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Unit of 1 Cardiovascular Rehabilitation and Exercise Physiology, 2 Hypertension, and 4 General Clinic of Cardiopathies, 3 School of Physical Education and Sports, InCor-Heart Institute, University of São Paulo Medical School, São Paulo, CEP 05403-000, Brazil; and 5 Department of Cardiology, University of California Medical School, Los Angeles, California 90095
The purpose of this study was to determine if abnormalities of sympathetic neural and vascular control are present in mild and/or severe heart failure (HF) and to determine the underlying afferent mechanisms. Patients with severe HF, mild HF, and age-matched controls were studied. Muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) in the nonexercising arm were measured during mild and moderate static handgrip. MSNA during moderate handgrip was higher at baseline and throughout exercise in severe HF vs. mild HF (peak MSNA 67 ± 3 vs. 54 ± 3 bursts/min, P < 0.0001) and higher in mild HF vs. controls (33 ± 3 bursts/min, P < 0.0001), but the change in MSNA was not different between the groups. The change in FVR was not significantly different between the three groups during static exercise. During isolation of muscle metaboreceptors, MSNA and blood pressure remained elevated in normal controls and mild HF but not in severe HF. During mild handgrip, the increase in MSNA was exaggerated in severe HF vs. controls and mild HF, in whom MSNA did not increase. In summary, the increase in MSNA during static exercise in severe HF appears to be attributable to exaggerated central command or muscle mechanoreceptor control, not muscle metaboreceptor control.
autonomic nervous system
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