TY - JOUR
T1 - Shear stress induced by acute heat exposure is not obligatory to protect against endothelial ischemia-reperfusion injury in humans
AU - Hemingway, Holden W.
AU - Richey, Rauchelle E.
AU - Moore, Amy M.
AU - Shokraeifard, Austin M.
AU - Thomas, Gabriel C.
AU - Olivencia-Yurvati, Albert H.
AU - Romero, Steven A.
N1 - Funding Information:
Funding was provided by the National Institutes of Health (R01 AG059314 and T32 AG020494) and the Texas Chapter of the American College of Sports Medicine Student Research Development Award.
Publisher Copyright:
© 2022 the American Physiological Society.
PY - 2022/1
Y1 - 2022/1
N2 - Acute heat exposure protects against endothelial ischemia-reperfusion (I/R) injury in humans. However, the mechanism/s mediating this protective effect remain unclear. We tested the hypothesis that inhibiting the increase in shear stress induced by acute heat exposure would attenuate the protection of endothelial function following I/R injury. Nine (3 women) young healthy participants were studied under three experimental conditions: 1) thermoneutral control; 2) whole body heat exposure to increase body core temperature by 1.2°C; and 3) heat exposure brachial artery compression to inhibit the temperature-dependent increase in shear stress. Endothelial function was assessed via brachial artery flow-mediated dilatation before (pre-I/R) and after (post-I/R) 20 min of arm ischemia followed by 20 min of reperfusion. Brachial artery shear rate was increased during heat exposure (681 ± 359 s-1), but not for thermoneutral control (140 ± 63 s-1; P < 0.01 vs. heat exposure) nor for heat brachial artery compression (139 ± 60 s_1; P < 0.01 vs. heat exposure). Ischemia-reperfusion injury reduced flow-mediated dilatation following thermoneutral control (pre-I/R, 5.5 ± 2.9% vs. post-I/R, 3.8 ± 2.9%; P = 0.06), but was protected following heat exposure (pre-I/R, 5.8 ± 2.9% vs. post-I/R, 6.1 ± 2.9%; P = 0.5) and heat arterial compression (pre-I/R, 4.4 ± 2.8% vs. post-I/R, 5.8 ± 2.8%; P = 0.1). Contrary to our hypothesis, our findings demonstrate that shear stress induced by acute heat exposure is not obligatory to protect against endothelial I/R injury in humans.
AB - Acute heat exposure protects against endothelial ischemia-reperfusion (I/R) injury in humans. However, the mechanism/s mediating this protective effect remain unclear. We tested the hypothesis that inhibiting the increase in shear stress induced by acute heat exposure would attenuate the protection of endothelial function following I/R injury. Nine (3 women) young healthy participants were studied under three experimental conditions: 1) thermoneutral control; 2) whole body heat exposure to increase body core temperature by 1.2°C; and 3) heat exposure brachial artery compression to inhibit the temperature-dependent increase in shear stress. Endothelial function was assessed via brachial artery flow-mediated dilatation before (pre-I/R) and after (post-I/R) 20 min of arm ischemia followed by 20 min of reperfusion. Brachial artery shear rate was increased during heat exposure (681 ± 359 s-1), but not for thermoneutral control (140 ± 63 s-1; P < 0.01 vs. heat exposure) nor for heat brachial artery compression (139 ± 60 s_1; P < 0.01 vs. heat exposure). Ischemia-reperfusion injury reduced flow-mediated dilatation following thermoneutral control (pre-I/R, 5.5 ± 2.9% vs. post-I/R, 3.8 ± 2.9%; P = 0.06), but was protected following heat exposure (pre-I/R, 5.8 ± 2.9% vs. post-I/R, 6.1 ± 2.9%; P = 0.5) and heat arterial compression (pre-I/R, 4.4 ± 2.8% vs. post-I/R, 5.8 ± 2.8%; P = 0.1). Contrary to our hypothesis, our findings demonstrate that shear stress induced by acute heat exposure is not obligatory to protect against endothelial I/R injury in humans.
KW - Endothelial ischemia-reperfusion injury
KW - Heat therapy
KW - Humoral factors
KW - Shear stress
UR - http://www.scopus.com/inward/record.url?scp=85123082457&partnerID=8YFLogxK
U2 - 10.1152/japplphysiol.00748.2021
DO - 10.1152/japplphysiol.00748.2021
M3 - Article
C2 - 34941435
AN - SCOPUS:85123082457
SN - 8750-7587
VL - 132
SP - 199
EP - 208
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 1
ER -