Mechanisms underlying the postexercise baroreceptor‐mediated suppression of heat loss

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% VO 2max ) each followed by a 45‐min recovery in the heat (35°C). Lower body positive ( LBPP ), negative ( LBNP ), or no (Control) pressure were 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) 4 mmol·L −1 Theophylline (inhibits adenosine receptors); (3) 10 mmol·L −1 Bretylium (inhibits noradrenergic transmitter release); or (4) 10 mmol·L −1 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.