Abstract
Recent data suggest that an increased muscle mitochondrial oxidative capacity is not a prerequisite for a marked metabolic effect of endurance training, but instead may represent an adaptive phenomenon to the new metabolic situation. The muscle content of the glucose transporter GLUT-4 increases after one or only a few exercise sessions. The ensuring enhancement of the insulin sensitivity allows faster replenishment of muscle glycogen stores following exercise bouts. There is evidence that the muscle content of GLUT-4 declines more slowly with inactivity than the muscle oxidative capacity. This may be a sign that, as in the chronically stimulated rabbit muscle, adaptive changes in human skeletal muscle follow a "first-in, last-out' sequence. There is evidence that muscle (and possibly also plasma) triacylglycerol is more important as an energy source during exercise than was previously recognized. Endurance training increases the content of slow isoforms of myosin in the muscle, and information on changes in muscle shortening velocity and on the molecular regulation of muscle volume is emerging. beta 2-agonists are well documented to enhance muscle mass, whereas creatine supplementation appears to enhance performance during high-intensity exercise.

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