Passive heat therapy improves cutaneous microvascular function in sedentary humans via improved nitric oxide-dependent dilation

Brunt, Vienna E.; Eymann, Taylor M.; Francisco, Michael A.; Howard, Matthew; Minson, Christopher T.

doi:10.1152/japplphysiol.00424.2016

Cited by 106 publications

(114 citation statements)

References 48 publications

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“…Blood pressure values in a neutral thermal environment, however, were not reported. Recent studies by Brunt et al 19,20 . found that cardiovascular function and blood pressure were remarkably improved after long-term passive heat therapy (daily hot baths over the course of 8 weeks).…”

Section: Discussionmentioning

confidence: 99%

“…In rats, it has been shown that heat treatment improves glucose tolerance 24 and shifts obesity-induced insulin resistance back to normal, healthy insulin sensitivity 25 . Heat therapy by means of water immersion in young healthy volunteers has been shown to significantly improve cardiovascular function 19,20 . However, it is not yet known if exposure to warm ambient air elicits comparable health effects in humans.…”

Section: Introductionmentioning

confidence: 99%

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Thermophysiological adaptations to passive mild heat acclimation

et al. 2017

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Passive mild heat acclimation (PMHA) reflects realistic temperature challenges encountered in everyday life. Active heat acclimation, combining heat exposure and exercise, influences several important thermophysiological parameters; for example, it decreases core temperature and enhances heat exchange via the skin. However, it is unclear whether PMHA elicits comparable adaptations. Therefore, this study investigated the effect of PMHA on thermophysiological parameters. Participants were exposed to slightly increased temperatures (∼33°C/22% RH) for 6 h/d over 7 consecutive days. To study physiologic responses before and after PMHA, participants underwent a temperature ramp (UP), where ambient temperature increased from a thermoneutral value (28.8 ± 0.3°C) to 37.5 ± 0.6°C. During UP, core and skin temperature, water loss, cardiovascular parameters, skin blood flow and energy expenditure were measured. Three intervals were selected to compare data before and after PMHA: baseline (minutes 30–55: 28.44 ± 0.21°C), T1 (minutes 105–115: 33.29 ± 0.4°C) and T2 (minutes 130–140: 35.68 ± 0.61°C). After 7 d of PMHA, core (T1: −0.13 ± 0.13°C, P = 0.011; T2: −0.14 ± 0.15°C, P = 0.026) and proximal skin temperature (T1: −0.22 ± 0.29°C, P = 0.029) were lower during UP, whereas distal skin temperature was higher in a thermoneutral state (baseline: +0.74 ± 0.77°C, P = 0.009) and during UP (T1: +0.49 ± 0.76°C, P = .057 (not significant), T2:+0.51 ± 0.63°C, P = .022). Moreover, water loss was reduced (−30.5 ± 33.3 ml, P = 0.012) and both systolic (−7.7 ± 7.7 mmHg, P = 0.015) and diastolic (−4.4 ± 4.8 mmHg, P = 0.001) blood pressures were lowered in a thermoneutral state. During UP, only systolic blood pressure was decreased (T2: −6.1 ± 4.4 mmHg, P = 0.003). Skin blood flow was significantly decreased at T1 (−28.35 ± 38.96%, P = 0.037), yet energy expenditure remained unchanged. In conclusion, despite the mild heat stimulus, we show that PMHA induces distinct thermophysiological adaptations leading to increased resilience to heat.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Thermophysiological adaptations to passive mild heat acclimation

et al. 2017

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“…The reason for this variability is unclear but may be due to other co‐existing factors that could affect blood flow mechanisms during the 1 week period of RIPC, such as physical activity or repeated exposures to heat (Brunt et al . ).…”

Section: Discussionmentioning

confidence: 97%

Seven consecutive days of remote ischaemic preconditioning improves cutaneous vasodilatory capacity in young adults

