PURPOSE: We evaluated whether hypocapnia achieved through voluntary hyperventilation diminishes the increases in oxygen uptake elicited by short-term (e.g., ~30 s) all-out exercise without affecting exercise performance. METHODS: Nine subjects performed 30-s Wingate anaerobic tests (WAnT) in control and hypocapnia trials on separate days in a counterbalanced manner. During the 20-min rest prior to the 30-s WAnT, the subjects in the hypocapnia trial performed voluntary hyperventilation (minute ventilation = 31 L min(-1)), while the subjects in the control trial continued breathing spontaneously (minute ventilation = 14 L min(-1)). RESULTS: The hyperventilation in the hypocapnia trial reduced end-tidal CO2 pressure from 34.8 ± 2.5 mmHg at baseline rest to 19.3 ± 1.0 mmHg immediately before the 30-s WAnT. In the control trial, end-tidal CO2 pressure at baseline rest (35.9 ± 2.5 mmHg) did not differ from that measured immediately before the 30-s WAnT (35.9 ± 3.3 mmHg). Oxygen uptake during the 30-s WAnT was lower in the hypocapnia than the control trial (1.55 ± 0.52 vs. 1.95 ± 0.44 L min(-1)), while the postexercise peak blood lactate concentration was higher in the hypocapnia than control trial (10.4 ± 1.9 vs. 9.6 ± 1.9 mmol L(-1)). In contrast, there was no difference in the 5-s peak (842 ± 111 vs. 850 ± 107 W) or mean (626 ± 74 vs. 639 ± 80 W) power achieved during the 30-s WAnT between the control and hypocapnia trials. CONCLUSIONS: These results suggest that during short-period all-out exercise (e.g., 30-s WAnT), hypocapnia induced by voluntary hyperventilation reduces the aerobic metabolic rate without affecting exercise performance. This implies a compensatory elevation in the anaerobic metabolic rate.
RCT Entities:
PURPOSE: We evaluated whether hypocapnia achieved through voluntary hyperventilation diminishes the increases in oxygen uptake elicited by short-term (e.g., ~30 s) all-out exercise without affecting exercise performance. METHODS: Nine subjects performed 30-s Wingate anaerobic tests (WAnT) in control and hypocapnia trials on separate days in a counterbalanced manner. During the 20-min rest prior to the 30-s WAnT, the subjects in the hypocapnia trial performed voluntary hyperventilation (minute ventilation = 31 L min(-1)), while the subjects in the control trial continued breathing spontaneously (minute ventilation = 14 L min(-1)). RESULTS: The hyperventilation in the hypocapnia trial reduced end-tidal CO2 pressure from 34.8 ± 2.5 mmHg at baseline rest to 19.3 ± 1.0 mmHg immediately before the 30-s WAnT. In the control trial, end-tidal CO2 pressure at baseline rest (35.9 ± 2.5 mmHg) did not differ from that measured immediately before the 30-s WAnT (35.9 ± 3.3 mmHg). Oxygen uptake during the 30-s WAnT was lower in the hypocapnia than the control trial (1.55 ± 0.52 vs. 1.95 ± 0.44 L min(-1)), while the postexercise peak blood lactate concentration was higher in the hypocapnia than control trial (10.4 ± 1.9 vs. 9.6 ± 1.9 mmol L(-1)). In contrast, there was no difference in the 5-s peak (842 ± 111 vs. 850 ± 107 W) or mean (626 ± 74 vs. 639 ± 80 W) power achieved during the 30-s WAnT between the control and hypocapnia trials. CONCLUSIONS: These results suggest that during short-period all-out exercise (e.g., 30-s WAnT), hypocapnia induced by voluntary hyperventilation reduces the aerobic metabolic rate without affecting exercise performance. This implies a compensatory elevation in the anaerobic metabolic rate.
Authors: Nicholas J Hanson; Dylan D Lothian; Christopher L Miller; Timothy J Michael; Michael G Miller Journal: J Exerc Sci Fit Date: 2018-08-17 Impact factor: 3.103