Exercise-Induced Muscle Damage and Potential Mechanisms for the Repeated Bout Effect

Abstract

Unfamiliar, predominantly eccentric exercise, frequently results in muscle damage. A repeated bout of similar eccentric exercise results in less damage and is referred to as the 'repeated bout effect'. Despite numerous studies that have clearly demonstrated the repeated bout effect, there is little consensus as to the actual mechanism. In general, the adaptation has been attributed to neural, connective tissue or cellular adaptations. Other possible mechanisms include, adaptation in excitation-contraction coupling or adaptation in the inflammatory response. The 'neural theory' predicts that the initial damage is a result of high stress on a relatively small number of active fast-twitch fibres. For the repeated bout, an increase in motor unit activation and/or a shift to slow-twitch fibre activation distributes the contractile stress over a larger number of active fibres. Although eccentric training results in marked increases in motor unit activation, specific adaptations to a single bout of eccentric exercise have not been examined. The 'connective tissue theory' predicts that muscle damage occurs when the noncontractile connective tissue elements are disrupted and myofibrillar integrity is lost. Indirect evidence suggests that remodelling of the intermediate filaments and/or increased intramuscular connective tissue are responsible for the repeated bout effect. The 'cellular theory' predicts that muscle damage is the result of irreversible sarcomere strain during eccentric contractions. Sarcomere lengths are thought to be highly non-uniform during eccentric contractions, with some sarcomeres stretched beyond myofilament overlap. Loss of contractile integrity results in sarcomere strain and is seen as the initial stage of damage. Some data suggest that an increase in the number of sarcomeres connected in series, following an initial bout, reduces sarcomere strain during a repeated bout and limits the subsequent damage. It is unlikely that one theory can explain all of the various observations of the repeated bout effect found in the literature. That the phenomenon occurs in electrically stimulated contractions in an animal model precludes an exclusive neural adaptation. Connective tissue and cellular adaptations are unlikely explanations when the repeated bout effect is demonstrated prior to full recovery, and when the fact that the initial bout does not have to cause appreciable damage in order to provide a protective effect is considered. It is possible that the repeated bout effect occurs through the interaction of various neural, connective tissue and cellular factors that are dependent on the particulars of the eccentric exercise bout and the specific muscle groups involved.

Effect of resistance training with different frequencies and detraining on muscular strength and oxidative stress biomarkers in older women

“…Additionally, anaerobic exercise, such as RT, can increase the synthesis of xanthine oxidase and NADPH oxidase enzymes both of which affect OS modulation (McHugh et al 1999). In response to this process, the antioxidant system adapts with adjustments favorable to the endogenous antioxidant system, thus increasing the body's defense capacity.…”

Repeated muscle damage blunts the increase in heat strain during subsequent exercise heat stress

“…It is plausible that reducing the degree of muscle damage encountered will also lessen the degree of heat strain encountered. One obvious, but unexplored avenue of investigation is the well-known repeated bout effect of muscle-damaging exercise, where a single session of eccentric exercise induces adaptations resulting in less evidence of damage when the exercise bout is repeated (Clarkson et al 1992;Clarkson and Hubal 2002;McHugh et al 1999). The mechanism to explain this repeated bout effect is not fully understood, though likely involves neural, cellular and mechanical mechanisms (Clarkson et al 1992;Clarkson and Hubal 2002;McHugh et al 1999).…”

Lower-volume muscle-damaging exercise protects against high-volume muscle-damaging exercise and the detrimental effects on endurance performance

“…CK activity after the second bout of high volume squatting was reduced by the initial lower volume bout, meaning it is unlikely that the RBE was exclusively due to the removal and replacement of weak sarcomeres as proposed by some studies (e.g. Armstrong et al 1983;Byrnes et al 1985;McHugh et al 2003;McHugh et al 1999). Indeed, if weak sarcomeres were still intact after the lower volume bout of squatting then they would have been damaged during the more strenuous high volume bout (Nosaka et al 2001).…”

“…Therefore, the lower CK in Bout 2 suggests that the initial stress in Bout 1, albeit of a lower intensity, provided a stimulus to strengthen the muscle cell membrane against further damage (Clarkson and Tremblay 1988;Howatson et al 2007). The protective effect of lower volume muscle-damaging exercise against subsequent high volume exercise could also be due to changes in motor unit recruitment during squatting Bout 2 (Chen 2003;Howatson et al 2007;McHugh 2003;McHugh et al 1999). Unfortunately EMG activity was measured during running and not the damaging exercise, which means that we are unable to confirm if alterations in motor unit activity occurred.…”

“…It is well established that the signs and symptoms of exercise-induced muscle damage (EIMD) are attenuated after a repeated bout of muscle-damaging exercise (McHugh 2003;McHugh et al 1999). These adaptations are now known to be extended to the observed effects of EIMD on running performance, whereby the negative alterations in the physiological, metabolic, perceptual and kinematic responses during fixed-intensity running are reduced after a repeated bout of EIMD performed two weeks later (Burt et al 2013).…”