Key result
Active exercise-induced heat stress and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge when skin temperatures are matched, with no significant difference in cumulative stress index (P=0.12).
Why the study?
Does exercise-induced heat stress reduce tolerance to simulated hemorrhage to a greater extent than passive heat stress when skin and core temperatures are matched in healthy adults?
RCT (n=8)
Open-label
Randomized crossover
No
Does exercise-induced heat stress reduce tolerance to simulated hemorrhage to a greater extent than passive heat stress when skin and core temperatures are matched in healthy adults?
Absolute Event Rate: 322% vs 383%
p-value: p=0.12
Tolerance to a simulated hemorrhagic challenge is similarly compromised by active and passive heat stress when skin and core temperatures are matched, highlighting the critical role of skin temperature elevation in orthostatic tolerance.
Skin temperature may primarily drive heat-related orthostatic intolerance; extends mechanistic insights but should not yet change practice.
Passive heat stress increases core and skin temperatures and reduces tolerance to simulated hemorrhage (lower body negative pressure; LBNP). We tested whether exercise-induced heat stress reduces LBNP tolerance to a greater extent relative to passive heat stress, when skin and core temperatures are similar. Eight participants (6 males, 32 ± 7 yr, 176 ± 8 cm, 77.0 ± 9.8 kg) underwent LBNP to presyncope on three separate and randomized occasions: 1) passive heat stress, 2) exercise in a hot environment (40°C) where skin temperature was moderate (36°C, active 36), and 3) exercise in a hot environment (40°C) where skin temperature was matched relative to that achieved during passive heat stress (∼38°C, active 38). LBNP tolerance was quantified using the cumulative stress index (CSI). Before LBNP, increases in core temperature from baseline were not different between trials (1.18 ± 0.20°C; P > 0.05). Also before LBNP, mean skin temperature was similar between passive heat stress (38.2 ± 0.5°C) and active 38 (38.2 ± 0.8°C; P = 0.90) trials, whereas it was reduced in the active 36 trial (36.6 ± 0.5°C; P ≤ 0.05 compared with passive heat stress and active 38). LBNP tolerance was not different between passive heat stress and active 38 trials (383 ± 223 and 322 ± 178 CSI, respectively; P = 0.12), but both were similarly reduced relative to active 36 (516 ± 147 CSI, both P ≤ 0.05). LBNP tolerance is not different between heat stresses induced either passively or by exercise in a hot environment when skin temperatures are similarly elevated. However, LBNP tolerance is influenced by the magnitude of the elevation in skin temperature following exercise induced heat stress.
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Pearson et al. (2014) conducted an RCT in Healthy volunteers (simulated hemorrhage) (n=8). Active heat stress (exercise in 40°C environment) vs. Passive heat stress (whole body heating via water-perfused suit) was evaluated on Lower body negative pressure (LBNP) tolerance quantified by cumulative stress index (CSI) (p=0.12). Active exercise-induced heat stress and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge when skin temperatures are matched, with no significant difference in cumulative stress index (P=0.12).
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