Experimental Evidences Supporting the Benefits of Exercise Training in Heart Failure

Abstract

Heart Failure (HF), a common end point for many cardiovascular diseases, is a syndrome with a very poor prognosis. Although clinical trials in HF have achieved important outcomes in reducing mortality, little is known about functional mechanisms conditioning health improvement in HF patients. In parallel with clinical studies, basic science has been providing important discoveries to understand the mechanisms underlying the pathophysiology of HF, as well as to identify potential targets for the treatment of this syndrome. In spite of being the end-point of cardiovascular derangements caused by different etiologies, autonomic dysfunction, sympathetic hyperactivity, oxidative stress, inflammation and hormonal activation are common factors involved in the progression of this syndrome. Together these causal factors create a closed link between three important organs: brain, heart and the skeletal muscle. In the past few years, we and other groups have studied the beneficial effects of aerobic exercise training as a safe therapy to avoid the progression of HF. As summarized in this chapter, exercise training, a non-pharmacological tool without side effects, corrects most of the HF-induced neurohormonal and local dysfunctions within the brain, heart and skeletal muscles. These adaptive responses reverse oxidative stress, reduce inflammation, ameliorate neurohormonal control and improve both cardiovascular and skeletal muscle function, thus increasing the quality of life and reducing patients' morbimortality.

Regulation of Cardiac-Specific Proteins Expression by Moderate-Intensity Aerobic Exercise Training in Mice With Myocardial Infarction Induced Heart Failure Using MS-Based Proteomics

“…It was shown that several preclinical studies have already provided molecular insights for the beneficial effect of exercise in various induced HF animal models. As a whole, exercise training can ameliorate HF-induced dysfunctions by acting on the current standard pharmacological care-targeted pathways (16,17) or non-pharmacological available targets correcting the inflammatory response, skeletal myopathy, and vagal outflow (16,17). More recently, exercise was demonstrated to activate cardio-myogenesis in adult mice and the robust cardiomyogenic response was also observed in the adjacent area of the infarcted zone (18).…”

Exercise Training Protects Against Heart Failure Via Expansion of Myeloid-Derived Suppressor Cells Through Regulating IL-10/STAT3/S100A9 Pathway

“…A large number of clinical and experimental data have confirmed that physical exercise can reduce the occurrence and development of chronic HF through its natural and powerful inflammatory inhibition, but its molecular mechanism for inhibiting inflammatory response is still inconclusive. [7][8][9] Existing evidence shows that exercise can effectively reduce the levels of inflammatory factors IL (interleukin)-1β, TNF-α (tumor necrosis factor-α), CRP (C-reaction protein) in the serum of patients with coronary heart disease, and effectively increase the content of anti-inflammatory factors IL-10, IL-1ra, and other cytokines. 10 Correspondingly, in the absence of exercise intervention, the treatment of HF with the IL-1 receptor antagonist-anakinra can effectively improve the exercise tolerance of patients.…”