Role of catecholamines and β-receptors in ventilatory response during hypoxic exercise

Abstract

The ventilatory response to moderate exercise in hypoxia is potentiated in goats, decreasing Pa CO 2 more than in normoxic exercise. We investigated the hypothesis that this potentiation results from a ventilatory stimulus provided by increased levels of circulating catecholamines (norepinephrine and/or epinephrine), acting via β-receptors. Plasma norepinephrine [NE] and epinephrine [E] concentrations, arterial blood gases and ventilation were measured in normoxia and hypoxia ( Pa O 2 = 34–38 Torr ) at rest and during moderate exercise (5.6 kph; 5% grade) in seven female goats. Pa CO 2 decreased from rest to exercise in normoxia ( 2.9 ± 0.7 Torr; P < 0.01 ), and decreased significantly more from rest during hypoxic exercise ( 6.4 ± 0.6 Torr; P < 0.01 ). [NE] increased in both normoxic ( 1.1 ± 0.4 ng/ml; P < 0.05 ) and hypoxic exercise ( 2.5 ± 0.5 ng/ml; p < 0.01 ); the [NE] increase in hypoxia was significantly greater ( P < 0.01). [E] increased in normoxic ( 0.3 ± 0.1 ng/ml; P < 0.05 ) but not hypoxic exercise ( 0.6 ± 0.5 ng/ml; P > 0.2 ). Experiments were repeated following administration of the β-adrenergic receptor blocker, propranolol (2 mg/kg, i.v.). After β-blockade, Pa CO 2 decreases from rest to exercise in normoxia ( 3.2 ± 0.7 Torr; P < 0.01 ) and hypoxia ( 8.1 ± 0.7 Torr; P < 0.001 ) were not significantly different from control. The data indicate that β-adrenergic receptor stimulation is not necessary for a greater decrease in Pa CO 2 during hypoxic versus normoxic exercise. The greater rise in [NE] suggests a possible role in ventilatory control during hypoxic exercise, perhaps via α-adrenergic receptors. However, recent evidence suggests that NE is inhibitory in goats, and that NE is unlikely to mediate extra ventilatory stimulation during hypoxic exercise.