI., 1990). Aftcr this stretching with no visible injury' on the surface point, there is a disintegration of the elastic proper- the nerve (Case Study 5-1). 12 11 10 9 8 In-situ strain: 11.0 :!:. 1.5% \"(L 7 In-situ stress: 0.05 :c: 0.3 MPa ~6 Ultimate stress: 11.7 :.:: 7 MPa ~ Ultimate strain: 38.5 :::: 2.0'% ~ 5 4 8 12 16 20 24 28 32 36 40 ~ iii 4 Strain ('%) 3 2 1 0 0 The stress-strain behavior of a rabbit tibial nerve. The nerve K\\·van, M.K., Myers, R.R., et al. (1990). An in. vitro mechanical an exhibits a low stiffness toe region of approximately 15 % histological study of acute stretching on rabbit tibial nerve. J Or- and begins to retain significant tension as the strain increases thop Res, 8, 694-707. beyond 20%. Reproduced with permission from Rydevik. 8.L.,
,-\"\" ----0 normal values during I-hour restitution. At 12 elongation, conduction was completely blocked by \" - -. B~ichial Plexus Palsy I hour and showed minimal recovery (Wall et a .\"ri.~.i-ipg the birth process, a newborn suffered a trac- 1992). Such data have clinical implication in ner rcpail~ limb trauma, and limb lengthening. ~fit9~. injury in his left brachial plexus. A few months '~t~~:·.h~'presents with the upper left arm in a static posi- A situation of even more gradual stretching, a '~i?r-.()fadduction, internal rotation of the shoulder, ex- i~h?i{)pof the elbow, pronation of the forearm, and flex- plied over a long time, is the growth or intraneu tumors such as schwannomas. In this situation, t i'9r'l9fthe wrist. He does not respond to sensory stimulus nerve fibers are forced into a circumferential Cou 'iri;~i~>shoulder and presents biceps and brachioradialis around the gradually expanding tumor. Function ~',-\"~fje.x.ia. A sudden deformation and high tensile stress in· changes in cases of sllch very gradual stretching a oftcn minimal or nonexistent. . . rr~~.in the (5-(6 nerve roots affected the mixed (motor :j'..''~'~.·'if'l,\"n\"d'··..s.en.sory) neural functions, mainly the muscles respon- ·\",-slbh~,'for the scapulohumeral rhythm (see Chapter 12). .1' ;:\\)'AHE.rb's palsy is diagnosed. The sudden elongation COMPRESSION INJURIES OF PERIPHERAL .-0'.> J7;r~uHer~~d during the traction can lead to structural dam- NERVES an9~;.~ge reduction in the transverse fascicular cross-sec- It hns long been known that compression of a ner can induce symploms stich as numbness, pain, a {ftio.f1~(area, producing impairment of the intraneural muscle weakness. Thc biological basis for the fun tional changes has been investigatcd eXlensiv .1,: :~\",,:vascu.lar flow and impulse transmission. (Rvdevik & Lundborg, 1977; Rydevik et aL, 1981), these investigations (Fig. 5-9), even mild compre 1~'., ·.In less severe cases, functional restoration may occur sion was observed lo induce structural and fun lion'll changes, and the significance of mechanic t.- within·weeks or months. In more severe cases, healing may \"i·i:~~X~k(place during the first 2 to 3 years, but if the structural :~r~erveJnjury is severe, considerable long-term functional :s<'disability can result, If structural derangement of the nerve :i·::i.trunk has taken place, nerve grafting may be required. ):i:' , \" High-energy plexus injuries represent an extreme Elongation type of stretching lesion caused by sudden violent J trauma. A differcm stretching situation of considerable Schematic representation of a peripheral nerve and its clinical interest is the sutllling of the two ends of a CuL blood supply at three stages during stretching. Stage I: T nerve under moderate tension. This situation occurs segmental blood vessels (S) are normally coiled to allow when a substantial gap exists in the continuity of a for the physiological movements of the nerve. Stage II: U nerve trunk and the restoration of the continuity re- der gradually increasing elongation, these regional vess quires the application of tension to bring the neryc ends become stretched and the blood flow in them is impaire back togethel: The moderate, gradual tension applied Stage III: The cross-sectional area of the nerve (represen to the nerve in these cases may stretch and angulate lo- within the circle) is reduced during stretching and the in cal feeding vessels. It ma.y also be sufficient to reduce traneural blood flow is further impaired, Complete cessa the transverse fascicular cross-seclional area and im- tion of all blood flow in the nerve usually occurs at ap- pair the intraneural nutritive capillary flow (Fig. 5-8). proximately 15% elongation. Adapted from Lundborg. G. Rydevik. 8. (1973). ENeas 0; strecching the tibial nerve of the As the sutured nelve is stretched, the perineurium rabbit: A preliminary study 0; (he intraneural circulation and l'ightens; as a result, the endoneurial fluid pressure is barrier (uncrion of the perineurium. J Bone Joint Surg, 558. 3 increased and the intrafascicular capillaries may' be obliterated. Also, the flow is impaired in lhe scgmcn· lal, feeding, and draining vessels, as it is in larger vessels in the epineudulll, and at a certain stage lhe intraneural microcirculation ceases. Intravital obser- vations of intraneural blood now in rabbit tibial nel'ves (Lundborg & Rydevik, 1973) showed that an elongation of 80M induced impaired venular no\\\\' and that even greater tension produced continuous im- pairment of capillary and arteriolar now until. at 15% elongation, all intraneural microcirculation ceased completely. For the same nerve, an elongation (strain) of 60/0 induced a reduction of nerve action po- tential amplitude by 709'0 at I hour with recover)' to
Recording sure levels (approximately 30 to 80 mm Hg) may in ducc intrancural edema. \\vhich in turn may becom electrodes organized into a fibrotic scar in the ncn'e (Ryclevi & Lundborg, 1977), and amplifier Compression at approxirnately 30 111m Hg als r1./,...,/ brings about changes in the axonal transport sys tems, and long-standing compression may thus lea Stimulating Compression to depletion of axonally transported proteins dista electrodes chamber to the compression site. Such blockage of axona I transport induced by local compression (pinching may cause the axons to be marc susceptible to ad Compressed ditional compression distally. the so-called double ajr inlets crush syndrome. Schematic drawing of an experimental setup for studying Slightly higher pressure (80 mm Hg, for example deterioration of nerve function during compression. causes complete cessation of intraneural blood flow the nerve in the locally compressed segment be Adapted from Dahlin, L.B.• Rydevik, 8.• & Lundborg. G. (1986). comes completely ischemic. Yel, even after 2 hour The pathophysiology of nerve entrapments and nerve compres' sian injuries. In A.R. Hargens (Ed.). Effeers of Mechanical Stress or more or compression, blood flo\\\\' is rapidly· re on Tissue Viability. New York: Springer- Verlag. stored whcn the pressure is released (Rydevik ct aI factors such as pressure level and mode of com- 1981), hen higher levels of pressure (200 to 40 pression became apparent. mm Hg, for example) applied directly to a nen'c ca induce structural nerve fiber damage and rapid de Critical Pressure Levels terioration of nerve function, with incomplete rc covel)· after even shortel· periods of compression Experimental and clinical observations have re· Hence, the magnitude of the applied pressure an vealed some data on the critical pressure levels at the severity of the induced compression lesion ap which disturbances occur in intraneural blood flow, pear to be correlated. axonal transport, and nerve function. Certain pres- sure levels seem to be well defined with respect to Mode of Pressure Application structural and functional changes induced in the nerve, The duration of the compression also influ- The pressure level is not the only faclOr that influ ences the development of these changes, ences the severity of nerve injlll)' brought about b compression, Experimental and clinical evidenc At 30 mm Hg of local compression, functional indicates that the mode of pressure application changes may occur in the nerve, and its viability also of major signiflcance. \"Its importance is illu may be jeopardized during prolonged compression trated by the fact that direct compression of a nerv (4 to 6 hours) at this pressure level (Lundborg et aI., at 400 mm Hg by means of a small inflatable cu 1982), Such changes appear to be caused by im- around the nCI've induces a more severe nerve injur pairment of the blood flow in the compressed part than does indirect compression of the nerve at 100 of the nerve (Rydevik et aI., 1981), Corresponding mrn Hg via a tourniquet applied around the extrem pressure levels (approximately 32 111111 Hg) were ity. Even though the hydrostatic pressure acting o recorded close to the median nen.re in the carpal the nerve in the former situation is less than ha tunnel in patients with carpal tunnel syndrome, that in the latter, the nerve lesion is more sever while in a group of control subjects the pressure in probably because direct compression causes a mor the carpal tunnel averaged onl~,.. 2 mm Hg. Long- pronounced deformation of the nerve (especially a standing or intermittent compression at lo\\\\' pres- its edges) than does indirect compression, in whic the tissue layers between the compression devic and the nerve \"bolster\" the nerve, One nlay also con clude that the nerve injllly caused by compression not directly related to the high hycfrostatic pl'essu in the center of the conipressed nerve segment bu instead is more dependent on the specific mechan cal deformation induced by the applied pressure,
Mechanical Aspects of Nerve Compression ing bone_ h may also occur when a spinal nerve Electron microscopic analysis of the deformation of compressed by a herniated elisc (Case Study 5·2). the nerve fibers in the peroneal nerve or the baboon The details of the deformation or a nerve may hind .limb induced b~,' tourniquet compression demonstrated the so-called edge effect; that is. a quite difTerent in these two cases of loading. In un form circumferential compression like that appli specific lesion was induced in the nerve fibers at both edges of the compressed nerve segment: the nodes of Ranvicr were displaced toward the non- ;!: I compressed parts of the nct·ve. The nerve fibers in Sciatic Pain the center of the compressed segment, where the A35-year-old male construction worker has chronic low back pain radiating below the- Ie-f! knee that is hydrostatic pressllt·c is highest. generally were nOl affected acutely. Tht.: large-diameter nerve fibers more severe with lifting activities and prolonged posi, were usually affected, but the thinner fibers were tions. After a careful examination. certain neurological spared. This finding confirms theoretical calcula- signs were found. Positive straight leg raising and L5 tions that indicate larger nerve fibers undergo a rd- motor and sensory functions were affected. atively greater deformation than do thinner fibers at A MRI shows a herniated disc at level L4-L5 with a given pressure. It is also known clinically that a posterolateral protrusion. which laterally compresses (he compression lesion of a nCI-vc IIrst affects the large left L5 nerve root. Compression of !he nerve deforms it fibers (e.g., those that can)' molOr function). while toward a more elliptical shape. increasing strain and the thin fibers (e.g.. those that mediate pain sensa- stress loads_ The effects of the pressure and mechanical lion) arc often preserved. The intraneural blood ves- deformation resultant from the load affects the nerve sels have also been shown to be injured at the cdges tissue, its nutrition, and the transmission function. in· of the compressed segment (Rydevik & Lundborg, flammation of the nerve root, induced by the nucleus 1977), Basically, the lesions of nerve libers and pu!posus, may sensitize the nerve rOOt so that mechani- blood vessels seem to be consequences of the pres- cal ne-rve root deformation causes SCiatic pain (Case sllre gradient. which is maximal just al the edges of Study Fig 5·2·1), the compressed segment. In considering the mechanical effects on nCI-ve compression, keep in mind that the effect of a given pressure depends on the way in which it is applied, ils magnitude and duration. Although pressure may be applied with a variety of spatial distributions. two basic types of pressure applications arc gener- ally encountered in experimental settings and in pathological conditions. One type is uniform pres- sure applied around the entire circumference of a longitudinal segment or a nerve or exu'emity. This is Ihe kind of purely radial pressure thai is applied by the common pneumatic tourniquet. It has also been used in miniature apparatlls to produce con- trolled compression of individual nerves (Rydevik & Lundborg, 1977) (Fig, 5-9). Clinically, Ihis Iype of loading on a nerve probably occurs when the pres- sure on the rnedian nenre is elevated in the carpal tunnel. producing a characteristic syndrome. orAnother type mechanical action takes place when the nerve is compressed laterally_ This is the kind of defol-mation that occurs if a nelve or ex- tremity is placed between two parallel nat rigid surR faces that arc then moved toward each othel~ squeezing the nerve or extremity. This type of defor- mation occurs if a sudden blow by a rigid object _.' Case Study Figure S-2·1. squeczes a nervc against the surface of an undcrly~ .:.-- ~I
y factor at both high and low pressures, but ischemia pl[t~·s a dominant role in longer-dunHion compres- i sion. This phenomcnon is illustraled b\\' the fact that direct ncr'vc compression at 30 111111 Fig for ) to 4 , hours produces reversible changes, whereas pro· longed compression a(}()\\'c this time period at this ,'.' . .-: I pressure level ma~' cause irreversible damage [0 the nCI\"e (Lundborg CI aI., 1982; Rydevik el aI., 1981), ,-,' .... --I------1I-- X Corn pression at 400 I11Ill Hg causes a much more se- vere nervc injur~1 arter 2 hours than after 15 min- ,-\",\";.:,, \".. ,\"/': Pressure I -ules. Such information indicalcs that Cn:n hiuh '•/,I:,'\". ::' ,\" '.:\"'f';;-,'i;:\":;\": dislribution ..--, ---c___ pressure has to \"acl\" for a certain period of lime for A B' C' E' injur.v to occur. These data also give some informa- F' lion about the viscoelastic (time-dependent) proper- ,. E G' x ties of\" peripheral nCI\"\\'t: tissue. Sufficient time OJ! f!51 F elapse for permanent deformation to develop. ---- G Biol17echal1ical Behavior (Jf ...\"\" ' .. \" :',:' I Spinal Nerve Roots ,, i,' . . '\",.,. The nerve roots in the thee;:d sac lack epinei\"fl-tl:lw and perin~uril1m, but under tensile loading they ex- B hibit both elasticity and tensile strength. The ulti- l11,tle load rnr ventral spinal nelye roots from the \"iG, 5-11 thecal sac is belween 2 and 22 ! , and 1'01' dorsal nerve roots from the thecal sac the load is between A, Theoretical displacement field under lateral compres- 5 and 33 N. The length of the nerve roots I'rorn the sion as a result of uniform clamping pressure. B, The origi, spinal corel to the foramina \\'aries From appro:d- nal and deformed cross-sections are shown for maximum I11ntely 60 mm at the L I level to approxilmllely 170 elongation in the x direction of 10. 30, and 50%. The vec- mm at the S I level. The mechanical propertics of human spinal nerve roots arc c1ifferelll for an~1 given tors shown from A to fJ:, B to a', and so forth, indicate the nerve roOl at its location in the cenlral spinal canal ancl in the lateral intel'vertebral foramina. The ulti- paths followed by the particular points A, B, and so forth nwtc load for the inrr4lthecal portion of human SI during the deformation. nel'VC rOOIS at the S I level is appro:\"\\imatcl~; 13 N, and thal 1'01' the roraminal portion is approximately I• 73 N. For human nCI'vc roots at the L5 level. the cor- responding values arc 16 Nand 71 N, respectively orthat this kind deformation can trigger r-iring of (Fig. 5-12). Thus, the \"allles ror ultimate load are approxil11«lel~\" five times higher ror the foraminal nerves, resulting in a sensation or pain when the segment of the spinal ner'vc roots than for the in- trathecal pan ion of the same nClVC roots under ten- ne\"'e Gbers are laterallv compressed. The details or sile loading. However, the cross-sectional area of the such deformation of nerves and their functional con- nerve root in the intervertebral fOI'(llllcn is sie:nifi- sequences have not been studied extensively and re- quire further research for their elucidation. -cantlv larger than that of the same nerve root in lhe . Duration of Pressure Versus Pressure Level thecal sac; thus, the ultimate tensile stress was more Knowledge is limited regarding the relalive impor- comparable for the two locations. The ultimate tance o[ pressure and time, rcspectively, in the pro- duction of nerve compression lesions. Mechanical -strain LInder tensile loading is 13 La 19% for the faclors seenl to be rehllively more imporlant al higher than at lo\\ver pressures. Time is a significant human ne,Ye root at the L5-S I level (Fig. 5-13), The nerve roots in the spine arc nol static slruc- lures: they 1110\\'C relati\\'e to the surrounding tissues
