Acute limb heating improves macro- and microvascular dilator function in the leg of aged humans

Romero, Steven A.; Gagnon, Daniel; Adams, Amy N.; Cramer, Matthew N.; Kouda, Ken; Crandall, Craig G.

doi:10.1152/ajpheart.00519.2016

Cited by 66 publications

(110 citation statements)

References 59 publications

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“…The notion of therapeutic benefits from controlled hyperthermia is not new (Lee Titsworth et al 2014) but has recently gained interest in large part after a 30 year prospective study (Laukkanen et al 2015) indicating that lifetime sauna use is associated with lower rates of cardiovascular system-related deaths. An acute vascular improvement (increased macro-and microvascular dilator function) with a single heat stress bout has also been shown in older men (Romero et al 2017). Remarkably, these vascular changes were comparable to improvements generally associated with aerobic exercise training (Wilson et al 2016).…”

Section: Discussionmentioning

confidence: 66%

“…These surprising findings potentially represent novel favourable effects that buttress the vascular benefits previously reported with non-pathophysiological hyperthermia (Umscheif et al 2010;Ohori et al 2012;Laukkanen et al 2015;Brunt et al 2016;Romero et al 2017). To our knowledge, this is the first study to determine the effects of passive heat stress on circulating microparticles.…”

Section: Discussionmentioning

confidence: 68%

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Passive heat stress reduces circulating endothelial and platelet microparticles

Bain

Ainslie

Bammert

et al. 2017

Experimental Physiology

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What is the central question of this study? Does passive heat stress of +2°C oesophageal temperature change concentrations of circulating arterial endothelial- and platelet-derived microparticles in healthy adults? What is the main finding and its importance? Concentrations of circulating endothelial- and platelet-derived microparticles were markedly decreased in heat stress. Reductions in circulating microparticles might indicate favourable vascular changes associated with non-pathological hyperthermia. Interest in circulating endothelial- and platelet-derived microparticles (EMPs and PMPs, respectively) has increased because of their potential pathogenic role in vascular disease and as biomarkers for vascular health. Hyperthermia is commonly associated with a pro-inflammatory stress but might also provide vascular protection when the temperature elevation is non-pathological. Circulating microparticles might contribute to the cellular adjustments and resultant vascular impacts of hyperthermia. Here, we determined whether circulating concentrations of arterial EMPs and PMPs are altered by passive heat stress (+2°C oesophageal temperature). Ten healthy young men (age 23 ± 3 years) completed the study. Hyperthermia was achieved by circulating ∼49°C water through a water-perfused suit that covered the entire body except the hands, feet and head. Arterial (radial) blood samples were obtained immediately before heating (normothermia) and in hyperthermia. The mean ± SD oesophageal temperature in normothermia was 37.2 ± 0.1°C and in hyperthermia 39.1 ± 0.1°C. Concentrations of circulating EMPs and PMPs were markedly decreased in hyperthermia. Activation-derived EMPs were reduced by ∼30% (mean ± SD; from 61 ± 8 to 43 ± 7 microparticles μl ; P < 0.05) and apoptosis-derived EMPs by ∼45% (from 46 ± 7 to 23 ± 3 microparticles μl ; P < 0.05). Likewise, circulating PMPs were reduced by ∼75% in response to hyperthermia (from 256 ± 43 to 62 ± 14 microparticles μl ). These beneficial reductions in circulating EMPs and PMPs in response to a 2°C increase in core temperature might partly underlie the reported vascular improvements following therapeutic bouts of physiological hyperthermia.

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 68%

Passive heat stress reduces circulating endothelial and platelet microparticles

Bain

Ainslie

Bammert

et al. 2017

Experimental Physiology

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“…; Romero et al . ). Further highlighting the clinical implications of heat therapy, recent data from a large prospective cohort study revealed that increased frequency of sauna bathing is associated with a reduced risk of fatal cardiovascular diseases and all‐cause mortality (Laukkanen et al .…”

Section: Discussionmentioning

confidence: 97%

Increased endothelial shear stress improves insulin‐stimulated vasodilatation in skeletal muscle

