Energy turnover in relation to slowing of contractile properties during fatiguing contractions of the human anterior tibialis muscle.

Slowing and loss of muscle power are major factors limiting physical performance but little is known about the molecular mechanisms involved. The slowing might be a consequence of slow detachment of cross bridges and, if this were the case, then a reduction in the ATP cost of an isometric contraction would be expected as the muscle fatigued. The human anterior tibialis muscle was stimulated repeatedly under ischaemic conditions at 50 Hz for 1.6 s with a 50% duty cycle and muscle metabolites measured by (31)P magnetic resonance spectroscopy. Over the course of 20 contractions the half-time of relaxation increased from 36.5 +/- 0.09 ms (mean +/- s.e.m.) to 113 +/- 17 ms and isometric force was reduced to 63 +/- 3% of the initial value. ATP turnover was determined from the change in high energy phosphates and lactate production, the latter estimated from the change of intracellular pH. ATP turnover over the first three contractions was 2.45 +/- 0.09 mM s(1) and decreased to 1.8 +/- 0.06 mm s(1) over the last five tetani. However, when this latter value was normalised for the decrease in isometric force, it became 2.56 +/- 0.3 mM s(1), which is the same as the turnover of the fresh muscle. The data suggest that the rate of cross bridge detachment is unaffected by fatigue and are consistent the suggestion that it is the rate of attachment which is slowed rather than the rate of detachment. The present results focus attention on stages in the cross bridge cycle concerned with attachment and the transition from low to high force states that may be influenced by metabolic changes in the fatiguing muscle.