Acute lower leg hot water immersion maintained macrovascular dilator function following ischaemia-reperfusion injury (post-I/R 5.3% vs pre 5.8%), whereas control immersion did not (3.6% vs 6.0%).
RCT (n=10)
randomized
Does acute lower leg hot water immersion prevent the decrease in macro- and microvascular dilator functions following ischaemia-reperfusion injury in young healthy humans?
Targeted lower leg heating protects against macrovascular ischaemia-reperfusion injury in humans, offering a potential alternative to whole-body heating.
Absolute Event Rate: 5.3% vs 3.6%
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.
Engelland et al. (Sun,) conducted a rct in Vascular ischaemia-reperfusion injury (n=10). Lower leg hot water immersion (~42°C) vs. Thermoneutral control immersion (~33°C) was evaluated on Macrovascular dilator function (brachial artery flow-mediated dilatation) post-ischaemia-reperfusion. Acute lower leg hot water immersion maintained macrovascular dilator function following ischaemia-reperfusion injury (post-I/R 5.3% vs pre 5.8%), whereas control immersion did not (3.6% vs 6.0%).
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