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vision chronically depress muscle glutamate and glutamine concentrations and thereby limit the ability of the Krebs cycle to accelerate rapidly enough. However, this is, at the moment, speculation. More research is needed.


It is well accepted that muscular activity has a marked effect on muscle composition and/or muscle bulk, depending upon the type of contractile activity involved. Moderate, repeated, long-term exercise causes increases in mitochondrial mass and alterations in myosin ATPase to isoforms appropriate to long-term aerobic exercise; and high resistance exercise causes increases in expression of actin and myosin and increased mixed muscle protein synthesis (Rennie, 1996) (Figure 11-2). The anabolic phase occurs in the post-exercise period and can be maximised by the provision of exogenous amino acids.

It has been difficult to make measurements of protein synthesis during exercise in human beings because of the difficulty of detecting Sufficient change over a short period of time but it seems likely that muscle protein synthesis is depressed (Rennie, 1996; Dohm et al., 1980); thus, the rebound observed post-exercise (Chesley et al., 1992; Biolo et al., 1995) appears to fulfill a homeostatic function as much as anything. The extent of this elevation is limited, with a return to baseline 36 hr after a stimulatory bout of exercise (MacDougall et al., 1995). This ability of contractile activity to stimulate anabolism probably

FIGURE 11-2 Notional scheme of changes in muscle protein synthesis and breakdown taking into account most of the current observations in the literature obtained from studies of human muscle.

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