Ultimate load: Human sinal nerve roots roots normally' adhere lo the surrounding tiss above and below the intervertebral disc they u n:rsc, compression may give rise to intraneural 2'\" sion, Spencer and associates (1984) measured r'n\" S contact force between a simulated disc herniat and a dclcwmed nerve 1'001 in cadavers. Taking § area of contact into aeCOUlll, they assumed a con pressure of approximately 400 mm Hg. \\<\\'ith 5 duced disc height. the contact force and pressure tween the experimental disc herniation and o' - - _ - ' - _ - ' ; : - = - - - - ' - ' - _ - ' - _ - ' ; - ; : \" ' - _ - ' - _ . . J nerve root was reduced, They suggested that th findings may explain in pan why sciatic pain is Sl LS lieved after chcmol1ucleolysis, and as disc degene tion progresses over time and the disc height ther N\"4 N~4 decreases, Diagram illustrating values for ultimate load obtained for [n central spinal stenosis, the mechanics or ne human spinal nerve roots under tensile loading. INR, in- root compression arc completely diFferent. Un trathecal nerve roots; FNR, foraminal nerve root. Note the these conditions, the pressure is applied circum marked difference in ultimate load for the intrathecal and cntially around the nerve roots in the cauda cqu the foraminal portions of the nerve roots. Error bars indi- at a slow, gradual rate, These different deformat factors, together with the fact that the nerve ro cate standard deviation. Reproduced with permission from centrally within the cauda equina differ comple Weinstein, IN., Latviotte, R.. Rydevik, B., er al. (1989), Nerve. In from the nerve roots located more laterally, clos the discs, ma.y explain some of the dillcrcnt syrm J, \\IV, Frymoyer & S.L. Gordon (Eds.). NevI Perspectives on Low toms found in spinal stenosis and disc herniatio Back Pain (Chapter 4, pp. 35-130). Park Ridge. IL: MOS. {Based Ultimate strain: Human spinal nerve roots on a workshop arranged by the National Institutes of Hea/rh (NIH) in Airlie, Virginia, USA, May 1988.} with every spinal motion. To allow for such motion _ 1S the nerve roots in the intervertebral foramina, for example. must have the capacity to glide. Chronic l ilTitation with subsequent fibrosis around the nerve roots. in association with conditions such as disc c herniation and/or Foraminal stenosis. can thus im- pair the gliding capacity of the nel\"VC roots. This .~ produces repeated \"microstretching\" injuries of the nerve roots even during normal spinal 1110Vcments, en 10 which might be speculated to induce yet FUrl her tis- sue iITitation in the nerve root components, The r\"n normal range of movements of nerve root.s in the human lumbar spine has been measured in cadaver § experiments. It was found that straight leg raising moved the nerve roots at the level of the interverte- 5 bral foramina approximately 2 to 5 mm. S Certain biomechanical Factors are obviollsly in- volved in the pathogenesis of val'ious symptoms in- o' - - - - ' - - - ' ; : - J ' - - - - - ' ' - - - - ' - - - - - - - ' , - : - ' - - - ' - - duced by nen'e root deformation in association with disc herniation and spinal stenosis and resulting in S1 LS radiating pain. In disc herniation, only one nerve root is usually compressed, Because individual nerve N.=4 N=4 Ultimate strain for human spinal nerve roots under ten loading. INR, intrathecal nerve root; FNR, foraminal ne root. Reproduced with permission from Weinstein, IN., L,1M otte, R\" Rydevik, 8., er at. (1989). Nerve. In I \\tV Fryrnoyer & Gordon (Eds.). New Perspectives on Low Bc1Ck Pain (Chapter pp. 35-130). Park RieJge, Ii: MOS. IBased on cl workshop arranged by the NatioTlallnstitut.es of Health (NIH) in Air/ie, ginia, USA, May /988.J
COMPRESSION OF SPINAL has been moderate interest in the past to Schematic drawing of an experimental model. The cau nerve root compression in experimental mod- equina (A) is compressed by an inflatable balloon (8) t Early sludies in the 1950s and 1970s found that is fixed to the spine by two l-shaped pins (C) and a ple roots seemed to be more susceptible La COI11- glass plate (0). Reproduced with permission from O/marke -';l;'pl'essie,n than did peripheral nerves. During recent Rydevik. 8., & Holm. S. (1989a). Edema (ormation in spina/ howevcl~ the interest in nerve rool patho- nerve roars inducecl by experimental. graded compression. ;ggph,ysiology has increased considerably and a oum- of studies have been performed thal arc rc- experimental srudy on the pig cauda eq'Jina ~'.Jirh special re ence co differences in effects between rapid and slow onsec .vic,\\Vc:ct below. Some years ago. a model was presented to eval- 1compression. Spine. ld. 579. the effects of compression of the cauda >------- in pigs, \\\\!hich for the first time allowed Howevcc with this protocol a full restoration or experimental, graded compression or cauda blood flow did not occur until thc compression lowcred from 5 to 0 mill Hg. This observation nCl\"Ve rOOlS at known pressure levels (01- ther supports the previous hypothesis that vasc marker. 1991) (Fig. 5-14). In this Illodel, ,he calida impairment is present even at low pressure leve equina was compressed by an inflatable balloon that was fixed to the spine. The cauda cquina A cornpression-induced impairmenl of the \"could also be observed through the translucent culature may thus be one mechanism for nerve balloon. This mndel made it possible to stud~' the dysfunction because the nutrition of the nerve flow in the intrinsic nerve roOl blood vessels at will be affected. However, the nerve rools will various pressure levels (Olmarkcr el aI., 1989a). derive a considerable nutritional supply via d The experiment was designed in a way that the sion from the cerebrospinal nuicl. To assess pressure in the compression balloon \\Vas in- compression-induced eFfects on the tolal conlr creased by 5 mm Hg evcry 20 seconds. Blood flow tion to the nerve rools. an experiment was desig and vessel diameters of the intrinsic vessels could in which jH-labelcd melhyl-glucose was allowe simultaneously be obsClycd through the balloon be transported to the nen/c tissue in the c using a vilal microscope. The average occlusion pressed segment via both the blood vessels and pressure for the arterioles was !\"ound to be slightly below and directly related to the systolic blood cerebrospinal fluid diffusion aflcI- systemic in pressure. and the blood Ilow in the capillary net- works was intimately depcndent on the blood flow tion. The results showed that no compensa of the adjacent venulcs. This corroborates the as- sumption that venular stasis may induce capillary stasis and thus changes in the microcirculation of the nerve tissue and is in accordance with previ- ous studies in which such a mechanism has been suggested as involved in carpal tunnel syndrome. The mean occlusion pressures for the venules demonstrated large val\"iations. However, a pres- sure of 5 to 10 mOl Hg was found to be sufficient for inducing venular occlusion. Because of retro- grade stasis, it is not unlikely to assume that the capillary blood flow will bc affected as well in slIch situations. In the same experimental SCt-lIp. the effects of gradual decompression, after initial acute compres- sion was maintained for only a short while. were studied. The average pressure for starting the blood lIow was slightly lower at decompression than at comprcssion For artcrioles. capillaries. and vcnulcs. _ . . . .'--->-->---
mechanism from cerebrospinal fluid diffusion ONSET RATE OF COMPRESSION could be expeclr:d at the low pressure levels. On the One faclor that has not been fully recognized COil Lntl)·, to 111m Hg compression was sufficient to compr-ession trauma of nerve tissue is the onset r of the compression. The onset rate, that is. the ti induce a 20 to 300/0 reduction of the transport or from start to full compression. may vnry clinica rrom fractions of seconds in lraUI11atic condition mClhyl·glucosc to the nerve r001S, as compared months or years in association with degenerat with the control. processes. Even in the clinically' rapid-onset ra there ma:v be a wide variation or onset rales. \\V \\·Ve know 1\"1'0111 experimental studies on peri ph- the presented model. it was possible to vary the end nen!cs that compression Illay also induce an set time of the applied compression, Two onset ra increase in the vascular permeability, leading to an have been investigated, Either the pressure is p intraneural edema formation. Such edema may' in- sent and compression is started by flipping crease the cndoncuriul Fluid pressure, which in switch of the compressed-air system used to inl turn may impair the endoneurial capillary blood the balloon or the compression pressure leve flow and jeopardize the nutrition of the ner'vc slowl~1 increased during 20 seconds. The first on rOOls. Because the edema Llsually persists for some rate was measured at 0.05 to 0.1 seconds. thus p lime after the rClllo\\'al of a compressive agenl. viding a rapid inflation of the balloon and a ra edema may negativel~r affect the nerve root for n compression onset. longer period than the compression itself. The presence of intraneural edema is also related to the Such a rapid-onset rate has been found to ind subsequent formation of intraneural fibrosis and more pronounced effects on eden1a formati may therefore contribute to the slow recaVCI)\" seen mcth~ll-glucose transport. and impulse propagat in some patients with nellie compression disor- lhan the slow-onser rale (Olmarker, 199 I). Rega ders. To assess if' intraneural edema also may form ing methyl-glucose transport, the results show t in nerve roots as the result of cornprcssion, the dis- the levels within the compression zone arc m tribution of Evan's blue-labeled albumin in the pronounced at the rapid than at the slow onSd r nerve tissue \\vas analyzed after compression at var- at corresponding pressure levels. There was als ious pressures and at various durations (Olmarker striking difference between the two onset ra el aI., 1989b). The study showed thal edema was when considering the segments ourside the co formed even at low pressure levels. The predomi· pression zones. 1n the slow-onset series, the le nant location was at the edges of the compression approached baseline values closer to the compr zone. sion zone than in the rapid-onsel series. This m indicate the presence of a more pronounced ed The function of the nelYC roots has been studied zone edema in the rapid-onset sel\"ics, with a sub by direct electrical stimulation and recordings ei- quent reduction of the nutritional transport in ther on the nenie itself or in the corresponding nerve tissue adjacent to the compression zone. muscular segments. During a 2- hour compression period, a critical pressure level for inducing a re- For the rapid-onset compression, which is lik duction uf MAP-amplitude seems to be located be- lo be more closely related to spine trauma or d tween 50 and 75 111m Hg. Higher pressure levels herniation than to spinal stenosis, a pressure of (100-200 mm Hg) may induce a tOlal conduction mill Hg maintained for only 1 second is surflcien block \\vith var.ying degrees of recovery after com- induce a gradual impairment of nc,'ve conduct pression release. To stud)! the effect's of compres- during the 2 hours studied aftcr the cornpress sion on sensory nerve fibers, electrodes in the was ended. Overall, the mechanisms for these p sacrum were used to record a compound nerve ac- nounced differences between the different on tion potential after stimulating the senso(v nerves rates arc not clear but may be related to dilTeren in the lail, that is, distal to the compression zone. in the displacement rates of the compressed ne The resuhs showed thaI the sensory fibers are tissue toward the uncompressed parts, as a resul slightly more susceptible to compression than are the viscoelastic propcnics of the nellie tissue, S the motor fibers. Also, the nerve roots are more phenomena may ICfld nOl only ro structural dam susceptible to compression injury if the blood to the nerve fibers but also to stn.lcturfll change pressure is lowered pharmacologically. This fur- the blood vcssels with subsequcnt edema formati ther indicates the importance of the blood supply to maintain the functional properties of the nerve roots.
orThe gradual formation intraneural edema may segment itself is ullcomprcssed. Regarding n conduction, the effects were much enhanced i also be closely\" related to observations of a graduall.\\' distance between the compression balloons wa increasing dilTcrcncc in nerve conduction impair- creased frorn one \\'cn~bral segment La two v ment between the two onset rates (Olmar-ker et al.. bral segments (Olmarker & Rydevik. 1992). Thi 1989b). dicates that the functional impairment may directl:v related to the distance between the MULTIPLE LEVELS OF SPINAL NERVE ROOT compression sites. COMPRESSION !'atients with double or multiple levcls of spinal CHRONIC NERVE ROOT COMPRESSION IN stenosis seem to have morc pronounced symptoms EXPERIMENTAL MODELS than do patients with stenosis only at one level. The presented model was modified to address this inter- Th~ discLlssion of compression-induced effect esting clinical question. Using two balloons at two nerve roots has deall primarily wiLh acute c adjacent disc levels. which resulted in a 10-mm un- pression, that is, compression that lasts for s compressed nerve segment bctwcen the balloons, hours and with no survival of [he animal. To be induced a much more pronounced impairment of mimic various clinical situations, compres nerve impulse conduction than previollsl~' had been must be applied over longer periods of time. T round at corresponding pressure levels (Olmarker & arc probably man.\" changes in the nerve Li Rydevik. 1992). For instancc. a pressurc of 10 mm such as adaptation ofaxons and vasculature, I-1g in two balloons induced a 60% reduction of will occur in patients but cannot be studied in nerve impulse amplitude during 2 hours of COIll- perimental models using only I to 6 hours of c pression, whereas 50 111m I-Ig in one balloon showed pression, Another important factor in this con no reduction. is the onset rale that was discllssed previousl) The mechanism ror the diFrerence between single clinical syndromes with nerve root compress and double compression may not simply be based lhe onset time may in many cases be quite s on the fact thal the nerve impulses have lo pass For instance, a gradual remodeling of the v more than one compression zone at double-level brae to induce a spinal stenosis probably lead .' . compression. There may also be a mechanism an onset lime of many years. Jt will of cours based on the local vascular anatomy of the nerve dirficult to mimic such a situation in an exp roots. Unlike for peripheral nerves, there are no re· mental modcl. It will also be impossible to gional nutritive arteries from the surrounding control over the pressure acting on the nerve r structures to the intraneural vascular system in in chronic models because or the remodeling spinal nerve roots. Compression at two levels might adaptation or the nerve tissue to the applied p therefore induce a nutritionally impaired region be- sure. However, knowledge of the exact pressur twcen the two compression sites. In this way. the probably of less importance in chronic tha :.~: segment nffected by the compression would be acute compression situations. Instead, chr \"', widened from one b,~lIoon diarneter (10 mm) to two models should induce a conLrolled compres balloon diameters including the inLCrjacent nerve with a slow onset time that is easily reproduc segment (30 mm). This hypothesis was partly con- Such models may be well suited for studies firmed in an experiment on continuous analyses of pathophysiological events as well as inlcrven the total blood flow in the ul1compresscd nerve scg· b~' surgery or drugs. Some attempts have b ment located between two compression balloons made to induce such compression. (Takahashi et al.. 1993). The results showed that a Dclamarlcr and collaborators (1990) present 64% reduction of total blood now in the uncoll1- model on dog cauda equina in which they appli pressed segment was induced when both balloons constricting plastic band. The band was tighte were inflated to 10 mm Hg. At a pressure close to nrollnd the thecal sac to induce a 25, 50, or 750/ the systemic blood pressure lhere was complete is- duction of the cross-sectional area. The band chemia in the nerve segment. Thus, experimental left in place for various limes. Analyses were evidence shows that the blood supply to the nerve ~forl1led and showed both stnlctural.and functi segment located between two compression sites in changes that were proportional to the degree of ••1. nerve roots is severely impaired although this Tlel'VC striction.
Experimental study to analyze the effects on nerve conduc· from Cornefjord, 1'11., 5ato, K., O/marker, K., et 011. (1997), tion velocity of nucleus pulposus (1), the combination of morJe! for chronic nerve root compression studies. Present nucleus pulposus and compression (2), and compression only (3). The nucleus pulposus and the constrictor were ap- of a porcine mode! (or controlled slow-onset compression plied to the first sacral nerve root in pigs. The contralateral nerve root served as a control. Reproduced with permission analyses of anatomic aspects, compression onser rate, and phologic and neurophysiologic effects. Spine, 22. 946-957 To induce a s!c)\\ver onset and more controlled in the nen'(' root and the dorsal root ganglio compression, Cornefjord and collaborators (1997) lowing such compression also has been fo used a constrictor to compress the nerve roots in Substance P is a neurotransmitter that is re the pig (Fig. 5-15). The constrictor was initially! in- to pain transmission. The study may thus pr tended for inducing vascular occlusion in experi- experimental evidence that compression of mental ischemic conditions in dogs. The constric- roots produces pain. tor consists of an outer metal' shell that on the inside is covered with a material called amaroid The constrictor model has also been use that expands when in contact with fluids. Because stud.\\' blood flow changes in the nerve root v of the metal shell, the amaroid expands inwards lature. It could then be observed that the b with a maximum expansion after 2 weeks, result- Flow is not reduced just outside the compre ing in compression of a nerve root placed in the zone but significantly reduced in parts o central opening of the constrictor. Compression of nerve roots located inside the constrictor. In the first sacral nerve root in the pig resulted in a context, note that in case of disc herniation significant reduction of nerve conduction velocity nerve root may become sensitized by substa and axonal injuries using a constrictor with a de- from the disc tissue (nucleus pulposus) so fined original diameter. An increase in substance P mechanical root deformation can induce nounced sciatic pain.
