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. We hypothesized that iNOS inhibition would augment sweating and cutaneous vasodilation in exercising older adults. Physically active younger (n = 12, 23 ± 4 yr) and older (n = 12, 60 ± 6 yr) adults performed two 30-min bouts of cycling at a fixed rate of metabolic heat production (400 W) in the heat (35°C). Sweat rate and cutaneous vascular conductance (CVC) were evaluated at four intradermal microdialysis sites with: 1) lactated Ringer (control), 2) nNOS inhibitor (nNOS-I, NPLA), 3) iNOS inhibitor (iNOS-I, 1400W), or 4) eNOS inhibitor (eNOS-I, LNAA). In younger adults during both exercise bouts, all inhibitors decreased sweating relative to control, albeit a lower sweat rate was observed at iNOS-I compared with eNOS-I and nNOS-I sites (all P < 0.05). CVC at the eNOS-I site was lower than control in younger adults throughout the intermittent exercise protocol (all P < 0.05). In older adults, there were no differences between control and iNOS-I sites for sweating and CVC during both exercise bouts (all P > 0.05). We show that iNOS and eNOS are the main contributors to NOS-dependent sweating and cutaneous vasodilation, respectively, in physically active younger adults exercising in the heat, and that iNOS inhibition does not alter sweating or cutaneous vasodilation in exercising physically active older adults.

Key pointsr Studies show that nitric oxide synthase (NOS) and cyclooxygenase (COX) are involved in sweating and cutaneous vascular regulation in young adults in a potentially interactive manner.r We evaluated the separate and interactive roles of NOS and COX in forearm sweating and cutaneous vasodilatation in older adults during intermittent exercise in the heat performed at a moderate fixed rate of metabolic heat production (400 W, ß48% V O 2 max ).r We demonstrated that neither NOS nor COX are functionally involved in the forearm sweating response in older adults during exercise, whereas only NOS contributed to cutaneous vasodilatation.r These results provide valuable insight into the age-related changes in heat loss and suggest that COX inhibitors (i.e. non-steroidal anti-inflammatory drugs) may not impair core body temperature regulation during exercise in the heat in older adults.Abstract This study evaluated the separate and combined roles of nitric oxide synthase (NOS) and cyclooxygenase (COX) in forearm sweating and cutaneous vasodilatation in older adults during intermittent exercise in the heat. Twelve healthy older (62 ± 7 years) males peformed two 30 min cycling bouts at a fixed rate of metabolic heat production (400 W) in the heat (35°C, 20% relative humidity). The exercise bouts were followed by 20 and 40 min of recovery, respectively. Forearm sweat rate (ventilated capsule) and cutaneous vascular conductance (CVC, laser Doppler perfusion units/mean arterial pressure) were evaluated at four skin sites that were continuously perfused via intradermal microdialysis with: (1) lactated Ringer solution (Control), (2) 10 mM ketorolac (non-selective COX inhibitor), (3) 10 mM N G -nitro-L-arginine methyl ester (L-NAME; non-selective NOS inhibitor) or (4) a combination of 10 mM ketorolac + 10 mM L-NAME. Sweating was not different between the four sites during either exercise bout (main effect P = 0.92) (average of last 5 min of second exercise, Control, 0.80 ± 0.06; ketorolac, 0.77 ± 0.09; L-NAME, 0.74 ± 0.07; ketorolac + L-NAME, 0.77 ± 0.09 mg min −1 cm −2 ). During both exercise bouts, relative to CVC evaluated at the Control site (average of last 5 min of second exercise, 69 ± 6%max), CVC was similar at the ketorolac site (P = 0.62; 66 ± 4%max) whereas it was attenuated to a similar extent at both the L-NAME (49 ± 8%max) and ketorolac + L-NAME (54 ± 8%max) sites (both P < 0.05). Thus, we demonstrate that NOS and COX are not functionally involved in forearm sweating whereas only NOS contributes to forearm cutaneous vasodilatation in older adults during intermittent exercise 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. Older males with (n = 12, 61 ± 9 years) and without (n = 12, 64 ± 7 years) T2D performed two 30‐min bouts of cycling at a fixed rate of metabolic heat production of 500 W (~70% peak oxygen uptake) in the heat (35°C); each followed by a 20‐ and 40‐min recovery, respectively. Cutaneous vascular conductance (CVC) and sweat rate were measured at four intradermal microdialysis sites treated with either (1) lactated Ringer (Control), (2) 10 mmol/L ascorbate (an antioxidant), (3) 10 mmol/L L‐NAME (non‐selective NOS inhibitor), or (4) a combination of ascorbate + L‐NAME. In both groups, ascorbate did not modulate CVC or sweating during exercise relative to Control (all P > 0.05). In comparison to Control, L‐NAME alone or combined with ascorbate attenuated CVC during exercise (all P ≤ 0.05) but had no influence on sweating (all P > 0.05). We show that in both healthy and T2D older adults, intradermal administration of ascorbate does not improve cutaneous vasodilation and sweating during exercise in the heat. However, NOS plays an important role in mediating cutaneous vasodilation.