Lang

Kim

Franke

et al. 2018

The Journal of Physiology

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Key points Remote ischaemic preconditioning (RIPC), induced by brief bouts of ischaemia followed by reperfusion, confers vascular adaptations that protect against subsequent bouts of ischaemia; however, the effect of RIPC repeated over several days on the human microcirculation is unknown. Using skin as a model, microvascular function was assessed at a control and a NO‐inhibited area of skin before 1 day after and 1 week after administering seven consecutive days of repeated RIPC on the contralateral arm. Maximal vasodilatation was increased by ∼20–50% following 7 days of repeated RIPC, and this response remained elevated 1 week after stopping RIPC; however, NO‐mediated vasodilatation was not affected by the RIPC stimulus. These data indicate that repeated RIPC augments maximal vasodilatation, but the underlying mechanism for this improvement is largely independent of NO. This finding suggests a role for other endothelium‐derived mediators and/or for endothelium‐independent adaptations with repeated RIPC. Abstract Remote ischaemic preconditioning (RIPC), induced by intermittent periods of ischaemia followed by reperfusion, confers cardiovascular protection from subsequent ischaemic bouts. RIPC increases conduit and resistance vessel function; however, the effect of RIPC on the microvasculature remains unclear. Using human skin as a microvascular model, we hypothesized that cutaneous vasodilatory (VD) function elicited by localized heating would be increased following repeated RIPC. Ten participants (23 ± 1 years, 6 males, 4 females) performed RIPC for seven consecutive days. Each daily RIPC session consisted of 4 repetitions of 5 min of arm blood flow occlusion interspersed by 5 min reperfusion. Before, 1 day after and 1 week after the 7 days of RIPC, two microdialysis fibres were placed in ventral forearm skin for continuous infusion of Ringer solution or 20 mM l‐NAME. Red blood cell flux was measured by laser Doppler flowmetry at each fibre site during local heating (Tloc = 39°C) and during maximal VD elicited by heating (Tloc = 43°C) and 28 mM sodium nitroprusside infusion. Data were normalized to cutaneous vascular conductance (flux/mmHg). Seven days of RIPC did not alter the nitric oxide (NO) contribution to the VD response to local heating (P > 0.05). However, the maximal VD was augmented (Pre: 2.5 ± 0.2, Post: 3.8 ± 0.5 flux/mmHg; P < 0.05) and remained elevated 1 week post RIPC (3.3 ± 0.4 flux/mmHg; P < 0.05). Repeated RIPC improves maximal VD but does not affect NO‐mediated VD in the cutaneous microvasculature. This finding suggests that other factors may explain the vasodilatory adaptations that occur following repeated RIPC.

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“…In humans, we showed that acute hot water immersion protects against reductions in brachial artery endothelial function induced by whole‐arm ischaemia‐reperfusion (Brunt et al . c ), a validated in vivo model of endothelial ischaemia‐reperfusion (Kharbanda et al . ; Loukogeorgakis et al .…”

Section: Introductionmentioning

confidence: 99%

Passive heat therapy protects against endothelial cell hypoxia‐reoxygenation via effects of elevations in temperature and circulating factors

Brunt

Wiedenfeld-Needham

Comrada

et al. 2018

The Journal of Physiology

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Repeated exposure to passive heat stress ('heat therapy') has widespread physiological benefits, including cellular protection against novel stressors. Increased heat shock protein (HSP) expression and upregulation of circulating factors may impart this protection. We tested the isolated abilities of mild heat pretreatment and serum from human subjects (n = 10) who had undergone 8 weeks of heat therapy to protect against cellular stress following hypoxia-reoxygenation (H/R), a model of ischaemic cardiovascular events. Cultured human umbilical vein endothelial cells were incubated for 24 h at 37°C (control), 39°C (heat pretreatment) or 37°C with 10% serum collected before and after 8 weeks of passive heat therapy (four to five times per week to increase rectal temperature to ≥ 38.5°C for 60 min). Cells were then collected before and after incubation at 1% O for 16 h (hypoxia; 37°C), followed by 20% O for 4 h (reoxygenation; 37°C) and assessed for markers of cell stress. In control cells, H/R increased nuclear NF-κB p65 protein (i.e. activation) by 106 ± 38%, increased IL-6 release by 37 ± 8% and increased superoxide production by 272 ± 45%. Both heat pretreatment and exposure to heat therapy serum prevented H/R-induced NF-κB activation and attenuated superoxide production; by contrast, only exposure to serum attenuated IL-6 release. H/R also decreased cytoplasmic haemeoxygenase-1 (HO-1) protein (known to suppress NF-κB), in control cells (-25 ± 8%), whereas HO-1 protein increased following H/R in cells pretreated with heat or serum-exposed, providing a possible mechanism of protection against H/R. These data indicate heat therapy is capable of imparting resistance against inflammatory and oxidative stress via direct heat and humoral factors.

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Passive heat therapy improves cutaneous microvascular function in sedentary humans via improved nitric oxide-dependent dilation

Cited by 106 publications

References 48 publications

Thermophysiological adaptations to passive mild heat acclimation

Thermophysiological adaptations to passive mild heat acclimation

Seven consecutive days of remote ischaemic preconditioning improves cutaneous vasodilatory capacity in young adults

Passive heat therapy protects against endothelial cell hypoxia‐reoxygenation via effects of elevations in temperature and circulating factors

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