Exercise-induced muscle injury in humans frequently occurs after unaccustomed exercise, particularly if the exercise involves a large amount of eccentric (muscle lengthening) contractions. Direct measures of exercise-induced muscle damage include cellular and subcellular disturbances, particularly Z-line streaming. Several indirectly assessed markers of muscle damage after exercise include increases in T2 signal intensity via magnetic resonance imaging techniques, prolonged decreases in force production measured during both voluntary and electrically stimulated contractions (particularly at low stimulation frequencies), increases in inflammatory markers both within the injured muscle and in the blood, increased appearance of muscle proteins in the blood, and muscular soreness. Although the exact mechanisms to explain these changes have not been delineated, the initial injury is ascribed to mechanical disruption of the fiber, and subsequent damage is linked to inflammatory processes and to changes in excitation-contraction coupling within the muscle. Performance of one bout of eccentric exercise induces an adaptation such that the muscle is less vulnerable to a subsequent bout of eccentric exercise. Although several theories have been proposed to explain this "repeated bout effect," including altered motor unit recruitment, an increase in sarcomeres in series, a blunted inflammatory response, and a reduction in stress-susceptible fibers, there is no general agreement as to its cause. In addition, there is controversy concerning the presence of sex differences in the response of muscle to damage-inducing exercise. In contrast to the animal literature, which clearly shows that females experience less damage than males, research using human studies suggests that there is either no difference between men and women or that women are more prone to exercise-induced muscle damage than are men.

Exercise-induced muscle damage in humans.

Objective:
To present recommendations to optimize the fluid-replacement practices of athletes.


Background:
Dehydration can compromise athletic performance and increase the risk of exertional heat injury. Athletes do not voluntarily drink sufficient water to prevent dehydration during physical activity. Drinking behavior can be modified by education, increasing accessibility, and optimizing palatability. However, excessive overdrinking should be avoided because it can also compromise physical performance and health. We provide practical recommendations regarding fluid replacement for athletes.


Recommendations:
Educate athletes regarding the risks of dehydration and overhydration on health and physical performance. Work with individual athletes to develop fluid-replacement practices that optimize hydration status before, during, and after competition.

/pdf/national-athletic-trainers-association-position-statement-5e9yw20d4i.pdf

National athletic trainers' association position statement: fluid replacement for athletes.

The repeated bout effect refers to the adaptation whereby a single bout of eccentric exercise protects against muscle damage from subsequent eccentric bouts. While the mechanism for this adaptation is poorly understood there have been significant recent advances in the understanding of this phenomenon. The purpose of this review is to provide an update on previously proposed theories and address new theories that have been advanced. The potential adaptations have been categorized as neural, mechanical and cellular. There is some evidence to suggest that the repeated bout effect is associated with a shift toward greater recruitment of slow twitch motor units. However, the repeated bout effect has been demonstrated with electrically stimulated contractions, indicating that a peripheral, non-neural adaptation predominates. With respect to mechanical adaptations there is evidence that both dynamic and passive muscle stiffness increase with eccentric training but there are no studies on passive or dynamic stiffness adaptations to a single eccentric bout. The role of the cytoskeleton in regulating dynamic stiffness is a possible area for future research. With respect to cellular adaptations there is evidence of longitudinal addition of sarcomeres and adaptations in the inflammatory response following an initial bout of eccentric exercise. Addition of sarcomeres is thought to reduce sarcomere strain during eccentric contractions thereby avoiding sarcomere disruption. Inflammatory adaptations are thought to limit the proliferation of damage that typically occurs in the days following eccentric exercise. In conclusion, there have been significant advances in the understanding of the repeated bout effect, however, a unified theory explaining the mechanism or mechanisms for this protective adaptation remains elusive.

Recent advances in the understanding of the repeated bout effect: the protective effect against muscle damage from a single bout of eccentric exercise.

