Mitochondrial function in human skeletal muscle is not impaired by high intensity exercise

The hypothesis that high-intensity (HI) intermittent exercise impairs mitoc hondrial function was investigated with different microtechniques in human muscle samples. Ten male students performed three bouts of cycling at 130% of peak O-2 consumption (V . O-2,O-peak). Muscle biopsies were taken from t he vastus lateralis muscle at rest, at fatigue and after 110 min recovery. Mitochondrial function was measured both in isolated mitochondria and in mu scle fibre bundles made permeable with saponin (skinned fibres). In isolate d mitochondria there was no change in maximal respiration, rate of adenosin e 5'-triphosphate (ATP) production (measured with bioluminescence) and resp iratory control index after exercise or after recovery. The ATP production per consumed oxygen (P/O ratio) also remained unchanged at fatigue but decr eased by 4% (P<0.05) after recovery. In skinned fibres, maximal adenosine 5 '-diphosphate (ADP)-stimulated respiration increased by 23% from rest to ex haustion (P<0.05) and remained elevated after recovery, whereas the respira tory rates in the absence of ADP and at 0.1 mM ADP (submaximal respiration) were unchanged. The ratio between respiration at 0.1 and 1 mM ADP (ADP sen sitivity index) decreased at fatigue (P<0.05) but after the recovery period was not significantly different from that at rest. It is concluded that mi tochondrial oxidative potential is maintained or improved during exhaustive HI exercise. The finding that the sensitivity of mitochondrial respiration to ADP is reversibly decreased after strenuous exercise may indicate that the control of mitochondrial respiration is altered.