The role of brain blood flow in thermoregulatory and respiratory control during exercise

Abstract

Introduction: The purpose of this study was to investigate the role of brain blood flow (BBF) on respiratory control during exercise-induced increases in body temperature. BBF is controlled largely by vascular responses to metabolic demand and arterial blood hydrostatic and carbon dioxide pressures. It has recently been found that hyperventilation occurs in response to a small rise in core temperature (Tc) during exercise, irrespective of exercise intensity, but potentially dependent on aerobic fitness. This ventilation drive appears to be independent from the aforementioned determinants of BBF. Furthermore, some of the vascular control of BBF is mediated by prostaglandins; impairing their production (e.g., pharmacologically, using Indomethacin) can reduce BBF. The effect of prostaglandins on brain blood flow and thus on thermoregulatory and ventilation drive during moderate to high intensity exercise is not known. This study tested the hypothesis that prostaglandin-mediated reductions in BBF would reduce the Tc thresholds for hyperventilation during exercise, thereby demonstrating the critical importance of BBF for ventilatory control in exercise. It was further hypothesised that trained individuals would show an absence of respiratory thresholds with normal BBF during exercise, but that these thresholds would become evident with Indomethacin-reduced BBF.

Methods: A single-blinded, randomised crossover design was used, with nine male participants spanning a wide range of aerobic power (42 – 75 mL . kg-1 . min-1). After an initial familiarisation session, participants undertook four testing sessions; two with ingestion of 1 g cornflour (CONTROL), and two with ingestion of an equivalent-looking pill containing 100 mg Indomethacin (INDO), 90 min before exercise. During the 90-min rest period, cerebrovascular reactivity, heart rate and Tc were measured alongside Middle Cerebral Artery velocity (MCAv) as a measure of BBF. Participants then completed (i) prolonged cycling at a standardised workload (40% V̇O2max) or (ii) ramped exercise to exhaustion (20 W per minute), thereby making four sessions. Paired t-tests were used to compare respiratory thresholds and slopes as functions of Tb and MCAv within each form of exercise, whereas two-way repeated measures ANOVAs were used to examine time-related changes in MCAv.

Results: MCAv was reduced by ~32% with INDO compared to CONTROL at rest (39 ± 6 vs. 57 ± 10 cm.s-1) and during steady state exercise (42 ± 6 vs. 64 ± 7 cm.s-1). Despite the marked reduction in MCAv, this had minimal impact on thresholds for ventilatory parameters (i.e. V̇E, V̇O2, V̇E/ V̇CO2, V̇E/ V̇O2, respiratory frequency or tidal volume, except for a possible small reduction in PETCO2 with INDO (39 ± 2 mm Hg) vs. CONTROL (40 ± 2 mm Hg; 95%CI of the difference: -1 ± 1 mm Hg; p=0.08)., whilst ventilatory parameters were unaltered and there was not a reliable presence of thresholds, which lead to not being able to formally test.

Conclusion: Marked reduction in MCAv, by way of Indomethacin, had minimal effect on ventilatory responses during exercise, indicating that MCAv per se is not a major factor in the control of ventilation during exercise (e.g., via its effects on H+ concentration or brain temperature).