No abstract

The mechanism responsible for the attenuated heart rate (HR) response to exercise in patients with congestive heart failure (CHF) was investigated in 46 normal subjects and 59 patients with CHF stratified by peak exercise oxygen consumption (Vo2). The peak exercise HR and the increment in HR from rest to peak exercise were decreased in CHF patients, and both correlated strongly with peak Vo2 (r=0.810, p<0.0001; r=0.863, p <0.0001, respectively). Peak exercise norepinephrine level (NE) and the increment in NE from rest to peak exercise were not attenuated in CHF patients. Resting NE was elevated in CHF patients and correlated inversely with peak Vo2 (r=-0.595, p<0.001). However, no significant correlation occurred between peak Vo2 and either peak exercise NE or the exercise increment in NE. The ratio of the exercise increments in HR and NE, an indirect index of sinoatrial node sympathetic responsiveness, was markedly reduced in CHF patients and was inversely related to the severity of exercise impairment. Likewise, the HR response to a graded isoproterenol infusion was markedly reduced in CHF patients. Age-matching of normal subjects and CHF patients did not affect the foregoing observations. Infusion of CHF patients with the phosphodiesterase inhibitor milrinone caused a significant increase in the ratio of the exercise increments in HR and NE. These data strongly suggest that the attenuated HR response to exercise in CHF patients is due, at least in part, to postsynaptic desensitization of the 8-adrenergic receptor pathway. (Circulation 1989;80:314-323) P eak heart rate response to exercise is determined primarily by the magnitude of increase in sympathetic drive to the heart and the ability of f-adrenergic receptors in the sinoatrial node to respond to catecholamines. In patients with congestive heart failure (CHF), the chronotropic response to peak exercise is reduced and may contribute significantly to the impaired cardiac output response to exercise.1-4The mechanism responsible for a reduced chronotropic response to exercise in patients with CHF is not known. Although it is known that both the reflex stimulation of sympathetic nervous system

Although lifestyle-induced weight loss improves insulin resistance in prediabetic individuals, postprandial hyperinsulinemia is reduced only when a low-GI diet is consumed. In contrast, a high-GI diet impairs pancreatic β cell and intestinal K cell function despite significant weight loss. These findings highlight the important role of the gut in mediating the effects of a low-GI diet on type 2 diabetes risk reduction.