View clinical trials related to Exercise Intolerance.
Filter by:Aim of investigators was to study whether abnormalities of lung diffusing capacity for nitric oxide (DLNO) and carbon monoxide (DLCO) in long COVID may have a clinical impact in relation to exercise intolerance.
Although the Covid-19 infection mainly manifests itself with respiratory symptoms, as early as two months after the onset of the pandemic, the presence of other symptoms, including muscle ones, became clear. With the disappearance of the emergency and the advancement of knowledge, medium- and long-term effects have been reported at the level of different organs and systems. Many patients, after several months from infection, report intolerance to exercise and many suffer from pain and muscle weakness. No studies has been carried out on the muscular consequences of the infection and on their possible contribution to intolerance to exercise. Since skeletal muscle possesses the ACE2 receptor (Angiotensin converting enzyme 2) to which SARS-Cov-2 binds, it follows that the involvement of the skeletal muscle could be due not only to the secondary effects of the infection (e.g. reduced oxygen supply from persistent lung disease, perfusion defects from cardiovascular defects and vascular damage), but also to the direct action of virus (SARS-Cov-2 myositis). The general purpose of the research is to quantify the spread of symptoms and signs of muscle weakness and pain among the patient population welcomed at the Cardiorespiratory Rehabilitation Department of the Alexandria Hospital which have been suffering from SARS-CoV-2, being discharged and healed for more than two months, and define the possible contribution of muscular modifications to exercise intolerance.
Myalgic encephalomyelitis/Chronic fatigue syndrome (ME/CFS), otherwise known as Chronic fatigue syndrome (CFS) or myalgic encephalomyelitis (ME), is an under-recognized disorder whose cause is not yet understood. Suggested theories behind the pathophysiology of this condition include autoimmune causes, an inciting viral illness, and a dysfunctional autonomic nervous system caused by a small fiber polyneuropathy. Symptoms include fatigue, cognitive impairments, gastrointestinal changes, exertional dyspnea, and post-exertional malaise. The latter two symptoms are caused in part by abnormal cardiopulmonary hemodynamics during exercise thought to be due to a small fiber polyneuropathy. This manifests as low biventricular filling pressures throughout exercise seen in patients undergoing an invasive cardiopulmonary exercise test (iCPET) along with small nerve fiber atrophy seen on skin biopsy. After diagnosis, patients are often treated with pyridostigmine (off-label use of this medication) to enhance cholinergic stimulation of norepinephrine release at the post-ganglionic synapse. This is thought to improve venoconstriction at the site of exercising muscles, leading to improved return of blood to the heart and increasing filling of the heart to more appropriate levels during peak exercise. Retrospective studies have shown that noninvasive measurements of exercise capacity, such as oxygen uptake, end-tidal carbon dioxide, and ventilatory efficiency, improve after treatment with pyridostigmine. To date, there are no studies that assess invasive hemodynamics after pyridostigmine administration. It is estimated that four million people suffer from ME/CFS worldwide, a number that is thought to be a gross underestimate of disease prevalence. However, despite its potential for debilitating symptoms, loss of productivity, and worldwide burden, the pathophysiology behind ME/CFS remains unknown and its treatment unclear. By evaluating the exercise response to cholinergic stimulation, this study will shed further light on the link between the autonomic nervous system and cardiopulmonary hemodynamics, potentially leading to new therapeutic targets.
Heart failure (HF) is a major public health problem. This is the first cause of hospitalization and mortality of about 65 years old. This syndrome is characterized by a poor prognosis and a high cost of care. Thus, new strategies for treatment and prevention of the HF are among the major challenges facing health sciences today. The management of HF requires multimodal approach it involves a combination of non-pharmacological and pharmacological treatment, Besides improvements in pharmacological treatment, supervised exercise programs are recommended for all patients with HF as part of a non-pharmacological management but many questions regarding exercise training in HF patients remain unanswered. Even simple questions such as the best mode of training for these patients are unclear. The aim of this study 1. First, to characterize the physiological functions involved in the genesis of exercise intolerance and dyspnea especially muscle function (respiratory and skeletal), and cardiopulmonary patients suffering from chronic HF. 2. Second, to study and compare the effects of different rehabilitation programs and prove the superiority of the combination of three training modalities program: aerobic training (AT), resistance training (RT) and inspiratory muscle training (IMT). These modalities are: Aerobic Training: It has been proven effective in improving muscle abnormalities on changing the ventricular remodeling, dyspnea, functional capacity, increasing the maximum performance and reducing hospitalization in subjects suffering HF. Resistance Training: It has been proven effective in improving skeletal muscle metabolism and angiogenesis; increasing capillary density and blood flow to the active skeletal muscles, promoting the synthesis and release of nitric oxide, and decreasing oxidative stress. Selective Inspiratory Muscle Training: It has been proven effective in improving the strength and endurance of the respiratory muscles and reduction of dyspnea during daily activities.
Heart failure with preserved ejection fraction (HFpEF) is a major public health problem that has no proven effective treatment. This study assessed the effects of acute nitrite administration on resting and exercise hemodynamics in patients with HFpEF.