Glabrous and non-glabrous vascular responses to mild hypothermia.

This study examined cutaneous vasoconstriction to whole-body hypothermia, specifically contributions of neural and endothelial vasomotor responses in glabrous and non-glabrous skin. Eleven participants were semi-recumbent at an ambient temperature of 22 °C for 30 min, after which ambient temperature was decreased to 0 °C until rectal temperature (Tre) had decreased by 0.5 °C. Laser-Doppler fluxmetry was measured at the forehead and thigh for measures of glabrous and non-glabrous skin, respectively; wavelet analysis was performed on the laser-Doppler signal to determine endothelial and neural activities. Hypothermia took on average 97 ±â€¯7 min and caused marked decreases at glabrous (42 ±â€¯5%baseline, p < 0.001) and non-glabrous (69 ±â€¯4%baseline, p < 0.001) skin. In glabrous skin, neural activity increased from 11 ±â€¯1% at thermoneutral to 18 ±â€¯1% (p < 0.001). In non-glabrous skin there was an initial decrease (p = 0.001) in neural activity from 13 ±â€¯2% to 9 ±â€¯1% (-0.2 °C decrease in Tre) and then increased (p = 0.002) to 21 ±â€¯2% baseline at -0.5 °C Tre. Endothelial activity decreased in both glabrous (16 ±â€¯3% to 6 ±â€¯1%, p < 0.001) and non-glabrous (15 ±â€¯1% to 7 ±â€¯1%, p = 0.003) skin. Hypothermia elicits large decreases in skin blood flow in both glabrous and non-glabrous skin that are related to increases in neural activity and a reduction of endothelial activity.

Cardiac autonomic function during hypothermia and its measurement repeatability.

This study examined the effect of mild hypothermia (a 0.5 °C decrease in rectal temperature) on heart rate variability (HRV), with the identical hypothermia protocol performed twice and compared using intraclass correlation coefficient (r) analysis to study the repeatability. Twelve healthy males each completed 1 neutral (23 °C) and 2 cold (0 °C) trials. In the neutral trial, participants sat quietly for 30 min. In the cold trials, baseline data were obtained from a 5-min sample following 30 min of quiet sitting at 23 °C, followed by passive exposure to 0 °C; hypothermic measures were taken from a 5-min period immediately prior to rectal temperature decreasing by 0.5 °C. HRV was obtained from a 3-lead electrocardiogram. There were no differences (all p > 0.05) in baseline measures between the neutral and the 2 cold trials, suggesting no precooling anxiety related to the cold trials. Heart rate, together with HRV measures (i.e., root mean square difference of successive normal RR intervals, triangular interpolation of NN interval histogram, low-frequency oscillations (LF), and high-frequency oscillations (HF)), increased (all p < 0.05) with mild hypothermia and showed excellent reliability between the 2 cold trials (all r ≥ 0.81). In contrast, the LF/HF ratio decreased (p < 0.05) and had only fair reliability between the 2 cold trials (r = 0.551). In general, hypothermia led to increases in heart rate, together with most measures of HRV. Although it was counterintuitive that both sympathetic and vagal influences would increase simultaneously, these changes likely reflected increased stress from whole-body cooling, together with marked cardiovascular strain and sympathetic nervous system activity from shivering to defend core body temperature. An important methodological consideration for future studies is the consistent and repeatable HRV responses to hypothermia.

Effects of mild whole body hypothermia on self-paced exercise performance.

This study examined self-paced, high-intensity exercise during mild hypothermia and whether hyperoxia might offset any potential impairment. Twelve trained males each completed 15-km time trials in three environmental conditions: Neutral (23°C, [Formula: see text] 0.21), Cold (0°C, [Formula: see text] 0.21), and Cold+Hyper (0°C, [Formula: see text] 0.40). Cold and Cold+Hyper trials occurred after a 0.5°C drop in rectal temperature. Rectal temperature was higher ( P ≤ 0.016) throughout Neutral compared with Cold and Cold+Hyper; Cold had a higher ( P ≤ 0.035) rectal temperature than Cold+Hyper from 2.5 to 7.5 km, and hyperoxia did not alter thermal sensation or comfort. Oxyhemoglobin saturation decreased from ~98% to ~94% with Neutral and Cold, but was maintained at ~99% in Cold+Hyper ( P < 0.01). Cerebral tissue oxygenation index (TOI) was higher in Neutral than in Cold throughout the time trial (TT) ( P ≤ 0.001), whereas Cold+Hyper were unchanged ( P ≥ 0.567) from Neutral by 2.5 km. Muscle TOI was maintained in Cold+Hyper compared with Neutral and was higher ( P ≤ 0.046) than Cold throughout the entire TT. Power output during Cold (246 ± 41 W) was lower than Neutral (260 ± 38 W) at all 2.5-km intervals ( P ≤ 0.012) except at 12.5 km. Power output during Cold+Hyper (256 ± 42 W) was unchanged ( P ≥ 0.161) from Neutral throughout the TT, and was higher than Cold from 7.5 km onward. Average cadence was higher in Neutral (93 ± 8 rpm) than in either Cold or Cold+Hyper (Cold: 89 ± 7 and Cold+Hyper: 90 ± 8 rpm, P = 0.031). In conclusion, mild hypothermia reduced self-paced exercise performance; hyperoxia during mild hypothermia restored performance to thermoneutral levels, likely due to maintenance of oxygen availability rather than any thermogenic benefit. NEW & NOTEWORTHY We examined self-paced, high-intensity exercise with 0.5°C rectal temperature decreases in a 0°C ambient environment, along with whether hyperoxia could offset any potential impairment. During a 15-km time trial, power output was lower with hypothermia than with thermoneutral. However, with hypothermia, hyperoxia of [Formula: see text] = 0.40 restored power output despite there being no thermophysiological improvement. Hypothermia impairs exercise performance, whereas hyperoxia likely restored performance due to maintenance of oxygen availability rather than any thermogenic benefit.