Human obesity is characterized by a selective potentiation of central chemoreflex sensitivity

The chemoreflexes are an important mechanism for regulation of both breathi ng and autonomic cardiovascular function. Obesity is associated with an inc reased risk of alveolar hypoventilation and carbon dioxide retention, sugge sting that abnormalities in chemoreflex control mechanisms may be implicate d. We tested the hypothesis that chemoreflex function is altered in obesity . We compared ventilatory, sympathetic, heart rate, and blood pressure resp onses to hypercapnia, hypoxia, and the cold presser test in 14 obese subjec ts and 14 normal-weight subjects matched for age and gender. During hyperca pnia, the increase in minute ventilation was significantly greater in obese subjects (7.0+/-0.3 L/min) than in normal-weight subjects (3.3+/-1.1 L/min ; P=0.03). Despite higher minute ventilation during hypercapnia in obese su bjects, the increase in muscle sympathetic nerve activity was similar in ob ese and normal-weight subjects. When the inhibitory influence of breathing during hypercapnia was eliminated by apnea, the increase in sympathetic ner ve activity in obese subjects (99+/-16%) was greater than in normal-weight subjects (44+/-16%; P=0.02). The magnitude of the ventilatory and autonomic responses to hypoxia and the cold presser test was similar in obese and no rmal-weight subjects. We conclude that chemoreflex responses to hypercapnia are potentiated in eucapnic obese subjects. In contrast, responses to hypo xia and to the excitatory cold presser stimulus in obese subjects are simil ar to those in normal-weight subjects. Thus, obesity is characterized by se lective potentiation of central chemoreflex sensitivity.