scholarly journals Apoptosis in the skeletal muscle of patients with heart failure: investigation of clinical and biochemical changes

Heart ◽  
2000 ◽  
Vol 84 (4) ◽  
pp. 431-437 ◽  
Author(s):  
G Vescovo
2012 ◽  
Vol 5 (6) ◽  
pp. 812-818 ◽  
Author(s):  
Stewart H. Lecker ◽  
Alexandra Zavin ◽  
Peirang Cao ◽  
Ross Arena ◽  
Kelly Allsup ◽  
...  

2015 ◽  
Vol 119 (6) ◽  
pp. 734-738 ◽  
Author(s):  
Satyam Sarma ◽  
Benjamin D. Levine

Patients with heart failure with preserved ejection fraction (HFpEF) have similar degrees of exercise intolerance and dyspnea as patients with heart failure with reduced EF (HFrEF). The underlying pathophysiology leading to impaired exertional ability in the HFpEF syndrome is not completely understood, and a growing body of evidence suggests “peripheral,” i.e., noncardiac, factors may play an important role. Changes in skeletal muscle function (decreased muscle mass, capillary density, mitochondrial volume, and phosphorylative capacity) are common findings in HFrEF. While cardiac failure and decreased cardiac reserve account for a large proportion of the decline in oxygen consumption in HFrEF, impaired oxygen diffusion and decreased skeletal muscle oxidative capacity can also hinder aerobic performance, functional capacity and oxygen consumption (V̇o2) kinetics. The impact of skeletal muscle dysfunction and abnormal oxidative capacity may be even more pronounced in HFpEF, a disease predominantly affecting the elderly and women, two demographic groups with a high prevalence of sarcopenia. In this review, we 1) describe the basic concepts of skeletal muscle oxygen kinetics and 2) evaluate evidence suggesting limitations in aerobic performance and functional capacity in HFpEF subjects may, in part, be due to alterations in skeletal muscle oxygen delivery and utilization. Improving oxygen kinetics with specific training regimens may improve exercise efficiency and reduce the tremendous burden imposed by skeletal muscle upon the cardiovascular system.


2020 ◽  
Vol 76 (1) ◽  
pp. 109-114
Author(s):  
Ippei Nakano ◽  
Masaya Tsuda ◽  
Shintaro Kinugawa ◽  
Arata Fukushima ◽  
Naoya Kakutani ◽  
...  

1996 ◽  
Vol 78 (7) ◽  
pp. 841-844 ◽  
Author(s):  
Tsutomu Sumimoto ◽  
Mutsuhito Kaida ◽  
Fumio Yuasa ◽  
Toshihiko Hattori ◽  
Toshimitsu Jikuhara ◽  
...  

2019 ◽  
Vol 21 (Supplement_L) ◽  
pp. L20-L23 ◽  
Author(s):  
Guilherme Wesley Peixoto da Fonseca ◽  
Stephan von Haehling

Abstract Sarcopaenia is defined as reduced skeletal muscle mass associated with either a decline in muscle strength or low physical performance. It has been shown to affect 17.5% of people worldwide, with a prevalence of 20% or higher in patients with heart failure (HF). Sarcopaenia has severe impact on mortality, physical capacity, and quality of life. Even though several mechanisms, such as autonomic imbalance, reduced muscle blood flow, increased inflammation, hormonal alterations, increased apoptosis, and autophagy have been proposed to fuel the pathogenesis of sarcopaenia, additional studies assessing the interaction of these conditions need to be conducted to elucidate how the presence of sarcopaenia can exacerbate the progression of HF and vice-versa. Resistance training combined with nutritional protein intake seems to be effective in the treatment of sarcopaenia, although current pharmacotherapies have not been extensively studied with this endpoint in mind. In conclusion, sarcopaenia is interwoven with HF and leads to worse exercise capacity in these patients. The mechanisms associated with this bilateral relationship between sarcopaenia and HF are still to be elucidated, leading to effective treatment, not only for the heart, but also for the skeletal muscle.


1997 ◽  
Vol 82 (5) ◽  
pp. 1488-1492 ◽  
Author(s):  
Stuart D. Katz ◽  
Jeannette Yuen ◽  
Rachel Bijou ◽  
Thierry H. Lejemtel

Katz, Stuart D., Jeannette Yuen, Rachel Bijou, and Thierry H. LeJemtel. Training improves endothelium-dependent vasodilation in resistance vessels of patients with heart failure. J. Appl. Physiol. 82(5): 1488–1492, 1997.—The effects of physical training on endothelium-dependent vasodilation in skeletal muscle resistance vessels were investigated in patients with heart failure. Forearm blood flows (ml ⋅ min−1 ⋅ 100 ml−1) in response to brachial arterial administration of acetylcholine (5 × 10−5 and 5 × 10−4 M at 1 ml/min) and nitroglycerin (5 × 10−6 and 5 × 10−5 M at 1 ml/min) were determined by strain-gauge venous occlusion plethysmography before and after 8 wk of daily handgrip exercise in 12 patients with chronic heart failure. After 8 wk of daily handgrip exercise, the vasodilatory responses to acetylcholine significantly increased from pretraining values, i.e., 16.6 ± 2.0 vs. 8.6 ± 1.3 ml ⋅ min−1 ⋅ 100 ml−1( P < 0.05) and 27.5 ± 1.5 vs. 14.6 ± 1.7 ml ⋅ min−1 ⋅ 100 ml−1( P < 0.05), respect- ively, whereas the vasodilatory responses to nitroglycerin did not change. Handgrip exercise training appears to specifically enhance endothelium-dependent vasodilation in the forearm skeletal muscle circulation of patients with heart failure.


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