NEW FINDINGS: • What is the central question of this study? What is the effect of lower leg hot water immersion on vascular ischaemia-reperfusion injury induced in the arm of young healthy humans? • What is the main finding and its importance? Lower leg hot water immersion successfully protects against vascular ischaemia-reperfusion injury in humans. This raises the possibility that targeted heating of the lower legs may be an alternative therapeutic approach to whole-body heating that is equally efficacious at protecting against vascular ischaemia-reperfusion injury. ABSTRACT: Reperfusion that follows a period of ischaemia paradoxically reduces vasodilator function in humans and contributes to the tissue damage associated with an ischaemic event. Acute whole-body hot water immersion protects against vascular ischaemia-reperfusion (I-R) injury in young healthy humans. However, the effect of acute lower leg heating on I-R injury is unclear. Therefore, the purpose of this study was to test the hypothesis that, compared with thermoneutral control immersion, acute lower leg hot water immersion would prevent the decrease in macro- and microvascular dilator functions following I-R injury in young healthy humans. Ten young healthy subjects (5 female) immersed their lower legs into a circulated water bath for 60 min under two randomized conditions: (1) thermoneutral control immersion (∼33°C) and (2) hot water immersion (∼42°C). Macrovascular (brachial artery flow-mediated dilatation) and microvascular (forearm reactive hyperaemia) dilator functions were assessed using Doppler ultrasound at three time points: (1) pre-immersion, (2) 60 min post-immersion, and (3) post-I/R (20 min of arm ischaemia followed by 20 min of reperfusion). Ischaemia-reperfusion injury reduced macrovascular dilator function following control immersion (pre-immersion 6.0 ± 2.1% vs. post-I/R 3.6 ± 2.1%; P < 0.05), but was well-maintained with prior hot water immersion (pre-immersion 5.8 ± 2.1% vs. post-I/R 5.3 ± 2.1%; P = 0.8). Microvascular dilator function did not differ between conditions or across time. Taken together, acute lower leg hot water immersion prevents the decrease in macrovascular dilator function that occurs following I-R injury in young healthy humans.
RCT Entities:
NEW FINDINGS: • What is the central question of this study? What is the effect of lower leg hotwater immersion on vascular ischaemia-reperfusion injury induced in the arm of young healthy humans? • What is the main finding and its importance? Lower leg hotwater immersion successfully protects against vascular ischaemia-reperfusion injury in humans. This raises the possibility that targeted heating of the lower legs may be an alternative therapeutic approach to whole-body heating that is equally efficacious at protecting against vascular ischaemia-reperfusion injury. ABSTRACT: Reperfusion that follows a period of ischaemia paradoxically reduces vasodilator function in humans and contributes to the tissue damage associated with an ischaemic event. Acute whole-body hotwater immersion protects against vascular ischaemia-reperfusion (I-R) injury in young healthy humans. However, the effect of acute lower leg heating on I-R injury is unclear. Therefore, the purpose of this study was to test the hypothesis that, compared with thermoneutral control immersion, acute lower leg hotwater immersion would prevent the decrease in macro- and microvascular dilator functions following I-R injury in young healthy humans. Ten young healthy subjects (5 female) immersed their lower legs into a circulated water bath for 60 min under two randomized conditions: (1) thermoneutral control immersion (∼33°C) and (2) hotwater immersion (∼42°C). Macrovascular (brachial artery flow-mediated dilatation) and microvascular (forearm reactive hyperaemia) dilator functions were assessed using Doppler ultrasound at three time points: (1) pre-immersion, (2) 60 min post-immersion, and (3) post-I/R (20 min of arm ischaemia followed by 20 min of reperfusion). Ischaemia-reperfusion injury reduced macrovascular dilator function following control immersion (pre-immersion 6.0 ± 2.1% vs. post-I/R 3.6 ± 2.1%; P < 0.05), but was well-maintained with prior hotwater immersion (pre-immersion 5.8 ± 2.1% vs. post-I/R 5.3 ± 2.1%; P = 0.8). Microvascular dilator function did not differ between conditions or across time. Taken together, acute lower leg hotwater immersion prevents the decrease in macrovascular dilator function that occurs following I-R injury in young healthy humans.
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