INCREASED PEAK OXYGEN-CONSUMPTION OF TRAINED MUSCLE REQUIRES INCREASED ELECTRON FLUX CAPACITY

The importance of the training-induced increase in mitochondrial capac ity in realizing the increase in maximal O-2 consumption (VO2max) of t rained muscle was evaluated using an isolated perfused rat hindlimb pr eparation at a high blood flow (similar to 80 ml.min(-1).100 g(-1)) du ring tetanic contractions. Rats trained for 8-12 wk by treadmill runni ng exhibited an similar to 25% increase in muscle VO2max (5.62 +/- 0.3 1 to 7.06 +/- 0.64 mu mol.min(-1).g(-1)), an increase in mitochondrial enzyme activity (similar to 70% for cytochrome oxidase and similar to 55% for NADH cytochrome-c reductase), and an increase in tissue capil larity (14%) that is expected to increase the O-2 exchange capacity of the tissue. Muscle VO2max of sedentary (n = 34) and trained (n = 30) animals was determined, and electron transport capacity was acutely ma naged with myxothiazol, a tight-binding inhibitor of complex III. Inhi bition of complex III was similar among 1) the low- and high-oxidative fibers and 2) the superficial and deep mitochondrial populations with in muscle. Inhibition of NADH cytochrome-c reductase activity resulted in reductions in muscle VO2max with similar dose responses (mean effe ctive dose of similar to 0.2 mu M) of myxothiazol added to the perfusi on medium. The extraction of O-2 by the contracting muscle decreased a s VO2max declined. The increase in muscle VO2max observed in the muscl e of trained animals was eliminated when its electron transport capaci ty was reduced to that observed in normal sedentary rat muscle. Thus, the exercise-induced adaptation of an increased muscle mitochondrial c ontent appears to be essential for trained muscle to exhibit its incre ased O-2 flux capacity. The results of the present experiment illustra te the importance of mitochondrial adaptations in muscle remodeled by exercise training.