Abstract
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.
Highlights
A growing body of empirical evidence indicates that postexercise thermoregulatory control is altered in humans
Consistent with our first hypothesis, lower body positive pressure (LBPP) was associated with increases in cutaneous vascular conductance (CVC) from a Control condition and this increase was blunted by the non-selective inhibition of nitric oxide synthase
CVC was reduced with LBNP which was not affected by inhibition of noradrenergic vasoconstriction
Summary
A growing body of empirical evidence indicates that postexercise thermoregulatory control is altered in humans. The cessation of exercise is associated with a suppression of heat loss responses (i.e., cutaneous blood flow and sweating) such that only ~50% of the heat gained during exercise is lost during the first hour of recovery (Kenny et al 2008). It is believed that nonthermal factors of central origin are involved in this response Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
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