Current Studies and Future Directions of Exercise Therapy for Muscle Atrophy Induced by Heart Failure

Abstract

Muscle atrophy is a common complication of heart failure. At present, there is no specific treatment to reverse the course of muscle atrophy. Exercise training, due to the safety and easy operation, is a recommended therapy for muscle atrophy induced by heart failure. However, the patients with muscle atrophy are weak in mobility and may not be able to train for a long time. Therefore, it is necessary to explore novel targets of exercise protection for muscle atrophy, so as to improve the quality of life and survival rate of patients with muscular atrophy induced by heart failure. This article aims to review latest studies, summarize the evidence and limitations, and provide a glimpse into the future of exercise for the treatment of muscle atrophy induced by heart failure. We wish to highlight some important findings about the essential roles of exercise sensors in muscle atrophy induced by heart failure, which might be helpful for searching potential therapeutic targets for muscle wasting induced by heart failure.

Exercise attenuates angiotensinⅡ-induced muscle atrophy by targeting PPARγ/miR-29b

“… 25 Exercise therapy currently represents the most commonly used and effective therapy for muscle atrophy. 9 , 10 However, patients with HF and muscle atrophy are characterized by decreased exercise capacity and may not be able to endure long periods of training. 3 , 4 Thus, it is important to investigate the key protective sensors of exercise as novel therapy targets for treatment of muscle atrophy.…”

“… 5 , 6 , 7 Skeletal muscle atrophy with HF can increase the risk of falls, osteoporosis, fractures, cachexia, hospitalizations, and mortality. 8 Except for exercise training, 9 , 10 there continues to be a lack of effective therapeutic strategies for reversing HF-induced muscle atrophy.…”

Non-coding RNA basis of muscle atrophy

“…Overexpression of miR-23a/miR-27a attenuated muscle loss by activating the AKT/FOXO1 pathway. 134 Aerobic exercise decreased miR-494 expression in gastrocnemius muscle of mice and promoted the upregulation of transcription factor A (TFAM) and FOXJ3, which are two regulatory factors of mitochondrial biogenesis, as well as increased mitochondrial biosynthesis. 135 As shown in Figure 2 , these findings suggest that exercise can delay muscle atrophy by regulating miRNAs.…”