Aerobic exercise elicits increases in cerebral blood flow (CBF), as well as core body temperature; however, the isolated influence of temperature on CBF regulation during exercise has not been investigated
The present study assessed CBF regulation and neurovascular coupling during submaximal cycling exercise and temperature-matched passive heat stress during isocapnia (i.e. end-tidal (Formula presented.) was held constant)
Submaximal cycling exercise and temperature-matched passive heat stress provoked ∼16% increases in vertebral artery blood flow, independent of changes in end-tidal (Formula presented.) and blood pressure
External carotid artery blood flow increased by ∼43% during both exercise and passive heat stress, with no change in internal carotid artery blood flow
Neurovascular coupling (i.e. the relationship between local increases in cerebral metabolism and appropriately matched increases in regional cerebral blood flow) is preserved during both exercise and temperature-matched passive heat stress.
Abstract: Acute moderate-intensity exercise increases core temperature (Tc; +0.7-0.8°C); however, such exercise increases cerebral blood flow (CBF; +10-20%) mediated via small elevations in arterial (Formula presented.) and metabolism. The present study aimed to isolate the role of Tc from (Formula presented.) on CBF regulation during submaximal exercise. Healthy adults (n = 11; 10 males/one female; 26 ± 4 years) participated in two interventions each separated by ≥48 h: (i) 60 min of semi-recumbent cycling (EX; 50% workload max) and (ii) 75 min of passive heat stress (HS; 49°C water-perfused suit) to match the exercise-induced increases in Tc (EX: Δ0.75 ± 0.33°C vs. HS: Δ0.77 ± 0.33°C, P = 0.855). Blood flow (Q) in the internal and external carotid arteries (ICA and ECA, respectively) and vertebral artery (VA) (Duplex ultrasound) was measured. End-tidal (Formula presented.) and (Formula presented.) were effectively clamped to resting values within each condition. The QICA was unchanged with EX and HS interventions (P = 0.665), consistent with the unchanged end-tidal (Formula presented.) (P = 0.327); whereas, QVA was higher throughout both EX and HS (EX: Δ16 ± 21% vs. HS: Δ16 ± 23%, time effect: P = 0.006) with no between condition differences (P = 0.785). These increases in QVA contributed to higher global CBF throughout both EX and HS (EX: Δ12 ± 20% vs. HS: Δ14 ± 14%, time effect: P = 0.029; condition effect: P = 0.869). The QECA increased throughout both EX and HS (EX: Δ42 ± 58% vs. HS: Δ53 ± 28%, time effect: P < 0.001; condition effect: P = 0.628). Including blood pressure as a covariate did not alter these CBF findings (all P > 0.05). Overall, these data provide new evidence for temperature-mediated elevations in posterior CBF during exercise that are independent of changes in (Formula presented.) and blood pressure.