Acute volume expansion preserves orthostatic tolerance during whole‐body heat stress in humans

Abstract

Whole-body heat stress reduces orthostatic tolerance via a yet to be identified mechanism(s). The reduction in central blood volume that accompanies heat stress may contribute to this phenomenon. The purpose of this study was to test the hypothesis that acute volume expansion prior to the application of an orthostatic challenge attenuates heat stress-induced reductions in orthostatic tolerance. In seven normotensive subjects (age, 40 ± 10 years: mean ± s.d.), orthostatic tolerance was assessed using graded lower-body negative pressure (LBNP) until the onset of symptoms associated with ensuing syncope. Orthostatic tolerance (expressed in cumulative stress index units, CSI) was determined on each of 3 days, with each day having a unique experimental condition: normothermia, whole-body heating, and whole-body heating + acute volume expansion. For the whole-body heating + acute volume expansion experimental day, dextran 40 was rapidly infused prior to LBNP sufficient to return central venous pressure to pre-heat stress values. Whole-body heat stress alone reduced orthostatic tolerance by ∼80% compared to normothermia (938 ± 152 versus 182 ± 57 CSI; mean ± s.e.m., P < 0.001). Acute volume expansion during whole-body heating completely ameliorated the heat stress-induced reduction in orthostatic tolerance (1110 ± 69 CSI, P < 0.001). Although heat stress results in many cardiovascular and neural responses that directionally challenge blood pressure regulation, reduced central blood volume appears to be an underlying mechanism responsible for impaired orthostatic tolerance in the heat-stressed human.

Active and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge

“…Such a challenge was not necessary to address the proposed hypotheses, and thus inclusion of a normothermic LBNP challenge would expose subjects to an unnecessary procedure and therefore some level of risk. That said, using a similar LBNP ramp, as well as CSI criteria to evaluate LBNP tolerance, we consistently observe CSI mean values in the ϳ900 -1,100 mmHg·min range in normothermic subjects (7,28,29,32), which is well above what was observed in any of the three trials in the present experiment.…”

“…Given that both passive heat stress (2,26,29,31,48,51) and exercise in a thermoneutral environment (6) impair tolerance to a hypotensive challenge, we hypothesized that the combination of exercise in the heat would further reduce LBNP tolerance, relative to passive heat stress alone, when controlling for internal and mean skin temperatures. Counter to that hypothesis, LBNP tolerance was not different between these two perturbations when mean skin temperatures were clamped at similar levels.…”

“…However, LBNP tolerance is influenced by the magnitude of the elevation in skin temperature following exercise induced heat stress. exercise; heat stress; orthostatic tolerance PASSIVE HEAT STRESS increases core and skin temperatures and is accompanied with profound reductions in tolerance to central hypovolemia [e.g., lower body negative pressure (LBNP)], which simulates a hemorrhagic state (2,26,29,31,48,51). This is due, in part, to a large displacement of blood to the cutaneous circulation and associated reductions in systemic vascular resistance (42) and central blood volume (12, 13), coupled with inadequate cutaneous vasoconstriction during the hypotensive challenge (11, 38).…”

End-tidal carbon dioxide tension reflects arterial carbon dioxide tension in the heat-stressed human with and without simulated hemorrhage

“…These physiological occurrences likely contribute to decreases in cerebral perfusion and thus the reduction in orthostatic tolerance that occur during heat stress (1,4,(11)(12)(13)25). The precise understanding of the relationship between carbon dioxide tension and the cerebral vasculature is dependent on the assumption that PET CO 2 accurately reflects Pa CO 2 , the latter of which is the physiologically relevant variable.…”

“…To our knowledge, however, there is no information regarding the relationship of PET CO 2 to Pa CO 2 in individuals with elevated internal temperatures. This information is important because heat stress-induced reductions in Pa CO 2 likely contribute to reductions in cerebral blood flow (3,5,15,26) and ultimately reduced orthostatic tolerance in this thermal condition (4,12,25). Because PET CO 2 is commonly used as an index of Pa CO 2 in heat-stressed individuals (3,5,15,26), it is important to identify the relationship between these variables in this thermal condition.…”