Endurance exercise training changes the limitation on muscle VO2max${\dot{V}}_{{{\mathrm{O}}}_{\mathrm{2}}{\mathrm{max}}}$ in normoxia from the capacity to utilize O₂ to the capacity to transport O₂

Abstract

Abstract Maximal oxygen (O 2 ) uptake () is an important parameter with utility in health and disease. However, the relative importance of O 2 transport and utilization capacities in limiting muscle before and after endurance exercise training is not well understood. Therefore, the present study aimed to identify the mechanisms determining muscle pre‐ and post‐endurance exercise training in initially sedentary participants. In five initially sedentary young males, radial arterial and femoral venous (blood samples), leg blood flow (thermodilution), and myoglobin (Mb) desaturation ( 1 H 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 using an O 2 half‐saturation pressure of 3.2 mmHg. Pre‐training muscle 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 gradients in normoxia (34 ± 3 mmHg) and hyperoxia (40 ± 7 mmHg) than hypoxia (29 ± 5 mmHg, both q < 0.024). Post‐training muscle 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 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 in normoxia from the mitochondrial capacity to utilize O 2 to the capacity to transport O 2 to the mitochondria. image Key points Maximal O 2 uptake is an important parameter with utility in health and disease. The relative importance of O 2 transport and utilization capacities in limiting muscle maximal O 2 uptake before and after endurance exercise training is not well understood. We combined the direct measurement of active muscle maximal O 2 uptake with the measurement of muscle intracellular before and after 8 weeks of endurance exercise training. We show that increasing O 2 availability did not increase muscle maximal O 2 uptake before training, whereas increasing O 2 availability did increase muscle maximal O 2 uptake after training. The results suggest that, in these initially sedentary participants, endurance exercise training changed the basis of limitation on muscle maximal O 2 uptake in normoxia from the mitochondrial capacity to utilize O 2 to the capacity to transport O 2 to the mitochondria.

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