E.A. Larson1, B.R. Ely1, M.A. Francisco1, V.E. Brunt1,2, C.T. Minson, FACSM1

1University of Oregon, Eugene, OR; 2University of Colorado Boulder, Boulder, CO

Spinal cord injury (SCI), which impacts both the afferent and efferent pathways of the thermoregulatory system and impairs sympathetically mediated blood flow redistribution, may compromise the thermoregulatory and cardiovascular response to heat stress. However, because the magnitude of these impairments is related to the level of injury, heat stress may be well tolerated in individuals with low-level SCI. PURPOSE: To compare the thermoregulatory and cardiovascular adjustments to acute passive heat exposure (APHE) in individuals with low-level SCI and able-bodied (AB) individuals. METHODS: Four individuals (1F) with low-level SCI (T8-T11) and 8 AB individuals (4F) completed a one-hour APHE session in 40°C water. Skin red blood cell (RBC) flux, rectal temperature (Tre), cardiac output (Q̇c) (open circuit acetylene uptake), and brachial mean arterial pressure (MAP) were measured during baseline rest and throughout APHE. RBC flux, measured at two sites on the ventral forearm (laser Doppler flowmetry), was divided by MAP 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). Data are reported as mean ± SEM. Statistical analyses were conducted via unpaired t-tests. RESULTS: CVC was similar between groups at baseline (SCI: 11 ± 6% CVCmax and AB: 9 ± 2% CVCmax, P= 0.54) and was similarly increased by 60 min APHE (both SCI and AB: 48 ± 4% CVCmax, P= 0.94). Trewas similar between groups at baseline (SCI: 36.98 ± 0.31°C and AB: 37.36 ± 0.11°C,P= 0.17) and after 60 min APHE (SCI: 38.45 ± 0.19°C and AB: 38.54 ± 0.08°C, P= 0.63).Q̇cwas similar between groups at baseline (SCI: 5.92 ± 0.35 L·min−1 and AB: 5.31 ± 0.24 L·min−1, P = 0.17) and was similarly increased by 60 min APHE (SCI: 8.70 ± 0.95 L·min−1 and AB: 9.80 ± 0.51 L·min−1, P = 0.29). MAP was similar between groups at baseline (SCI: 85 ± 3 mmHg and AB: 85 ± 2 mmHg,P= 0.95) and was similarly reduced throughout heating (SCI: 74 ± 3 mmHg and AB: 77 ± 4 mmHg by 60 min APHE, P= 0.63). CONCLUSION: Individuals with SCI and AB individuals initiate similar increases in skin blood flow above the lesion level and cardiac output in response to whole-body heat stress, allowing both groups to maintain Treand MAP within safe ranges during a one-hour APHE session.

Supported by American Heart Association: 16GRNT31330014.

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