The relative contribution of α‐ and β‐adrenergic sweating during heat exposure and the influence of sex and training status

Abstract

While human eccrine sweat glands respond to adrenergic agonists, there remains a paucity of information on the factors modulating this response. Thus, we assessed the relative contribution of α-and β-adrenergic sweating during a heat exposure and as a function of individual factors of sex and training status. α-and β-adrenergic sweating was assessed in forty-eight healthy young men (n = 35) and women (n = 13) including endurance-trained (n = 12) and untrained men (n = 12) under non-heat exposure (temperate, 25°C; n = 17) and heat exposure (hot, 35°C; n = 48) conditions using transdermal iontophoresis of phenylephrine (α-adrenergic agonist) and salbutamol (β-adrenergic agonist) on the ventral forearm, respectively. Adrenergic sweating was also measured after iontophoretic administration of atropine (muscarinic receptor antagonist) or saline (control) to evaluate how changes in muscarinic receptor activity modulate the adrenergic response to a heat exposure (n = 12). α-and β-adrenergic sweating was augmented in hot compared with temperate conditions (both P ≤ .014), albeit the relative increase was greater in β (~5.4-fold)-as compared to α (~1.5-fold)adrenergic-mediated sweating response. However, both α-and β-adrenergic sweating was abolished by atropinization (P = .001). Endurance-trained men showed an augmentation in α-(P = .043) but not β (P = .960)-adrenergic sweating as compared to untrained men. Finally, a greater α-and β-adrenergic sweating response (both P ≤ .001) was measured in habitually active men than in women. We show that heat exposure augments α-and β-adrenergic sweating differently via mechanisms associated with altered muscarinic receptor activity. Sex and training status modulate this response.

Effects of Medications on Heat Loss Capacity in Chronic Disease Patients: Health Implications Amidst Global Warming

“…A likely reason for such conflicting evidence is the differing localised and systemic effects of oral βadrenoreceptor blockers that may indirectly modulate sweating during passive and exercise-induced sweating (Buono et al, 2010(Buono et al, , 2011. Local β-adrenergic blockade has been found to suppress local sweat rates during exercise-induced heat stress (Amano et al, 2017(Amano et al, , 2020. Recent in vivo evidence during exercise demonstrated that locally administered propranolol attenuated local sweat response, albeit only during higher-intensity submaximal exercise (80 -90% of maximum workload) in habitually active men, with no attenuation in untrained men (Amano et al, 2017).…”

Effects of tetraethylammonium‐sensitive K+ channel blockade on cholinergic and thermal sweating in endurance‐trained and untrained men

“…Regular exercise training is associated with an increase in cardiorespiratory fitness, which is paralleled by an enhanced sweating response leading to improve performance during exercise, especially in the heat. It is believed that the exercise‐training‐induced activation of sweat glands may be responsible for the high sweat rate given the observation that pharmacological assessment of cholinergic sweating can be two times greater in endurance‐trained as compared to non‐endurance‐trained individuals (Amano et al., 2013, 2020b; Buono & Sjoholm, 1988; Inoue et al., 2014). Our findings confirm this hypothesis, but also advance new knowledge by demonstrating that the activity of TEA‐sensitive K + channels such as those associated with Ca 2+ ‐activated and possibly voltage‐gated K + channels, and therefore efflux of K + to extracellular space through these channels, does not modulate the underlying mechanisms mediating the augmented cholinergic sweat production in endurance‐trained men.…”

“…They were all members of the University Track and Field Club and were participating in regular competitions in both middle (e.g., 800–1500 m) and long (more than 1500 m) distance events. We limited the inclusion of endurance‐trained participants to those engaged in these events given prior reports demonstrating that middle‐ and long‐distance runners (Amano et al., 2020b; Tokizawa et al., 2016) but not sprinters (less than 400 m) (Amano et al., 2013) demonstrate an adaptive sweating response to regular exercise training. The non‐endurance participants were not engaged in any structured exercise activities for the previous 2 years.…”

“…Exercise training has been shown to augment thermoregulatory sweating during both exercise heat stress and passive heat stress (Amano et al, 2013(Amano et al, , 2020cLamarche et al, 2018;Yamazaki et al, 1994). This response is in large part mediated by cholinergic mechanisms as evidenced by the observation that sweating induced by transdermal administration of cholinergic agonists is augmented in endurance-trained as compared to non-endurance-trained individuals (Amano et al, 2013(Amano et al, , 2020bBuono & Sjoholm, 1988;Inoue et al, 2014). However, the ionic mechanisms that underlie the greater sweat production in endurance-trained individuals remain largely unresolved.…”

Effects of Isomaltulose Ingestion on Thermoregulatory Responses during Exercise in a Hot Environment

“…Local sweat rates on the forearm and chest were measured using the ventilated capsule method according to the methods used in our laboratory and described elsewhere [ 36 , 37 ]. A 3.14 cm 2 plastic capsule was affixed using topical glue (Collodion; Kanto chemical, Tokyo, Japan).…”