Skeletal muscle ATP turnover by 31P magnetic resonance spectroscopy during moderate and heavy bilateral knee extension

During constant-power high-intensity exercise, the expected increase in oxygen uptake (V-O2) is supplemented by a V-O2 slow component (V-O2sc), reflecting reduced work efficiency, predominantly within the locomotor muscles. The intracellular source of inefficiency is postulated to be an increase in the ATP cost of power production (an increase in P/W). To test this hypothesis, we measured intramuscular ATP turnover with P-31 magnetic resonance spectroscopy (MRS) and whole-body V-O2 during moderate (MOD) and heavy (HVY) bilateral knee-extension exercise in healthy participants (n=14). Unlocalized P-31 spectra were collected from the quadriceps throughout using a dual-tuned (H-1 and P-31) surface coil with a simple pulse-and-acquire sequence. Total ATP turnover rate (ATP(tot)) was estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling. Between 3 and 8min during MOD, there was no discernable V-O2 sc (mean +/- SD, 0.06 +/- 0.12 l min(-1)) or change in [PCr] (30 +/- 8 vs. 32 +/- 7mm) or ATP(tot) (24 +/- 14 vs. 17 +/- 14 mm min(-1); each P=n.s.). During HVY, the V-O2sc was 0.37 +/- 0.16 l min(-1) (22 +/- 8%), [PCr] decreased (19 +/- 7 vs. 18 +/- 7mm, or 12 +/- 15%; P<0.05) and ATP(tot) increased (38 +/- 16 vs. 44 +/- 14 mm min(-1), or 26 +/- 30%; P<0.05) between 3 and 8min. However, the increase in ATP(tot) (ATP(tot)) was not correlated with the V-O2sc during HVY (r(2)=0.06; P=n.s.). This lack of relationship between Delta ATP(tot) and V-O2sc, together with a steepening of the [PCr]-V-O2 relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial sources (the O-2 cost of ATP resynthesis; P/O).