Reports indicate that postexercise heat loss is modulated by baroreceptor input; however, the mechanisms remain unknown. We examined the time-dependent involvement of adenosine receptors, noradrenergic transmitters, and nitric oxide (NO) in modulating baroreceptor-mediated changes in postexercise heat loss. Eight males performed two 15-min cycling bouts (85% VO2max) each followed by a 45-min recovery in the heat (35°C). Lower body positive (LBPP), negative (LBNP), or no (Control) pressure was applied in three separate sessions during the final 30-min of each recovery. Four microdialysis fibres in the forearm skin were perfused with: 1) lactated Ringer’s (Ringer’s); 2) 4mM Theophylline (inhibits adenosine receptors); 3) 10mM Bretylium (inhibits noradrenergic transmitter release); or 4) 10mM L-NAME (inhibits NO synthase). We measured cutaneous vascular conductance (CVC; percentage of maximum) calculated as perfusion units divided by mean arterial pressure, and local sweat rate. Compared to Control, LBPP did not influence CVC at L-NAME, Theophylline or Bretylium during either recovery (P>0.07); however, CVC at Ringer’s was increased by ~5-8% throughout 30 min of LBPP during Recovery 1 (all P<0.02). In fact, CVC at Ringer’s was similar to Theophylline and Bretylium during LBPP. Conversely, LBNP reduced CVC at all microdialysis sites by ~7-10% in the last 15 min of Recovery 2 (all P<0.05). Local sweat rate was similar at all treatment sites as a function of pressure condition (P>0.10). We show that baroreceptor input modulates postexercise CVC to some extent via adenosine receptors, noradrenergic vasoconstriction, and NO whereas no influence was observed for postexercise sweating.
Identifer | oai:union.ndltd.org:uottawa.ca/oai:ruor.uottawa.ca:10393/32992 |
Date | January 2015 |
Creators | McGinn, Ryan |
Contributors | Kenny, Glen |
Publisher | Université d'Ottawa / University of Ottawa |
Source Sets | Université d’Ottawa |
Language | English |
Detected Language | English |
Type | Thesis |
Format | application/pdf |
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