Sodium bicarbonate ingestion mitigates the heat-induced hyperventilation and reduction in cerebral blood velocity during exercise in the heat

Hyperthermia during exercise in the heat causes minute ventilation (VE) to increase, which leads to reductions in arterial CO2 partial pressure (PaCO2) and cerebral blood flow. On the other hand, sodium bicarbonate ingestion reportedly results in metabolic alkalosis, leading to decreased and increased PaCO2 during prolonged exercise in a thermoneutral environment. Here, we investigated whether sodium bicarbonate ingestion suppresses heat-induced hyperventilation and the resultant hypocapnia and cerebral hypoperfusion during prolonged exercise in the heat. Eleven healthy men ingested a solution of sodium bicarbonate (0.3 g/kg body weight) (NaHCO3 trial) or sodium chloride (0.208 g/kg) (NaCl trial). Ninety minutes after the ingestion, the subjects performed a cycle exercise for 60 min at 50% of peak oxygen uptake in the heat (35°C and 40% relative humidity). Esophageal temperature did not differ between the trials throughout (P = 0.56, main effect of trial). VE gradually increased with exercise duration in the NaCl trial, but the increases in VE were attenuated in the NaHCO3 trial (P = 0.01, main effect of trial). Correspondingly, estimated PaCO2 and middle cerebral artery blood velocity (an index of anterior cerebral blood flow) were higher in the NaHCO3 than the NaCl trial (P = 0.002 and 0.04, main effects of trial). Ratings of perceived exertion were lower in the NaHCO3 than the NaCl trial (P = 0.02, main effect of trial). These results indicate that sodium bicarbonate ingestion mitigates heat-induced hyperventilation and reductions in PaCO2 and cerebral blood velocity during prolonged exercise in the heat.

Assessment of single-vessel cerebral blood velocity by phase contrast fMRI

Current approaches to high-field functional MRI (fMRI) provide 2 means to map hemodynamics at the level of single vessels in the brain. One is through changes in deoxyhemoglobin in venules, i.e., blood oxygenation level–dependent (BOLD) fMRI, while the second is through changes in arteriole diameter, i.e., cerebral blood volume (CBV) fMRI. Here, we introduce cerebral blood flow–related velocity-based fMRI, denoted CBFv-fMRI, which uses high-resolution phase contrast (PC) MRI to form velocity measurements of flow. We use CBFv-fMRI in measure changes in blood velocity in single penetrating microvessels across rat parietal cortex. In contrast to the venule-dominated BOLD and arteriole-dominated CBV fMRI signals, CBFv-fMRI is comparable from both arterioles and venules. A single fMRI platform is used to map changes in blood pO2 (BOLD), volume (CBV), and velocity (CBFv). This combined high-resolution single-vessel fMRI mapping scheme enables vessel-specific hemodynamic mapping in animal models of normal and diseased states and further has translational potential to map vascular dementia in diseased or injured human brains with ultra–high-field fMRI.