Evidence for temperature‐mediated regional increases in cerebral blood flow during exercise

KEY POINTS: 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 P C O 2 was held constant) Submaximal cycling exercise and temperature-matched passive heat stress provoked approximately 16% increases in vertebral artery blood flow, independent of changes in end-tidal P C O 2 and blood pressure External carotid artery blood flow increased by approximately 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 degrees C); however, such exercise increases cerebral blood flow (CBF; +10-20%) mediated via small elevations in arterial P C O 2 and metabolism. The present study aimed to isolate the role of Tc from P C O 2 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 degrees C water-perfused suit) to match the exercise-induced increases in Tc (EX: Delta0.75 +/- 0.33 degrees C vs. HS: Delta0.77 +/- 0.33 degrees 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 P C O 2 and P O 2 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 P C O 2 (P = 0.327); whereas, QVA was higher throughout both EX and HS (EX: Delta16 +/- 21% vs. HS: Delta16 +/- 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: Delta12 +/- 20% vs. HS: Delta14 +/- 14%, time effect: P = 0.029; condition effect: P = 0.869). The QECA increased throughout both EX and HS (EX: Delta42 +/- 58% vs. HS: Delta53 +/- 28%, time effect: P 0.05). Overall, these data provide new evidence for temperature-mediated elevations in posterior CBF during exercise that are independent of changes in P C O 2 and blood pressure.