Reductions in cerebral blood flow during passive heat stress in humans: partitioning the mechanisms
- 15 August 2011
- journal article
- research article
- Published by Wiley in Journal Of Physiology-London
- Vol. 589 (16), 4053-4064
- https://doi.org/10.1113/jphysiol.2011.212118
Abstract
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 degrees C (Protocol I; n = 10) and 1.8 +/- 0.1 degrees 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, r(2) = 0.81; PCAv, r(2) = 0.83; P < 0.05) and stroke volume (MCAv, r(2) = 0.38; PCAv, r(2) = 0.43), but not with cardiac output. Protocol II consisted of severe heat stress which resulted in much greater reductions in end-tidal CO2 (-87.5 +/- 31.5%) and CBF (MCAv, -36.4 +/- 6.1%; PCAv, -30.1 +/- 4.8%; P < 0.01 for all variables), while end-diastolic volume and stroke volume decreased to a similar extent as for mild heat stress. Importantly, isocapnia restored MCAv and PCAv back to normothermic baseline. This investigation therefore produced two novel findings: first, that venous return and stroke volume are related to CBF during mild heat stress; and second, that hyperventilatory hypocapnia has a major influence on CBF during severe passive heat stress.This publication has 44 references indexed in Scilit:
- The distribution of blood flow in the carotid and vertebral arteries during dynamic exercise in humansJournal Of Physiology-London, 2011
- End-tidal carbon dioxide tension reflects arterial carbon dioxide tension in the heat-stressed human with and without simulated hemorrhageAmerican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2011
- Alterations in cerebral blood flow and cerebrovascular reactivity during 14 days at 5050 mJournal Of Physiology-London, 2011
- Different blood flow responses to dynamic exercise between internal carotid and vertebral arteries in womenJournal of Applied Physiology, 2010
- The effects of reduced end‐tidal carbon dioxide tension on cerebral blood flow during heat stressJournal Of Physiology-London, 2009
- Dynamic cerebral autoregulation during passive heat stress in humansAmerican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2009
- Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stressJournal of Applied Physiology, 2008
- Effects of passive heating on central blood volume and ventricular dimensions in humansJournal Of Physiology-London, 2008
- Heat stress reduces cerebral blood velocity and markedly impairs orthostatic tolerance in humansAmerican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2006
- Middle cerebral artery blood velocity depends on cardiac output during exercise with a large muscle massActa Physiologica Scandinavica, 1998