A classical physiological question is whether central and/or local circulatory factors limit maximal aerobic capacity (V_O2,max) in humans. The skeletal muscle has been thought to play a crucial role in the etiology of V_O2,max as it receives 80-95 % of the peripheral O₂ delivery during intense exercise. The two major competing hypotheses predict that V_O2,max would drastically decline if either O₂ delivery or O₂ diffusion to skeletal muscle is impaired. A marked reduction in O₂ delivery could occur during intense exercise if cardiac output and skeletal muscle decline significantly, particularly in conditions of hyperthermia (Gonzçlez-Alonso et al. 1998). Since hyperthermia exacerbates the reductions in stroke volume and cardiac output, we determined whether declining systemic and skeletal muscle O₂ delivery is the main factor limiting V_O2,max in trained humans under normal and heat stress conditions.

Eight healthy subjects with a mean (± S.E.M.) age of 24 ± 2 years and V_O2,max of 4.7 ± 0.1 l min^-1, gave written informed consent to participate in this study, which was approved by the Copenhagen and Frederiksberg Ethics Committee. The subjects completed two cycle ergometer exercise tests until fatigue (356 ± 14 W, which elicited V_O2,max after 4-5 min under normal conditions) starting with either an elevated (~38 °C; hyperthermia) or a normal (~37 °C: normal) body temperature. During exercise arterial and femoral venous blood was sampled, heart rate, mean arterial pressure and body temperature were recorded, and leg blood flow (LBF) and cardiac output were measured using the thermodilution and the cardio-green dye dilution techniques, respectively. Statistical significance (P < 0.05) was tested using Student’s paired t tests.

Performance time was reduced by 30 % (327 ± 14 vs. 458 ± 25 s, respectively, P < 0.05), despite heart rate (193 ± 3 vs. 191 ± 2 beats min^-1) and core temperature (39.7 ± 0.1 vs. 39.5 ± 0.1°C) having similar values at the time of exhaustion, when comparing hyperthermia with control conditions. Before exhaustion in both trials, systemic O₂ delivery and O₂ delivery to the locomotive skeletal muscles declined 5-8 %, due largely to the decline in cardiac output and skeletal muscle blood flow (Fig. 1A and B).

In sharp contrast, leg a-vO₂ difference and leg O₂ extraction increased progressively until the end of exercise (Fig. 1C), thus precluding any abrupt limitation in O₂ diffusion to contracting muscle in either trial. Therefore, leg V_O2 declined 5-7 % before exhaustion in both trials as a result of the greater decline in O₂ delivery (Fig. 1D). These findings support the hypothesis that reduced delivery of O₂ to the contracting skeletal muscle, largely associated with the falling stroke volume under normal or elevated heat stress, precedes exhaustion during maximal aerobic exercise.

This work was supported by the Danish National Research Foundation (504-14), the Gatorade Sports Science Institute and Team Denmark.