Exercise-induced muscle damage (EIMD) can be caused by novel or unaccustomed exercise and results in a temporary decrease in muscle force production, a rise in passive tension, increased muscle soreness and swelling, and an increase in intramuscular proteins in blood. Consequently, EIMD can have a profound effect on the ability to perform subsequent bouts of exercise and therefore adhere to an exercise training programme. A variety of interventions have been used prophylactically and/or therapeutically in an attempt to reduce the negative effects associated with EIMD. This article focuses on some of the most commonly used strategies, including nutritional and pharmacological strategies, electrical and manual therapies and exercise. Long-term supplementation with antioxidants or β-hydroxy-β-methylbutyrate appears to provide a prophylactic effect in reducing EIMD, as does the ingestion of protein before and following exercise. Although the administration of high-dose NSAIDs may reduce EIMD and muscle soreness, it also attenuates the adaptive processes and should therefore not be prescribed for long-term treatment of EIMD. Whilst there is some evidence that stretching and massage may reduce muscle soreness, there is little evidence indicating any performance benefits. Electrical therapies and cryotherapy offer limited effect in the treatment of EIMD; however, inconsistencies in the dose and frequency of these and other interventions may account for the lack of consensus regarding their efficacy. Both as a cause and a consequence of this, there are very few evidence-based guidelines for the application of many of these interventions. Conversely, there is unequivocal evidence that prior bouts of eccentric exercise provide a protective effect against subsequent bouts of potentially damaging exercise. Further research is warranted to elucidate the most appropriate dose and frequency of interventions to attenuate EIMD and if these interventions attenuate the adaptation process. This will both clarify the efficacy of such strategies and provide guidelines for evidence-based practice.

The prevention and treatment of exercise-induced muscle damage.

Eccentric exercise commonly results in muscle damage. The primary sequence of events leading to exercise-induced muscle damage is believed to involve initial mechanical disruption of sarcomeres, followed by impaired excitation-contraction coupling and calcium signaling, and finally, activation of calcium-sensitive degradation pathways. Muscle damage is characterized by ultrastructural changes to muscle architecture, increased muscle proteins and enzymes in the bloodstream, loss of muscular strength and range of motion and muscle soreness. The inflammatory response to exercise-induced muscle damage is characterized by leukocyte infiltration and production of pro-inflammatory cytokines within damaged muscle tissue, systemic release of leukocytes and cytokines, in addition to alterations in leukocyte receptor expression and functional activity. Current evidence suggests that inflammatory responses to muscle damage are dependent on the type of eccentric exercise, previous eccentric loading (repeated bouts), age and gender. Circulating neutrophil counts and systemic cytokine responses are greater after eccentric exercise using a large muscle mass (e.g. downhill running, eccentric cycling) than after other types of eccentric exercise involving a smaller muscle mass. After an initial bout of eccentric exercise, circulating leukocyte counts and cell surface receptor expression are attenuated. Leukocyte and cytokine responses to eccentric exercise are impaired in elderly individuals, while cellular infiltration into skeletal muscle is greater in human females than males after eccentric exercise. Whether alterations in intracellular calcium homeostasis influence inflammatory responses to muscle damage is uncertain. Furthermore, the effects of antioxidant supplements are variable, and the limited data available indicates that anti-inflammatory drugs largely have no influence on inflammatory responses to eccentric exercise. In this review, we compare local versus systemic inflammatory responses, and discuss some of the possible mechanisms regulating the inflammatory responses to exercise-induced muscle damage in humans.

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Characterization of inflammatory responses to eccentric exercise in humans.

The primary purpose of the study was to examine circulating neutrophils and monocytes and their plasma membrane expression of CD64, CD11b, and CD18 after two bouts (B1 and B2) of eccentric exercise...

Adaptation to eccentric exercise: effect on CD64 and CD11b/CD18 expression

The purpose of this study was to determine the effect of a high vs. a low preexercise carbohydrate (CHO) diet on performance during multiple sets of resistance exercise. Eleven resistance-trained males performed cycle ergometry to deplete quadriceps muscle glycogen stores, followed by 48 hr of a high (HICHO) or a low (LOCHO) CHO diet. Subjects then performed five sets each of squats, leg presses, and knee extensions (resistance = 15 RM) to failure. Blood samples were taken before and during exercise for determination of glucose and lactate (LA). No differences in performance (repetitions x weight lifted) were observed (HICHO = 15,975 +/- 1,381 and LOCHO = 15,723 +/- 1,231 kg). Blood glucose was significantly higher after exercise for HICHO compared to LOCHO (HICHO = 4.8 +/- 0.2 vs. LOCHO = 3.9 +/- 0.2 mmol.L-1). No differences in LA accumulation were observed. The data indicated that preexercise CHO status did not affect resistance exercise performance. Further, the differences in blood glucose and the similarity in LA responses suggest that glycolysis was maintained in the LOCHO condition, and there may have been an increased reliance on blood glucose when preexercise CHO status was low.

Paul C. DiLauro

Papers

Adaptation to eccentric exercise: effect on CD64 and CD11b/CD18 expression

The Effect of Preexercise Carbohydrate Status on Resistance Exercise Performance