Screening criteria for increased susceptibility to heat stress during work or leisure in hot environments in healthy individuals aged 31-70 years.

Population aging and global warming generate important public health risks, as older adults have increased susceptibility to heat stress (SHS). We defined and validated sex-specific screening criteria for SHS during work and leisure activities in hot environments in individuals aged 31-70 years using age, anthropometry, and cardiorespiratory fitness. A total of 123 males and 44 females [44 ± 14 years; 22.

Effect of P2 receptor blockade on cutaneous vasodilation during rest and exercise in the heat in young men.

We assessed the role of purinergic P2 receptors in the regulation of cutaneous vasodilation in young adults at rest and during intermittent moderate-intensity exercise in the heat (35 °C). P2 receptor blockade augmented resting cutaneous vasodilation but had no influence during and following exercise. This increase was partly diminished by nitric oxide synthase inhibition.

Fitness-related differences in the rate of whole-body evaporative heat loss in exercising men are heat-load dependent.

What is the central question of this study? Aerobic fitness modulates heat loss, but the heat-load threshold at which fitness-related differences in heat loss occur in young healthy men remains unclear. What is the main finding and its importance? We demonstrate using direct calorimetry that aerobic fitness modulates heat loss in a heat-load-dependent manner, with fitness-related differences occurring between young men who have low and high fitness when the heat load is ∼≥500 W. Although aerobic fitness has been known for some time to modulate heat loss, our findings define the precise heat-load threshold at which fitness-related differences occur.

Increasing age is a major risk factor for susceptibility to heat stress during physical activity.

We evaluated the extent to which age, cardiorespiratory fitness, and body fat can independently determine whole-body heat loss (WBHL) in 87 otherwise healthy adults. We show that increasing age is a major predictor for decreasing WBHL in otherwise healthy adults (aged 20-70 years), accounting for 40% of the variation in the largest study to date. While greater body fat also had a minor detrimental impact on WBHL, there was no significant role for cardiorespiratory fitness.

No effect of ascorbate on cutaneous vasodilation and sweating in older men and those with type 2 diabetes exercising in the heat.

Aging and chronic disease such as type 2 diabetes (T2D) are associated with impairments in the body's ability to dissipate heat. To reduce the risk of heat-related injuries in these heat vulnerable individuals, it is necessary to identify interventions that can attenuate this impairment. We evaluated the hypothesis that intradermal administration of ascorbate improves cutaneous vasodilation and sweating in older adults via nitric oxide synthase (NOS)-dependent mechanisms during exercise in the heat and whether these improvements, if any, are greater in individuals with T2D.

Individual variations in nitric oxide synthase-dependent sweating in young and older males during exercise in the heat: role of aerobic power.

We evaluated the association between aerobic power (defined by peak oxygen consumption; O) and the contribution of nitric oxide synthase (NOS) to the sweating response in young and older individuals during exercise in the heat. Data from 44 young (24 ± 1 years) and 48 older (61 ± 2 years) males with mean VO of 47.8 ± 2.

The roles of K, K, and K channels in regulating cutaneous vasodilation and sweating during exercise in the heat.

We recently showed the varying roles of Ca-activated (K), ATP-sensitive (K), and voltage-gated (K) K channels in regulating cholinergic cutaneous vasodilation and sweating in normothermic conditions. However, it is unclear whether the respective contributions of these K channels remain intact during dynamic exercise in the heat. Eleven young (23 ± 4 yr) men completed a 30-min exercise bout at a fixed rate of metabolic heat production (400 W) followed by a 40-min recovery period in the heat (35°C, 20% relative humidity).

Mechanisms of nicotine-induced cutaneous vasodilation and sweating in young adults: roles for K, K, and K channels, nitric oxide, and prostanoids.

We evaluated the influence of K channels (i.e., Ca-activated K (K), ATP-sensitive K (K), and voltage-gated K (K) channels) and key enzymes (nitric oxide synthase (NOS) and cyclooxygenase (COX)) on nicotine-induced cutaneous vasodilation and sweating.

The roles of the Na+/K+-ATPase, NKCC, and K+ channels in regulating local sweating and cutaneous blood flow during exercise in humans in vivo.

Na/K-ATPase has been shown to regulate the sweating and cutaneous vascular responses during exercise; however, similar studies have not been conducted to assess the roles of the Na-K-2Cl co-transporter (NKCC) and K channels. Additionally, it remains to be determined if these mechanisms underpinning the heat loss responses differ with exercise intensity. Eleven young (24 ± 4 years) males performed three 30-min semirecumbent cycling bouts at low (30% VO), moderate (50% VO), and high (70% VO) intensity, respectively, each separated by 20-min recovery periods.

