Do nitric oxide synthase and cyclooxygenase contribute to the heat loss responses in older males exercising in the heat?

Abstract

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. 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, ∼48% VO2 max). 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. 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. 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 NG-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.