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How muscles know how to adapt

Michael J. Rennie

At a meeting some years ago I saw Professor Sam Perry of Birmingham University, one of the pioneers of British muscle biochemistry, present a slide juxtaposing two brothers who were identical twins. One had gone in for body-building and the other had decided to become a distance runner. The point was, of course, that despite having identical genomes, these men had managed to sculpt their bodies in completely different ways by training. The plasticity of muscle has long been recognised but apart from some biologically trivial generalisations (resistance exercise causing an increase in muscle bulk and repeated moderate dynamic exercise causing an increase in muscle oxidative capacity) we have made slow progress in understanding the mechanisms involved. Most of our information is about the distal processes involved (e.g. selective hypertrophy of particular fibres, alterations in mitochondrial density and changes in myosin heavy chain phenotypes). Some of the changes appear to be almost immediate, for example the changes in the rate of translation of mRNA for muscle proteins, which falls during exercise and rebounds during recovery (Rennie & Tipton, 2000). Others take days to months and involve changes in gene expression, both of the type and the amount of particular proteins such as myosin subtypes or cytochrome C (Pette, 2000). The difficult question to answer is, what is the nature of the proximal processes that act, both acutely and chronically, to link the pattern of contractile activity with the cellular changes, allowing adaptation to new circumstances? There have been many conjectures in the past involving alterations in such things as ATP/ADP concentration ratios, availability of free creatine, the redox state of muscle, its pH, etc. There has also been speculation based upon the degree of tension experienced by muscle membranes and the intracellular cytoskeletal system and their connections with the extracellular matrix and other muscle cells through, for example, integrins. It is relatively trivial to conceive of a scheme which involves alterations in transcription and translation as a result of force signals due to contractile activity being transmitted, for example, to the muscle membrane and to integrin anchors and thereby retransmitted to the interior of muscles via membrane-associated sensor and signalling elements, these signals being modulated by cross-talk with metabolic signals. However, such a model still has to account for the two major modes of response, i.e. hypertrophy and increases in oxidative capacity, and how, under certain circumstances, these can even be combined (e.g. in well-trained distance runners type 1 fibres are not only more oxidative but they are bigger than in untrained individuals).

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