Sweating During Intermittent Exercise in the Heat in Young and Older Adults: A Role for P2 Receptors

Recent findings have identified nitric oxide synthase (NOS) as an important modulator of sweating during exercise. Additionally, in vitro studies have identified the presence of P2 receptors (a subgroup of purinergic receptors) on human eccrine sweat glands, which may indicate that these receptors can modulate sweating. If so, these receptors may influence sweating through NOS‐dependent mechanisms, given that P2 receptor activation can increase calcium ion concentration, which in turn can activate NOS. Studies also demonstrate that NOS‐dependent sweating is impaired in older adults during exercise in the heat. In parallel, P2 receptors are down regulated in older adults, suggesting the contribution of P2 receptors, if any, to sweating may also be impaired. Thus, we assessed the separate and combined contribution of NOS and P2 receptors to the sweating response during exercise in the heat. Additionally, we evaluated whether ageing influences these responses. Eight young (24±4 years) and nine older (57±6 years) adults performed an intermittent cycling protocol consisting of two 30 min bouts of exercise (Ex) at a fixed rate of heat production of 400 W in the heat (35°C); followed by 20 and 40 min of recovery respectively. Sweat rate (ventilated capsule) was monitored at four forearm skin sites continuously perfused via intradermal microdialysis: 1) lactated Ringer (Control), 2) 10 mM N G ‐nitro‐ L ‐arginine methyl ester ( L ‐NAME, a non‐selective NOS inhibitor), 3) 100 mM pyridoxine (PDX, non‐selective P2 receptor blocker), or 4) a combination of PDX and L ‐NAME. We show that in young adults, administration of L ‐NAME attenuated sweat rate (Ex1: 0.65 mg min −1 cm −2 ; Ex2: 0.67 mg min −1 cm −2 ) in comparison to Control (Ex1: 0.79 mg min −1 cm −2 ; Ex2: 0.82 mg min −1 cm −2 ) at the end of both exercise bouts (both P≤0.05). Further, infusion of PDX, both independently (Ex1: 0.69 mg min −1 cm −2 , P=0.07; Ex2: 0.73 mg min −1 cm −2 , P=0.04) and in combination with L ‐NAME (Ex1: 0.69 mg min −1 cm −2 , P=0.04; Ex2: 0.74 mg min −1 cm −2 , P=0.09), tended to reduce sweat rate relative to Control; albeit, these responses were not all statistically significant. However, the magnitude of reduction at each site compared to Control were not different (P=0.32). Finally, no differences in local sweat rate were observed between treatment sites in older adults (P=0.20). In summary, our findings indicate that P2 receptor activation can contribute to sweating in young adults through a NOS‐dependent mechanism. However, the contribution of these pathways to the sweating response is diminished in older adults. Support or Funding Information Funding support: This study was supported by grants from the Natural Sciences and Engineering Research Council of Canada (Discover grant, RGPIN‐06313‐2014; Discovery Grants Program ‐ Accelerator Supplement, RGPAS‐462252‐2014; funds held by Dr. Glen P. Kenny).

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