',:\",f;1>Thc peripheral nerves arc composed of nerve Myc:rs. R.R .. ~Itlrabmi, H., .& \"(}WI:I!. H.C. (1986), Red }t;,,:rs, layers or connective tissue, and blood vessels. uel\"\\'l' hlood flow in l.'delllatous nCllropathics-A bi ;~{2 The nCIYC f'ibers arc extremely susceptible 10 chanica I lIle(,:h.lOism . .11;LTol'tlscu!al' Ues. 32. 145-151 ruuma but because they arc surrounded by slicces- Myi.'rs, R.R\" 8.: Powell, H.e. (1981). Endoncuri,d fluid sive layers of connective tissue (the epineuriulll and 1?~rinc·urillm)J they arc 111cchanically protected. sure in peripheral neuropathies. In A.R. Hargens Ti..;SIIC flilid PreSSl/re tlml C01lllJOsithm (p. 193). Balti ;:.'$§';}Strctching induces changes in intraneural Willi.II11S &. Wilkins. Olillarkl\"', K., Rydc\\·ik. B., &: Holm. S. (1989a). Edema r( bl~~d noll' m~d nerve Iiber S[;'llctllre before the lion in spin£llnl'l'\\'l' roots induced by experimelltal. g compression, An experirnenud Sllld~' on lhe: pig c trunk ruptures. equina with special reference 10 dilTerences in effec 1\\\\,(.'(.'11 rapid ..Iud slow onset of compression. Spiw:, I..J Comrression of a nerve can cause ItlJury to nerve fibers and blood vessels in the nerve, Olmarkcr. K., Rydc\\'ik. B.. Holm. S .. 1..'1 ill. (l9&9b). EffcC 'mail,lv at the edges of the compressed nerve seg- CXpl'l'illlental graded compression on blood flow in s V>:ment. but also by ischemic mechanisms. nl,.·l'vc roms. r\\ vilal microscopic study 011 Ihe po caudn equinll. J Orthop Res, 7,8Ii. 5- Pressure level, duration of compression. and mode of preSSllre application arc signillcant vari- Olmarkcl'. K. {1991l. Spinal nerve rOOl compression. ables in the development of nen'c injury, compression of dle cauda equina studied in pigs . ..IeU f/mp Scallll, 62. Suppl 2·n. j\".\"'j Ollllarker. K. 6.: Rydc\\·ik. B. (1992). Single: \\'('rstls doubk· 6.. Spinal nerve roots arc anatomically different COllllll·l,.·ssion. '\\n experimental slud.... un till..' porcine c from peripheral nerves and therefore react differ- l'qUill,1 with 'lll.t1ySl'S of nen·c impulse condu<:lion pr ently to mechanical defonnalion, lies. Cfill On/lOp. 279, 3539. T: Spinal nerve roots arc morc susceptible than Olmarker. K. & Hasuc, :\\1. (1995). Classificalion and p peripheral ncrves to mechanical dcformation, orphysiology of spinal pain syndromes. III J.1'$. \\\\\\:inSl mainly because of the lack of protective connective tissue layers in nerve roots. B. Rydl'\\'ik (Eds.), Essc/llial... Ihe Spillt'. RJ\\'l'n REFERENCES !\\l,.·w York. NY. R~·(!l'\\'ik. B.L., Kw~n, \\I.K., ;-\"'Iyel's, R.R .. l'l al. (1990). CorndjonJ. lVi., Saw. K.. Olmarkcr. K.. ci :d. (1997). A nHldcl ror chronic n('IT\":\" roOI compression studies. PrCSi..'IlI~llion vitro mechanical and histological study of <ll..:lHe stret of a porcine model for contrnllt·d slow-onset comprl'ssion on r;,hbit tibial nerve . .I Onhop Ucs. B, 694-701. \\\\\"ith an.tlyscs of anatomic ::lSPCCIS. comprl,.·ssion onSel r~lle, and morphologic and neurophysiologic crfeels. Ryd(·\\·ik. B. & Lundborg. G. (1977). Pl:rIllt.'ahilily of SpilIC, 22. 946-957, ncur:ll micl'U\\'l'ssels :lnd perineurium following : gradl,.·d cxpl'l'illlenlal ncrn: cOlllprcs~ion. SC(/Iu} J Na:> [hillin. L.B .. Ry(kvik, B.. &: Lundborg. G. (1986). Thc p.IIIHI' COI1Slr Sl/\".~. II. 179. orphysiology of nelTe eHtrapmellis and nervi..' cOlllpr\":\"ssion Rydc\\'ik, B., Lundborg. G., &. Bagge, U. (1981). Eff(,., gra<k·d compr('ssion nn inlr,1I1cural blood flow. An in injuries. In A.R. Hargens (Ed.). E!l;'cIS .\\kclwllic:al sllld.... 011 rabbil tihi.tl ner\\'e. J flawl Sure;. 6. 3. Stress 011 Tisslle Viability. New York: Springer-Verlag. Ryd\":\"\\'ik, B.. Bro\\\\'ll, :\\I.D .. &: Lundborg, G. (1 Delamartcr, R.B\" Bohlman. I-U-I., Dodge, L.D\" el a!. (1990). P<llhoanatolll~' and pathoph ....siolog.\\· of nel'\\'e root Experimental lumbar spinal SlCllosis. Analysis of the cor- pression. Sp;Ilt.'. 9. 7. tic~d evoked potentials, microvasculature and histop<1thCII· Ryd(.·\\'ik. B.L.. Kw<tn, M.K .. Myers R.R., et :11. (1990). ogy. J BOIlt: JOillf SI/r:.:, 72:\\. 110-120. Lundbor!!, G., &: Rvdcvik, B. (1973), Effecls of strctchin!! Ihe vitro mechanical :\\n(\\ histological study of ,H:llle strel on r.. hbil tibi:ll nen·l'. J Orrhop U,·.... 8. 694. libial ~\\cl\"\\\"e of lill,.· rabbic: :\\ prdimin.ary slUdy of tilt: i;llra- Spencer. D.L.. ~'lillcr. J.I\\., .& BCriolini. J.E. (198·.J). Th fects of intervertebral disc space narrO\\\\\"ing nil the co neural cin:ul~lliol1 and Ihe b.uTicr funclion of Ihe per· inelll'iul11. J BOllI: JOill1 SlIrg, 558, 390. force bl·twcen the Ill'rn' rOOt and a simlll:llcd disc p Lundborg. G. (1975). Structure :\\Jld flllll:tioll of the inlra· sion. Spille 9, 422. ncural micrO\\'essl,:ls as related lO Iraum:l. edcma formation SUl1ckrbnd. S. (1978). Nen'c.>: alld Nave III;tlri(~s (2nd and nerve fUllclion.) !JOIII.' )oim Surg. 57..1. 938. Edinburgh: Churchill Livingslone. Lundborg, G., e{ .11, (1982). Median nel'\\'e compression ill the Takah;lshi, K.. Olm:-.rkc.·r. K., Holm, S .. cl £II. (1993). Do C,I1'p,ll tunnel: The fUllclion:l1 respons(.· 10 cxpcrillH.'nlally induced controlll·d pressure . .f f-/mu} SlIrg, 7, 152. I('vel cauda ('quina cqmprcssion. An experimenlal Myers, R.R. (1998). :\\Iorphology or the peripheral nervous wilh conlinuous monitoring of intraneural blood fl System nnd its relntiollship to neuropathic pain. In T.L Onhop Res, II, 104, ';aksh. C. Lynch III. W.M. Zapol.:-\"-1. ~'1azc, J.E Bicbuyck . .& L.J. Saidman (Eds.\"J. Aw:...tht'S;u: Bio}o~ic FouI/datiolls (pp. TOrlora, GJ., & Anagnoslakos. N.r. (1984). Prillci\"l 483-514). Phil'lCldphia: LippiIKOll·R~I\\,l,.'n. AlUlIOI1lY (/ltd Physio}ogl' (41h cd.). N(.·w York: Harper & Wall. E.J .. M:ISSic, J.B.. Kwan. M.K .. CI 011. (1992). E lllcnta! stretch neurop'lthy. Changcs in nerve condu under tension,) BOllt' .foitlf Stl,.~, N-B. 126, Weinstein. J.N\" L.li\\lotll'. R.. Rydcdk, B. el 011., (1989). N In J.W. Frymoyer 8.: S.L. Gordon (Eds.)_ Nell' 1'('I\"spccti 1.0\\1' Back Paill (Chapll'r 4, pp, 3S-130). Park Ridg( '\\AOS. [Based 011 a workshop ,IIT,lngcu by Ihe N:llion stiwtes of Health (NIH) in AirJil'_ Virginia, USA. May
Nerve structure Structural Protects -Biochemical 'Axon's D composition from barrier protector o and function -Nutrition external properties affected trauma 'Preserves ionic environment .. Illness or injury _ Peripheral nerve's structure and alteration. Clinica \"This flow (hart is designed for classroom or group discussion. Flow chart is not mean
Delivery Local Returned Tl<lnsmission of Of importJ.nce Myelin of blood oxygen supply blood flow impulses; (or impulse production and transmission intl<lcellular synthesis of tl<lnspon of trophic factors material D al examples.* nt to be exhaustive.
Biomechanics o Skeletal Muscle Tobias Lorenz, Marco Campel/o adapred fr Mark I. Pieman, Lars Peters Introduction Composition and Structure of Skeletal Muscle Structure and Organization of Muscle Molecular Basis of Muscle Contraction The MOtor Unit The Musculotendinous Unit Mechanics of Muscle Contraction Summation and Tetanic Contraction Types of Muscle Contraction Force Production in Muscle Length-Tension Relationship Load-Velocity Relationship Force·Time ReJ(ltionship Effect of Skeletal lvIuscie Architecture Effect of Prestretching Effect of Temperature Effect of Fatigue Muscle Fiber Differentiation Muscle Injuries Muscle Remodeling Effects of Disuse and Immobilization Effects of Physical Training Summary References Flow Charts IJ ~S'.r'
Introduction ton. The myofibril is made lip of several sarcome that contain thin (actin), thick (myosin), clas The muscular sYSlCll1 consists of three III usc Ie.:: l.ypes: (titin), and inelastic (ncbulin) filaments. Actin a the cardiac muscle, which composes the hc[trt; the myosin are the contractile part of the myofibr whereas titin and nebulin nrc part of the intramy Sl1100th (nonstriated or involuntary) muscle, which fibrillar cytoskelcton (Stromer et aI., 1998). T lines the hollow internal organs; and the skeletal myof-ibrils are the basic unit of contraction. (striated or voluntary) muscle, which auaches to the Each fiber is encompassed b:y a loose connect skeleton via the tendons. The focus of this chapter is tissue called the endomysium and the fibers arc the role and function of skeletal muscle. ganized into various-sized bundles, or Fascicles (F 6·1, A & B), which arc in (urn encased in a den Skeletal muscle is the most abundant tissue in connective tissue sheath known as the perimysiu the human body, accounting for 40 to 45% of the to- The muscle is composed of several fascicles s lal body weighL. The human body has morc than rounded by a fascia of fibrous connective tis 430 skeletal !TIuscles, found in pairs on the right and called the epimysium. left sides of the body. The most vigorolls movements are produced by fewer than 80 pairs. The muscles In general, each end of a muscle is attached provide strength and protection to the skeleton by bone by tendons, which have no active contract distributing loads and absorbing shock; they enable properties. The muscles form the contractile co Ihe bones to move at the joints and provide the ponent and the tendons the series clastic comp nent. The collagen fibers in the perimysium a maintenance or body posture against force. Such epimysium are continuous with those in the t dons: together these fibers act as a stnlctural fr,\\I abilities usuall~' represent the action of muscle work for the attachment of bones and muscle fibe groups, not of individurll mllscles. The perim)'sium, endomysium, epimysium, and s colemma act as parallel elastic components. T The skeletal muscles perform both dynamic and forces produced by the contracting muscles static work. Dynamic work permits locomotion and transmitted to bone through these connective the positioning of the body segments in space. Sta- sucs and tendons (Kassel'. 1996). tic work maintains body posture or position. In this chapter we describe the composition and structure Each muscle fiber is composed of a lal'ge nu of skeletal muscle. the mechanics of muscle con- ber of delicate strands, thc mvol'ibrils. These traction. force production in muscle. Illuscle fiber the contractile clements of muscle. Their structu differentiation, and muscle remade-ling. and function have been studied cxhausti\\'c1y Iighl and eleclron microscopy, and [heir his Composition and Structure chemistr~' and biochclllistry have been explain o( Skeletal Muscle elsewhel'c (Alvidson et aI., 1984; Guvton, 198 Approximately I p.m in c1iamctcl: the myofibrils An understanding of the biorncchanics of Illuscle parallel to each other within the cytoplasm (s function requires knowledge of the gross anatomi- coplasm) of the muscle fiber and extend throug cal structure and function of the musculotendinous out its length. They vary in number from a few unit and the basic microscopic structure and chem- several thousand depending on the diameter of ical composition of the muscle fiber. ll1uscle fibel~ which depcnds in turn on thc type ll1usclc fiber. STRUCTURE AND ORGANIZATION OF MUSClE The transverse banding pattern in striated m cles repeats itself along (he length of (he mus The slructuralunit of skeletal muscle is thc muscle fiber. each repeat being known as a sal'comerc (F fiber, a long cylindrical cell with many hundreds of 6-IC). These striations are caused by thc individ nuclei. Muscle fibers range in thickness from ap- myofibrils, which are aligned continuously throu proximately 10 to 100 fim and in Icngth from ap- Ollt the muscle fiber. The sarcomere is the fu proximately 1 to 30 cm. A muscle fiber consists of tional unit of the contractile syslem in muscle. a many myofibrils, which are invested by a delicate the events that take place in one sarcomere arc plasma membl·ane called the sarcolemma. The sar- plicated in the others. Various sarcomere build colemma is connected via vinculin- and dystrophin- myofibril, various myof\"ibrils build the muscle fi rich costameres with the sarcon1ctric Z lines, which and various muscle fibers build the muscle. represent a pan of the cxtramyofibrillar cytoskcle- 1
Schematic drawings of the structural organization of mus- / Epimysium cle. A, A fibrous connective tissue fascia. the epimysium. surrounds the muscle, which is composed of many bun- A dles. or fascicles. The fascicles are encased in a dense con· nective tissue sheath, the perimysium. B, The fascicles are S',glc [ composed of muscle fibers, which are long, cylindrical, muscle multinucleated cells. Between the individual muscle fibers are capillary blood vessels. Each muscle fiber is sur· Ilber rounded by a loose connective tissue called the endomy- (cetl) sium. Just beneath the endomysium lies the sarcolemma. a thin elastic sheath with infoldings that invaginate the B fiber interior. Each muscle fiber is composed of numerous delicate strands-myofibrils, the contractile elements of c Cross section a muscle. C. Myofibrils consist of smaller filaments that form Thin level of a band a repeating banding pattern along the length of the my- ofibril. One unit of this serially repeating pattern is called IllamentlJl a sarcomere. The sarcomere is the functional unit of the (actin) .;.....,,''''':'' contractile system of muscle. D, The banding pattern of \", , . the sarcomere is formed by the organization of thick and , thin filaments, composed of the proteins myosin and actin, respectively. The actin filaments are attached at one ThICK : \" ,,':'.' ',:: :.:: : end but are free along their length to interdigitate with the myosin filaments. The thick filaments are arranged in o filament ' ..... a hexagonal fashion. A cross-section through the area of (mYOSin) overlap shows the thick filaments surrounded by six Sa(comer,:, organilalion equally spaced thin filaments. E, The lollipop-shaped mol· ecules of each myosin filament are arranged so that the Myosin { long tails form a sheaf with the heads, or cross-bridges, Mamenl projecting from it. The cross· bridges point in one direc- tion along half of the filament and in the other direction E \\ along the other half. Only a portion of one half of a fila- ment is shown here. The cross-bridges are an essential ele- Troponin ment in the mechanism of muscle contraction, extending outward to interdigitate with receptor sites on the actin filaments. Each actin filament is a double helix, appearing as two strands of beads spiraling around each other. Two additional proteins, tropomyosin and troponin, are associ- ated with the actin helix and play an important role in regulating the interdigitation of the actin and myosin fila- ments. Tropomyosin is a long polypeptide chain that lies in the grooves between the helices of actin. Troponin is a globular molecule attached at regular intervals to the tropomysin. Adapted from Williams, P & War\".vick. R, (1980). Gray's Anatomy (36ch ed., pp. 506-515). Edinburgh: Cht/rdlill Livingstone. Each sarcomere is composed of the Following: 3, The elastic filaments composed of the protei titin (Fig, 6-2) I, The thin filaments (approximately 5 nm in di- ameter) composed of the protein actin A, The inelastic filaments composedof the pro- teins nebulin and tilin 2, The thick filaments (approximately 15 nm in diameter) conlposed of the protein myosin Aetin, the chief component or the thin filamen (Fig, 6-1, D & E) has the shape of a double helix and appears as tw
strands of beads spiraling around t.:ach othcl: Two with a globular \"head\" projecting from a long sha additional proteins, troponin and tropomyosin, are or \"tail.\" Several hundred slIch molecules are pack important constituents of the actin helix because tail to tail in a sheaf with their heads pointed in on direction along half of the filament and in the opp thev appear to regulate the making and breaking of site dircction along the other half, leaving a hca cOI~taclS between the actin and myosin filamel1ls free region (the H zone) in between. The globul heads spiral about the myosin filament in the regio during contraction. Tropomyosin is a long polypep- where actin and myosin ovcrlap (the A band) and e tcnd as cross-bridges to interdigitate with sites o tide chain that lies in the grooves between the he- the actin filaments, thus forming the structural an iices of actin. Troponin is a globular molecule at- I'unctionallink between the two filament types. laehed at regular intcr'vals to the tropomyosin (Fig. The intramyofibrilh.,r cvtoskeleton includes i 6-1, D & E). elastic nebulin filaments, which span from the The thick filaments are located in the central re- line to the actin filaments. Ncbulin might also act a template for the thin filament assembly. gion of the sarcomere, where their ordcrl.y, parallcl arrangemcl1l gives rise to dark bands known as A Titin is I j.1m long. It is the largest polypepti bands because they arc strongly anisotropic. Thc and spans from the Z line to the IVI line. Titin is a thin filaments arc atlachcd at either end of the sar- clastic filament. The part between the Z linc an comere to a structurL' known as the Z line, which myosin has a string-likL' appearance. Titin has be consists of shon elements that link the thin fila- suggested to contdbutc greatly to the passh'c for ments of adjacent sarcomcres. defining the limits development of muscle during stretch (Fig. 6·2). of each sarcomere. The thin filaments cxtcnd From also might act as a template for the thick filame the Z line toward the center of the sarcomere, assembly (Linke et aI., 1998; Squire et al., 199 Stromer et aI., 1998), where they overlap with the thick fibmcnts. Re- The I bane! is bisected by the Z lines, which conta cently it was shown thal there is a third set or n1YO- the portion of the thin filaments that does not overl with the thick filaments and the clastic part of tit in. fibril filaments in the vertebrate striated Illuscles. the center of the A ballet. in the gap between the en This connecting filament, named titin, links the thick Filaments with the Z line (elastic I band re- or the thin filaments, is the H zone, a light band co gion of titin) and is part of the thick filaments (A band region o[ titin). This filament maintains the taining only thick filaments and that part of tilin th central position of the A band throughout contrac- is integrated in the thick filaments. A narrow, da tion and relaxation and might act as a template area in the center of the H zone is the M line, 1'1 during myosin ~,sselllbly. Myosin, the thicker filament, is composed of indi- vidual molecules, each of which resembles a lollipop M-line A-band part 01 titin Extent of one !!lin molecule The arrangement of titin molecules within the sarcomere. Adapted from Craig. R.(J994). The stftJ(ture of the contract filaments. In A.G. Engel & Fraflzini·Armscrong (eds.). !vlyology (2nd ed.• p. 150). New York: McGr<)w-Hill, Inc. •..-,r; •.. __.
