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Abnormal neurovascular control during exercise is linked to heart failure severity
135
Citations
12
References
2001
Year
HypertensionHeart FailurePeak Msna 67Cardiovascular FunctionBlood PressureDiastolic FunctionKinesiologyExerciseHeart Failure SeverityApplied PhysiologyNeurologyMicrovascular DysfunctionSport PhysiologyCardiologyCardiac MechanicHealth SciencesAutonomic SystemRehabilitationCardiovascular DiseaseExercise PhysiologyPhysiologyVascular ControlCardiovascular PhysiologyMedicineAbnormal Neurovascular Control
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.
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