Purpose: We investigated the effects of pre-exercise voluntary
hyperventilation and the resultant
hypocapnia on metabolic and cardiovascular responses during and after high-intensity exercise. Methods: Ten healthy participants performed a 60-s cycling exercise at a workload of 120% peak
oxygen uptake in control (spontaneous breathing),
hypocapnia and normocapnia trials.
Hypocapnia was induced through 20-min pre-exercise voluntary
hyperventilation. In the normocapnia trial, voluntary hyperpnea was performed with CO2 inhalation to prevent
hypocapnia. Results: Pre-exercise end-tidal CO2 partial pressure was lower in the
hypocapnia trial than the control or normocapnia trial, with similar levels in the control and normocapnia trials. Average V˙O2 during the entire exercise was lower in both the
hypocapnia and normocapnia trials than in the control trial (1491 ± 252vs.1662 ± 169vs.1806 ± 149 mL min-1), with the
hypocapnia trial exhibiting a greater reduction than the normocapnia trial. Minute ventilation during exercise was lower in the
hypocapnia trial than the normocapnia trial. In addition, minute ventilation during the first 10s of the exercise was lower in the normocapnia than the control trial. Pre-exercise
hypocapnia also reduced heart rates and arterial blood pressures during the exercise relative to the normocapnia trial, a response that lasted through the subsequent early recovery periods, though end-tidal CO2 partial pressure was similar in the two trials. Conclusions: Our results suggest that pre-exercise hyperpnea and the resultant
hypocapnia reduce V˙O2 during high-intensity exercise. Moreover,
hypocapnia may contribute to voluntary
hyperventilation-mediated cardiovascular responses during the exercise, and this response can persist into the subsequent recovery period, despite the return of arterial CO2 pressure to the normocapnic level.