Thermoregulatory Response to Acute Passive Heat Exposure in Individuals with Low‐level Spinal Cord Injury

Spinal cord injury (SCI) impacts both the afferent and efferent pathways of the thermoregulatory system and may result in delayed and/or diminished sweating, skin blood flow, and ventilatory responses to whole body heating. Because the magnitude of these impairments is largely related to the level and severity of injury, it is possible that individuals with low‐level SCI initiate an appropriate thermoregulatory response that supports the maintenance of core temperature within a safe range during acute heat exposure. Purpose To characterize and compare the thermoregulatory response to acute passive heat exposure (APHE) in individuals with low‐level SCI and the able‐bodied (AB) population. We hypothesized that individuals with low‐level SCI would display attenuated skin blood flow and ventilatory responses to heating compared to AB individuals, but that these responses would be sufficient to maintain core temperature within a safe range during a one‐hour bout of APHE. Methods Four individuals (1F) with low‐level SCI (T8‐T11) and 8 AB individuals (4 F) completed a one‐hour APHE session immersed to the level of the sternum in 40°C water. During a period of seated rest, baseline values of skin red blood cell (RBC) flux, ventilation (V̇ E ), and rectal temperature (T re ) were measured. RBC flux, measured at two sites on the ventral forearm (laser Doppler flowmetry), was divided by mean arterial pressure to calculate cutaneous vascular conductance (CVC). Local heating to 44°C was performed following APHE, and data are presented as a percentage of maximal CVC (% CVCmax). Throughout APHE, average CVC was assessed every 5 minutes, V̇ E was measured every 20 minutes, and T re was recorded every 5 minutes. Data are reported as mean ± SEM. Statistical analyses were conducted via paired and unpaired t‐tests where appropriate. Results Baseline CVC was similar between groups at rest (SCI: 11 ± 6% CVCmax and AB: 9 ± 2% CVCmax, P = 0.54) and after 60 minutes of APHE (both SCI and AB: 48 ± 4% CVCmax, P = 0.94). However, the time course of cutaneous vasodilation was delayed in individuals with SCI as CVC increased to only 19 ± 6% CVCmax in individuals with SCI by 20 minutes APHE compared to 39 ± 3% CVCmax in AB individuals ( P = 0.01). Baseline V̇ E was similar between groups (SCI: 7.9 ± 0.8 L·min −1 and AB: 9.4 ± 1.1 L·min −1 , P = 0.39). Within group comparisons revealed that V̇ E increased with heating in AB individuals (12.2 ± 1.4 L·min −1 at 60 minutes APHE, P < 0.01) but not in individuals with SCI (SCI: 9.2 ± 0.5 L·min −1 at 60 minutes APHE, P = 0.15). There was no difference in baseline T re between groups (SCI: 36.98 ± 0.31°C and AB: 37.36 ± 0.11°C, P = 0.17). T re tended to increase more in individuals with SCI (+1.48 ± 0.36°C) than AB individuals (+1.18 ± 0.04°C) ( P = 0.25) throughout heating, but by 60 minutes APHE T re increased to a similar, safe level in both groups (SCI: 38.45 ± 0.19°C and AB: 38.54 ± 0.08°C, P = 0.63). Conclusion These data indicate that although individuals with low‐level SCI exhibit a delayed rise in skin blood flow and an attenuated ventilatory response to heating compared to AB individuals, both groups similarly maintain T re within a safe range during a one‐hour APHE session. Support or Funding Information American Heart Association 16GRNT31330014 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .