Hypocapnia Contributes To The Development Of Post-exercise Hypotension After High-intensity Intermittent Exercise

INTRODUCTION: A single bout of exercise accompanying strenuous muscle work sometimes leads to postexercise reductions in arterial blood pressure below resting levels (post-exercise hypotension: PEH), but the mechanism(s) by which this response is mediated is still unclear. After high-intensity exercise, hyperventilation-induced reduction in arterial CO2 pressure (hypocapnia) can occur. Previous work reported that hypocapnic hyperventilation reduces arterial blood pressure at rest and during exercise. Thus, PEH after high-intensity exercise may in part be elicited by hyperventilation induced-hypocapnia. However, it remains unclear whether hypocapnia modulates PEH after high-intensity exercise. PURPOSE: To investigate the influence of hyperventilation induced-hypocapnia on PEH after high-intensity intermittent exercise. METHODS: Healthy young 18 (4 females) participants performed three 30-s bouts of high-intensity cycling exercise (Ex1 and 2: constant-workload at 80% of the power output in the Wingate anaerobic test (WAnT), Ex3: WAnT) interspaced with 4-min recovery periods. After completing Ex 3, the participants rested in a semi-recumbent position for 25 min under spontaneous breathing condition with room air (hypocapnia: Hypo) or a high-fraction (3.05 ± 0.90 %) of CO2 (normocapnia: Normo). RESULTS: During recovery period, end-tidal CO2 partial pressure, an index of arterial CO2 partial pressure was decreased from the pre-exercise (Baseline) value in Hypo trial, whereas it was clamped at Baseline level in Normo trial. Eleven participants [responder group] showed a substantial PEH during recovery [Δmean arterial pressure (MAP): -12.7 ± 7.3 mmHg, P < 0.001] from Baseline. The other seven participants did not show a reduction in MAP from the Baseline during the recovery period (ΔMAP: 3.3 ± 4.4 mmHg, P = 0.097)(non-responder group). In the responder group, MAP in Normo trial was similar to the level observed at pre-exercise (ΔMAP: 2.5 ± 9.7 mmHg, P = 0.414). In non-responder group, the MAP was similar between Hypo and Normo trials (P = 0.424). CONCLUSIONS: Our results suggest that there is a large individual variation in PEH response after high-intensity intermittent exercise, and hypocapnia may contribute to the development of PEH after the high-intensity intermittent exercise.