Endurance exercise training changes the limitation on muscle VO2max in normoxia from the capacity to utilize O2 to the capacity to transport O2

Maximal oxygen (O-2) uptake (V-O2max) is an important parameter with utility in health and disease. However, the relative importance of O-2 transport and utilization capacities in limiting muscle V-O2max before and after endurance exercise training is not well understood. Therefore, the present study aimed to identify the mechanisms determining muscle V-O2max pre- and post-endurance exercise training in initially sedentary participants. In five initially sedentary young males, radial arterial and femoral venous V-O2max (blood samples), leg blood flow (thermodilution), and myoglobin (Mb) desaturation (H-1 nuclear magnetic resonance spectroscopy) were measured during maximal single-leg knee-extensor exercise (KE) breathing either 12%, 21% or 100% O-2 both pre and post 8 weeks of KE training (1 h, 3 times per week). Mb desaturation was converted to intracellular V-O2max using an O-2 half-saturation pressure of 3.2 mmHg. Pre-training muscle V-O2max was not significantly different across inspired O-2 conditions (12%: 0.47 +/- 0.10; 21%: 0.52 +/- 0.13; 100%: 0.54 +/- 0.01 L min(-1), all q > 0.174), despite significantly greater muscle mean capillary-intracellular V-O2max gradients in normoxia (34 +/- 3 mmHg) and hyperoxia (40 +/- 7 mmHg) than hypoxia (29 +/- 5 mmHg, both q < 0.024). Post-training muscle V-O2max was significantly different across all inspired O-2 conditions (12%: 0.59 +/- 0.11; 21%: 0.68 +/- 0.11; 100%: 0.76 +/- 0.09 mmHg, all q < 0.035), as were the muscle mean capillary-intracellular V-O2max gradients (12%: 32 +/- 2; 21%: 37 +/- 2; 100%: 45 +/- 7 mmHg, all q < 0.029). In these initially sedentary participants, endurance exercise training changed the basis of limitation on muscle V-O2max in normoxia from the mitochondrial capacity to utilize O-2 to the capacity to transport O-2 to the mitochondria.