Isometric handgrip exercise (IHG) increases sweating rate without changing core or skin temperatures. The contribution of central command resulting in increases in sweating rate during IHG is unknown. To investigate this question, seven subjects performed IHG (35% maximum voluntary contraction (MVC) for 2 min) followed by 2-min of post-exercise ischaemia (PEI), with and without partial neuromuscular blockade (PNB). PNB was performed to augment central command during the IHG bout. These trials were conducted while the subject was normothermic, mildly heated, and moderately heated. On the non-exercising arm, forearm sweating rate was monitored over a microdialysis membrane perfused with neostigmine (acetylcholinesterase inhibitor), and at an adjacent untreated site. In normothermia with PNB, despite reduced force production during IHG (17 ± 9 versus 157 ± 13 N; P < 0.001), the elevation in sweating rate at the neostigmine-treated site was greater relative to the control IHG bout (P < 0.05). During subsequent PEI, for the PNB trial mean arterial blood pressure (MAP) and sweating rate returned towards pre-IHG levels, while during the control trial these variables remained elevated. During IHG while mildly heated, the elevation in sweating rate was greater during the PNB trial relative to the control trial. In contrast, during moderate heating sweating increased during IHG for both trials, however the elevation in sweating rate during the PNB trial was not greater than during the control trial. These results suggest that central command is capable of modulating sweating rate in all thermal conditions, however its effect is reduced when body temperatures and/or sweating rate are substantially elevated.
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