Journal of applied physiology
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Recent studies suggest that arousal is the dominant factor acutely increasing blood pressure in obstructive sleep apnea and that neither stimulation of chemoreceptors nor mechanical factors associated with large negative swings in intrapleural pressure substantially contribute to the rise in blood pressure associated with each obstructive apneic event. A canine model of obstructive sleep apnea was used to examine the relative contributions of these mechanisms in the blood pressure response to induced airway obstruction during non-rapid-eye-movement sleep. In part A of the study, the arousal response was eliminated from an obstructive event by restoring airway patency just before the expected arousal, allowing blood pressure responses to be compared between obstructive events with and without arousal. ⋯ In comparison, when arousal was allowed to occur, MAP increased by a further 11.8 +/- 1.2 mmHg (P < 0.01). In part B (n = 3 dogs), there was no change in MAP during the obstructive apneic event, and MAP fell by > 10 mmHg in the postobstruction period whether or not arousal occurred (P < 0.05). We conclude that neural reflexes, but not mechanical factors, substantially contribute to the acute blood pressure response to an obstructive apneic event and that arousal produces a separate, additional acute hypertensive response.
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The effects of hypoglycemia on sweating, skin blood perfusion, and shivering responses were investigated in 10 healthy male volunteers. They exercised on an underwater cycle ergometer while immersed to the neck in 28 degrees C water for 20 min at 50% of their maximal work rate. The exercise-induced elevation in esophageal temperature (T(es)) initiated the sweating response (Esw) and increased skin blood perfusion (SkBP) as measured at the forehead. ⋯ Whereas the exercise delta T(es) response was unaffected by hypoglycemia, the decrease in T(es) was greater (P < or = 0.005) during the hypoglycemic than during the euglycemic condition. Hypoglycemia did not alter the delta T(es) threshold for cessation of sweating and passive vasodilation but reduced (P < or = 0.001) the delta T(es) threshold for onset of shivering (from -0.09 +/- 0.07 degrees C in the euglycemic condition to -0.65 +/- 0.12 degrees C in the hypoglycemic condition). The present results indicate that hypoglycemia (2.8 mM) does not affect the delta T(es) threshold for cessation of thermoregulatory sweating or the threshold for passive vasodilation during recovery from exercise-induced moderate heat stress but that it decreases the core temperature threshold for shivering during cold exposure.