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% VO2max) 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.