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1999 Publications

Exercise-induced muscle damage and potential mechanisms for the repeated bout McHugh MP, Connolly DA, Eston RG, Gleim GWSchool of Sport, Health and Physical Education Sciences, University of Wales, Bangor, Gwynedd, Wales.; NISMAT, Lenox Hill Hospital, N.Y., N.Y - last modified 2013-02-10 00:00
Sports Med 1999 Mar;27(3):157-70


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.