Reductions in cerebral blood flow during passive heat stress in humans: partitioning the mechanisms

• Published in: The Journal of physiology 2011-08, Vol.589 (16), p.4053-4064
• Main Authors: Nelson, Michael D., Haykowsky, Mark J., Stickland, Michael K., Altamirano‐Diaz, Luis A., Willie, Christopher K., Smith, Kurt J., Petersen, Stewart R., Ainslie, Philip N.
• Format: Article
• Language: English
• Subjects: Adult; Blood Flow Velocity - physiology; Blood Pressure - physiology; Body Temperature - physiology; Cerebrovascular Circulation - physiology; Heart Rate - physiology; Heat Stress Disorders - physiopathology; Heat Stress Disorders - prevention & control; Heat-Shock Response - physiology; Humans; Indexing in process; Integrative; Male; Severity of Illness Index; Stroke Volume - physiology; Young Adult
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2011.212118

Non‐technical summary  Heat stress reduces brain blood flow and impairs orthostatic tolerance. Brain blood flow is largely controlled by the partial pressure of arterial . Indeed, hyperthermia‐induced over‐breathing and related reductions in arterial account for ∼50% of the reduction in brain blood flow. This investigation tested the unique hypothesis that the distribution of cardiac output during heat stress (challenged by thermoregulatory increases in skin blood flow and sweat loss) contributes to the remaining 50%. We show that cardiac output is not related to brain blood flow, but rather arterial plays a much larger role than previously suggested. These findings help us understand the mechanisms relating heat stress with an increased likelihood of fainting, and are also relevant to pathological conditions that are accompanied by elevations in body temperature.   Cerebral blood flow (CBF) is reduced during passive heat stress, with 50% of this reduction associated with hyperventilatory‐induced hypocapnia and subsequent cerebral vasoconstriction. It remains unknown, however, what other factors may contribute to the remaining 50%. We tested the hypothesis that the distribution of cardiac output plays an important role in maintaining cerebral perfusion during mild and severe heat stress. Middle cerebral artery and posterior cerebral artery blood flow velocity (MCAv and PCAv; transcranial Doppler) and left ventricular end‐diastolic and end‐systolic volumes (2‐D echocardiography) were measured under conditions of normothermia and mild and severe passive heat stress (core temperature +0.8 ± 0.1°C (Protocol I; n= 10) and 1.8 ± 0.1°C (Protocol II; n= 8) above baseline). Venous return was manipulated by passive tilt table positioning (30 deg head‐down tilt (HDT) and 30 deg head‐up tilt (HUT)). Measurements were made under poikilocapnic and isocapnic conditions. Protocol I consisted of mild heat stress which resulted in small reductions in end‐tidal CO2 (−5.6 ± 3.5%), MCAv/PCAv (−7.3 ± 2.3% and −10.3 ± 2.9%, respectively) and stroke volume (−8.5 ± 4.2%); while end‐diastolic volume was significantly reduced (−16.9 ± 4.0%) and cardiac output augmented (17.2 ± 7.4%). During mild heat stress, CBF was related to left ventricular end‐diastolic volume (MCAv, r2= 0.81; PCAv, r2= 0.83; P < 0.05) and stroke volume (MCAv, r2= 0.38; PCAv, r2= 0.43), but not with cardiac output. Protocol II consisted of severe heat stress which resulted in much greater reductions in end‐tidal