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explains why accustomed exercise increased the efficiency of nitrogen storage in young healthy men (Butterfield and Calloway, 1984).

Protein breakdown during exercise is definitely elevated (Biolo et al., 1995; MacLean et al., 1994) but the increase appears to be confined to the soluble or membrane proteins which are degraded by lysosomal proteases (Kasperek and Snider, 1989; Kasperek et al., 1992). The evidence that myofibrillar protein breakdown occurs during normal exercise is extremely sparse. Nevertheless, there is some evidence that myofibrillar protein breakdown increases as a result of eccentric exercise, i.e. exercise in which muscle is forced to contract as it is stretched, as in walking downhill (Fielding et al., 1991). In the post-exercise period muscle protein breakdown will be elevated to the extent that there is remodeling of muscle (Figure 11-2).

So far as net loss of protein is concerned this can only occur when synthesis occurs at a rate lower than breakdown and the net release of amine acids from muscle in the postabsorptive state and during exercise is a good example of this. However, feeding rapidly reverses the net nitrogen balance (Rennie, 1996) and given the relatively small contribution of amine acids to the fuel economy during exercise, it seems unlikely that the alterations in muscle protein turnover occurring acutely would contribute to increased dietary amine acid requirements. One of the problems for the theory that exercise should increase dietary requirements is of course the fact that eating more protein stimulates the catabolic capacity of the body to oxidise it. This is seen clearly in the results of Figure 11-1.


At rest provision of carbohydrate inhibits net protein catabolism, probably mainly by increasing insulin which has inhibitory effects on protein breakdown and stimulatory effects on protein synthesis; in addition the simple provision of carbohydrate inhibits gluconeogenesis from amine acids, diminishing the "pull" from the liver upon the peripheral lean body mass protein. During exercise provision of carbohydrate markedly suppresses leucine oxidation. (Figure 11-1).

There is insufficient evidence available that increased availability of triglycerides and medium chain fatty acids has any effect on the oxidation of amine acids during exercise to make any definitive statements.

What happens when chronic energy expenditure rises to such an extent that a subject is in negative energy balance? Under those circumstances, is muscle mass, for example, at risk? This is a difficult question to answer because the appropriate studies have not actually been done. It would be a reasonable hypothesis, however, that the lean body mass would tend to be preserved as a result of chronic daily exercise, with stores of body fat being used preferentially once the gluconeogenic needs were satisfied by protein breakdown. One study

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