Whole-body heating augmented (-48.7 ml) and cooling attenuated (-10.3 ml) orthostatic-induced decreases in stroke volume compared to normothermia (-33.2 ml; P<0.05).
Does thermal stress alter orthostatic-induced decreases in stroke volume via the Frank-Starling mechanism in humans?
Thermal stress modulates orthostatic tolerance by altering the operating position on the Frank-Starling curve, with heating steepening and cooling flattening the relationship.
Absolute Event Rate: -48.7% vs -33.2%
p-value: p=<0.05
The Frank-Starling 'law of the heart' is implicated in certain types of orthostatic intolerance in humans. Environmental conditions have the capacity to modulate orthostatic tolerance, where heat stress decreases and cooling increases orthostatic tolerance. The objective of this project was to test the hypothesis that heat stress augments and cooling attenuates orthostatic-induced decreases in stroke volume (SV) via altering the operating position on a Frank-Starling curve. Pulmonary artery catheters were placed in 11 subjects for measures of pulmonary capillary wedge pressure (PCWP) and SV (thermodilution derived cardiac output/heart rate). Subjects experienced lower-body negative-pressure (LBNP) of 0, 15 and 30 mmHg during normothermia, skin-surface cooling (decrease in mean skin temperature of 4.3 +/- 0.4 degrees C (mean +/- s.e.m.) via perfusing 16 degrees C water through a tubed-lined suit), and whole-body heating (increase in blood temperature of 1.0 +/- 0.1 degrees C via perfusing 46 degrees C water through the suit). SV was 123 +/- 8, 121 +/- 10, 131 +/- 7 ml prior to LBNP, during normothermia, skin-surface cooling, and whole-body heating, respectfully (P = 0.20). LBNP of 30 mmHg induced greater decreases in SV during heating (-48.7 +/- 6.7 ml) compared to normothermia (-33.2 +/- 7.4 ml) and to cooling (-10.3 +/- 2.9 ml; all P < 0.05). Relating PCWP to SV indicated that cooling values were located on the flatter portion of a Frank-Starling curve because of attenuated decreases in SV per decrease in PCWP. In contrast, heating values were located on the steeper portion of a Frank-Starling curve because of augmented decreases in SV per decrease in PCWP. These data suggest that a Frank-Starling mechanism may contribute to improvements in orthostatic tolerance during cold stress and orthostatic intolerance during heat stress.
Wilson et al. (Wed,) reported a other. Thermal stress (whole-body heating and skin-surface cooling) with lower-body negative-pressure vs. Normothermia was evaluated on Decrease in stroke volume during LBNP of 30 mmHg (p=<0.05). Whole-body heating augmented (-48.7 ml) and cooling attenuated (-10.3 ml) orthostatic-induced decreases in stroke volume compared to normothermia (-33.2 ml; P<0.05).