duced by transversely and longitudinally oriented allel to the myofibrils and lend to enlarge and f at the level of the junctions between the A an proteins that link adjacent thick filaments, maintain- bands, forming transverse sacs, or the terminal ing their parallel Hrrangclllel1L The various areas of ternae, that surround the individual myofi the banding patlern arc apparent in the photomicro- completely, graph of human skeletal muscle shown in Figure 6-3. The terminal cisternae enclose a smaller tub Closely correlated with the rcpealing pattern or tha1 is scpanllcd from them by its own membra The smaller tubule and the terminal cisternae ab the sarcomcrcs is an organized network of tubules and below it are known as a triad. The enclo and sacs known as the sarcoplasmic reticulum. The tubules of the sarcoplasmic reticulum lie par- A ----\"'....Sarcomere r _--~\"\" _~ } Sarcoplasmic reticulum Mitochondrion { I~M t --- Line z H Zone Line B A. Single muscle fiber with three protruding myofibrils. B. Electron photomicrograph of a cross·section of human skeletal m c1e. The sarcomeres are apparent along the myofibrils. Characteristic regions of the sarcomere ar~ indicated.
Myo,libril Mitochondrion hence of the muscle, results from the relative m Sarcolemma ment of the actin and myosin filaments past on other while each retains its original length. ' lBand force of contraction is developed by the m heads, or cross-bridges, in the region of overla ~ tween actin and myosin (the A band), These c bridges swivel in an arc around their fixed pos ill on the surface of the m,vosin filament, much the oars of a boat. This movement of the c EA bridges in contact with the actin filaments duces the sliding of the actin filaments tc)\\var mu0 Band center of the sarcomere, A muscle fiber con If) \\vhen all sarcomere shorten simultaneously all-or-nothing fashion, which is called a twitch I Because a single movement of a cross-bridge Band I z· duces only' a small displacement of the actin ment relative to the myosin filament, each in Triad ual cross-bridge detaches itself from one rec ! \\j site on the actin filament and reattaches itself other site further along, repeating the process f Sarcotubule Terminal six tirnes, \"with an action similar to a man p on a rope hand over hand\" (Wilkie, 1968). I cisternae cross-bridges do not act in a s)-'nchronized ma each acts independently, Thus, at any given mo DD-------- (mly approximately half of the cross-bridges ac generate force and displacement, and when Diagram of a portion of a skeletal muscle fiber illustrating detach, others take up the task so that shorten the sarcoplasmic reticulum that surrounds each myofibril. maintained, The shortening is reflected in th The various regions of the sarcomere are indicated on the comere as a decrease in the I band and a decre left myofibril to show the correlation of these regions with the H zone as the Z lines move closer togethe the sarcoplasmic reticulum, shown surrounding the middle width of the A band remains constant. and right myofibrils. The transverse tubules represent an infolding of the sarcolemma, the plasma membrane that A key..' to the sliding mechanism is the calciu encompasses the entire muscle fiber. Two transverse (Ca~'), which turns the contractile activity on tubules supply each sarcomere at the level of the junctions off. Muscle contraction is iniliated \\vhen calci of the A band and I bands. Terminal cisternae are located made available to the contractile elements on each side of the transverse tubule, and together these ceases when calcium is removed, The mecha structures constitute a triad. The terminal cisternae con- that regulate the availability of calcium ions nect with a longitudinal network of sarcotubules spanning contractile machinery are coupled to electric e the region of the A band. Adapted from Ham, A.W & Cor- occurring in the muscle membrane (sarcolem An action potential in the sarcolemma provid 1 mack, D.H, (7979). Histology (8th ed.J. PiJifadefphia: IS, Lippincott electric signal for the initiation of contractile it,v. The mechanism by which the electric signa tubule is part or the transverse tubule system, or T gel'S the chemical events of contraction is kno system, which are invaginatio!1s of the surface excitationNcontraction coupling. membrane of the fiber. This membrane, the sar- colemma, is a plasma membrane that invests every \\Vhen the motor neuron stimulates the m striated muscle (Fig. 6-4). at the neuromuscular junction (Fig, 6-5A) an propagated action potential depolarizes the Molecular Basis of Muscle cle cell membrane (sarcolemma), there is a \\vard spread of the action potential along Contraction system. (Details of this process arc given in F 6-5, A-C and in Box 6-1, which summarize The most widely..' held theory of muscle contraction events during the excitation, contraction, an is the sliding filament theory, proposed simultane- laxation of muscle, Figure 6-5D shows the ously by A.F. Huxley and H.E. Huxley in 1964 and subsequently refined (Huxley, 1974). According to this theory, active shortening of the sarcomere, and
Molor end plate A B (1 ) Synaptic vesicles (3) co Schematic representation of the innervation of muscle fibers. area in this section is shown in detail in C. C. Ultrastructu A, An axon of a motor neuron (originating from the cell body the junction of an axon terminal and the sarcolemma. Th in the anterior horn of the spinal cord) branches near its end vagination of the sarcolemma forms the synaptic trough to innervate several skeletal muscle fibers, forming a neuro- which the axon terminal protrudes. The invaginated sar- muscular junction with each fiber. The region of the muscle colemma has many folds, or subneural clefts, which grea membrane (sarcolemma) lying directly under the terminal crease its surface area. Acetylcholine is stored in synaptic branches of the axon has special properties and is known as cles in the axon terminal. Band C. adapted from Brobeck, I the motor end plate, or motor end plate membrane. The rec- (Ed.) (/979). Best and Taylor's Physiological Basis of Medical Pra tangular area is shown in detail in B. B, The fine terminal (10(h ed., pp. 59-1/3). Baltimore: Williams & Wilkins. D. Cros branches of the nerve (axon terminals), devoid of myelin bridge cycle of muscle contraction. sheaths, lie in grooves on the sarcolemma. The rectangular
Events During Excitation, Contraction, and Relaxation of Muscle Fiber 1. An action potential is initiated and propagated in a mo- 1 1. Actin activates the myosin ATPase found on the myosin tor axon. cfOss-bridge, enabling ATP to be split (hydrolyzed.) This 2. This action potential causes the release of acetylcholine process releaSES energy used to produce movement 01 irom the axon terminals at the neuromuscular junction. the myosin cross~br;dges: 3. Acetylcholine is bound to receptor sites on the motor end plate membrane. A, I'll ' ATP --; A ' Iv1 + ADP + P, 4. Acetylcholine increases the permeability of the motor 12. Oar-like movements of the cross4 bridges produce rela- end plate to sodium and potassium ions. producing an tive sliding of the thick and thin filaments past each end-plate potential. other. S. The end-plate potential depolarizes the muscle mem- 13. Fresh AT? binds to the myosin cross-bridge, breaking brane (sarcolemma), generating a muscle action pOlen- tiallhat is propagated over the membrane suriaee. the actin-myosin bond and allowing the cross-bridge to dissociate from aGin: 6. Acetylcholine is rapidly destroyed by acetylcholinesterclse on the end plate membrclne. A . rv1 .;-. ATP -) A + tvl . ATP 7. The muscle aGion potential depolarize') the transverse 14. The ATPase hydrolyzes the myosin ATP complex to rhe tubules. M . AlP complex, which represents rhe relaxed state of the sarcomere: 8. Depolarization of the transverse tubules leads to the re- lease of calcium Ions from the terminal cisternae of the M' ATP -) Iv1 ' ATP sarcoplasmic reticulum surrounding the myofibrils. 15. Cycles of binding and unbinding of actin with the These ions are released imo the sarcoplasm in the direct myosin cross-bridges at successive sites along the actin vicinitY of the regulatory proteins tropomyosin and tro- filament (steps 11, 12, 13, CH'\\d 14) continue as long as ponin. ii)e concentration of calcium remains high enough to 9. Calcium ions bind to troponin, allowing movement of inhibit the action of the troponin-rropomyosin system. the tropomyosin molecule away from the myosin recep- tor sites on the actin filament that it had been blocking 16. Concentration of calcium ions falls as they are pumped and releasing the inhibition tilat had prevented actin into the terminal cisternae of the sarcoplasmic reticulum from combining with myosin. by an energy-requiring process that splits ATP, 10. Actin (A) combines with myosin ATP (M-ATP). In this state, ATP has been hydrolyzed to ADP and phosphate 17. Calcium diSSOCIates from troponin. restoring the in- bUt the products are still attached to myosin (receptor hibitory action of troponin-tropomyosin. The actin fila- sites on the myosin cross-bridges bind to receptor sites ment slides back and rhe muscle lengthens. In the pr~s-, on the actin chain): ence of ATp, actin and myosin remain in tll~ dissociated; relaxed stale. A + Iv1 ' ATP --; A ' M ' ATP (,l.,!odiiied from Luciano er ,l!. (I 978j, In HUIl1\"n FuncliOn <1nd Structure (Fig 5,5D/ New York: ,\\,'1cGril~·/·Hi,ll: and ,jdiJpted from (I'dlg. R. 099.:1). Myology (2nd ed.. p. 162) New York: McGra:'1·;·/iIl.) lural features between actin and the cross-bridges tract independently. \\Vhcn stimulated, all mu of mvosin.) fibers in the mOlor unit respond as one. The fi of a Illotor unit arc said to show an all-or·none THE MOTOR UNIT sponse to stimulation: the),..' contract either m mally or not at aIL The functional unit of skeletal 111uscle is the mOlor unit. which includes a single motor neuron and all The number of muscle fibers forming a -m of the muscle rlbers innervated by it. This unit is the unit is closely I\"elated to the degree of contro smallest part of the muscle that can be made to CO!l4 quirccl of the muscle, In small muscles thal perf vcr~' fine movements, such as the extraocular I
des, each motor unit may contain less than a dozen PEC SEC muscle fibers; in large n'lUscies that perform coarse movements. such as the gastrocnemius, the motor ,OOOOOH unil may contain 1,000 to 2,000 muscle fibers. CC The fibers or each motor unit arc not contiguous I but dispersed throughout the muscle with fibers of I other units. Thus. if a single motor unit is stimu- The musculotendinous unit may be depicted as consisti latex!. a large ponion or the muscle appears to con· of a contractile component ((C) in parallel with an elas component (PEQ and in series with another elastic com (rae£. If additional motor units of the nerve inner· nent {SEQ_ The contractile component is represented b vating the muscle are stimulated, the muscle the contractile proteins of the myofibril, actin, and myo corHracls with greater force. The calling in of adeli· (The myosin cross-bridges may also exhibit some elastic tional motor units in response to greater stimula- The parallel elastic component comprises the connectiv tion of the motor nClvc is called recruitment. tissue surrounding the muscle fibers (the epimysium, pe mysium, and endomysium) and the sarcolemma. The se THE MUSCULOTENDINOUS UNIT elastic component is represented by the tendons. Adap hom Keefe. CA.. Neil, E., & Joels. N (1982). I.;lvsc!e and the The tendons and the connective tissues in and lle!Voll$syslem. In Samson 1/</rI911(5 f.\\ppli(~cJ PhySiology (i3th around the muscle belly are viscoelastic structures ed, fJP, 248~259). Oxford: Oxford Unlversiry Press that help determine the mechanical characteristics of whole muscle during contraction and passive ex· 4. The viscous property of the series and para tension. Hill (1970) showed that the tendons repre- sent a spring-like elastic component located in se· lel clastic components allows lIk'lll to abso rics with the contractile component (the contractile proteins or the m~yofibril, actin, and myosin), while energy proportional to the rate of force app the epimysium, perimysium, endomysium, and sm'· cation and to dissipate energy in a timc~ dependent manner. (For a discussion of vis colcmma represent a second elastic component 10· coelasticity, see Chaptcl- 4.) cated in parallel with the contractile component Thb viscoLIs property. combined with the ela (Fig. 6-6). properties of the musculotendinous unit. is dem slI-atcd in everyday activities. For example, whe When the parallel and series elastic components person altempts to stretch and touch the toes, stretch during active contraction 01- passive exten- stretch is initially elastic. As the stretch is held, h sion of a muscle, tension is produced and energy is ever, further elongation or the muscle results fr stored; when they recoil with muscle relaxation, this the viscosity of the Illuscle-tendon structure, energy is released_ The series elastic fibers are more the fingers slo\\\\'I~' reach closer to the noor. important in the production of tension than are lhe parallel elastic fibers (Wilkie, 1956). Several investi- Mechanics of iVluscle gators have suggested that the cross-bridges of the Contraction myosin filaments have a spring-like property and also contdbutc to the elastic properties of muscle _Electromyography' provides a mechanism for ev (Hill, 1968). ating and comparing neural effects on muscle the contractile activity or the muscle itself in v The distensibility! and elasticity of the clastic com· and in vitro. Much has been learned by using c ponents arc valuable to the muscle in severnl wavs: I. Thev tend to keep the muscle in readiness for contraction and assure that muscle tension is produced and transillittcd smoothly during contraction. 2. They assure that the contractile elements re- turn to their original (resting) positions when contraction is terminated. 3. They may help prevent the passive over- stretch of the contractile elements when these elements are relaxed, thereby lessening the danger of Illuscle injUl)'.
tromyography Lo study various aspects or the con- time of the rnuscle so that little or no relax tractile process, particularly the time relationship can occur before the next contraction is ini between the onset of electrical activity in the muscle and aClltal contraction of the muscle or muscle (Fig. 6-8). fiber. The following sections discuss the mechanical response of a muscle to electrical (neural) stimula- The considerable gradation of COlllraction e ited by wholc muscles is achic\\·ed by the differ tion and the various ways in which the muscle con- tracts to move a joint, control its motion, or main- tain its position. SUMMATION AND TETANIC IIL,L,U--. CONTRACTION o tOO 200 300 400 500 t tI;+-<- - - I > The mechanical response of a muscle to a single s\\ 8 2 S3 stimulus of its molar nerve is known as a twitch, which is the fundamental unit of recordable mus- A cle activity. Following stimulation there is an in- terval of a few milliseconds known as the latency Ilh t~ I period before the tension in the muscle fibers be- 0 100 200 300 400 500 gins to rise. This period represents the timc re· quit'cd for the \"slack\" in the elastic components to be taken up. The time from the start of tension de- velopment to peak tension is the contraction time, t I-t and the time from peak tension ulltil the tension S, S2 S3 drops to zero is the relaxation time. The contrac- B tion time and relaxation time vary an10ng muscles, !I~ ,~ depending largely on the muscle fibcr makeup (de· I scribed below). Some muscle fibers contracl with a speed of only 10 mscc; others ma~; take 100 Illsec 0 100 200 300 400 500 or longer. t ..tI.- An action potential lasts only approximately I to 2 msec. This is n small fraction of the time taken for S, 5,S3 the subsequent mechanical response, or twitch, even in muscles that contract quickly; thus it is pos- Time (msec) sible for a series of action potentials to be initiated C f ' before the first twitch is completed if the activity of the motor axon is maintained. \\'\\Then mechanical re- sponses to successive stimuli arc added to an initial Summation of contractions in a muscle held at a cons response, the result is knc)\\vn as summation (Fig. length. A, An initial stimulus (51) is applied to the mu 6-7). If a second stimulus occurs during the latencyl and the resulting twitch lasts 150 msec. The second (5 period of the first muscle twitch, it produces no ad- third (5J) stimuli are applied to the muscle after 200-m ditional response and the muscle is said to be com- intervals when the muscle has relaxed completely, thu pletely refractory. summation occurs. 8.5 1 is applied 60 msec after 51, w The frequency of stimulation is variable and is the mechanical response from 5.. is beginning to decr modulated by individual motor units. The greater the frequency of stimulation of the muscle fibers. The resulting peak tension is greater than that of the the greater the tension produced in the muscle as gle twitch. C. The interval between 5.. and 5J is furthe a whole. However, a maximal frequency will be duced to 10 msec. The resulting peak tension is even reached beyond which the tension of the muscle no greater than in S, and the increase in tension produce longer increases. \\\"'hen this maximallension is sus- smooth curve. The mechanical response evoked by 5J tained as a result or summation, the muscle is said pears as a continuation of that evoked .by 51' Adapted to contract tetanically. In this case, the rapidity of Luciano, 0.5., Vander. AJ.• & Sherman. J.H. (1978). Huma stimulation olltstrips the contraction~relaxation tion and Structure (pp. J J3-(36). New York: McGraw,Hill.
