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Short term effects of exercise training on exercise capacity and quality of life in patients with pulmonary arterial hypertension: protocol for a randomised controlled trial

DOI: 10.1186/1471-2466-11-25

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Abstract:

This randomised controlled trial will determine whether a 12 week, outpatient-based, supervised, whole body exercise training program, followed by a home-based exercise program, is safe and improves exercise capacity and quality of life in individuals with pulmonary arterial hypertension. This study aims to recruit 34 subjects who will be randomly allocated to the exercise group (supervised exercise training 3 times a week for 12 weeks, followed by 3 sessions per week of home exercise for 12 weeks) or the control group (usual medical care). Subjects will be assessed at baseline, 12 weeks and 24 weeks.This study will determine whether outpatient-based, whole body exercise training is beneficial and safe in individuals with pulmonary arterial hypertension. Additionally, this study will contribute to clinical practice guidelines for this patient population.Australia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12609000502235Pulmonary arterial hypertension (PAH) is characterised by pathological changes in the pulmonary vasculature that cause an increase in pulmonary vascular resistance (PVR) thereby restricting blood flow through the pulmonary circulation [1,2]. To maintain blood flow, pulmonary artery pressure (PAP) increases [2]. Disease progression leads to right ventricular dysfunction and right heart failure [3,4]. The physiologic response of the pulmonary vasculature to exercise is markedly different from normal in individuals with PAH [1,5]. The pulmonary arteries and arterioles have an impaired capacity to vasodilate and distend, and the increase in cardiac output required to accommodate the metabolic requirements of exercise is limited [1]. As a result, oxygen delivery to the peripheral muscles is impaired [6], contributing to the symptoms of muscle fatigue and dyspnoea [1,5]. Whilst the impairment in cardiac output to meet peripheral oxygen demands during exercise largely contributes to the reduction in exercise capacity [7], skeletal muscle dysfunc

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