Abstract
Spinal cord injured (SCI) individuals show an altered hemodynamic response to metaboreflex activation due to a reduced capacity to vasoconstrict the venous and arterial vessels below the level of the lesion. Exercise training was found to enhance circulating catecholamines and to improve cardiac preload and venous tone in response to exercise in SCI subjects. Therefore, training would result in enhanced diastolic function and capacity to vasoconstrict circulation. The aim of this study was to test the hypothesis that one year of training improves hemodynamic response to metaboreflex activation in these subjects. Nine SCI individuals were enrolled and underwent a metaboreflex activation test at the beginning of the study (T0) and after one year of training (T1). Hemodynamics were assessed by impedance cardiography and echocardiography at both T0 and T1. Results show that there was an increment in cardiac output response due to metaboreflex activity at T1 as compared to T0 (545.4 ± 683.9 mL·min−1 versus 220.5 ± 745.4 mL·min−1, P < 0.05). Moreover, ventricular filling rate response was higher at T1 than at T0. Similarly, end-diastolic volume response was increased after training. We concluded that a period of training can successfully improve hemodynamic response to muscle metaboreflex activation in SCI subjects.
Highlights
During dynamic exercise, arterial blood pressure is regulated by the central nervous system through a balance between systemic vascular resistance (SVR) and cardiac output (CO) [1, 2]
It has recently been found that control over the cardiovascular system in response to muscle “metaboreflex,” a cardiovascular reflex evoked by those afferent nerve endings in the muscle that are sensitive to accumulation of muscle metabolic end-products [8], is altered in these patients, as demonstrated by their reduced blood pressure increment to this reflex
The aim of this study was to test the hypothesis that hemodynamic response to muscle metaboreflex activation could be improved in spinal cord injured subjects with one-year training
Summary
Arterial blood pressure is regulated by the central nervous system through a balance between systemic vascular resistance (SVR) and cardiac output (CO) [1, 2]. It has recently been found that control over the cardiovascular system in response to muscle “metaboreflex,” a cardiovascular reflex evoked by those afferent nerve endings in the muscle that are sensitive to accumulation of muscle metabolic end-products [8], is altered in these patients, as demonstrated by their reduced blood pressure increment to this reflex This phenomenon is to be ascribed to an impaired capacity to elevate SVR and to enhance ventricular filling rate (VFR) and SV [3]. These findings strengthen the concept that, in SCI individuals, there is a dearrangement in cardiovascular control, and this fact may be partly responsible for their difficulty in achieving normal CO levels during exercise
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