3 c 0 'iii c 2 ><-l-> 'g><l> 0; a: 0 Jumnmrnmmnnrrmnnmi t I i i is s s s s s ssssssssssssssssssssssssssssssssss 100 200 300 400 500 600 700 800 900 1000 Time (msec) Generation of muscle tetanus. As the frequency of stimula- becomes maximal and the muscle contracts tetanically, tion (5) increases (Le., the intervals shorten from 200 to 100 ing sustained peak tension. Adapled from Luciano, OS. msec), the muscle tension rises as a result of summation. AI, 8 Sherman, IN (978). Human Function and Structure When the frequency is increased to lOO/second, summation I i 3-136). New York: McGraw-Hi//. activity' of their motor units, in both stimulation fre- Although no motion is accomplished and n quency' and the number of units activated. The chanical \\vork is performed during an isom repetitive twitching of all recruited motor units of a contraction, muscle work (physiological wo muscle in an as:vnchronous manner results in brief performed: energy is expended and is Illostly summations or more prolonged subtetanic or paled as heat, which is also called the isornetric tetanic contractions of the muscle as a whole and is production. All dynamic contractions involve a principal Factor responsible for the smooth move- ma.y be considered an initial static (isometric) ments produced by the skeletal muscles. as the muscle first develops tension equal to th it is expected to overcome. TYPES OF MUSCLE CONTRACTION The tension in a muscle varies with the t.y During contraction, the force exerted by a contract- contraction. Isometric contractions pro ing muscle on the bony lever(s) to which it is at- greater tension than do conccntric contrac tached is known as the muscle tension, and the ex- Studies suggest that the tension developed ternal force exerted on the muscle is known as the eccentric contractIon may even exceed that resistance, or load. As the muscle exerts its force, it oped during an isometric contraction. Thes generates a turning erFect, or moment (torque), on ferences arc thought to be due in large part the involved joint because the line of application of vat'ying amounts of supplemental tension the muscle force usually lies at a distance from the duced in the series clastic component of the center of motion of the joint. The moment is calcu- cle and to diFferences in contraction time lated as the product of the muscle force and the per~ longer contraction time of the isometric an pendicular distance between its point of application centric contractions allows greater cross~ and the center of motion (this distance is known as formation by the contractile components, thu the lever arm, or moment arm, of the force), mitting greater tension to be generated ( 1987). More time is also available for this te Muscle contractions and the resulting muscle to be transmitted to the series elastic comp work can be classified according to the relationship as the muscle-tendon unit is stretched. The l bet\\veen either the muscle tension and the resis- contraction time allo\\vs the recruitment of tance to be overcome or the muscle moment gener- tional nlotor units. ated and the resistance to be overcome, as shown in Box 6-2 (Krocmcr e! 'II., 1990), Komi (1986) has pointed oul that concentri metric, and eccentric muscle contractions se
_ Types of Muscle Work and Contraction Dynamic work: Mechanical work is performed and joint mo- 4. Iseinenial (iso, constant; inertial, resistance) contraction: tion is produced through the following forms of muscle con- traction: This is a type of dynamic muscle work wherein the resis tance against which the muscle must contract remains 1. Concentric (con, together; cemrum, center) contrac- constant. If the moment (torque) produced by the musc tion: When muscles develop sufficient tension to over- is equal to or less than the resistance to be overcome, come the resistance of the body segment, the mus- cles shorten and cause joint movement. The net the mllscle length remains unchanged and the muscle moment generated by the muscle is in the same di· rection as the change in joint angle. An example of a contracts isomelfically. If the moment is greater than th concentric contraction is the action of the quadriceps resistance, the muscle shortens (contracts concentrically in extending the knee when ascending stairs. and causes acceleration of the body part. Isoinertial con~ traction occurs, for example, when a constant external 2. Eccentric (e.g., out of-, centrum, center) contraction: load is lifted. At the extremes of motion, the inertia of When a muscle cannot develop sufficient tension and the load must be overcome; the involved muscles con- is overcome by the external load, it progressively tract isometrically and muscle torque is maximal. In the lengthens instead of shortening. The net muscle mo- midrange of the motion, with the inenia overcome, the ment is in the opposite direclion irom the change in mU'jcles contract concentrically and the torque is sub- joint angle. One purpose of eccenlric contraction is to maximal. decelerate the motion oi a joint. For example, when one descends stairs, the quadriceps works eccentri- 5. Isotonic (iso, constant; tonic, iorce) contraction: This ter cally to decelerate flexion of the knee, thus decelerat- ing the limb. The tension that il applies is less than is commonly used to define muscle contraction in which the force of gravity pulling the body downward, but it is sufficient to allow controlled lowering of the body. the tension is constant throughout a range of joint m()~ 3. Isokinetic (iso, constant; kinetic, motion) contraction: tion. This term does not take into aCCOLlnt the leverage'\" eilects at the joint. Ho\\,vever, because the muscle force This is a type of dynamic muscle work in which move- moment arm changes throughout the range oi joint mo ment of the joint is kept at a constan I velocity. and lion, the muscle tension must also change. Thus, isoton hence rhe velocity of shortening or lengthening of the muscle contraction in the truest sense does not exist in muscle is constant. Because velocity is held constant, the production of joint motion (Kroll, 1987). muscle energy cannot be dissipated through accelera- Static work: No mechanical work is performed and posture lion of the body part and is entirely converted to a re- or joint position is maintained through the following form sisting moment. The muscle force varies with changes muscle contraction: in its lever arm throughout the range of joint motion 1. Isometric (iso, constant; metric, length) contra(ti()~,;,.:~~s. (Hislop & Perrine. 1967). The muscle contracts con- centrically and eccentrically with different directions of c1es are not always directly involved in the prod~qi~~:-Pr. joint motion. For example, the i1exor muscles of a joint contract concentrically during flexion and eccen- joint movements. They may exercise either a rest'ra(ning trically during extension, acting as decelerators during the latter. or a holding action, such as that needed t~ ~aint~i~ th body in an upright position in opposing the force of gravity. In this case the muscle attempts to shorten (i.e., the myofibrils shorten and in doing so stretch the series elastic componenr. thereby producing tension), but it does not overcome the load and cause movement; in- stead. it produces a moment that supports the load in a iixed position (e.g., maintains posture) because no ,\" change takes place in the distance between the mlJsc!le points of attachment.
occur alone in normal human movement. Instead, c one type of contraction or load is preceded by a dif- .2 ferent type. An example is the eccentric loading mc '.0 I prior to the concentric contraction that occurs at I the ankle frolll miclstance to toe-off during gait. \"f- I ~, \".~ I Because muscles normally' shorten or lengthen at 0.5 I \"at)!ing velocities and with valying amoullls of tcnsion, <i I perfolll1ance and measurement of isokinetic work re- 0; I quire the lise of an isokinetic dynamon1ctcl: This device I provides constant velocity of joint motion and maxi- a: I mum cxtcIllal resistance throughout the range of 010- II lion of the involved joint. thereby requiJing maximal muscle torque. The use of the isokinctic dynamometer 1.27 1.65 2.0 2.25 provides a method of selective training and measure- ment, but physiological movement is not simulated. Sarcomere Length (JIm) 2.25-3.6 I'm c==:jr=z=J~\\:~::\\g:;:~;::~:::~\\==i/i== Ir==z M A Z 20-225\"m=9! i':::\": :::!::~ <1.65\"m==j~F= Force Production in Muscle Tension·length curve from part of an isolated muscle f stimulated at different lengths. The isometric tetanic t The total force that a muscle can produce is influ- sion is dosely related to the number of cross-bridges o enced by its mechanical properties, which can be the myosin filament overlapped by the actin filament. described by examining the length-tension. load- tension is maximal at the slack length, or resting lengt velocity, and force-time relationships of the muscle the sarcomere (2 p.m), where overlap is greatest, and f and the skeletal muscle architecture. Other princi- to zero at the length where overlap no longer occurs pal factors in force production arc muscle tempera- ,....m). The tension also decreases when the sarcomere ture, muscle fatigue, and prestrclching. length is reduced below the resting length. falling sha at 1.6S IJ.m and reaching zero at 1.27 IJ.ffi as the exten LENGTH-TENSION RELATIONSHIP overlap interferes with cross-bridge formation. The str tural relationship of the actin and myosin filaments at The force, or tension, that a muscle exerts varies ous stages of sarcomere shortening and lengthening is with the length at which it is held when stimulated. portrayed below the curve. A. actin filaments; M. myo This relationship can be observed in a single fiber filaments; Z, Z lines. Adapted from CriJ....,;ord. CN.C & J~ contracting isometrically and tetanically, as illus- trated by the length-tension curve in Figure 6-9. N. T. (1980). The design of muscfes. In R. Owen, J. Goodfelfo Maximal tension is produced when the muscle fiber P. Buffough (Eds.), Scientific Foundations of Orthopaedics an is approximately at its \"slack,\" or resting, length. ,If the fiber is held at shorter lengths. the tension falls Trmilllalology (pp. 67·-74). London.' William Heinemann;')5 off slowly at first and then rapidly. If the fiber is modified from Gordon, A.M., rluxley, A.F.I., & JlIlian, F.l. (1 lengthened beyond the resting length, tension pro- Tile variation in isometric tension with SMcomere length in gressively decreases. tebr~lre muscle fibers. J Physiol, 184, 170. The changes in tension when the fiber is sian because it allows ovedapping of the thin stretched or shortened primarily are caused by ments at opposite ends of the sarcomere, which structural alterations in the sarcomere. Maximal functionally polarized in opposile directions. isometric tension can be exerted when the sarcom- sarcomere length of less than 1.65 fJ.m. the thic eres arc at their resting length (2.0-2.25 /J.m), be- aments on the Z line and the tension dimi cause the actin and myosin fllamcnts overlap along sharply. their entire length and the number of cross-bridges is maximal. If the sareo meres arc lengthened. there Thc length-tension relationship illustrated in are fewer junctions between the marnents and the ure 6-9 is for an individual muscle fiber. If this active tension decreases. At a Sarcomere length of ,lionship is measured in a whole mus.de contrac approximately 3.6 J.Lm, there is no overlap and isometrically and tetanically, the tension produ hence no active tension. Sarcomcl·e shortening to by both active components and passive compon less than its resting length decreases the acLive ten- must be taken into account (Fig. 6-10).
The cun/e labeled \"active tension\" in Figure Eccenlric Concentric 6-10 represents the tension developed by the con- tractile elements of the muscle. and it resembles --~ the curve for the individual fiber. The curve labeled u \"passive tension\" reflects the tension developed when the muscle surpasses its resting length and -'o\"' the noncontractile muscle belly is stretched. This passive tension is mainly developed in the parallel o .. and series elastic components (Fig. 6-6). When the belly contracts, the combined active and passive Velocity tensions produce the total tension excrled. The curve demonstrates that as a muscle is progl'cs· sivdy stretched beyond its resting length, the pas· sive tension rises and the active tension decreases. Most rnuscles that cross only one joint normally are not stretched enough fOl- the passive tension 10 play an important role, but the case is different for lwo-joint muscles. in which the extremes of the load-velocity curve generated by plotting the veloci motion of the muscle lever arm against the external When the external load imposed on the muscle is ne ble, the muscle contracts concentrically with maxima speed. With increasing loads the muscle shortens mo slowly. When the external toad equals the maximum that the muscle can exert, the muscle fails to shorten has zero velocity) and contracts isometrically. When load is increased further, the muscle lengthens eccen cally. This lengthening is more rapid with greater loa L Length length-tension relationship may be functi (Crawford & James, 1980). For example, the ~------ strings shorten so much when the knee is Hexed that the tension they can exert decreases The active and passive tension exerted by a whole muscle siderably. Conversely, when the hip is nexed an knee extended. the Illuscles arc so stretched t I contracting isometrically and tetanically is plotted against the is the magnitude of their passive tension tha muscle's length. The active tension is produced by the con· vents flirt her elongation and causes the knee t tractile muscle components and the passive tension by the se- if hip flexion is increased. ries and parallel elastic components, which develop stress LOAD-VELOCITY RELATIONSHIP I when the muscle is stretched beyond its resting length. The greater the amount of stretching, the larger the contribution The relationship between the velocity of shOl· of the elastic component to the total tension. The shape of or eccentric lengthening of a muscle and dif the active curve is generally the same in different muscles. constant loads can be determined by plolLing t but the passive curve, and hence the total curve, varies de- locil)' of motion of the muscle lever arm a1 va pending on how much connective tissue (elastic component) external loads. thereby generating a load-ve the muscle contains. Adapted from Crawford. CN.C & James. curve (Fig. 6-11). The velocity of shortening N. T. (1980). Tile design of muscles. III R. Owen. 1. Goodfel/o;,t~ & p. muscle contracting concentrically' is inverse Bulfough (£els.), Scientific Foundations of Orthopaedics and TraurnJ· lated to the external load applied (Guyton, tology (pp. 67-74). London: William Heinemann. The velocity' of shortening is grealest when th •I
~~~·_----_·_-------T tcrnalload is zero, but as the load increases th ele shortens morc and more slowly. \\Vhcn the Gastrocnemius Muscie Tear nul load equals the mnximal force that the can exen, the velocity of shortening becom - -. ·. 22·year-old male professional athlete tears his ga5- and the muscle contracts isometrically. \\,\\fl A___ trocnemius during a race (Fig. (56-1-1). The tensile load is increased still further, th~ muscle co eccel1Lrically: it elongates during contractio overload that happens during strenuous eccentric and load~velocity relationship is reversed from the concentri-cally contracting rnuscle; the c6n~entric contractions increases the risk of injury. espe- eccentrically lengthens more quickl)! with inc ciallywhen the forces involve bj-articular muscles such load (Kroll. 1987) (Case Study 6-1). :asthe gastrocnemius. This indirect trauma is associated FORCE-TIME RElATIONSHIP :wi!~ 111gh tensile forces during rapid contraction (high The force, or tension, generated by a muscle v~l_()~ity) and continued changes in muscle length. The portional to the contraction time: the long status of muscle contracrion at the time of overload is contraction lime, the greater is the force deve uS!Jally eccentric, and failure most often occurs at or lip to the point of maximurn tension. In Figur near the myotendinous junction unless the muscle has this relationship is illustrated by a force-lime for a whole muscle contl\"acting isomet Q.eef1. previously injured (Kasser, 1996). Swelling from Slower contraction leads to greaLcr force p lion because time is allowed for the tensio ·h~~{br'rh~ge occurs initially in the inflammatory phase. duced b.y thL' cornractilc clements to be trans through the parallel clastic components to t ,The cellu.lar response is more rapid and repair is (rlore don. AltlH)Ugh tension production in the cont complete'if the vascular channels are not disrupted and component can reach a maximum in as little ·thenutritioo.of ihe tissue is not disturbed. The degree mscc. lip to 300 ITlSeC ma~' be needed for th of injury from a tensile overload will dictate the poten· sion to be transferred to the clastic compo The tension in the tendon will reach the max tia/hos< r~sponse and the time needed iar repair. tension developed by the contractile element the aClive contraction process is of sufficien lion (Olloson, 1983). C~;-\";~-e. -Study Fig~re 6-1-1, EFFECT OF SKElETAL MUSCLE ARCHITECTURE The Illuscles consist of the contractile comp the sarcomere, which produces active tensio arrangement of the contractile components the contractile propcnies of the muscle dr cally. The more sarcomere lie in series, the the myofibril will be; the more sarCOlllere lie lel. the larger the cross-sectional area 01\" the m ril will be. These two basic architectural patte myofibrils (long or thick) affect the contractile erties of the llluscies in the following ways: 1. The force the muscle can produce is pro lion'll to the cross-section of the myofibr (Fig_ 6-13A). 2. The velOcity and the excursion (working range) that the muscle can produce are portional to the length of the I11vofibril (Fig. 6-138).
