|
pubmed:abstractText |
We examined whether oropharyngeal stimulation by drinking released the dehydration-induced suppression of cutaneous vasodilatation and decreased mean arterial pressure (MAP) in exercising subjects, and assessed the effects of hypovolaemia or hyperosmolality alone on these responses. Seven young males underwent four hydration conditions. These were two normal plasma volume (PV) trials: normal plasma osmolality (P(osmol), control trial) and hyperosmolality (DeltaP(osmol) = +11 mosmol (kg H(2)O)(-1)); and two low PV trials: isosmolality (DeltaPV = -310 ml) and hyperosmolality (DeltaPV = -345 ml; DeltaP(osmol) = +9 mosmol (kg H(2)O)(-1)), attained by combined treatment with furosemide (frusemide), hypertonic saline and/or 24 h water restriction. In each trial, the subjects exercised at 60% peak aerobic power for approximately 50 min at 30 degrees C atmospheric temperature and 50% relative humidity. When oesophageal temperature (T(oes)) reached a plateau after approximately 30 min of exercise, the subjects drank 200 ml water at 37.5 degrees C within a minute. Before drinking, forearm vascular conductance (FVC), calculated as forearm blood flow divided by MAP, was lowered by 20-40% in hypovolaemia, hyperosmolality, or both, compared with that in the control trial, despite increased T(oes). After drinking, FVC increased by approximately 20% compared with that before drinking (P < 0.05) in both hyperosmotic trials, but it was greater in normovolaemia than in hypovolaemia (P < 0.05). However, no increases occurred in either isosmotic trial. MAP fell by 4-8 mmHg in both hyperosmotic trials (P < 0.05) after drinking, but more rapidly in normovolaemia than in hypovolaemia. PV and P(osmol) did not change during this period. Thus, oropharyngeal stimulation by drinking released the dehydration-induced suppression of cutaneous vasodilatation and reduced MAP during exercise, and this was accelerated when PV was restored.
|
