Background and Purpose   Exercise training is known to have positive effects on cerebrovascular health, and in particular there is a growing interest surrounding high-intensity exercise and cerebrovascular function. Cerebrovascular reactivity (CVR) is one measure of cerebrovascular function, and refers to the ability of the cerebral blood vessels to dilate and constrict in response to acute changes in the partial pressure of arterial CO₂. However, little is known about the acute effect of sprint exercise on CVR.  Therefore, the purpose of this study was to investigate the acute effect of maximal sprint exercise on CVR in healthy young adults.

Methods   Twenty-one healthy adults (mean ± SD age, height and weight: 22.7 ± 3.1 years, 173.4 ± 8.4 cm and 70.3 ± 10.1 kg, respectively, 13 males, 8 females) volunteered to participate in this study. Participants visited the laboratory for one experimental visit, having refrained from caffeine, alcohol and vigorous physical activity for 24 hours, and arrived at the laboratory >2 hours postprandial. CVR of the middle cerebral artery to hypocapnia was determined through one minute of voluntary hyperventilation, performed at 25 breaths.min^-1. Middle cerebral artery blood velocity (MCAv) was measured using transcranial Doppler ultrasonography, and the partial pressure of end-tidal carbon dioxide (P_ETCO₂) was measured breath-by-breath using a gas analyser. Participants completed the CVR protocol at baseline, and 30 minutes following a maximal, 30 second Wingate test completed on a cycle ergometer. CVR was quantified as both the absolute (cm.s^-1) and relative (%) change in MCAv from baseline per 1 mmHg change in P_ETCO₂, taken from the final 10 s of hyperventilation. The effect of the Wingate test on MCAv, P_ETCO₂ and CVR was explored using paired samples t-tests.

Results   Baseline MCAv was significantly lower following the Wingate test (60.8 ± 11.0 vs 66.2 ± 11.5 cm.s^-1, P<0.01), as was baseline P_ETCO₂ (32.4 ± 4.3 vs 36.8 ± 4.2 mmHg, P<0.01). During the hyperventilation protocol, both MCAv and P_ETCO₂ fell by a significantly smaller magnitude following the Wingate test, compared to baseline (20.6 ± 8.9 vs 26.0 ± 9.7 cm.s^-1 and 12.3 ± 5.1 vs 14.5 ± 5.7 mmHg, respectively, P<0.01). However, CVR remained unaltered following the Wingate test, when expressed in both absolute (1.7 ± 0.4 vs 1.9 ± 0.4 cm.s^-1.mmHg^-1, P=0.16) and relative (2.9 ± 0.6 vs 2.8 ± 0.6 %.mmHg^-1, P=0.70) terms.

Conclusion   These findings indicate that both resting MCAv and P_ETCO₂ are not fully recovered 30 minutes following maximal sprint exercise in healthy young adults. However, despite these marked changes in baseline values, the reactivity of MCAv to hypocapnia remained unaltered 30 minutes following a Wingate test. Future research investigating the time-course of CVR responses following sprint exercise is warranted to further our understanding of high-intensity exercise on cerebrovascular function.