Muscles with shoner fibers and a Im'ger cross- 100 10 15 20 sectional area are designed to produce [orce, Muscle Length (cm) whereas muscles \\vith long fibers are designed for 80 excursion and velocity. The quadriceps muscle con- 10 15 20 tains shorter myofibrils and appears to be special- ~ Muscle Velocity (cm/s) ized ror force product ion. The sartorius muscle has longer fibers and a smaller cross-sectional arca and ~ 60 is better suited for high excursion (Barana et aI., ~ 1998; Lieber & Bodine-Fowler, 1993), ~ EFFEa OF PRESTRETCHING ~ 40 It has been demonstrated in amphibians and in hu- mans (Cuillo & Zarins, 1983) that a muscle per- :\":; forms more work when it shortens inlmediatcly af- ter being stl'etched in the concentrically contracted 20 state than when it shortens from a state of isomet- ric contraction. This phenomenon is not entirely ac- B 100 counted for by the elastic energ~' stored in the series clastic component during stretching but must also 80 be caused by energy stored in the contractile com· ~ ~ 60 uo. ~ '0 40 ~ :\":; 20 5 0F----------- Isometric and isotonic properties of muscles with differ architecture. A. Force-length relationship. B. Force-veloc Time relationship. PSCA. physiological cross-sectional area. iI B mL - _ Reprinted with permission of the AmeriC<Jn Physical Therapy Force-time curve for a whole muscle contracting isometri· sociation from Lieber, RL (J 993). Skeletal muscle rnec!wnics cally. The force exerted by the muscle is greater when the Implications for rehabilitation. Physical Therapy, 73(2). 852. contraction time is longer because time is required for the tension created by the contractile components to be trans- • ferred to the parallel elastic component and then to series elastic component as the musculotendinous unit is pon~nl. 'It has been suggested [hat changes in the stretched. trinsic mechanical properties of l11)'oflbrils are ponant in the stretch-induced enhancement work production (Takarada et aI., 1997), EFFECT OF TEMPERATURE A rise in muscle temperature causes an incre in conduction velocity across the sarcolem (Phillips & PeLrorsky, 1983), increasing the quency of stimulntion and hence tbe product of muscle force. Rising of the muscle temperat from 6 La 34u C results in an almost linear incre or the tension/stirrness raLio (Callcr et al\" 199
A rise in temperature also causes greater enzy- Fatigue in a muscle contracting isometrically. Prolong matic activity of muscle metabolism, thus in- stimulation occurs at a frequency that outstrips the m creasing the efficiency of rnusclc contraction. A cle's ability to produce suHicient ATP for contraction. further effect of a rise in temperature is the in- result, tension production declines and eventually ce creased elasticity of the collagen in the series and parallel elastic components. which enhances the Adapted from Luciano. 0.5., Vander. A.i., &- Sherman. J.H extensibility of the muscle-tendon unit. This in- (1978). Human Function and Structure (pp. 113-136). Ne creased prestrclch incrcases the force production of the muscle. York: McGraw-Hili. Muscle temperature increases by rneans of two • mechanisms: myosin ATPase rapidly breaks down ATP. Th I. Increase in blood now, which occurs when an crease in adenosine diphosphate (ADP) and athlete \"warms up\" his or her muscles phate (Pi) concentralions resulting from this b down ultimately leads to increased rale 2. Production of the heal of reaction generated oxidative phosphorylation and glycolysis. A by metnbolism. by the release of the energy short lapsc. however. lhese metabolic palhway of contraction, and by friction as the contrac- gin lO deliver ATP at a high rate. During this tile components slide over each other vaL lhc energy for AT? formation is provided b atine phosphate, which offers the most rapid m However, at low tenlperaturc (1 O('C), it has been of forming ATP in the muscle cell. shown that the maximum shortening velocity and the isometric tension are inhibited significantly. At moderate rates of muscle aClivity, most o This is caused by decreased pH (acidosis) in Ihe required ATP can be formed by the process o muscle. The 1'1-1 plays a much less important role at idalive phosphorylation. During intense exe temperatures close to the physiological level (Pate et when ATP is being broken down rapidly, the aI., 1995). abilitv to replace ATP by oxidalive phosphory may be limited. primarily by inadequate deliv EFFECT OF FATIGUE oxygen to the muscle b.y lhe circulatory system The ability of a muscle to contract and relax is de- Even \\vhcn oxygen delivery is adequate, th pendent on the availability of adenosine triphos- al which oxidative phosphorylation can pro phate (ATP) (Box 6-1). If a muscle has an adequate ATP may be insufficient to sustain inlense ex supply of oxygen and nutrients that can be broken because the enzymatic machinery of this pathwC down to provide ATP, it can sustain a series of low- relatively slow. Anncrobic glycolysis then beg frequency twitch responses for a long time. The rre- contribute an increasing portion of the ATP. Th quency must be low enough to allow the muscle to colytic pathway, although it produces much sr synthesize AT? at a rate sufficient to keep up with amounts of ATP h-om the breakdown of glucos the rate of ATP breakdown during contraction. If erates at a Illuch faster rate. It can also proce the fTequency of stimulation increases and outstrips the absence of oxygen, with the formation of the rate of replacement of ATP, the twitch responses acid as ils end product. Thus, during intense soon grow progressively \\veaker and eventually fall cise, anaerobic glycolysis becomes an addi to zero (Fig. 6-14). This drop in tension following source for rapidly supplying the muscle with A prolonged stimulation is muscle fatigue. If the fre- quency is high enough to produce tetanic contrac- The glycolytic pathway has the disadvanta tions, fatigue occurs even sooner. [f a period of rest requiring large amounts of glucose for the pr is allowed before stimulation is continued, the ATP tion of small amounts of\" ATP. Thus, even th concenln.l.lion rises and the muscle briefly recovers muscle stores glucose in the form of glycogen, its contractile ability before again undergoing fa- ing glycogen supplies rnay be depicted quickly tigue. Three sources supply ATP in muscle: creatine phosphate, oxidative phosphorylation in Ihe mito- chondria. and substrate phosphor:ylation during anaerobic glycolysis. \\'Vhen contraction begins, the
muscle aconty is intense, Finally, myosin ATPase Jvlany methods of classifying muscle fibers may break down AT? faster than even glycolysis can been devised. As early' as 1678, Lorenzini obse r~p'lace it, and fatigue occurs rapidly as AT? con- anatomically the gross dilTcrence bel\\\\,Icen red centrations drop. white muscle. and in 1873 Ranvier typed muscl the basis of speed of contractility and fatigab After a period of intense exercise, creatine phos- Although considerable confusion has existed phate levels have become low and much of the mus- cCl'ning the method and terminology for classif cle glycogen may have been convened to lactic acid. skeletal muscle, recenl histological and histoch For the muscle to be returned to its original state, cal observations have led to the identificatio creatine phosphate must be resynthesized and the three distinct typcs or muscle fibers on the bas u1vcofLcn stores must be replaced. Because both differing contractile and metabolic prope pl:oce~ses require energy, the muscle will continue (Brandstater & Lambert, 1969; Buchtah! & Soh to consumc oxygen at a rapid rate cven though it burch, 1980) (Table 6-1). has stopped contracting. This sustained high oxy- !:rell uptake is demonstrated by the fact that a person The fiber t~'pes are distinguished mainly by ~ontinues to breathe heavily and rapidly aher a pe- metabolic pathways by which they can gene riod of strenuous exercise. AT? and the rate at which its energy is made a able to the conrractilc system of the sarcom v\"hen the energy necessary to return glycogen which determines the speed of contraction. and creatine phosphate to their original levels is three fiber types are termed type I, slow-twitch taken into account, the ef(-icienc~.. with which mus- idative (SO) fibers; type lIA, fast-twilCh oxida cle coovens chemical energy to work (movement) is glycolvtic (FOG) fibers; and type liB, fast-twitch usually no more than 20 to 250/0, the majority of the colytic (FG) fibers. energy being dissipated as heat. Even when Illuscle is operating in its most efficient stnte, a maximum Typc I (SO) fibers are characterized by a low ()f only approxinwtel)! 45{>~ of the energy is used for tivity of my'osin ATPase in the muscle fiber contraction (Arvidson ct 'II., 1984; Guyton, !986). thcrefore, a relatively slow contraction time. glycolytic (anaerobic) aClivity is low in this In growth biomechanics, muscle fatigue is flrst lype, but a high content of mitochondria produc observed by the lack of coorclinalion or movement high potential for oxidative (aerobic) activity. Ty and its effect in the increasing of loads in tissue. Re- fibers are difficult to fatigue because the high ra searchers including Bates et al. (1977) have indi- blood now to these fibers delivers oxygen and n cated that the skill of the person in performing a ents at a sufficient rate to keep up with the relati given action is affected by fatigue, They studied the slow rate of ATP breakdown by myosin ATP fatigue effect on runners and absented that runners Thus, the fibers are well suited for prolonged, decrease their knee extension when fatigue occurs intensity work. These fibers are relatively sma (Bates et aI., 1977). Parnianpour (1988) studied the diameter and so produce relatively little tens motion coupling of the spine at exhaustive extension The high myoglobin content of type I fibers give Oexion. This study showed that when an individual muscle a red color, became fatigued, the coupled motion increased and therefore the spinaltorquc increased. The most dele- Type II muscle fibers arc divided into two n terious component of the ncurornuscular adaptation subgroups, IIA and IlB, on the basis of differing to the fatiguc state was the reduction in accuracy ceptibility to treatment with different buffers p control and speed of contraction, \\vhich may predis- to incubation (Brooke & Kaiser, 1970). A third pose an individual to injury if muscle fatigue occurs. group, the typc lIe fibers, are rare, undifferenti Muscle Fiber Differentiation. fibers, which are usually seen before the 30th w In the preceding section, we described the major of gestalion. This fiber type is infrequent in hu ractors that determine the total tension developed muscle (Banker, 1994). Tvpe IIA and 11 B fibers b.v the whole rnuscle when it COlllracts. Individual characterized by a high activity of myosin ATP muscle fibers also display distinct differences in which results in relatively fast contraction. their rates of contraction, development of tension. and susceptibility to fatigue. Type lIA (FOG) fibers are considered interm ate between type 1 and type lIB because their contt-action time is combined with a modera well-developed capacity for both aerobic (ox tive) and anaerobic (glycolytic) activity. T
Properties of Three Types of Skeletal Muscle Fibers TYPE 1 TYPE JlA TYPE JIB Slow-Twitch Fast-Twitch Fast-Twitch Oxidative Oxidative- Glycolytic (SO) Glycolytic (fG) (fOG) Fast Speed of contraction Slow Fast Primary source of ATP Oxidative Oxidative Anaerobic production phosplloryla tion phosphorylation glycolysis Glycolytic enzyme activity Intermediate Capillaries low Many High Myoglobin conlent High Glycogen content Many Intermediate few Fiber diameler High Intermediate Rate of fatigue Intermediate low Low High Small Slow Large Fast fiber's also have a well-developed blood supply. tractile and histochemical properties and the They can maintain their contractile activity for rel- twitch fibers became slow. <Hively long periods; ho\\vevcr, at high rates of ac- tivity. the high rate of ATP splitting exceeds the ca- The fiber composition of a given muscle pacity of both oxidative phosphorylation and pends on the function 01\" that muscle. Some m glycolysis to supply ATP, and these fibers thus cles perform predominantly one form of cont eventually fatigue. Because the myoglobin conlCIH tile activity' and arc often composed mostl 01\" this muscle type is high, the muscle is oflen cat- one muscle fiber t}'pc. An example is the so egorized as red III lIscl e. muscle in the calf, which prirnarily maint posture and is composed of a high percentag T:vpe liB (FG) libers rely primarily on glycolvtic type I fibers. More commonly', however, a mu (anaerobic) activity for ATP production. Few capil- is reqllir'cd to perform endurance-type act laries are found in the vicinity of these fibers and be- unde)' some cirClllTlstances and high-inten cause they contain little myoglobin (hey are ohen strength activity under others. These mus referred to as white muscle. Although Lype liB fibers generally contain a mixture of the three mu are able to producc ATP rapidly, they fatigue easily fiber types. because their high rate of ATP splitting quickly de- pletes the glycogen needed for glycolysis. These (n a typical mixed muscle exerting low tens fibers generally are of large diameter and are thus some of the small motor units, composed of ty able to produce great tension, but only for short pe- fibers, contract. As the muscle force increa riods before they fatigue. more motor units are recruited and their quency of stimulation increases. As the frequ It has been well demonstrated that the nerve in- becomes maximal. greater muscle force nervating the muscle fibcr determines its t.ypc achieved by recruitment of larger motor u (Burke el aI., 1971); thus, the muscle fibers of each composed of type 11;\\ (FOG) fibers ancl eventu motor unit are of a single type. In humans and other type lIB (FG) fibers. As the peak muscle force species, electrical stimulation was found to change creases, the larger units are the first to cease the fiber type (Munsal, McNeal, & Waters, 1976). In tivity (Guyton. 1986; Luciano, Vander. & Sherm animal studies, transecting the nerves that inner- 1978). vate slow8 twitch and fast-twitch muscle fibers and then crossing these nen;es was noted to reverse the It is generally, but not universally, accepted fiber types. After recovery from the cross-innerva- fiber types are genetically det~rmined (Costi tion, the slow-twitch fibers became fast in their con- aI., 1976; Gollnick, 1982). In the average pop tion, approximatel.'Y' 50 to 55% of muscle fi
are type I, approximately 30 to 35 Cj(; are type IrA, physical constraint of the surrounding tissues, t and approximately' 15 rJr; are t.\\'Pe lIB, but these extent and condition of extracellular matrices, a percentages vary greatly among individuals. the development of repair cells. Muscle injuries a important but the topic is not \\vithin the scope In elite athletes, the relative percentage of fiber this chapter. Injuries should be investigated ca types differs from that in the general population and fully if suspicion arises that a patient has mus appears to depend on whether the athlete's principal damage. activit)' requires a short, explosive, maximal effort or involves submaximal endurance. Sprinters and Muscle Remodeling shot putters, for example, have a high percentage of tvpe II flbers, whereas distance runners and cross- The remodeling of muscle tissue is similar to that ~ountry skiers have a higher percentage of type I other skeletal tissues such as bone, articular car fibers. Endurance athletes may have as man.v as lage, and ligaments. Asin these other tissues, mu 80% t.ype I fibers, and those engaged in short, ex- cle atrophies in response to disuse and immobili plosive efforts as few as 300/e of these fibers (Saltin tion and hypertrophies when subjected to grea et 'II., 1977). use than usual. The genetically determined fiber typing may be EFFECTS OF DISUSE AND responsible for the natural selective process by IMMOBILIZATION which athletes are drawn to the type of sport for which they are most suited. Because fiber types are Disuse and immobilization have detrimental effe determined by the nerve that innervates the muscle on muscle ftbers. These effects include loss of fiber, there may be some cortical control of this in- durance and strength and muscle atrophies on a m nervation that influences an athlete to choose the crostructural and macrostructural level, such as sport in which he or she is genetical I)' able to excel. creased numbers and size of fiber. Biochemi changes occur and affect aerobic and anaerobic Muscle Injuries erg}' production. These effects are dependent fiber type and muscle length during immobilizati iVluscle injuries comprise contusion, laceration, Immobilization in a lengthened position has a l ruptures, ischemia, compartment syndromes, and deletet-ious effect (Appell, 1997; Kassel', 1996; Oh denervation. These injuries weaken the muscles and et 'II.. 1997; Sandmann, et 'II., 1998). can cause significant disability'. Blunt trauma can diminish muscle strength, limit joint motion, and fl- Clinical and laboratory studies of human and nally lead to myositis ossiflcans. lVlusclc laceration, imal muscle tissue suggest that a program of surgical incisions, and traumatic lesion to muscle mediate or early motion may prevent Illuscle at tissue and denervation weaken the ITmsclcs, some- phy after injury or surgery. In a study of cn times significantly. Ruptures in muscles also can injuries to rat muscle, the effect of immobilizat cause weakness. Like the other injuries, they rnay of the crushed limb was compared with that of result from direct trauma, but muscle contractions mediate motion. The muscle fibers \\vere found against resistance also can lead to tears in muscle regenerate in a more parallel orientation in the m tissue. bilized animal than in the immobilized anim capillarization occurred more rapidly, and tens Acute muscle ischemia and compartment syn- strength returned more quickly. Similar resu dromes can cause extensive muscle necrosis. The were found in a later study on the effect of imm many potential causes of compartment s}'ndrome bilization on the IT'lOrphology of rat calf musc all result in increased pressure \\vithin a confined (Kannus et aI., 1998a). muscle compartment. In this case, failure to relieve the pressure rapidl.y ma}' cause complications that It has been found clinically that atrophy of range from weakness and decreased motion to loss quadriceps muscle that develops while the limb of an entire limb. immobilized in a rigid plaster cast cannot be v'ersed through the use of isometric exercises. Studies have shown that healthy skeletal muscle rophy may be limited by allowing early mot has a substantial capacity to repair itself. This re- such as that permitted by a partly mobile c pair process following a specific injury is inferred by the prior innovation pattern, vascularization,
brace. In this case, dynamic exercises can be per- stood (Gollnick, 1982; Guyton, 1986). It ap formed. that these evcnts arc controlled or modifi both the intrafusal muscle spindles, located Human muscle biopsy studies have shown that allel with the extrafusal fibers of the muscle it is mainly' the type I fibers that atrophy with im- and the Go!gi tendon organs, located in serie mobilization; their cross-sectional area decreases and their potential for oxidative enzyme activity is Ruptured Left Anterior eruciate Ligam reduced (Kannus et aI., 1998b). Earl)' motion may' prevent this atrophy. It appears that if the muscle A 25-year-old male, status postsurgical repair of the is placed under tension when the body segment - ruptured left anterior cruciale ligament, had torqu moves, afferent (sensory) impulses from the intra- measurements taken from the involved and uninvolved fusal muscle spindles will increase, leading to in- limb 10 weeks after the surgical procedure (Fig. (56-2-1 creased stimulation of the type I fiber. Although in- and repeated 6 weeks after the training began (Fig. (56 termittent isometric exercise may be sufficient to 2-1 B). An increase of muscle torque is shown in the re- maintain the metabolic capacity of the t.vpe II peated isokinetic test. The initial deficit of the involved fibel~ the type I fiber (the postural fiber) requires a side was approximately 63~o when compared with the more continuous impulse. Evidence also suggests uninvolved side. After 6 '.Neeks of trainin~J. the deficit o that electric stimulation may prevent the de- the involved side compared with tho uninvolved side de crease in type I fiber size and the decline in its oxi- dative enzyme activity caused b:v immobilization creased to 43%. (Eriksson et ai., 1981). 187,------------- In elite athletes, inactivity following injury, surgery, or immobilization rapidly decreases the 163 size and aerobic capability of muscle fibers, partic- ularly in the fiber type affected bv the chosen 140 sport. Tn endurance athletes, type I fibers are af- fected, while in athletes engaged in an explosive <cEn 116 ----- activity such as sprinting, type II fibers are af- 93 fected. ;o: 47 / EFFECTS OF PHYSICAL TRAINING z\" 69 23 Physical training increases the cross-sectional area o J-~c_-----__:-~:-''''-'---- of all muscle fibers, accounting for the increase in o 16 32 48 64 80 96 112 muscle bulk and strength. Some evidence suggests that the relative percentage of fiber types compos- Knee motion degrees ing a person's muscles rna:v also change with phys- A ical training (Arvidson, Eriksson, & Pitman, 1984). The cross-sectional area of the fibers affected by 294 the athlete's principal activit).' increases. For exam- ple, in endurance athletes, the arca of muscle taken 239 up by type I and type IIA fibers increases at the ex- pense of the total area of type lIB fibers (Case ~ 204 Study 6-2). 192 c Stretching incrcases muscle Oexibility, maintains \";0: 136 \" \" \"- and augmcnts the range of joint motion, and in- 108 /. \"- creases the elasticity and length of the musculo- z 68 , tendinous unit (Brobeck, 1979; Cuillo & Zarins, .< 1983). It also permits the musculotendinous unit to store more energy in its viscoelastic and contractile 33 / components. 0 0 16 32 48 64 80 96 112 The events that take place during muscle stretching are complex and incompletely under- Knee motion degrees B Case Study Figure 6-2-1 Isokinetic test at 180~/sec. A Measurement of the quadriceps femoris torque produc tion at 10 weeks postsurgical procedure. The dashed fi represents torque output by the involved limb. The so line represents torque output by the noninvolved limb B. Measurements of the quadriceps femoris torque pro duction at 16 weeks postsurgical procedure and 6 wee after training sessions. The dashed line represents torq output by the involved limb. The solid line represents torque output by the noninvolved limb.
