scholarly journals Acylated ghrelin treatment normalizes skeletal muscle mitochondrial oxidative capacity and AKT phosphorylation in rat chronic heart failure

2017 ◽  
Vol 8 (6) ◽  
pp. 991-998 ◽  
Author(s):  
Rocco Barazzoni ◽  
Gianluca Gortan Cappellari ◽  
Sandra Palus ◽  
Pierandrea Vinci ◽  
Giulia Ruozi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Oxidative Capacity ◽  
Acylated Ghrelin ◽  
Akt Phosphorylation ◽  
Mitochondrial Oxidative Capacity

scholarly journals Maximal oxygen uptake is proportional to muscle fiber oxidative capacity, from chronic heart failure patients to professional cyclists

2016 ◽  
Vol 121 (3) ◽  
pp. 636-645 ◽  
Author(s):  
Stephan van der Zwaard ◽  
C. Jo de Ruiter ◽  
Dionne A. Noordhof ◽  
Renske Sterrenburg ◽  
Frank W. Bloemers ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Ex Vivo ◽  
Vastus Lateralis ◽  
Oxidative Capacity ◽  
Heart Failure Patients ◽  
Mitochondrial Oxidative Capacity

V̇o2 max during whole body exercise is presumably constrained by oxygen delivery to mitochondria rather than by mitochondria's ability to consume oxygen. Humans and animals have been reported to exploit only 60-80% of their mitochondrial oxidative capacity at maximal oxygen uptake (V̇o2 max). However, ex vivo quantification of mitochondrial overcapacity is complicated by isolation or permeabilization procedures. An alternative method for estimating mitochondrial oxidative capacity is via enzyme histochemical quantification of succinate dehydrogenase (SDH) activity. We determined to what extent V̇o2 max attained during cycling exercise differs from mitochondrial oxidative capacity predicted from SDH activity of vastus lateralis muscle in chronic heart failure patients, healthy controls, and cyclists. V̇o2 max was assessed in 20 healthy subjects and 28 cyclists, and SDH activity was determined from biopsy cryosections of vastus lateralis using quantitative histochemistry. Similar data from our laboratory of 14 chronic heart failure patients and 6 controls were included. Mitochondrial oxidative capacity was predicted from SDH activity using estimated skeletal muscle mass and the relationship between ex vivo fiber V̇o2 max and SDH activity of isolated single muscle fibers and myocardial trabecula under hyperoxic conditions. Mitochondrial oxidative capacity predicted from SDH activity was related ( r2 = 0.89, P < 0.001) to V̇o2 max measured during cycling in subjects with V̇o2 max ranging from 9.8 to 79.0 ml·kg−1·min−1. V̇o2 max measured during cycling was on average 90 ± 14% of mitochondrial oxidative capacity. We conclude that human V̇o2 max is related to mitochondrial oxidative capacity predicted from skeletal muscle SDH activity. Mitochondrial oxidative capacity is likely marginally limited by oxygen supply to mitochondria.

scholarly journals Decreased mitochondrial oxidative capacity or reduced metabolic efficiency in skeletal muscle in congestive heart failure?

1996 ◽  
Vol 27 (2) ◽  
pp. 114
Author(s):  
Graham Kemp ◽  
Stamatis Adamopoulos ◽  
Campbell Thompson ◽  
John Stratton ◽  
Françoise Brunotte ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Congestive Heart Failure ◽  
Oxidative Capacity ◽  
Metabolic Efficiency ◽  
Mitochondrial Oxidative Capacity

scholarly journals Chronic heart failure reduces Akt phosphorylation in human skeletal muscle: relationship to muscle size and function

2011 ◽  
Vol 110 (4) ◽  
pp. 892-900 ◽  
Author(s):  
Michael J. Toth ◽  
Kimberly Ward ◽  
Jos van der Velden ◽  
Mark S. Miller ◽  
Peter VanBuren ◽  
...  
Keyword(s):  
Physical Activity ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Protein Content ◽  
Muscle Mass ◽  
Receptor Activation ◽  
Disease Exacerbation ◽  
Akt Phosphorylation ◽  
And Function

Patients with chronic heart failure (HF) frequently lose muscle mass and function during the course of the disease. A reduction in anabolic stimuli to the muscle has been put forth as a potential mechanism underlying these alterations. The present study examined the hypothesis that skeletal muscle tissue from HF patients would show reduced IGF-1 expression and phosphorylation of signaling molecules downstream of receptor activation. To isolate the unique effect of HF on these variables, we limited the confounding effects of muscle disuse and/or acute disease exacerbation by recruiting controls ( n = 11) with similar physical activity levels as HF patients ( n = 11) and by testing patients at least 6 mo following any bouts of disease exacerbation/hospitalization. IGF-1 expression in skeletal muscle was similar between patients and controls. Despite this, HF patients were characterized by reduced levels of phospho-Akt/Akt (S473; −43%; P < 0.05), whereas no differences were found in total Akt protein content or phospho- or total protein content of mammalian target of rapamycin (mTOR; S2448), glycogen synthase kinase-3β (GSK-3β; S9), eukaryotic translation initiation factor 4E binding protein-1 (eIF4E-BP; T37/46), p70 ribosomal S6 kinase (p70 S6K; T389), or eIF2Bε (S540). Reduced phospho-Akt/Akt levels and phospho-mTOR/mTOR were related to decreased skeletal muscle myosin protein content ( r = 0.602; P < 0.02) and knee extensor isometric torque ( r = 0.550; P < 0.05), respectively. Because patients and controls were similar for age, muscle mass, and physical activity, we ascribe the observed alterations in Akt phosphorylation and its relationship to myosin protein content to the unique effects of the HF syndrome.

162 PGC-1alpha correlates with cardiac and skeletal muscle oxidative capacity in heart failure

2003 ◽  
Vol 2 (1) ◽  
pp. 29-30
Author(s):  
A GARNIER ◽  
D FORTIN ◽  
C DELOMENIE ◽  
I MOMKEN ◽  
V VEKSLER ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Oxidative Capacity ◽  
Muscle Oxidative Capacity

Soothing the sleeping giant: improving skeletal muscle oxygen kinetics and exercise intolerance in HFpEF

2015 ◽  
Vol 119 (6) ◽  
pp. 734-738 ◽  
Author(s):  
Satyam Sarma ◽  
Benjamin D. Levine
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Functional Capacity ◽  
Oxidative Capacity ◽  
Exercise Intolerance ◽  
Aerobic Performance ◽  
Muscle Oxygen ◽  
Oxygen Kinetics ◽  
Patients With Heart Failure

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.

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