Effects of Pre-Exercise Voluntary Hyperventilation on Metabolic and Cardiovascular Responses During and After Intense Exercise

ABSTRACT

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 $\dot{V}{\mathrm{O}}_2$ 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 $\dot{V}{\mathrm{O}}_2$ 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.

KEYWORDS:

• Aerobic metabolism
• anaerobic metabolism
• chemoreflex deactivation
• respiratory alkalosis
• respiratory muscle(s)

Acknowledgments

We would like to sincerely thank the volunteer subjects. We also greatly appreciate the help of Dr. William Goldman (English editing and critical comments).

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This study was supported by the grants from Japan Society for the Promotion of Science [JSPS KAKENHI; grant number18J20086]. K.Dobashi is the recipient of a research fellowship for young scientists from the JSPS.