these fibers. The spindles respond to an increase in 5 A key (0 (he sliding mechanism is the calciu muscle length and the Golgi apparatus to an in- ion, which lu)-ns the contractile activity on and a crease in TllUSc!C tension. The resulting spindle re- flex increases muscle contraction, while the Goigi 6 The mOlOr unit, a single motor neuron and reflex inhibits contraction and enhances muscle musclc fibers inncrvatcd by it, is the smallesl pan relaxation. the muscle thal can contral:t independently. T calling in of additional motor units in response The intrafusal muscle spindles are or t\\Vo types: greater stimulation of thc rnotor nerve is known primary and secondary. The primary spindles re- recruitment. spond to changes in the rate of muscle lengthen- ing (dynamic response) and the actual amount or 7 The tendons and the endomysium, perim lengthening. The secondary spindles respond only sium, sarcolemma, and epimysium reprcsent par (0 the actual length change (static response). The lel and series clastic components dUll stretch w static response is weak and the dynarnic response aClive contraction or passive muscle extension a is strong: therefore, keeping the rate of stretch recoil with muscle relaxation. low may allow the dynamic response to be by- passed, essentially negating dte effect of the spin- 8 Summation occurs whcn mcchanical dles. Conversely, the increase in rnusclc tcnsion sponscs of the muscle to successivc stimuli a during stretching may activate the relaxing effect added to an initial response. \\Vhen maximal tensi of the Golgi apparatus and thus enhancc further is sustained as a result of summation, the mus stretching. The various 111ethods and theories of\" contracts tetanically. The muscle fiber contracts stretching all have as a common goal inhibition of an all-or-nothing fashion. the spindle effect and cnhanccrnent or the Golgi 9 Muscles may contract concentrically, eccent cally, or isometricaH)' depending on the relationsh effect to relax the muscle and promote further belween the muscle lension and thc rcsistance to lcngt hen ing. overcome. Concentric and eccentric contractio involve dynamic work, in which the muscle move Sllmm.ary joint or controls its 111ovcn1cnl. i!;< The structural unil of skeletal muscle is the ',10 Force production in muscle is influenced fil.;·c'r, which is encompassed by the endomysium the length-tension, load-velocity. nne! rorce-time and organized into fascicles encased in the perirny- lationships of the muscle. The length-tension re slum. The epimysium surrounds the entire musclc. tionship in a whole Illuscle is influenced by both tive (contractile) and passive (series and paral 2 The fibers are composed of myofibrils. aligned elastic) components. so as to create a band pallern. Each repeat of this 11 Two other factors that increase force produ pattern is a sarcomere, the functional unit 01\" the tion are prestretching or the muscle and a rise muscle tempenllure. contractile system. 12 The energy for muscle contraction and its 3 The myofibrils arc composed or thin filaments lease is provided by the hydrolytic splitting of AT of the protein actin and thick filaments of the pro- Muscle fatigue occurs \\\\'!hen the ability of the mu tein myosin, and the intramyofibrillar cytoskeleton cle to synthesize ATP is insufficient to keep is composed 01\" the clastic filaments titin and the in- with the rate of ATP breakdown during contra elastic filarnents ncbulin. tion. 4· According to the sliding filament theOl)\" active 13 Three main fiber types have been identifie shortening of the muscle results from the reiativL' type I, slow-twitch oxidative; type IIA, fast-twit movement of the actin and myosin filaments past one anothel: The force of contnlClion is developed oxidative-glycolytic; and type liB. fast-twitch g by movement of the myosin heads, or cross-bridges, in contact with the aclin filaments. Troponin and colytic fibers. Most muscles contain a mixture tropomyosin, two proteins in the actin helix, regu- these types. Iatc the making and breaking of the contacts be- tween r-ilamenls. .,14 Muscle atrophies occur under disuse and i mobilization; muscle trophism can' be restor through early and active rcmobilization.
REFERENCES Hi!ilop, H.J. ~ Perrine, J. (1967). The isokinelic I.:Olltl.'p Appell, H.J. (1997). Thl' muscle in the rch'lbilit~l!ion pro(\"e~s. cn:isc. Ph.\"..; Ther, -Ii. 114. OnJlOp{/{!t'. 26( 11).930-934. Huxley, A.F (1974). Muscul\"r contraction. J Physi<:d, 2- AITidson. I., Eriksson. E.. 6.:. Pitman, M. (1984). Neuromuscu- Huxley. A.F &. Huxll.'Y, H.E. (196-1). Organizcrs of:t disc orlar basis of n:. habilit'llioll. In E. Hunter & J. Funk (Eds.), of Ihe physical and chemical basis of l1l11st.:lllar tO RelllI!JiUtarioll the \"ljlt/wl I\\.\"m'c (pp. 210-234). SI. Louis: ntion. Pmc Sec. 8160. -433. C. V. Mosby. Kannus. P., JOI.5\", L.. K\\·j:.;1. ,\\1., Jarvinen, T\" J;lninc B;:lnkcr, B.O. (1994). Basic reaction of 1ll1lSt:!t:. In A.G. ErH!cl (1998aL EHeus of immobilizaLion and sllbseqm'n & C. Franzini-Al'fllstrong (Eds.), Myology (2nd cel.). N~\\\\' and high. intensity excrcise on morphology of I'~\\t tal )'ork: McGraw-HilI. Inc. cles. Scal/t! J ,\\Jed Sci Sports. 8(3), 160-171. Baratta R.V., Solornono\\\\', \\1., Z!lOtl, S.H. (1998), Frequency Kant1us. P., J~\\o't.zs(a1,99L8.b. ).JaFrn\\':ientm'n,obTil.Liz.,atiKo\\n'is,1t.1ld1\\'l1o.. wV- iteo domain-based llwdds of skeletal llluscle. J ElcclroJllyogr Jilrvinen, Kilu:siol, 8(1}, 79·91. Billes. B.T.. Ostl,.'l'lling. L.R., James. S,L. (1977). Fati!!uc ef· intensity exercise ill immobili/.ation-indllccd muscl phy. J ..\\ppl P/I\\'s;ol, 8-1(4), 1418-1424. feels in running. ) MOlor Be/ull'. 9. 203-107. - Kassel', l.R. (1996). Celleral Knowledge. III J.R. Ka5sI.. Brobeck, J. R. (Ed.) (1979). Bes/ lIml Ttl.do,.:, Physiological Bt/· Onltop{lcdic Kllou·l....d~i! lIpt/tltf! 5: I-Ioml.' Sr/flh- S\\' sis of :\\let/iclIl Practice (10th cd., pp. 59-113). B~llimore: Illinois: American :\\cad('my of Orthopaedic Su;·!!c(; \\\\'illinms &. Wilkins. Kedc. C.r\\ .• Nl.'il. E., ..\\: Jock N, (1982). \\Iusch: a,;d Ih Brooke. ;\\'1.1-1. &. K~iscr, K.K. (1970). Thn:e lllyosin adenosine vo u s system. In StllJl:WI/ W,.ighl~ AUpnpilni.e'ld'siPLh\\:rsPiroelso~\"~\\'\" Iriphosphat~sl: systcms: The nature of t1~cir pH liability cd .. pp. 248-259 ). Oxford : O.xford Komi, P. V. (1986). Tbl,.' slrl,.'tch-shorti.'nin~ t:v~le and and sulfhydryl depi.'nd\"llce. J l-listodl/!JIl Cy/oclli:lll. 18, power OUlpUt. In N.L. JOllCS, N. McCan·!lt.'\\·, ~ A. 670. Con~s (Eds.) I-ItlIIltlJl \"'//SciI.' POII'a (PI'. 2'7-39). Blll;ht~lhJ. F & Sohl1li.\\lburch, H. (1980). Motor unilS of Ill;llll- paign. IL: 1-lull1an Kin .... tics Publishers. 11l;llian Illusdt.'. Phniol Ret'. 60. 90. r\\.I'Oellll,.'l', I\\..H.E., Marr:ls. \\V.M., McGlothlin, J.D., Burh-, R.E .. Levinc, D.N.. Z~lj~~C. F.E. (1971). M~lnlllwlinn mo· (1990). On the IlH::ISUl'l..'lllent of hllm~\\ll stf'I..'Il!.nh. III ~ tor unils: Physiological hislochemic~ll corrckltion in Ihrce elliS! [;'/\",!!,OIlOlllics, 6, 199-21 O. types of motor units in cal gastrocllemius. Seicllct.', 17-1, Kroll. P.G. (1987). The <fjfi:Cl oFpl\"t.'l'iolls co!//rac/ioll cO 709. 011 SU!lS(,({IIl'11I l..'cn'Jllric PO\\\\'('I\" production iu dhol\\' Cost ill, D.L.. Coyle, E.F., Fink. W.F., l.. eslllcs, G.R .. Wilzmann. EA. (1979). Adapt.uioll in skeletal llluscles following IIIIISC!CS. Unpllbli~lwd doctoral dissertaLioll, New strengLh Lraining. J .-Ippl Pln'siol, 46.96·9, ~ University. Nt::\\\\· York. Craig. R. (199-4), The structur~ of (he contract filaments. In Lkbcr, RL. &. Bodine·Fowler, S.c. (1993). Sh'Il,.,t~d 1ll1lS A.~. ~ngd ,&. C. Fr<lnzini-Annstrong (Eds.), ,\\(mlogy (2nd ~hanics. ImpliGllions for n.'hahilit<ltion.l'h.l's Tho: t.'cI.). New )ork: i\\1cGraw·Hill, Inc 844-856. Crawford. C.N.C. &. J<101es. N.T. (1980). The dl'sign of mus- Linke, W.A .• In:·l1lcyl,.'l', ~L '\\-llInde!. P., Stockm,·icl'. orcles .. In R. O\"\". 'n, J. Goodfellow, ~ fl. Bullollgh (Eds.) Sci· Kolml,.·rL'r, B. (1998). N~lturl,.· of PEVK-titill e1asli skclet~ll muscle. PJ'(l(: NIlt! '-\\1.:lId Sci liS..\\. ~1!.lilie FOtllldaliOll.' Onltopacdics (lIId Tnl1lll/tllO!ogy (pp. 8052-8057. 0/-74). London: Willi.lm Heinemann. Luciano, D.S., Vander, :\\.1 .. .& Sherman, J.H. (1978). I Cuillo, J.V. & Zarins, B. (1983). Bioml,.'chanics of the mLlSt:U- I-'Il.I/clio/1 alll! Strl/('ltlrt' (pp. 113-136). New York: \\k lotcndinous unit: Relation 10 athk-lic performance and in· Hill. jury. Clilt Sports ,\\lcd, 2. 71. \\'lul1s.al. TL. NcNl.'al. D.. & Wat(-rs. R. (1976). Eff Eriksson, E., Hagglll;uk, T, Kiessling, K.H., l,.'t;:\\1. (1981). Ef- lll,.'l\"\\,e stimulation on human must-Ie. :lrcll N<'lI.rol, 3 feCI of dectrie:ll slimulation on human skelt.-Ial musde. 1m Sports :lIed. 2, IS. Ohir~l. Y.. Y~\\slli, w., Roy, R.R., Edgerlon, \\f.R. (199;). Galler, S.. Hilbcr. K. (1998). Tension/stirrncl-is ratio of skinned of mllscl\\: ll:ngLh on 1111: r('spons\\: to unloadirH2. ..le! rat skelcLallllllsde fibn.' types at v:\\l'iolls lCl11pCratllrt's. Ac/ ([Jasen. 159(2-3), 90-98. - Physio! Sctlml, 162(2), 119-126. Ottoson, D. (1983). I'hysio!o.!,:y of lhi' NO\"l'IllIS 8\"SI<,1 Gollnick, P.O. (1982). Ri..'lationship or strcngth and cndllr<lIlce 78-116), New York: Oxford Univcrsitv Press. . with skeletal muscle structure and llll,.·tabolic potential. lilt Parnianpou[\", ~...I.. Nordin, M .. Kahano\\\"iLz. N.. \"'I al. J Spons ,\\1t:tI (SliP!'!]. 3, 26. The triaxial collpling torque generation of trunk m Gordon, A.M., Huxley, A.F.!., &. Julian, FJ. (1966). The varia- during isometric I..'xl,.'nioI1S and tlti.' l,.'fb.:1 of fat tion in isol1\\l,.'tric 1i..'nsiOll with s;trC<llllt.'rt.' kngth in \\'I:.'rte- isoinerlial mOH'ltIents on the molor output <lnd mOH orbratc Illuscle fibers. J Physiol, 18-1, 170. pallcrns. Spillt.', 13(9). Guylon, A.C. (1986). Tex/book ,\\ledieal Pltysiolog\\' (7th e(l.). Pate, E., Bhimani, i\\l., Fnmks-Skib'l, K., Cook. R. (199 duced ('ffCCI of pH on skinned r~lhbit jlSO:lS musc Philndelphia: \\V.B. Saunders. . chanics at high temperatures: Implications for f\"l -' Hnm,. A.W. &. Corm:lck, D.H. (I979). Nis{olo~y (Sth cd.). Phl1adclphia: J.B. Lippincott. P!lysiol (Loud), -I86(Pt 3), 689-694. Hill, A. V. (1970). Firsl (//Ill L{lsi £'\\\"/1(:ri1l11:11/:; ;11 ,\\fl/sell! ,lh'· Phillips, C.,x. &. Pctrofsky, 1.5. (1983) . .\\lrchfUlics of S dUlllies. Cambridgl..': C;imbridgl: Uni\\'cl\"sitv Press. alltl e(mliut.' ,\\fuse/e. Springfield; Charles C. Thon1<ls Hill, O.K. (1968), Tl.:nsion due 10 interaction bt.~lween lhe slid- S\"ltin. B.• el al. (1977). Fiber types and I1K'tabolk polt ing filal1lt.'nts of resting $lriatcd museit.-. Thl,.' dft.'cr of of skdelal Illuscles in sedcntal\"}' m;m and enduranc stimulatinn. Pltysio! (LOllll], /99,637. n(;rs. :11111 NV ..lead Sd, 301. 3.
