The physiology of injured skeletal muscle

The functional unit responsible for bodily movement or the generation of static force is composed of a skeletal muscle, its tendonous attachments and the bones onto which these tendons are inserted. In this article, attention will be focused on the response of muscle tissue to injury, to the exclusion of a coverage of injuries to tendon and bone.

Skeletal muscle accounts for about 40 per cent of the total bodyweight of the average adult male, and a slightly lower proportion in the adult female. Most of this muscle tissue is located close to the body surface, usually overlying the rigid components of the skeletal system. Because of this, it is likely that the application of external violence to the body will result in muscular damage. Newman et al (1969) found that in a population of 1847 patients suffering from sports injuries, 14 per cent of the cases involved injury to skeletal muscle. The implications of this for the athlete are obvious, since all sporting activity requires involvement of at least part of the muscle mass. The competitive athlete is also particularly susceptible to muscular injury as a result of acute or chronic overuse. Inability to train or compete due to injury is a personal catastrophe for the serious athlete, and the aim of treatment must be to minimise the initial damage and to maximise recovery. An understanding of the physiological effects of trauma on skeletal muscle must form the basis of successful treatment.

STRUCTURE AND FUNCTION OF MUSCLE

In cross-section, the light microscope reveals the muscle as consisting of bundles of individual fibres enclosed within the fascia, a tough collagenous sheet which forms an outer connective tissue sheath. Within this outer sheath, the epimysium, the fibres are grouped in bundles, each normally containing 20 to 40 fibres and each being surrounded by a less substantial envelope of connective tissue, the perimysium. Each fibre is enclosed within a fine collagen network, the endomysium. Large muscles may contain many thousands of fibres, although the very smallest muscles consist of only a few fibres grouped together. Irrespective of the size of the muscle, each fibre is between and Sofx in diameter (Bendall, 1969).

In longitudinal sections of skeletal muscle, the light miscroscope reveals the characteristic cross-striations of the fibres: further detail can be resolved by use of the electron microscope . Each fibre is composed of a large number of myofibrils, each 1 to 1.5/u. in diameter. The myofibril can be considered as the basic contractile unit of the muscle cell. The myofibril itself is composed of bundles of microfilaments. The striated appearance of the muscle is due to the composition of the microfilaments, the light region is due to the presence of the protein actin, the dark region being composed of another protein, myosin. It is the physical and chemical properties of these proteins which enable the muscle to shorten or to generate tension. These phenomena occur not as a result of contraction of any of the physical structures of the muscle but because of a relative sliding motion of the microfilaments.

Also present within the fibre are other structures essential for the normal functioning of the cell. All striated muscle cells contain nuclei located along the length of the cell immediately under the cell membrane. Mitochondria within the cell are responsible for the maintenance of the oxidative energy supply. Also present is a delicate internal membrane system, the sarcotubular system, which is involved in the control of the initiation of contraction in response to a nervous impulse. Substrate depots are present in the form of glycogen granules and lipid droplets. The blood supply to the muscle consists of an extensive network of capillaries which surrounds the fibre, the capillary density being higher in trained than in untrained muscle (Andersen, 1975).

The mechanical properties of the muscle depend upon the existence of the contractile apparatus, but the activity of the contractile components is modified by the presence ofjelastic components in the muscle. The series elastic component lies not within the muscle itself but within the tendons into which the muscle fibres are inserted and which attach the muscle to the bone. The parallel elastic component is due to the presence of the non-contractile structures of the muscle, including the cell membranes, sarcotubular system and connective tissue. These elastic elements have the effect of damping the contractions produced by the contractile apparatus which must first stretch the elastic tissue before shortening or load bearing can occur.

EFFECTS OF TRAUMA ON SKELETAL MUSCLE Muscle injuries can occur as a result of intrinsic factors generated from within the muscle, or from extrinsic factors which originate outside the tissue. Both of these types of factors can result in damage to the muscle fibres, to the associated connective tissue or to the vascular system. Tearing or rupture of the muscle as a result of excessive stretch or of a direct blow on the surface of the muscle may be complete, in which case loss of function is also complete due to loss of structural continuity. Such cases are, however, relatively rare. Rupture of the muscle appears to be most common in the region of the muscle-tendon junction (Burry, 1973) and will be visible as a bunching of the muscle due to retraction from the severed region. It is not clear why the muscle-tendon junction should be weaker than the belly of the muscle itself. Tears, strains and pulls of the muscle describe cases of partial rupture in which the damage is restricted to a limited number of fibres.