Pregnant women are recommended to engage in 150 min of moderate-intensity physical activity per week to reduce pregnancy complications. Many women struggle to remain physically active throughout pregnancy, and there is no consensus about whether women adopt a less efficient movement pattern as they progress through pregnancy and experience gestational weight gain. This study assessed the change in energy expenditure and mechanical efficiency in pregnant women (PREG; n = 10) when performing a walking treadmill task in early, mid, and late pregnancy and also compared with an age- and body mass index-matched, nonpregnant (CON; n = 10) group. On average, the PREG group gained within the Institute of Medicine’s gestational weight gain guidelines (11.6 ± 3.6 kg) and were all inactive (measured using accelerometry), except for 1 participant, by the third trimester, as per the 2019 Canadian physical activity guidelines for pregnant women. Energy expended to complete the walking task increased throughout pregnancy and was higher than the controls (111.5 ± 24.6 kcal) in mid and late pregnancy (139.0 ± 22.2 kcal, p = 0.02, and 147.3 ± 24.6 kcal, p = 0.005, respectively), but not early pregnancy (129.9 ± 18.9 kcal, p = 0.08). Walking mechanical efficiency was similar within pregnant women at each time point and compared to nonpregnant controls. Our findings add to the growing body of evidence demonstrating that pregnant women can safely perform physical activity by showing that walking mechanical efficiency is unchanged at low to moderate intensities. Novelty Energy demand during exercise increases proportionally to weight gain across pregnancy trimesters. However, mechanical efficiency remains unchanged during low- to moderate-intensity walking.

It is unclear if angiotensin II, which can increase the production of reactive oxygen species (oxidative stress), modulates heat loss responses of cutaneous blood flow and sweating. We tested the hypothesis that angiotensin II-induced increases in oxidative stress impair cutaneous perfusion and sweating during rest and exercise in the heat. Eleven young (24 ± 4 yr) healthy adults performed two 30-min cycling bouts at a fixed rate of metabolic heat production (400 W) in the heat (35°C). The first and second exercises were followed by a 20- and 40-min recovery. Four microdialysis fibers were placed in the forearm skin for continuous administration of either: 1) lactated Ringer (control), 2) 10 μM angiotensin II, 3) 10 mM ascorbate (an antioxidant), or 4) a combination of 10 μM angiotensin II + 10 mM ascorbate. Cutaneous vascular conductance (CVC; laser-Doppler perfusion units/mean arterial pressure) and sweating (ventilated capsule) were evaluated at each skin site. Compared with control, angiotensin II reduced both CVC and sweating at baseline resting and during each recovery in the heat (all P < 0.05). However, during both exercise bouts, there were no differences in CVC or sweating between the treatment sites (all P > 0.05). When ascorbate was coinfused with angiotensin II, the effect of angiotensin II on sweating was abolished (all P > 0.05); however, its effect on CVC at baseline resting and during each recovery remained intact (all P < 0.05). We show angiotensin II impairs cutaneous perfusion independent of oxidative stress, while it impairs sweating through increasing oxidative stress during exposure to an ambient heat stress before and following exercise.