Heat stress significantly reduces orthostatic tolerance (i.e. fainting) in humans resulting in a high probability of injury when these two stressors are combined. The mechanism(s) causing this response are unknown. In the parent grant we tested the hypothesis that human baroreflex function was impaired during hyperthermic exposure and this contributed to the reduction of orthostatic tolerance observed in this thermal condition. As a result of that work we identified that whole body heating did not alter baroreflex control of heart rate or muscle sympathetic nerve activity. However, preliminary data suggested that heating might attenuate vasoconstrictor responsiveness. Thus, despite an appropriate neural drive during a hypotensive challenge in the heat, the elevation in vascular resistance may be impaired and thereby predispose the individual to fainting. This hypothesized blunted elevation in vascular resistance becomes even more detrimental in maintaining orthostatic tolerance when coupled with proposed heat induced alterations in the Frank-Starling curve, that likely contribute to a greater fall in blood pressure during orthostasis, as well as impaired cerebrovascular autoregulation. Given this background, the primary objective of this proposal is to test the following hypotheses. A) Heat stress shifts the operating point on the Frank-Starling curve to a steeper location such that for the same reduction in ventricular filling pressure during orthostasis there will be a greater reduction in stroke volume, and thus blood pressure, in the heated condition. B) Heat stress impairs pre- and post-synaptic responses such that during an orthostatic challenge the elevation in vascular resistance is attenuated, relative to normothermia, and thus blood pressure regulation will be further impaired. C) Heat stress shifts the cerebrovascular autoregulatory curve, that when combined with a reduction in blood pressure during orthostasis, result in the blood pressure operating point residing on the descending limb of the autoregulatory curve. Upon completion of these studies valuable information will be obtained regarding the etiology of heat-induced reductions in orthostatic tolerance in humans.
| Huang, Mu; Brothers, R Matthew; Ganio, Matthew S et al. (2018) Tolerance to a haemorrhagic challenge during heat stress is improved with inspiratory resistance breathing. Exp Physiol 103:1243-1250 |
| Pearson, James; Lucas, Rebekah A I; Schlader, Zachary J et al. (2017) Elevated skin and core temperatures both contribute to reductions in tolerance to a simulated haemorrhagic challenge. Exp Physiol 102:255-264 |
| Schlader, Zachary J; Wilson, Thad E; Crandall, Craig G (2016) Mechanisms of orthostatic intolerance during heat stress. Auton Neurosci 196:37-46 |
| Schlader, Zachary J; Gagnon, Daniel; Lucas, Rebekah A I et al. (2015) Baroreceptor unloading does not limit forearm sweat rate during severe passive heat stress. J Appl Physiol (1985) 118:449-54 |
| Schlader, Zachary J; Gagnon, Daniel; Adams, Amy et al. (2015) Cognitive and perceptual responses during passive heat stress in younger and older adults. Am J Physiol Regul Integr Comp Physiol 308:R847-54 |
| Wingo, Jonathan E; Low, David A; Keller, David M et al. (2015) Combined facial heating and inhalation of hot air do not alter thermoeffector responses in humans. Am J Physiol Regul Integr Comp Physiol 309:R623-7 |
| Shibasaki, Manabu; Umemoto, Yasunori; Kinoshita, Tokio et al. (2015) The role of cardiac sympathetic innervation and skin thermoreceptors on cardiac responses during heat stress. Am J Physiol Heart Circ Physiol 308:H1336-42 |
| Crandall, Craig G; Wilson, Thad E (2015) Human cardiovascular responses to passive heat stress. Compr Physiol 5:17-43 |
| Lucas, Rebekah A I; Sarma, Satyam; Schlader, Zachary J et al. (2015) Age-related changes to cardiac systolic and diastolic function during whole-body passive hyperthermia. Exp Physiol 100:422-34 |
| Schlader, Zachary J; Gagnon, Daniel; Rivas, Eric et al. (2015) Fluid restriction during exercise in the heat reduces tolerance to progressive central hypovolaemia. Exp Physiol 100:926-34 |
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