Associated with the damage to the contractile components of the muscle, rupture of connective tissue and blood vessels normally occurs at the site of the injury, leading to the formation of a haematoma. If the epimysium remains intact, blood escaping from damaged capillaries is retained within the muscle, leading to a rise in intramuscular pressure and associated pain and loss of function. Because the blood remains within the muscle such an outcome is termed an intramuscular haematoma. If the injury has resulted in splitting of the fascia, an interstitial haematoma is formed, in which the increase in pressure is avoided due to the escape of blood into the interstitial spaces. As a result, the effects of an interstitial haematoma in terms of pain and disability are generally less severe than those produced by an intramuscular haematoma, although it may produce rather spectacular discolouration of the skin either in the region of the wound or further down the limb.

RECOVERY AND REPAIR OF DAMAGED TISSUE The repair of damage to skeletal muscle involves two separate processes which shall be dealt with separately; the first of these involves the formation of non-contractile collagenous fibres, the second depends on the capacity of the muscle tissue for regeneration.

Following injury, the tissue is infiltrated by macrophages. These cells are converted to fibroblasts which proliferate rapidly in the damaged area. Existing fibroblasts also rapidly divide. This proliferation appears to result from the inactivation of inhibitory substances which are normally present in healthy tissues. An increase in the number of fibroblasts in the region of a wound has been observed to occur within 24 hours of wound infliction (Dunphy and Udupa, 1955). These fibroblasts secrete a soluble protein precursor of collagen and, in their mature form, these cells remain in the tissue as fibrocytes. The process of maturation is accompanied by an irreversible shortening of the fibrocytes, leading to the tendency of muscle wounds to heal short. The strength of this scar tissue progressively increases, reaching a maximum some months after its initial formation (Douglas, 1966). Because it is non-contractile, this fibrous tissue cannot contribute to the generation of tension by the muscle, but it allows the undamaged muscle to fulfil its normal function.

It was established by Gay and Hunt (1954) that skeletal muscle possesses the capacity of regeneration to the extent that complete reunion of transected fibres is possible if the cut ends of the fibres are closely opposed following sectioning. They suggested that the majority of the cut fibres in the muscles which they studied had successfully reunited. It should, of course, be realised that surgical sectioning of muscle produces a clean cut through the fibres, whereas muscle lacerations sustained in the sporting situation seldom involve simple transection of the fibres, but are usually associated with considerable damage, which makes it impossible to oppose accurately the damaged ends of the fibres.

There is a widespread misconception that muscle is incapable of regenerative repair. Experimental work on animals has, however, demonstrated that skeletal muscle possesses a high capacity for regeneration (Carlson, 1968; Carlson and Gutman, 1972). Carlson performed a series of experiments in which complete animal muscles were removed, minced into small (lmm3) pieces and re-implanted in their original sites. He showed recovery of the muscle begins almost immediately and follows a sequence of events similar to those undergone by normal muscle in the post-natal period. Morphological changes can be observed within two to three days, with the appearance of myoblasts around the edges of the minced tissue. Progressive regeneration takes place during the succeeding weeks, spreading through the muscle mass, and re-attachment to the existing tendon stumps takes place. The original fibres degenerate and disappear, and cross-striations begin to appear in the new developing fibres. The contractile properties of the muscle also gradually return, the first responses being observed about seven to eight days after the operative procedure; it is at about this time that the presence of cross-striations in the immature fibres is first noted. Although functional re-innervation of the regenerating muscle occurs, complete recovery in terms of strength is not achieved. Each of the new fibres possesses almost normal functional characteristics, but the new muscle contains relatively few fibres and large amounts of connective tissue. The total tension which the muscle is capable of producing is therefore less than that of normal muscles. These experiments do, however, demonstrate that mature muscle is capable of recovery by regeneration. The experiments quoted here were done, for obvious reasons, on animals rather than on human subjects, but there seems to be little doubt that the results are generally applicable to mammalian skeletal muscle.

Occasionally, the process of recovery and repair is complicated by bacterial infection of the wound or by the formation of serum filled cysts resulting from incomplete re-absorbtion of the haematoma. In such cases, surgical drainage may be required. A more serious complication is the development of myositis ossificans. This ossification process is due to the invasion of the haematoma formed at the time of injury by osteoblasts which are probably derived from the damaged periosteum. Maturation of these cells leads to the formation in the muscle of an open network of bone. The patient will experience symptoms of pain, swelling and disability. If this condition is present, exercise of the affected limb should be strictly avoided, as this may result in further damage and increased ossification (Ellis and Franck, 1966). It is quite probable that the associated pain will result in disinclination on the part of the subject, but it should be realised that vigorous massage may be equally dangerous.