Intradermal administration of endothelin-1 attenuates endothelium-dependent and -independent cutaneous vasodilation via Rho kinase in young adults.

We recently showed that intradermal administration of endothelin-1 diminished endothelium-dependent and -independent cutaneous vasodilation. We evaluated the hypothesis that Rho kinase may be a mediator of this response. We also sought to evaluate if endothelin-1 increases sweating.

Nicotinic receptor activation augments muscarinic receptor-mediated eccrine sweating but not cutaneous vasodilatation in young males.

What is the central question of this study? Acetylcholine released from cholinergic nerves can activate both muscarinic and nicotinic receptors. Although each receptor can independently induce cutaneous vasodilatation and eccrine sweating, it remains to be elucidated whether the two receptors interact in order to mediate these responses. What is the main finding and its importance? We show that although nicotinic receptor activation does not modulate muscarinic cutaneous vasodilatation, it lowers the muscarinic receptor agonist threshold at which onset for eccrine sweating (augmentation of muscarinic eccrine sweating) occurs in young men in normothermic resting conditions.

The effect of endothelin A and B receptor blockade on cutaneous vascular and sweating responses in young men during and following exercise in the heat.

During exercise, cutaneous vasodilation and sweating responses occur, whereas these responses rapidly decrease during postexercise recovery. We hypothesized that the activation of endothelin A (ET) receptors, but not endothelin B (ET) receptors, attenuate cutaneous vasodilation during high-intensity exercise and contribute to the subsequent postexercise suppression of cutaneous vasodilation. We also hypothesized that both receptors increase sweating during and following high-intensity exercise.

K+ channel mechanisms underlying cholinergic cutaneous vasodilation and sweating in young humans: roles of KCa, KATP, and KV channels?

Acetylcholine released from cholinergic nerves is involved in heat loss responses of cutaneous vasodilation and sweating. K(+) channels are thought to play a role in regulating cholinergic cutaneous vasodilation and sweating, though which K(+) channels are involved in their regulation remains unclear. We evaluated the hypotheses that 1) Ca(2+)-activated K(+) (KCa), ATP-sensitive K(+) (KATP), and voltage-gated K(+) (KV) channels all contribute to cholinergic cutaneous vasodilation; and 2) KV channels, but not KCa and KATP channels, contribute to cholinergic sweating.

Exploring the mechanisms underpinning sweating: the development of a specialized ventilated capsule for use with intradermal microdialysis.

Many studies have aimed to identify the controllers of sweating using ventilated capsules with intradermal microdialysis. It is unclear, however, if the surface area covered by the capsule influences the observed response as a result of differences in the number of sweat glands affected by the infused pharmacological agent relative to the total glands captured by the capsule. We evaluated the area of skin perfused with agents delivered via microdialysis.

The interactive contributions of Na(+) /K(+) -ATPase and nitric oxide synthase to sweating and cutaneous vasodilatation during exercise in the heat.

Key Points: Nitric oxide synthase (NOS) contributes to sweating and cutaneous vasodilatation during exercise in the heat. Similarly, reports show that Na(+) /K(+) -ATPase activation can modulate sweating and microvascular circulation. In light of the fact that NO can activate Na(+) /K(+) -ATPase, we evaluated whether there is an interaction between Na(+) /K(+) -ATPase and NOS in the regulation of heat loss responses during an exercise-induced heat stress.

iNOS-dependent sweating and eNOS-dependent cutaneous vasodilation are evident in younger adults, but are diminished in older adults exercising in the heat.

Nitric oxide synthase (NOS) contributes to sweating and cutaneous vasodilation during exercise in younger adults. We hypothesized that endothelial NOS (eNOS) and neuronal NOS (nNOS) mediate NOS-dependent sweating, whereas eNOS induces NOS-dependent cutaneous vasodilation in younger adults exercising in the heat. Further, aging may upregulate inducible NOS (iNOS), which may attenuate sweating and cutaneous vasodilator responses.

Local infusion of ascorbate augments NO-dependent cutaneous vasodilatation during intense exercise in the heat.

Recent work demonstrates that nitric oxide (NO) contributes to cutaneous vasodilatation during moderate (400 W of metabolic heat production) but not high (700 W of metabolic heat production) intensity exercise bouts performed in the heat (35°C). The present study evaluated whether the impairment in NO-dependent cutaneous vasodilatation was the result of a greater accumulation of reactive oxygen species during high (700 W of metabolic heat production) relative to moderate (500 W of metabolic heat production) intensity exercise. It was shown that local infusion of ascorbate (an anti-oxidant) improves NO-dependent forearm cutaneous vasodilatation during high intensity exercise in the heat.