Limitations to oxygen transport and utilization during sprint exercise in humans: evidence for a functional reserve in muscle O2 diffusing capacity

Key points Severe acute hypoxia reduces sprint performance. Muscle V̇O2 during sprint exercise in normoxia is not limited by O2 delivery, O2 offloading from haemoglobin or structure‐dependent diffusion constraints in the skeletal muscle of young healthy men. A large functional reserve in muscle O2 diffusing capacity exists and remains available at exhaustion during exercise in normoxia; this functional reserve is recruited during exercise in hypoxia. During whole‐body incremental exercise to exhaustion in severe hypoxia, leg V̇O2 is primarily dependent on convective O2 delivery and less limited by diffusion constraints than previously thought. The kinetics of O2 offloading from haemoglobin does not limit V̇O2 peak in hypoxia. Our results indicate that the limitation to V̇O2 during short sprints resides in mechanisms regulating mitochondrial respiration. To determine the contribution of convective and diffusive limitations to V̇O2 peak during exercise in humans, oxygen transport and haemodynamics were measured in 11 men (22 ± 2 years) during incremental (IE) and 30 s all‐out cycling sprints (Wingate test, WgT), in normoxia (Nx, PIO2: 143 mmHg) and hypoxia (Hyp, PIO2: 73 mmHg). Carboxyhaemoglobin (COHb) was increased to 6–7% before both WgTs to left‐shift the oxyhaemoglobin dissociation curve. Leg V̇O2 was measured by the Fick method and leg blood flow (BF) with thermodilution, and muscle O2 diffusing capacity (DMO2) was calculated. In the WgT mean power output, leg BF, leg O2 delivery and leg V̇O2 were 7, 5, 28 and 23% lower in Hyp than Nx (P