Snndm<tnn, ~I.E.. Shoemanll. J.A .. Thompson. L. V, (1998). T:lbrad~l, Y., (wnll\\oto, 1-1., Sugi. 1-1 .. Hir~ln(), Y.. Ishi (1997). Strctch-ilH.luccd l'nhanCCIllc.'Jll of m':\"chanical Th..:- fib1.'r·typ ...·spccific effcct of inactivity and intcrmillellt production in long frog single fihers and hUIll<ln mus App! Physio!, 83(5),1741-17-4$. wci2ht·henring on the !!aslroc!lcmius of 30'lllollth-old rats~ Arch PI/\\'~ ,lied UCllllb;/, 79(6), 658-662. Wilkie. D.R. (J956). The mechanical propenies of llluscl Squire. J.~1. (1997). Architecture and fUllction in thl.: muscl~ .\\It'd BIIII, /2, 177. s~lI·comcrl·. e/ln Opill Stl'llCI Bio!. 7(2). 247-257. Strom~r, M.H. (1998). Thc cytoskelelon in skckt;-.l. c:lI'di:1C Wilkie, D.R. (1968) . .\\lusc/c. london: Edward Arnold. :lIId smooth muscl~ (dis. His/o! f/islOpa/llOl, / 3( I). Williams, P. &. Warwick. R. (1980). Gray:.; rlJlll/om.\" 06tl1 283-291. pp. 506-5(5). Edinburgh: Churchill Livingstone. -'::' ' '-'\" i.: \",' '''\"
--:----- ,.... ,.' ,·_-------·1· . ···~ -- .......... -
---------1 z o ·--. --------1'',.\". ,. ;0= .~ ~ ~ e- \"0 Z 0 u0 \"9 1< \"'\"v~ \" >z!' ~ :> =E <; =<;; ~ -0; >0 .0,;; ~ ~I6~ , '\"(; 'g\" c .~ .:2;; .~ .c~ \":=c,- ~ '<\"; -0 <; e<=; C l'\"' ~< t ~ § 2 ~ ~ .\"=0~ \".~ -\",5 g ;::
,~:':,i$;\\') \",:tt:./ ;1~& .:)~;;;: ,.', u.... '.;'x. j,t-:;:\". . e2? ij <~- .-,~, :\". \"., ~.
. \"c~. s.~ E .2 ~ XX ~0 :s;;; .0a v £ 0c 0 ''\"\" 0 ~ E-c0 E .-~ .\" \"v~ ~ .0;; ~ 3 E ;0;: -S \".~ .\" .~ .!!i ~ .,.~ '5 ,c,~ ~ 0 0. 0 ~ § i; .ev E v e0 :~ ~ v0 wx 2 .\" 0 C .'~\" .\" .~ \".0;; .g3 ..0a '\"
~ Intrinsic disord *This flow chart is designed for classroom or
ders associated with muscle damage. Clinical examples. * r group discussion. Flow chart is not meant to be exhaustive.
Biomechanics of Joints
Biomechanics of the Knee Margareta Nordin, Victor H. Franke Introduction Kinematics Range of Motion Surface Joint ~J1otion Tibiofemoral Joint Patellofemoral Joint Kinetics Statics of the Tibiofemoral Joint Dynamics of the Tibiofemoral Joint Stability of the Knee JOint Function of the Patella Statics and Dynamics of the Patellofemoral Joint Summary References
Introduction The knce is particularl... \\vell suited for dem strating biomechanical anal.vscs of joints beca The knee transmits loads, part III pales in motion, these anal..,scs can be simplified in the knee and aids in conservation of momentum, and provides a yield useful data. Although knee motion occurs force couple for activities involving the leg. The hu- multancous!y\" in three planes, thc motion in man knee, the largest and perhaps 1110st complex planc is so great that it accounts for nearly all of joint in the bod)!, is a two-joint structure composed motion. Also, although many muscles prod 'of the tibiofemoral joint and the patellofcmoral forces on the knee, at any particular instant joint (Fig. 7-1). The knee sustains high forces and muscle group predominates, generating a force moments and is situated between the body's two great that it accounts for most of the muscle fo longest lever arms (the femur and the tibia), making acting on the knee. Thus, basic biomedwni it particularly' susceptible to injury. This d18ptcr uti- analyscs can be limited to motion in one plane lizes the knee to introduce the basic terms, explain to the force produced by a single muscle group the methods, and demonstrate the calculations nec- still give an understanding of kncc mc)tion and essary for analyzing joint motion and the forces and estimation of the magnitude of the principal for moments acting on a joint. This information is np· and moments on the knee. Advanced bioIllcchan plied to other joints in subsequcnt chaptcrs. d.\\'namic anal,\\'ses of thc knee joint that include Anterior cruclate ligament Popliteus Medial tendon collateral Fibular ligament collateral Semimembrano ligament Superficial Biceps medial collat femoris ligament (cu tendon Transverse ligament Iliotibial Gracillis band (cut) Semitendinosus Sartorius Interosseous -cr--l'- membrane Patellar tendon B Two-joint structure of the knee. A, Lateral view of a knee joint with open growth plates. B, Anterior view without patella.
soft tissue structures are complex and still under in- Kinematics vestigation. Kinematics defines thl..' range of motion an Analysis or motion in any joint requires the lise of scribes the sw-facc motion of a joint in three p kinematic daw. Kinematics is the branch of mc- frontal (coronal or longitudinal), sagittal, and crlanics thal deals with Illotion of a body without verse (horizonlal) (Fig. 7H 2, A & B). Clinical reference to force or mass. Anal:vsis of the forces surements of joint range 01\" motion defin and momenl~ acting on a joint necessitates the anatomical position as a zero position for mc usc of both kinematic and kinetic data. Kinetics is ment. This laxonomy will be uscd for joint m the branch of mechanics that deals with the motion throughout this book. Other taxonomies and of a body under the action of given forces and/or ence systems exist (Ant!riacchi et aI., 1979; Gr moments. ~!1j\"~~;;:~i..k~~~i===::::=Frpolannelal Proximal/ I~.•., -Sagittal dislal o ;,.j ~ plane Internal/external k'. ~)1 Varus! valgus AB A, Frontal (coronal or longitudinal), sagittal. and transverse tion and proximal distal translation, flexion-extension (horizontal) planes in the human body performed easily for tion, internal-external rotation, varus-valgus rotation. both the tibiofemoral and the patellofemoral joint. B, Depic- Adapted from Wilson, S.A., Vigorita, V.J., & Scott, W.N tion and nomenclature of the six degrees of freedom of knee (1994). Anacomy. In N. Scott (Ed.), The Knee (p. 17). Philad motion: anterior posterior translation, medial/lateral transla- Mosby- Year Book. .,...<:, \";'~,' I?:A
Sun tal' 1983; Kroemer ct aL. 1990; bzkaya & -20 !:=------;!':---7::----==---:'::-- Nordin, 1999), but the anatomical reference system bv far is the mOSl commonlv lIsed among clinicians. 100 20 40 60 80 10 O'r the two joints composing the kne'; the tibio- Percentage of Cycle femoral joint lends itself particularly well to an Range of motion of the tibiofemoral joint in the sagittal analysis of range orjoinl motion. Analysis of surface plane during level walking in one gait cycle. The shaded joint motion can be performed easily For both the dred indicates variation among 60 subjects (age range 20 tibiofemoral and the P<'11cllofcmoral joint. An~' im- to 65 years). Adapted {rom MtJ((a}~ M.P., Drought, A.B., Kor} pediment of range of motion or surface joint 'motion R. C. (1964j. I/o/alking patterns of norma! men. J Bone Joint Su will disturb the normal loading pattern of' a joint 46A,335, a.nd bear consequences. in this joint during walking has been measured RANGE OF MOTION all planes. The range of motion in the sagittal pla during level walking was measured with an e1ectr orThe range motion of any joint can be measured in goniometer by Lamoreaux (1971) and MUlTay et (1964). Full or nearly Full extension was noted at t any plane. Gross measurements can be made with a beginning of the stance phase (0% of cycle) at he goniometer, but more specific measurements re- strike, and at the end of the stance phase before LO off (around 60% of cycle) (Fig, 7-3), Maximum fle quire the lise or more precise methods such as elcc- ion (approximately 60°) was observed during t middle of the swing phase (sec Chapter 18, Biom lrogoniomelr~·. roenlgenogJ\"aphy. stcreopllologralll- chanics of Gait. For more detailed inFormation metr)'. or photographic and video techniques using These measurements are velocit.y-c1ependent an skeletal pins, must be interpreted with caution. In the tibiofcmoral jail'll. nlOtion takes place in all ~\"lotion in the transverse plane during walking h three planes, but the range of motion is greatest by been measured by several investigators. Using a ph far in the sagittal plane. Motion in this plane from lOgraphic technique involving the placement full extcnsion to Fulillexion of the knee is from 0' to skeletal pins through the femur and tibia, Leve approximately 140°. and associates (1948) Found that total rotation of t tibia with respect to the fernur ranged from appro Motion in the transverse plane. intel-nnl and ex- imately 4 to 13' in 12 subjects (mean 8,6'). Great ternal rotation. is inOuenced by the position of the rotation (mean 133') was noted by Kettclkamp an joint in the sagittal plane, With the knee in Full ex- coworkers (1970). who used electrogoniollletry o tension. rOHHion is almost completely restl'ictcd b~f 22 subjects. In both studies, external rotation beg the interlocking of the femoral and tibial condyles. during knee extension in the stance phase an which occurs mainly because the medial femoral reached a peak value at the end of th~ swing pha condyle is longer than the lateral condyle. The range just before heel strike. Internal rotation was note of rotation increases as the knee is flexed, reaching during Ilexion in the swing: phase. a maximum at 90° of nexion; with the knee in this :- position. external rotation ranges from 0° to ap- proximately 45° and internal rotation ranges from 0' to appmximatcly 3D'. Beyond 90' of Ilexion. the range of internal and external rotation decreases, primarily because the soft tissues restrict rOlation. Motion in the frontal plane. abduction and ad- duction. is similarly aFfected by the amount of joint flexion, Full extension of the knee precludes almost all motion in the frontal plane. Passive abduction and adduction increase with knee Oexion up to 30°. but each reaches a maximum of only a few degrees. With the knee flexed beyond 3D'. motion in the frontal plane again c1ecre~lses because of the limit- ing function of the sol't tissues. The range of tibiofernoral joint motion required For the performance of various physical activities can be determined from kinematic anal~lsis. MOlion
Search
Read the Text Version
- 1
- 2
- 3
- 4
- 5
- 6
- 7
- 8
- 9
- 10
- 11
- 12
- 13
- 14
- 15
- 16
- 17
- 18
- 19
- 20
- 21
- 22
- 23
- 24
- 25
- 26
- 27
- 28
- 29
- 30
- 31
- 32
- 33
- 34
- 35
- 36
- 37
- 38
- 39
- 40
- 41
- 42
- 43
- 44
- 45
- 46
- 47
- 48
- 49
- 50
- 51
- 52
- 53
- 54
- 55
- 56
- 57
- 58
- 59
- 60
- 61
- 62
- 63
- 64
- 65
- 66
- 67
- 68
- 69
- 70
- 71
- 72
- 73
- 74
- 75
- 76
- 77
- 78
- 79
- 80
- 81
- 82
- 83
- 84
- 85
- 86
- 87
- 88
- 89
- 90
- 91
- 92
- 93
- 94
- 95
- 96
- 97
- 98
- 99
- 100
- 101
- 102
- 103
- 104
- 105
- 106
- 107
- 108
- 109
- 110
- 111
- 112
- 113
- 114
- 115
- 116
- 117
- 118
- 119
- 120
- 121
- 122
- 123
- 124
- 125
- 126
- 127
- 128
- 129
- 130
- 131
- 132
- 133
- 134
- 135
- 136
- 137
- 138
- 139
- 140
- 141
- 142
- 143
- 144
- 145
- 146
- 147
- 148
- 149
- 150
- 151
- 152
- 153
- 154
- 155
- 156
- 157
- 158
- 159
- 160
- 161
- 162
- 163
- 164
- 165
- 166
- 167
- 168
- 169
- 170
- 171
- 172
- 173
- 174
- 175
- 176
- 177
- 178
- 179
- 180
- 181
- 182
- 183
- 184
- 185
- 186
- 187
- 188
- 189
- 190
- 191
- 192
- 193
- 194
- 195
- 196
- 197
- 198
- 199
- 200
- 201
- 202
- 203
- 204
- 205
- 206
- 207
- 208
- 209
- 210
- 211
- 212
- 213
- 214
- 215
- 216
- 217
- 218
- 219
- 220
- 221
- 222
- 223
- 224
- 225
- 226
- 227
- 228
- 229
- 230
- 231
- 232
- 233
- 234
- 235
- 236
- 237
- 238
- 239
- 240
- 241
- 242
- 243
- 244
- 245
- 246
- 247
- 248
- 249
- 250
- 251
- 252
- 253
- 254
- 255
- 256
- 257
- 258
- 259
- 260
- 261
- 262
- 263
- 264
- 265
- 266
- 267
- 268
- 269
- 270
- 271
- 272
- 273
- 274
- 275
- 276
- 277
- 278
- 279
- 280
- 281
- 282
- 283
- 284
- 285
- 286
- 287
- 288
- 289
- 290
- 291
- 292
- 293
- 294
- 295
- 296
- 297
- 298
- 299
- 300
- 301
- 302
- 303
- 304
- 305
- 306
- 307
- 308
- 309
- 310
- 311
- 312
- 313
- 314
- 315
- 316
- 317
- 318
- 319
- 320
- 321
- 322
- 323
- 324
- 325
- 326
- 327
- 328
- 329
- 330
- 331
- 332
- 333
- 334
- 335
- 336
- 337
- 338
- 339
- 340
- 341
- 342
- 343
- 344
- 345
- 346
- 347
- 348
- 349
- 350
- 351
- 352
- 353
- 354
- 355
- 356
- 357
- 358
- 359
- 360
- 361
- 362
- 363
- 364
- 365
- 366
- 367
- 368
- 369
- 370
- 371
- 372
- 373
- 374
- 375
- 376
- 377
- 378
- 379
- 380
- 381
- 382
- 383
- 384
- 385
- 386
- 387
- 388
- 389
- 390
- 391
- 392
- 393
- 394
- 395
- 396
- 397
- 398
- 399
- 400
- 401
- 402
- 403
- 404
- 405
- 406
- 407
- 408
- 409
- 410
- 411
- 412
- 413
- 414
- 415
- 416
- 417
- 418
- 419
- 420
- 421
- 422
- 423
- 424
- 425
- 426
- 427
- 428
- 429
- 430
- 431
- 432
- 433
- 434
- 435
- 436
- 437
- 438
- 439
- 440
- 441
- 442
- 443
- 444
- 445
- 446
- 447
- 448
- 449
- 450
- 451
- 452
- 453
- 454
- 455
- 456
- 457
- 458
- 459
- 460
- 461
- 462
- 463
- 464
- 465
- 466
- 467
- 468
- 469
- 470
- 471
- 472
- 473
- 474
- 475
- 476
- 477
- 478
- 479
- 480
- 481
- 482
- 483
- 1 - 50
- 51 - 100
- 101 - 150
- 151 - 200
- 201 - 250
- 251 - 300
- 301 - 350
- 351 - 400
- 401 - 450
- 451 - 483
Pages:
