The objective of this review is to evaluate the measurement tools currently used in the study of eccentric contraction-induced muscle injury, with emphasis on their usefulness for quantifying the magnitude and duration of the injury and as indicators of muscle functional deficits. In studies in humans, it was concluded that measurements of maximal voluntary contraction torque and range of motion provide the best methods for quantifying muscle injury. Similarly, in animal studies, the in vitro measurement of electrically elicited force under isometric conditions was considered to be the best of the measurement tools currently in use. For future studies, more effort should be put into measuring other contractile parameters (e.g. force/torque-velocity and force/torque-length relationships maximal shortening velocity and fatigue susceptibility) that may reflect injury-induced functional impairments. The use of histology, ratings of soreness and the measurement of blood or bath levels of myofibre proteins should be discouraged for purposes of quantifying muscle injury and/or functional impairment.

The purpose of this study was to estimate the absolute and relative masses of the three types of skeletal muscle fibers in the total hindlimb of the male Sprague-Dawley rat (Rattus norvegicus). For six rats, total body mass was recorded and the following weights taken from dissection of one hindlimb: 32 individual major muscles or muscle parts, remaining skeletal musculature (small hip muscles and intrinsic foot muscles), bone, inguinal fat pad, and skin. The fibers from the 32 muscles or muscle parts (which constituted 98% of the hindlimb skeletal muscle mass) were classified from histochemistry as fast-twitch oxidative glycolytic (FOG), fast-twitch glycolytic (FG), or slow-twitch oxidative (SO), and their populations were determined. Fiber cross-sectional areas from the same muscles were measured with a digitizer. Mass of each of the fiber types within muscles and in the total hindlimb was then calculated from fiber-type population, fiber-type area, and muscle-mass data. Skeletal muscle made up 71% of the total hindlimb mass. Of this, 76% was occupied by FG fibers, 19% by FOG fibers, and 5% by SO fibers. Thus, the FG fiber type is clearly the predominant fiber type in the rat hindlimb in terms of muscle mass. Fiber-type mass data are compared with physiological (blood flow) and biochemical (succinate dehydrogenase activities) data for the muscles taken from previous studies, and it is demonstrated that these functional properties are closely related to the proportions of muscle mass composed of the various fiber types.

These experiments were designed to study skeletal muscle pathology resulting from eccentric-biased exercise in rats. The effects on the muscles of running on a treadmill on a 0 degrees incline (similar amounts of concentric and eccentric contractions), down a 16 degrees incline (primarily eccentric contractions), and up a 16 degrees incline (primarily concentric contractions) at 16 m . min-1 for 90 min were assessed by following postexercise changes in 1) plasma creatine kinase and lactate dehydrogenase activities, 2) glucose-6-phosphate dehydrogenase (G-6-PDase) activity (bio- and histochemically) in the physiological extensor muscles, and 3) histological appearance of the muscles. The data indicate the following. 1) Whereas all exercise protocols resulted in elevations of plasma enzymes immediately after running, only eccentric exercise caused late phase elevations 1.5-2 days postexercise. 2) Significant increases in muscle G-6-PDase activity, which were always associated with accumulations of mononuclear cells, always occurred within some muscles of each extensor group 1-3 days following downhill and uphill running and did not occur following level running; the increases in activity were usually of lower magnitude in the muscles of uphill runners than in those of downhill runners; the deeply located, predominantly slow-twitch muscles were most affected by both down- and uphill running. 3) Muscle histology demonstrated localized disruption of normal banding patterns of some fibers immediately after exercise and accumulations of macrophages in the interstitium and in some (less than 5%) muscle fibers by 24 h postexercise in the deep slow muscles of the antigravity groups. Although the data generally indicated that eccentric exercise causes greater injury to the muscles, questions remain.

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Exercise for which a skeletal muscle is not adequately conditioned results in focal sites of injury distributed within and among the fibres. Exercise with eccentric contractions is particularly damaging. The injury process can be hypothesised to occur in several stages. First, an initial phase serves to inaugurate the sequence. Hypotheses for the initial event can be categorised as either physical or metabolic in nature. We argue that the initial event is physical, that stresses imposed on sarcolemma by sarcomere length inhomogeneities occurring during eccentric contractions cause disruption of the normal permeability barrier provided by the cell membrane and basal lamina. This structural disturbance allows Ca++ to enter the fibre down its electrochemical gradient, precipitating the Ca++ overload phase. If the breaks in the sarcolemma are relatively minor, the entering Ca++ may be adequately handled by ATPase pumps that sequester and extrude Ca++ from the cytoplasm ('reversible' injury). However, if the Ca++ influx overwhelms the Ca++ pumps and free cytosolic Ca++ concentration rises, the injury becomes 'irreversible'. Elevations in intracellular Ca++ levels activate a number of Ca(++)-dependent proteolytic and phospholipolytic pathways that are indigenous to the muscle fibres, which respectively degrade structural and contractile proteins and membrane phospholipids; for instance, it has been demonstrated that elevation of intracellular Ca++ levels with Ca++ ionophores results in loss of creatine kinase activity from the fibres through activation of phospholipase A2 and subsequent production of leukotrienes. This autogenetic phase occurs prior to arrival of phagocytic cells, and continues during the inflammatory period when macrophages and other phagocytic cells are active at the damage site. The phagocytic phase is in evidence by 2 to 6 hours after the injury, and proceeds for several days. The regenerative phase then restores the muscle fibre to its normal condition. Repair of the muscle fibres appears to be complete; the fibres adapt during this process so that future bouts of exercise of similar type, intensity, and duration cause less injury to the muscle.

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The objectives of this research were to determine the contribution of excitation-contraction (E-C) coupling failure to the decrement in maximal isometric tetanic force (Po) in mouse extensor digitorum longus (EDL) muscles after eccentric contractions and to elucidate possible mechanisms. The left anterior crural muscles of female ICR mice (n = 164) were injured in vivo with 150 eccentric contractions. Po, caffeine-, 4-chloro-m-cresol-, and K+-induced contracture forces, sarcoplasmic reticulum (SR) Ca2+ release and uptake rates, and intracellular Ca2+ concentration ([Ca2+]i) were then measured in vitro in injured and contralateral control EDL muscles at various times after injury up to 14 days. On the basis of the disproportional reduction in Po (approximately 51%) compared with caffeine-induced force (approximately 11-21%), we estimate that E-C coupling failure can explain 57-75% of the Po decrement from 0 to 5 days postinjury. Comparable reductions in Po and K+-induced force (51%), and minor reductions (0-6%) in the maximal SR Ca2+ release rate, suggest that the E-C coupling defect site is located at the t tubule-SR interface immediately after injury. Confocal laser scanning microscopy indicated that resting [Ca2+]i was elevated and peak tetanic [Ca2+]i was reduced, whereas peak 4-chloro-m-cresol-induced [Ca2+]i was unchanged immediately after injury. By 3 days postinjury, 4-chloro-m-cresol-induced [Ca2+]i became depressed, probably because of decreased SR Ca2+ release and uptake rates (17-31%). These data indicate that the decrease in Po during the first several days after injury primarily stems from a failure in the E-C coupling process.