The Effects of Local NOS‐inhibition and Ascorbate Administration on Cutaneous Vasodilation and Sweating During Exercise‐heat Stress in Adults With and Without Hypertension
Authors: Schmidt Madison D. , Meade Robert D. , Muia Caroline M. , Fujii Naoto , Boulay Pierre , Sigal Ronald J. , Kenny Glen P. 
Published: April 2020

Aging is associated with oxidative stress in the skin resulting from an accumulation of radical oxygen species. Hypertension exacerbates oxidative stress, leading to a reduced contribution of nitric oxide (NO) to cutaneous vasodilation during whole‐body passive heat stress. We recently demonstrated that local administration of the non‐selective anti‐oxidant ascorbate did not modify NO‐dependent cutaneous vasodilation and sweating in older adults exercising in the heat (35°C). The effect of ascorbate on those responses in individuals with hypertension, however, remains uncertain. We therefore evaluated the hypothesis that local ascorbate administration improves NO‐dependent cutaneous vasodilation and sweating in adults with hypertension. Middle‐aged adults with (HYPE, mean [SD] age: 60 [5] years; n=7, 5 women) and without (CON, age: 63 [6] years; n=7, 2 women) hypertension performed two 30‐min bouts of cycling in the heat (35°C, 20% RH) at an external work rate eliciting ~50% peak aerobic power. The first (Ex1) and second (Ex2) bouts were separated by a 20‐min recovery. Four skin sites were perfused continuously via microdialysis with either 1) lactated Ringer’s (control site); 2) 10 mM ascorbate (anti‐oxidant treated); 3) 10 mM L‐NAME (NO‐inhibited); or 4) a combination of both agents. Cutaneous vascular conductance (CVC; presented as a % of maximum during sodium nitroprusside administration, CVCmax) and sweat rate were measured at each site. The effect of each treatment (i.e., change from the control site) was evaluated separately within each group. No differences in CVC at the control site were observed between HYPE (Ex1: 68 [20]%CVCmax; Ex2: 74 [25]%CVCmax) and CON (Ex1: 63 [16]%CVCmax; Ex2: 68 [20]%CVCmax; both p>.74). In the HYPE, ascorbate augmented CVC during Ex1 (7 [4]%CVCmax, P=.003) and Ex2 (8 [6]%CVCmax, P=.014‐‐). By contrast, L‐NAME reduced CVC alone (Ex1: −26 [19]%CVCmax; Ex2: −29 [16]%CVCmax; both p<.013) and when administered with ascorbate (Ex1: −19 [15]%CVCmax; Ex2: −19 [14]%CVCmax; both p<.017). In CON, an effect of ascorbate was not observed (Ex1: −5 [20]%CVCmax; Ex2: −11 [21]%CVCmax; both p>.18) and L‐NAME attenuated CVC with (Ex1: −22 [18]%CVCmax; Ex2: −23 [22]%CVCmax; both p<.026) and without ascorbate (Ex1: −24 [14]%CVCmax; Ex2: −22 [23]%CVCmax; both p<.031). Sweat rate was reduced in the HYPE compared to CON group during Ex1 (.39 [15] vs .78 [.31] mg·min−1 ·cm−2; p=.011) and Ex2 (.39 [15] vs .78 [.31] mg·min−1 ·cm−2; p=.011) at the control site. Sweating was not influenced by any treatment in HYPE (all p>.07). In CON, ascorbate augmented sweating during Ex 1 (.14 [.16] mg·min−1 ·cm−2; p=.038) but not Ex2 (.09 [.23] mg·min−1 ·cm−2; p=.31). No effect on sweating was seen at either NO‐inhibited site in CON (all p>.13). Therefore, in individuals with hypertension exercising in the heat, local administration of ascorbate augments NO‐dependent cutaneous vasodilation but not sweating, while in individuals without hypertension, ascorbate did not affect either heat loss response.

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