PHYSIOLOGICAL EFFECTS OF TREATMENT The object of any treatment given to the injured athlete must be to minimise damage in the short term and to maximise recovery in the long term. In the immediate post-injury phase, this should be accomplished by attempting to eliminate bleeding at the site of injury and by preventing movement which might aggravate muscular damage. The first of these objectives is normally achieved by the application of cold or pressure, or both. By increasing the local tissue pressure as a result of bandaging to the point at which it exceeds the systolic pressure, occlusion of the blood vessels in the area below the bandage will occur. Application of cold in the form of proprietary cold packs, sprays or ice has a two-fold effect. Firstly, blood flow is decreased as a result of a decrease in local metabolic rate due to the decreased temperature of the tissues. This mechanism, however, is of little importance compared with the reflex inhibition of blood flow which occurs. In response to stimulation of cold receptors, probably in the form of free nerve endings in the skin, a reflex mechanism exists whereby local vasoconstriction takes place as a result of contraction of the smooth muscle lining the arterioles. If the application of cold is too severe and prolonged, accumulation of vasoactive metabolities will occur as a result of anaerobic metabolism. This will normally overcome the cold-induced reflex vasoconstriction, and a period of high local blood flow ensues. This in turn gives way to vasoconstriction and a cyclical pattern of alternate high and low blood flow is observed. However, the net effect is an overall decrease in local blood flow, and a combination of cold and pressure is strongly recommended if intramuscular bleeding is suspected. The American Medical Association Committee on the Medical Aspects of Sports recommended application of cold during the first 24 to 48 hours after injury (Hein, 1969). Williams and Sper-ryn (1976) advised that pressure be applied and maintained for 48 to 72 hours.

Most injuries are presented for treatment only after some time has elapsed, and are consequently too late for first aid treatment. The aim in these cases, as indeed in all cases, must be to obtain maximum restoration of function, normally in the shortest time possible, as the sportsman is invariably anxious to return to training and competition. A wide choice of treatments is available, and each case must be considered on an individual basis. The aim of these treatments is generally to stimulate local blood flow, and in this respect, local heating, massage and exercise are all effective.

Application of heat from infra-red sources is widely used, but for heating of deep tissue structures, this method is rather ineffective. Ultrasound treatment is effective in producing localised heating in deep structures, but tends to produce its effects most markedly in underlying bone rather than in muscle (Bass, 1969). Dyson et al (1970), however, showed that ultrasound therapy was effective in promoting healing of experimental lesions.

Massage with ice (cryokinetics) has been suggested as a treatment for chronic injuries in addition to its use in the immediate post-injury phase (Grant, 1964; Laing et al, 1973). There is no satisfactory explanation for the beneficial effects which this treatment has been reported to produce.

Surface massage has a two-fold effect, by promoting re-absorption of any haematoma which may be present and by stimulating blood flow in the affected area. In conjunction with massage, a gradual return to exercise should be undertaken. This can take the form initially of stretching exercises against gentle resistance and may take the form of active stretching of the muscle by the patient or of externally applied manipulation to the joints. Rylander (1969) has proposed that a more vigorous exercise programme than that normally recommended is effective in promoting recovery. Except in cases of myositis ossificans, rest will normally delay recovery, and is not to be recommended.

It has been suggested that administration of antiinflammatory drugs, such as oxyphenbutazone (Blazina, 1969), indomethacin, phenylbutazone, meferamic acid and flufenamic acid (Bass, 1969) are effective in aiding rehabilitation. In contrast to these reports, a double-blind study by Huskisson et al (1973) showed that indomethacin treatment was not superior to a placebo administered to injured football players.

EFFECTS OF TRAINING AND DISUSE ON SKELETAL MUSCLE Sports injuries, by definition, occur to sportsmen and sportswomen, and it should be recognised that the muscle of the trained athlete is different in some respects from that of the normal non-athletic individual. The aim of a training regime is to produce an adaptive response which will facilitate the performance of exercise. If the athlete is prevented from training by injury, these processes are reversed, and a detraining effect is observed. Training and fitness are obviously specific to individual sports, and the characteristics of the endurance athlete are quite different from those of the heavyweight weightlifter. The endurance athlete has a highly developed cardiovascular system: the increased dimensions of this system facilitate an increased oxygen delivery to the working muscles. In addition, the oxidative capacity of the muscle is enhanced by an increased concentration of the enzymes and co-factors involved in oxidative energy supply. These adaptations result in an improved ability to maintain a high level of energy production without the onset of fatigue. The training programme of the athlete whose event is based on strength rather than endurance is designed to increase both muscle mass and the strength of the muscle per unit cross-sectional area. These aims can be achieved independently by a careful choice of the training stimulus. The full effects of a training programme become apparent over a period of months or years rather than weeks. It is of interest, therefore, to note that Salt in et al (1968) found that the maximum oxygen uptake, a measure of endurance capacity, was decreased by approximately 26 per cent in response to 21 days bed rest. In the rat, immobilisation of a limb resulted in a rapid decrease in the concentration of enzymes involved in oxidative energy production; these responses to disuse occurred in an exponential fashion, one half of the total decrease being complete in four to six days (Booth, 1977). Similar changes in the weights of individual muscles in the immobilised limb were also recorded. Thus the decrease in both endurance and strength is extremely rapid when compared with the time necessary to produce the training effect. It is for these reasons that absence from training due to injury should be minimised.

