The Roles of Nitric Oxide, Oxidative Stress, and Angiotensin II Type 1 Receptor in Regulating Cutaneous Blood Flow and Sweating During Prolonged Exercise in the Heat with and without Fluid Replacement
The current study evaluated whether NO synthase (NOS) contributes to cutaneous vasodilation and sweating during prolonged exercise in the heat. In addition, we determined if prolonged exercise-induced increases in reactive oxygen species (ROS) and activation of angiotensin II type 1 receptors (AT1R)...
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ndltd-uottawa.ca-oai-ruor.uottawa.ca-10393-365272018-01-05T19:03:06Z The Roles of Nitric Oxide, Oxidative Stress, and Angiotensin II Type 1 Receptor in Regulating Cutaneous Blood Flow and Sweating During Prolonged Exercise in the Heat with and without Fluid Replacement McNeely, Brendan Kenny, Glen Heat Loss Prolonged Exercise Nitric Oxide Reactive Oxygen Species The current study evaluated whether NO synthase (NOS) contributes to cutaneous vasodilation and sweating during prolonged exercise in the heat. In addition, we determined if prolonged exercise-induced increases in reactive oxygen species (ROS) and activation of angiotensin II type 1 receptors (AT1R) impair heat loss responses. On two separate days, eleven young men completed 90-min of continuous cycling at ~600W of metabolic heat production followed by 40-min of recovery in the heat (40ºC). To evaluate the role of excess fluid loss via sweating, participants completed a second session of the same protocol while receiving fluid replacement (FR) determined during the first session (No-FR). Cutaneous vascular conductance (CVC) and local sweat rate (LSR) were measured at four intradermal microdialysis forearm sites perfused with either: (1) lactated Ringer (Control); (2) 10 mM NG-nitro-L-arginine methyl ester (L-NAME, NOS inhibition); (3) 10 mM ascorbate (non-selective anti-oxidant); or (4) 4.34 nM Losartan (AT1R inhibition). Ascorbate treatment increased CVC at 60- and 90-min of exercise versus Control during the FR (P < 0.02), but not the No-FR condition (P > 0.31). CVC was reduced at the L-NAME treated site (P < 0.02), but was not different relative to Control at the Losartan treated site (P > 0.19) irrespective of condition. LSR did not differ between sites or as a function of condition (all P > 0.10). We conclude that NO regulates cutaneous vasodilation but not sweating, irrespective of fluid replacement, and ascorbate sensitive ROS impair cutaneous vasodilation during prolonged exercise in the heat with FR. 2017-08-18T18:35:24Z 2017-08-18T18:35:24Z 2017 Thesis http://hdl.handle.net/10393/36527 http://dx.doi.org/10.20381/ruor-20807 en Université d'Ottawa / University of Ottawa |
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language |
en |
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topic |
Heat Loss Prolonged Exercise Nitric Oxide Reactive Oxygen Species |
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Heat Loss Prolonged Exercise Nitric Oxide Reactive Oxygen Species McNeely, Brendan The Roles of Nitric Oxide, Oxidative Stress, and Angiotensin II Type 1 Receptor in Regulating Cutaneous Blood Flow and Sweating During Prolonged Exercise in the Heat with and without Fluid Replacement |
description |
The current study evaluated whether NO synthase (NOS) contributes to cutaneous vasodilation and sweating during prolonged exercise in the heat. In addition, we determined if prolonged exercise-induced increases in reactive oxygen species (ROS) and activation of angiotensin II type 1 receptors (AT1R) impair heat loss responses. On two separate days, eleven young men completed 90-min of continuous cycling at ~600W of metabolic heat production followed by 40-min of recovery in the heat (40ºC). To evaluate the role of excess fluid loss via sweating, participants completed a second session of the same protocol while receiving fluid replacement (FR) determined during the first session (No-FR). Cutaneous vascular conductance (CVC) and local sweat rate (LSR) were measured at four intradermal microdialysis forearm sites perfused with either: (1) lactated Ringer (Control); (2) 10 mM NG-nitro-L-arginine methyl ester (L-NAME, NOS inhibition); (3) 10 mM ascorbate (non-selective anti-oxidant); or (4) 4.34 nM Losartan (AT1R inhibition). Ascorbate treatment increased CVC at 60- and 90-min of exercise versus Control during the FR (P < 0.02), but not the No-FR condition (P > 0.31). CVC was reduced at the L-NAME treated site (P < 0.02), but was not different relative to Control at the Losartan treated site (P > 0.19) irrespective of condition. LSR did not differ between sites or as a function of condition (all P > 0.10). We conclude that NO regulates cutaneous vasodilation but not sweating, irrespective of fluid replacement, and ascorbate sensitive ROS impair cutaneous vasodilation during prolonged exercise in the heat with FR. |
author2 |
Kenny, Glen |
author_facet |
Kenny, Glen McNeely, Brendan |
author |
McNeely, Brendan |
author_sort |
McNeely, Brendan |
title |
The Roles of Nitric Oxide, Oxidative Stress, and Angiotensin II Type 1 Receptor in Regulating Cutaneous Blood Flow and Sweating During Prolonged Exercise in the Heat with and without Fluid Replacement |
title_short |
The Roles of Nitric Oxide, Oxidative Stress, and Angiotensin II Type 1 Receptor in Regulating Cutaneous Blood Flow and Sweating During Prolonged Exercise in the Heat with and without Fluid Replacement |
title_full |
The Roles of Nitric Oxide, Oxidative Stress, and Angiotensin II Type 1 Receptor in Regulating Cutaneous Blood Flow and Sweating During Prolonged Exercise in the Heat with and without Fluid Replacement |
title_fullStr |
The Roles of Nitric Oxide, Oxidative Stress, and Angiotensin II Type 1 Receptor in Regulating Cutaneous Blood Flow and Sweating During Prolonged Exercise in the Heat with and without Fluid Replacement |
title_full_unstemmed |
The Roles of Nitric Oxide, Oxidative Stress, and Angiotensin II Type 1 Receptor in Regulating Cutaneous Blood Flow and Sweating During Prolonged Exercise in the Heat with and without Fluid Replacement |
title_sort |
roles of nitric oxide, oxidative stress, and angiotensin ii type 1 receptor in regulating cutaneous blood flow and sweating during prolonged exercise in the heat with and without fluid replacement |
publisher |
Université d'Ottawa / University of Ottawa |
publishDate |
2017 |
url |
http://hdl.handle.net/10393/36527 http://dx.doi.org/10.20381/ruor-20807 |
work_keys_str_mv |
AT mcneelybrendan therolesofnitricoxideoxidativestressandangiotensiniitype1receptorinregulatingcutaneousbloodflowandsweatingduringprolongedexerciseintheheatwithandwithoutfluidreplacement AT mcneelybrendan rolesofnitricoxideoxidativestressandangiotensiniitype1receptorinregulatingcutaneousbloodflowandsweatingduringprolongedexerciseintheheatwithandwithoutfluidreplacement |
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