Thermoregulatory and Cardiovascular Adjustments to Acute Passive Heat Exposure in Low‐level Spinal Cord Injury
Authors: Larson Emily A. , Ely Brett R. , Francisco Michael A. , Wright Elise S. , Halliwill John R. , Minson Christopher T. 
Published: June 2021

Spinal cord injury (SCI) results in complete or partial loss of sensory, motor, and autonomic function below the level of the lesion. Because SCI impacts both the afferent and efferent pathways of the thermoregulatory system, it can impair the accurate sensation of and adequate response to heat stress. Impairments in heat dissipation through vasodilation of cutaneous microvessels and sweating could lead to unsafe rises in core temperature in individuals with SCI during heat stress. Due to the reduced muscle pump activity and attenuation of sympathetically mediated redistribution of blood flow in individuals with SCI, heat stress may also present a challenge to blood pressure regulation. However, because the magnitude of these impairments is related to the level and severity of injury, heat stress may be well tolerated in individuals with low‐level SCI. Therefore, this study sought to characterize and compare the thermoregulatory and cardiovascular adjustments to acute passive heat exposure (APHE) in individuals with low‐level SCI and the able‐bodied (AB) population. We hypothesized that a one‐hour water immersion APHE session in 40°C water would result in similar core temperature and blood pressure responses in subjects with low‐level SCI and AB subjects. Two individuals (1F) with low‐level SCI (below T6 vertebra) (Body Mass: 70.45 ± 2.57 kg) and 8 AB individuals (4F) (Body Mass: 70.18 ± 2.53 kg) underwent APHE. Resting and APHE values of rectal temperature (Tre), brachial mean arterial pressure (MAP), and cardiac output (Q̇c) (open circuit acetylene uptake) were collected. Tre and MAP were recorded every 5 minutes and Q̇c was measured every 20 minutes throughout APHE. Total peripheral resistance (TPR) was calculated as (MAP/Q̇c). Due to the low number of volunteers with SCI, no statistical comparisons were made between groups. Subjects with SCI and AB subjects had a similar Tre at rest, but Tre increased slightly more in those with SCI (+1.70°C) than AB (+1.18°C) throughout heating. However, by 60 minutes APHE Tre remained within safe limits in both groups (SCI: 38.75 ± 0.05°C and AB: 38.54 ± 0.08°C). Those with SCI had a slightly lower MAP at rest than AB subjects (SCI: 80 ± 4 mmHg vs AB: 85 ± 2 mmHg) and MAP was similarly reduced throughout heating (SCI: 70 ± 4 mmHg and AB: 74 ± 3 mmHg by 60 minutes APHE). In subjects with SCI compared to AB subjects, resting Q̇c was slightly higher (SCI: 6.58 ± 0.97 L·min−1 vs AB: 5.65 ± 0.31 L·min−1) and TPR was slightly lower (SCI: 12.34 ± 1.21 mmHg·min·L−1 vs AB: 15.30 ± 0.86 mmHg·min·L−1). Heating similarly impacted Q̇c and TPR in subjects with SCI and in AB subjects as Q̇c nearly doubled (SCI: 10.86 ± 1.45 L·min−1 and AB: 10.15 ± 0.56 L·min−1) and TPR fell by ~50% (SCI: 6.49 ± 0.53 mmHg·min·L−1 and AB: 7.41 ± 0.52 mmHg·min·L−1) by 60 minutes APHE in both groups. Consistent with our hypothesis, one‐hour APHE elicits similar changes in Tre, Q̇c, MAP, and TPR in individuals with SCI and in AB subjects. These findings are of particular relevance as chronic passive heat therapy emerges as a means of improving cardiometabolic health in patient populations.

Support or Funding Information

Supported by American Heart Association 16GRNT31330014

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.