Skeletal muscle is a highly specialised tissue, adapted for the performance of physical work in the form of movement or tension generation. Injury to muscle may result from acute or chronic overuse, or from the application of external violence. Injury may take the form of damage to the contractile apparatus, but often also involves rupture of the vascular system, and consequent extravasation of blood leading to an increase in intramuscular pressure and associated pain. The repair and recovery processes involve a degree of regeneration of muscular tissue and the formation of fibrous scar tissue.

Treatment should aim to eliminate further damage by restricting movement in the immediate post-injury phase and limit bleeding by application of cold and pressure. During the recovery phase, massage and heat application should be used in conjunction with a gradual return to normal activity. The return to full training should be accomplished as rapidly as is possible in order to minimise the de-training effect which accompanies muscular disuse.

REFERENCES

Andersen, P. (1975). Capillary density in skeletal muscle of man. Acta Physiologia Scandinavica, 95, 203-205. Bass, A. L. (1969). Treatment of muscle, tendon and minor joint injuries in sport. Proceedings of the Royal Society of Medicine, 62, 925-928. Bendall, J. R. (1969). Muscles, molecules and movement.

Heinemann, London. Blazina, M. E. (1969). Oxyphenbutazone as an adjunct to the conventional treatment of athletic injuries.

Clinical Medicine, 161, 19-22. Booth, F. W. (1977). Time course of muscular atrophy during immobilisation of hind limbs in tats. Journal of Applied Physiology, 43, 656-661. Burry, H. C. (1973). Soft tissue injury in sport. In J. H.

Wilmore (ed). Exercise and sports sciences reviews.

Academic Press, New York.

Carlson, B. M. (1968). Regeneration of the completely excised gastrocnemius muscle in the frog and rat from minced muscle fragments. Journal of Morphology, 125, 447-471.

Carlson, B. M. and Gutmann, E. (1972). Development of contractile properties of minced muscle regenerates in the rat. Experimental Neurology ,36,239-249.

Douglas, D. M. (1966). Wound healing. Churchill, London.

Dunphy, J. E. and Udupa, K. N. (1955). Chemical and histochemical sequences in the normal healing of wounds. New England Journal of Medicine, 253, 847-851.

Dyson, M. Ford, J. B., Joseph J. and Warwick, R. (1970). Stimulation of tissue regeneration by pulsed planewave ultrasound. Institute of Electrical and Electronic Engineers Transactions of Sonics and Ultrasound, 17, 133-140.

Ellis, M. and Frank, H. G. (1966). Myositis ossificans traumatica: with special reference to the quadriceps femoris muscle. The Journal of Trauma, 6,724-738.

Gay, A. J. and Hunt, T. E. (1954). Reuniting of skeletal muscle fibres after transection. Anatomical Record, 120, 853-871.

Grant, A. E. (1964). Massage with ice (cryokinetics) in the treatment of painful conditions of the musculoskeletal system. Archives of Physical Medicine and Rehabilitation, 45, 233-238.

Hein, F. V. (1969). Continuous cold application for athletic injuries. Journal of the American Medical Association, 207, 962.

Huskisson, E. K., Berry, H., Street, F. G. and Medhurst, H. E. (1973). Indomethacin for soft tissue injuries. Rheumatology and Rehabilitation, 12, 159-160.

Laing, D. R., Dalley, D. R. and Kirk, J. A. (1973). Ice therapy in soft tissue injuries. New Zealand Medical Journal, 78, 155-158.

Newman, P. H., Thompson, J. P. S., Barnes, J. M. and Moore T. M. C. (1969). A clinic for athletic injuries. Proceedings of the Royal Society of Medicine, 62, 939-941.

Rylander, C. R. (1969). Rehabilitation of the injured athlete. Delaware Medical Journal, 41, 271-273.

Saltin, B., Blomqvist, C, Mitchell, J. H., Johnson, R. L., Wildenthal, K. and Chapman, C. B. (1968). Response to exercise after bedrest and after training. Circulation, Supplementum, 7.

Williams, J. G. P. and Sperryn, P. N. (1976). Sports medicine. Edward Arnold, London.

Sorry, comments are closed for this post.

Share On Facebook
Share On Twitter
Share On Google Plus
Share On Pinterest