Walsh

Ghiarone

Olver

et al. 2018

The Journal of Physiology

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Key points It has been postulated that increased blood flow‐associated shear stress on endothelial cells is an underlying mechanism by which physical activity enhances insulin‐stimulated vasodilatation. This report provides evidence supporting the hypothesis that increased shear stress exerts insulin‐sensitizing effects in the vasculature and this evidence is based on experiments in vitro in endothelial cells, ex vivo in isolated arterioles and in vivo in humans. Given the recognition that vascular insulin signalling, and associated enhanced microvascular perfusion, contributes to glycaemic control and maintenance of vascular health, strategies that stimulate an increase in limb blood flow and shear stress have the potential to have profound metabolic and vascular benefits mediated by improvements in endothelial insulin sensitivity. Abstract The vasodilator actions of insulin contribute to glucose uptake by skeletal muscle, and previous studies have demonstrated that acute and chronic physical activity improves insulin‐stimulated vasodilatation and glucose uptake. Because this effect of exercise primarily manifests in vascular beds highly perfused during exercise, it has been postulated that increased blood flow‐associated shear stress on endothelial cells is an underlying mechanism by which physical activity enhances insulin‐stimulated vasodilatation. Accordingly, herein we tested the hypothesis that increased shear stress, in the absence of muscle contraction, can acutely render the vascular endothelium more insulin‐responsive. To test this hypothesis, complementary experiments were conducted using (1) cultured endothelial cells, (2) isolated and pressurized skeletal muscle arterioles from swine, and (3) humans. In cultured endothelial cells, 1 h of increased shear stress from 3 to 20 dynes cm−2 caused a significant shift in insulin signalling characterized by greater activation of eNOS relative to MAPK. Similarly, isolated arterioles exposed to 1 h of intraluminal shear stress (20 dynes cm−2) subsequently exhibited greater insulin‐induced vasodilatation compared to arterioles kept under no‐flow conditions. Finally, we found in humans that increased leg blood flow induced by unilateral limb heating for 1 h subsequently augmented insulin‐stimulated popliteal artery blood flow and muscle perfusion. In aggregate, these findings across models (cells, isolated arterioles and humans) support the hypothesis that elevated shear stress causes the vascular endothelium to become more insulin‐responsive and thus are consistent with the notion that shear stress may be a principal mechanism by which physical activity enhances insulin‐stimulated vasodilatation.

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“…We demonstrated that FMD% improved acutely after a single bout of HEAT, which agrees with a previous report (Tinken et al., ). The increase in FMD% with acute heating has often been attributed to elevated anterograde shear rate (Tinken et al., ), although this has not been unanimously reproducible thus far (Romero et al., ; Thomas et al., ). Differences in heating protocols and the artery examined in them might explain some of the inconsistencies observed.…”

Section: Discussionmentioning

confidence: 99%

Peripheral artery endothelial function responses to altered shear stress patterns in humans

Cheng

MacDonald

2019

Experimental Physiology

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New Findings What is the central question of this study?What is the effect of altered shear stress pattern, with or without concurrent neurohumoral and metabolic activation, on the acute endothelial function response assessed via brachial artery flow‐mediated dilatation? What is the main finding and its importance?Despite generating distinctive shear stress patterns (i.e. increases in anterograde only, anterograde only with neurohumoral and metabolic activation, and both anterograde and retrograde), similar acute improvements were observed in the brachial artery flow‐mediated dilatation response in all conditions, indicating that anterograde and/or turbulent shear stress might be the essential element to induce acute increases in endothelial function. Abstract Endothelial function is influenced by both the direction and the magnitude of shear stress. Acute improvements in endothelial function have mostly been attributed to increased anterograde shear, whereas results from many interventional models in humans suggest that enhancing shear stress in an oscillatory manner (anterograde and retrograde) might be optimal. Here, we determined the acute brachial artery shear stress (SS) and flow‐mediated dilatation (FMD) responses to three shear‐altering interventions [passive heat stress (HEAT), mechanical forearm compression (CUFF) and handgrip exercise (HGEX)] and examined the relationship between changes in oscillatory shear index (OSI) and changes in FMD. During separate visits, 10 young healthy men (22 ± 3 years old) underwent 10 min of HEAT, CUFF or HGEX in their left forearm. Anterograde and retrograde SS, Reynolds number, OSI and FMD were assessed at rest and during/after each intervention. Anterograde SS increased during all interventions in a stepwise manner (P < 0.05 between interventions), with the change in HGEX (∆37.7 ± 12.2 dyn cm−2, P < 0.05) > CUFF (∆25.1 ± 11.9 dyn cm−2, P < 0.05) > HEAT (∆14.5 ± 7.9 dyn cm−2, P < 0.05). Retrograde SS increased during CUFF (∆−19.6 ± 4.3 dyn cm−2, P < 0.05). Anterograde blood flow was turbulent (i.e. Reynolds number ≥ |2000|) during all interventions (P < 0.05). The relative FMD improved after all interventions (P = 0.01), and there was no relationship between ∆OSI and ∆FMD. We elicited changes in SS profiles including increased anterograde SS (HEAT and HGEX) and both increased anterograde and retrograde SS (CUFF); regardless of the SS pattern, FMD improved to the same extent. These findings suggest that the presence of anterograde and/or turbulent SS might be the key to optimizing endothelial function in acute assessment protocols.

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Acute limb heating improves macro- and microvascular dilator function in the leg of aged humans

Cited by 66 publications

References 59 publications

Passive heat stress reduces circulating endothelial and platelet microparticles

Passive heat stress reduces circulating endothelial and platelet microparticles

Increased endothelial shear stress improves insulin‐stimulated vasodilatation in skeletal muscle

Peripheral artery endothelial function responses to altered shear stress patterns in humans

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