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

Abstract

To determine the contribution of convective and diffusive limitations to V̇(O2peak) 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, P(IO2): 143 mmHg) and hypoxia (Hyp, P(IO2): 73 mmHg). Carboxyhaemoglobin (COHb) was increased to 6-7% before both WgTs to left-shift the oxyhaemoglobin dissociation curve. Leg V̇(O2) was measured by the Fick method and leg blood flow (BF) with thermodilution, and muscle O2 diffusing capacity (D(MO2)) was calculated. In the WgT mean power output, leg BF, leg O2 delivery and leg V̇(O2) were 7, 5, 28 and 23% lower in Hyp than Nx (P < 0.05); however, peak WgT D(MO2) was higher in Hyp (51.5 ± 9.7) than Nx (20.5 ± 3.0 ml min(-1) mmHg(-1), P < 0.05). Despite a similar P(aO2) (33.3 ± 2.4 and 34.1 ± 3.3 mmHg), mean capillary P(O2) (16.7 ± 1.2 and 17.1 ± 1.6 mmHg), and peak perfusion during IE and WgT in Hyp, D(MO2) and leg V̇(O2) were 12 and 14% higher, respectively, during WgT than IE in Hyp (both P < 0.05). D(MO2) was insensitive to COHb (COHb: 0.7 vs. 7%, in IE Hyp and WgT Hyp). At exhaustion, the Y equilibration index was well above 1.0 in both conditions, reflecting greater convective than diffusive limitation to the O2 transfer in both Nx and Hyp. In conclusion, muscle V̇(O2) during sprint exercise is not limited by O2 delivery, O2 offloading from haemoglobin or structure-dependent diffusion constraints in the skeletal muscle. These findings reveal a remarkable functional reserve in muscle O2 diffusing capacity.

Figure 1. Power output, O₂ delivery and O₂ uptake during sprint exercise

Power output (A), pulmonary oxygen uptake (${\dot{V}}_{{\mathrm{O}}_2}$) (B), two‐legged O₂ delivery (C), and two‐legged ${\dot{V}}_{{\mathrm{O}}_2}$ (D) during isokinetic Wingate tests at 80 rpm performed in normoxia ($P_{\mathrm{I}{\mathrm{O}}_2}$ ≈ 143 mmHg) and acute hypoxia ($P_{\mathrm{I}{\mathrm{O}}_2}$ ≈ 73 mmHg). *P < 0.05 normoxia (triangles pointing up) vs. hypoxia (triangles pointing down); n = 10 (one subject did not perform the Wingate test in hypoxia).

Figure 2. Muscle gas exchange during sprint exercise

Mean capillary oxygen pressure ($P_{\mathrm{c}{\mathrm{O}}_2}$) and femoral vein (FV) $P_{{\mathrm{O}}_2}$ (A), muscle O₂ diffusing capacity (B), equilibration index Y (dimensionless) (C), leg fractional O₂ extraction (D), in vivo femoral vein P ₅₀ (corrected for the Bohr effect) (E), femoral vein pH (F), femoral vein $P_{\mathrm{C}{\mathrm{O}}_2}$ (G), and femoral vein blood temperature (H) during isokinetic Wingate tests at 80 rpm performed in normoxia ($P_{\mathrm{I}{\mathrm{O}}_2}$ ≈ 143 mmHg) and acute hypoxia ($P_{\mathrm{I}{\mathrm{O}}_2}$ ≈ 73 mmHg). *P < 0.05 normoxia (triangles pointing up) vs. hypoxia (triangles pointing down); n = 10 (one subject did not perform the Wingate test in hypoxia).

Figure 3

Wagner plot showing convection versus diffusion limitations during sprint exercise in normoxia ( P_IO ${}_{{}_2}$ ≈ 143 mmHg) and hypoxia (P_IO ${}_{{}_2}$ ≈ 73 mmHg) Two‐leg ${\dot{V}}_{{\mathrm{O}}_2}$ during the Wingate test in normoxia (filled symbols) and hypoxia (open symbols) represented by Fick's law of diffusion (${\dot{V}}_{{\mathrm{O}}_2}$ = $D_{{\mathrm{O}}_2}$ × ($P_{{\mathrm{O}}_2\mathrm{cap}}$ − $P_{{\mathrm{O}}_2\mathrm{mit}}$)) and the Fick principle (${\dot{V}}_{{\mathrm{O}}_2}$ = $\dot{Q}$($C_{\mathrm{a}{\mathrm{O}}_2}$ − $C_{\mathrm{v}{\mathrm{O}}_2}$)). The lines from the origin through the data points (${\dot{V}}_{{\mathrm{O}}_2}$) reflect Fick's Law of diffusion with their corresponding values for normoxia and hypoxia. The sigmoid curves represent ${\dot{V}}_{{\mathrm{O}}_2}$ defined by the Fick principle. Despite lower O₂ delivery in hypoxia (vertical displacement in sigmoid curve), the steeper slope of the relationship between ${\dot{V}}_{{\mathrm{O}}_2}$ and $P_{\mathrm{v}{\mathrm{O}}_2}$ (Fick diffusion) shows the higher $D_{\mathrm{M}{\mathrm{O}}_2}$ in hypoxia. $\dot{Q}$, two‐legged blood flow; $C_{\mathrm{a}{\mathrm{O}}_2}$, arterial [O₂]; $C_{\mathrm{v}{\mathrm{O}}_2}$, venous [O₂]; $D_{{\mathrm{O}}_2}$, O₂ diffusing capacity; P _cap, mean capillary $P_{{\mathrm{O}}_2}$; P _mito, $P_{{\mathrm{O}}_2}$ at cytochrome c oxidase of mitochondria (assumed to approach zero at muscle ${\dot{V}}_{{\mathrm{O}}_2\max }$). n = 9.