The acute effect of exercise intensity on peripheral and cerebral vascular function in healthy adults

Abstract

The acute effect of exercise intensity on cerebrovascular reactivity and whether this mirrors changes in peripheral vascular function have not been investigated. The aim of this study was to explore the acute effect of exercise intensity on cerebrovascular reactivity (CVR) and peripheral vascular function in healthy young adults (n = 10, 6 females, 22.7 ± 3.5 yr). Participants completed four experimental conditions on separate days: high-intensity interval exercise (HIIE) with intervals performed at 75% maximal oxygen uptake (V̇o_2max; HIIE1), HIIE with intervals performed at 90% V̇o_2max (HIIE2), continuous moderate-intensity exercise (MIE) at 60% V̇o_2max and a sedentary control condition (CON). All exercise conditions were completed on a cycle ergometer and matched for time (30 min) and average intensity (60% V̇o_2max). Brachial artery flow-mediated dilation (FMD) and CVR of the middle cerebral artery were measured before exercise, and 1- and 3-h after exercise. CVR was assessed using transcranial Doppler ultrasonography to both hypercapnia (6% carbon dioxide breathing) and hypocapnia (hyperventilation). FMD was significantly elevated above baseline 1 and 3 h following both HIIE conditions (P < 0.05), but FMD was unchanged following the MIE and CON trials (P > 0.33). CVR to both hypercapnia and hypocapnia, and when expressed across the end-tidal CO₂ range, was unchanged in all conditions, at all time points (all P > 0.14). In conclusion, these novel findings show that the acute increases in peripheral vascular function following HIIE, compared with MIE, were not mirrored by changes in cerebrovascular reactivity, which was unaltered following all exercise conditions in healthy young adults.NEW & NOTEWORTHY This is the first study to identify that acute improvements in peripheral vascular function following high-intensity interval exercise are not mirrored by improvements in cerebrovascular reactivity in healthy young adults. High-intensity interval exercise completed at both 75% and 90% V̇o_2max increased brachial artery flow-mediated dilation 1 and 3 h following exercise, compared with continuous moderate-intensity exercise and a sedentary control condition. By contrast, cerebrovascular reactivity was unchanged following all four conditions.

Keywords: HIIE; cerebrovascular reactivity; endothelial function; flow-mediated dilation.

Graphical abstract

Figure 1.

Experimental conditions. The numbers refer to cycling intervals at a percentage of maximal oxygen uptake for each individual. The average intensity of each exercise trial was designed to be 60% maximal oxygen uptake, and all exercise trials were 30 min in duration. CON, resting control trial; HIIE, high-intensity interval exercise; MIE, moderate-intensity exercise.

Figure 2.

Mean ± 95% CI (shaded) middle cerebral artery blood velocity (MCAv) across the four experimental trials [control (A), moderate-intensity exercise (B), high-intensity interval exercise 1 (C), high-intensity interval exercise 2 (D)]. The shading shows the pattern of the exercise stimulus. n = 9 (5 female) due to signal loss in 1 participant. Analysis of between trial differences are presented in Table 2. CI, confidence interval.

Figure 3.

Peripheral vascular outcomes [baseline diameter (A), absolute change in brachial artery diameter (B), allometrically adjusted FMD (C), area under the shear rate curve until time of peak dilation (D)] before (pre) and 1 and 3 h after the four experimental trials (n = 10, 6 female). A repeated-measures ANOVA revealed a significant time by trial interaction effect for the change in brachial artery diameter after occlusion (P = 0.025; B) and the allometrically adjusted flow-mediated dilation statistic (P = 0.014; C). Only the within-trial significant differences are denoted. *Different from pre within the high-intensity interval trial 1. #Significantly different from pre within the high-intensity interval trial 2. CON, control; FMD, flow-mediated dilation allometrically adjusted to baseline diameter; HIIE, high-intensity interval exercise; MIE, moderate-intensity exercise; SR_AUC, area under the shear rate curve until time of peak dilation.

Figure 4.

Physiological responses to 5 min of 5% carbon dioxide inhalation (n = 10, 6 female). A: MCAv change reflects the difference between resting baseline and the highest 30 s rolling average during the hypercapnic stimulus. B: the $\text{P}\text{E}{\text{T}}_{\text{C}{\text{O}}_2}$ change is calculated as the difference between baseline and this time point. C: cerebrovascular reactivity A repeated-measures ANOVA revealed no significant time by trial interaction for any of these outcomes (P > 0.605, η² < 0.078). CON, control; CVR, cerebrovascular reactivity; HIIE, high-intensity interval exercise; MCAv, middle cerebral artery blood velocity; MIE, moderate-intensity exercise; $\text{P}\text{E}{\text{T}}_{\text{C}{\text{O}}_2}$, end tidal partial pressure of carbon dioxide.

Figure 5.

Physiological responses to 1 min of deep hyperventilation (n = 10, 6 female). The change in MCAv (A) and $\text{P}\text{E}{\text{T}}_{\text{C}{\text{O}}_2}$ (B) reflects the difference between resting baseline and the final 10 s of the hyperventilation stimulus, used to calculate cerebrovascular reactivity (C). A repeated-measures ANOVA revealed no significant time by trial interaction for any of these outcomes (P > 0.594, η² < 0.079). CON, control; CVR, cerebrovascular reactivity; HIIE, high-intensity interval exercise; MCAv, middle cerebral artery blood velocity; MIE, moderate-intensity exercise; $\text{P}\text{E}{\text{T}}_{\text{C}{\text{O}}_2}$, end tidal partial pressure of carbon dioxide.