New Findings: What is the central question of this study? Do regional differences exist in nitric oxide synthase (NOS)-dependent cutaneous vasodilatation and sweating during exercise-heat stress in young men. What is the main finding and its importance? Exercise-induced increases in cutaneous vasodilatation and sweating were greater on the chest and upper back compared to the forearm, although the NOS contribution to cutaneous vasodilatation was similar across all regions. Conversely, there was a greater NOS-dependent rate of change in sweating on the chest compared to the forearm, with a similar trend on the back.
Abstract: While it is established that nitric oxide synthase (NOS) is an important modulator of forearm cutaneous vasodilatation and sweating during an exercise-heat stress in young men, it remains unclear if regional differences exist in this response. In 15 habitually active young men (24 ± 4 (SD) years), cutaneous vascular conductance (CVC) and local sweat rate (LSR) were assessed at three body regions. On each of the dorsal forearm, chest and upper-back (trapezius), sites were continuously perfused with either (1) lactated Ringer solution (control) or (2) 10 Mm N -nitro-l-arginine (l-NNA, NOS inhibitor), via microdialysis. Participants rested in the heat (35°C) for ∼75 min, followed by 60 min of semi-recumbent cycling performed at a fixed rate of heat production of 200 W m (equivalent to ∼42% ). During exercise, the chest and upper-back regions showed higher CVC and LSR responses relative to the forearm (all P < 0.05). Within each region, l-NNA attenuated CVC and LSR relative to control (all P < 0.05). However, the NOS contribution was not different across regions for the rate of change and plateau for CVC or for the LSR plateau (all P > 0.05). Conversely, there was a greater NOS contribution to the rate of change for LSR at the chest relative to the forearm (P < 0.05) with a similar trend for the back. In habitually active young men, NOS-dependent cutaneous vasodilatation was similar across regions while the NOS contribution to LSR was greater on the chest relative to the forearm. These findings advance our understanding of the mechanisms influencing regional variations in cutaneous vasodilatation and sweating during an exercise-heat stress.
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http://dx.doi.org/10.1113/EP088388 | DOI Listing |
Am J Physiol Heart Circ Physiol
January 2025
Department of Kinesiology & Applied Physiology, University of Delaware, Newark DE.
The endothelin-B receptor (ETR) mediates vasodilation in young women, an effect that is absent in postmenopausal women. We have previously demonstrated that ETR-mediated vasodilation is regulated by estradiol (E) in young women; however, the impact of E on ETR function in postmenopausal women remains unknown. Accordingly, the objective of this study was to test the hypothesis that E exposure restores ETR-mediated dilation in postmenopausal women.
View Article and Find Full Text PDFJ Therm Biol
December 2024
School of Psychology, Sport and Health Science, Faculty of Science and Health, University of Portsmouth, UK; Diabetes and Endocrinology Department, Portsmouth Hospitals University NHS Trust, Portsmouth, UK. Electronic address:
PLoS One
November 2024
Univ. Grenoble Alpes, Inserm U1300 -HP2, CHU Grenoble Alpes, Grenoble, France.
Cureus
September 2024
Internal Medicine, Centro Médico Nacional Siglo XXI, Mexico City, MEX.
Chronic liver disease is a major cause of morbidity and mortality. The most common extrahepatic manifestations are dermatological. The pathophysiology of these dermatological manifestations is not clear, but it is postulated that the mechanisms involved include generalized vasodilatation, hyperdynamic blood circulation, and altered estrogen metabolism.
View Article and Find Full Text PDFJ Appl Physiol (1985)
November 2024
Department of Health and Human Physiology, The University of Iowa, Iowa City, Iowa, United States.
Human cutaneous microdialysis approaches for assessing nitric oxide (NO)-dependent blood flow include local heating (LH) of the skin until a plateau is reached, followed by infusion of a NO synthase inhibitor such as -nitro-l-arginine methyl ester (l-NAME); however, varied methods of quantifying and expressing NO-dependent vasodilation can obfuscate data interpretation and reproducibility. We retrospectively assessed NO-dependent vasodilation during LH to 39°C or 42°C, calculated as the ) absolute contribution of the NO-dependent component (along with baseline and the non-NO-dependent component) to the total cutaneous vascular conductance (CVC) response to LH, normalized to maximal CVC (%CVC); ) difference in %CVC (Δ%CVC) between the LH plateau and post-NO synthase inhibition (l-NAME plateau; Δ%CVC = LH plateau - l-NAME plateau); ) percentage of the LH plateau attributable to Δ%CVC (%plateau = Δ%CVC/LH plateau × 100); and ) %plateau when correcting for baseline. The LH plateaus during 39°C and 42°C were 48 ± 17%CVC (9 ± 5% baseline; 2 ± 4% non-NO dependent; 36 ± 15% NO dependent) and 88 ± 10%CVC (15 ± 8% baseline; 9 ± 10% non-NO dependent; 64 ± 13% NO dependent), respectively.
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