Effects of dynamic changes in arterial pressure and carbon dioxide on middle cerebral artery blood velocity during high-intensity interval exercise

Cerebral autoregulation at rest is enhanced at lower arterial partial pressure of carbon dioxide (P a CO 2 ), and P a CO 2 progressively decreases during high-intensity interval exercise (HIIE). Therefore, we investigated whether cerebrovascular control changes across a bout of HIIE. We hypothesized that cerebral autoregulation would improve during the later stages of HIIE when estimated P a CO 2 (eP a CO 2 ) is reduced. Fourteen young healthy adults (5 women) performed 18.5 min of pseudorandom HIIE, where work rate alternated between 25 W and 50% of the difference between the ventilatory threshold and peak oxygen uptake. Autoregressive moving-average (ARMA) analysis quantified indices of cerebral autoregulation and cerebrovascular reactivity to CO 2 for the first and second halves of HIIE. Mean arterial pressure at the level of the middle cerebral artery (MAP MCA ; 89±9 vs. 83±10 mmHg; p<0.001), eP a CO 2 (40.9±2.9 vs. 38.4±3.3 mmHg; p<0.001), and mean middle cerebral artery blood velocity (MCAv; 61.1±16.1 vs. 56.5±15.8 cm·s −1 ; p<0.001) were all higher during the first half of the test. ARMA analysis revealed lower ( p=0.004) steady-state changes in MCAv in response to a step increase in MAP in the second half of HIIE (0.15±0.11 cm·s −1 ·mmHg -1 ) compared to the first half (0.23±0.14 cm·s -1 ·mmHg -1 ), suggesting improved autoregulation in the later stages of HIIE when eP a CO 2 was lower. Large transient increases in MCAv at the onset of high-intensity intervals were temporally linked to spikes in MAP, which were exacerbated by shorter recovery intervals. These results suggest a dynamic change in the regulation of cerebrovascular and systemic hemodynamics as a function of time and work rate pattern during HIIE.