Int J Sports Med 1981; 02(4): 216-219
DOI: 10.1055/s-2008-1034612
© Georg Thieme Verlag Stuttgart · New York

Hormonal and Metabolic Responses to Exercise in Insulin-Dependent Diabetics with and Without Autonomic Neuropathy and in Normal Subjects

J. Hilsted, H. Galbo, B. Tronier, N. J. Christensen, T. W. Schwartz
  • Institute of Medical Physiology B, University of Copenhagen; Hvidøre Hospital; NOVO Research Institute; Medical Department F, Herlev Hospital; and Institute of Medical Biochemistry, University of Aarhus, Denmark
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Publication History

Publication Date:
14 March 2008 (online)

Abstract

The responses to exercise of hormones [free insulin, noradrenaline, adrenaline, renin, glucagon, growth hormone, Cortisol, and pancreatic polypeptide (PP)] and metabolites (glucose, lactate, free fatty acids, glycerol and (β-hydroxy-butyrate) were measured during exercise at 50 W and 100 W on an ergometer cycle. Seven normal subjects, eight insulin-dependent diabetics without neuropathy, eight with slight autonomic neuropathy (decreased beat-to-beat variation in heart rate, a cardiac parasympathetic defect), and seven with severe autonomic neuropathy including orthostatic hypotension were studied in the postabsorptive state. The capacity for exercise (expressed as duration of exercise until exhaustion) was reduced in both patient groups with autonomic neuropathy. During exercise, the concentrations of hormones (apart from renin) and metabolites were higher in diabetics without neuropathy than in normal subjects. In patients with severe neuropathy, the concentrations of hormones (apart from Cortisol) and of metabolites (apart from lactate) deviated less from those of normals. PP and renin did not increase at all in patients with severe autonomic neuropathy, suggesting that autonomic activity normally is involved in the responses of PP and renin to exercise. In conclusion, the hormonal and metabolic responses to exercise depend on the previous metabolic states. Furthermore, autonomic neuropathy may significantly attenuate the alterations in hormonal and metabolic responses induced by uncomplicated diabetes.

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