Training partially reverses skeletal muscle metabolic abnormalities during exercise in heart failure

1994 ◽  
Vol 76 (4) ◽  
pp. 1575-1582 ◽  
Author(s):  
J. R. Stratton ◽  
J. F. Dunn ◽  
S. Adamopoulos ◽  
G. J. Kemp ◽  
A. J. Coats ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Atp Synthesis ◽  
Exercise Duration ◽  
Oxidative Capacity ◽  
Voluntary Contraction ◽  
Resonance Spectroscopy ◽  
Metabolic Abnormalities ◽  
Maximal Rate ◽  
Muscle Training

Using 31P-magnetic resonance spectroscopy during and after exercise, we studied whether forearm metabolic responses to exercise were improved by 1 mo of training in 10 males with heart failure. In the control (untrained) arm, there were no changes in any of the measured variables. In the trained arm, maximal voluntary contraction increased 6% (P = 0.05). During incremental exercise, duration increased 19% (P < 0.05) and submaximal responses improved for pH (6.78 +/- 0.13 pretraining vs. 6.85 +/- 0.17 posttraining; P < 0.01) and PCr/(PCr+Pi) (where PCr is phosphocreatine; 0.48 +/- 0.09 pretraining vs. 0.52 +/- 0.07 posttraining; P < 0.01). The PCr resynthesis rate increased by 48% (P < 0.01), and estimated effective maximal rate of mitochondrial ATP synthesis increased by 37% (P < 0.05). Endurance exercise duration increased by 67% (P < 0.01), and submaximal levels of PCr/(PCr+Pi) (P < 0.05) and pH (P = 0.07) improved. The PCr resynthesis rate (P < 0.01) and the effective maximal rate of mitochondrial ATP synthesis (P < 0.05) also improved. These findings document that impaired oxidative capacity of skeletal muscle can be improved by local muscle training in heart failure, which is compatible with the hypothesis that a part of the abnormality present in heart failure may be due to inactivity.

Skeletal muscle beta-adrenoreceptors and phosphate metabolism abnormalities in heart failure in rats

1996 ◽  
Vol 271 (5) ◽  
pp. H1739-H1745
Author(s):  
Z. Chati ◽  
C. Michel ◽  
J. M. Escanye ◽  
P. M. Mertes ◽  
C. Ribuot ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Adrenergic Receptor ◽  
Gastrocnemius Muscle ◽  
Atp Synthesis ◽  
Initial Slope ◽  
Resonance Spectroscopy ◽  
Metabolic Abnormalities ◽  
Phosphate Metabolism ◽  
Coronary Ligation

To investigate the mechanisms leading to skeletal muscle metabolic abnormalities in chronic heart failure (CHF), we studied phosphate metabolism and skeletal muscle beta-adrenoreceptors (beta-AR) in rats 12-14 wk after coronary ligation (CL). We performed 31P magnetic resonance spectroscopy in the gastrocnemius muscle during motor activity produced by electrical stimulation (5 Hz). The initial slope of phosphocreatine (PCr) depletion was higher in the CL rats compared with sham-operated rats (Pi/PCr/time: 0.211 +/- 0.045 vs. 0.113 +/- 0.029; P < 0.05). During recovery, both PCr resynthesis rate and maximal rate of oxidative ATP synthesis were reduced threefold in the CL rats compared with controls (11 +/- 2 vs. 37 +/- 7 mmol.l-1.min-1, P < 0.04; and 20 +/- 3 vs. 79 +/- 18 mmol.l-1.min-1, P < 0.03, respectively). There were no significant differences either for the skeletal muscle density (13 +/- 6 vs. 15 +/- 3 fM/mg) or for the affinity (0.244 +/- 0.149 vs. 0.246 +/- 0.146 nM) of beta-AR between the two groups. This study showed that, although in moderate CHF skeletal muscle metabolic abnormalities can be demonstrated, these changes could not be explained by skeletal muscle beta-adrenergic receptor alterations in this experimental model.

Use of intramuscular triacylglycerol as a substrate source during exercise in humans

2004 ◽  
Vol 97 (4) ◽  
pp. 1170-1187 ◽  
Author(s):  
Luc J. C. van Loon
Keyword(s):  
Skeletal Muscle ◽  
Effective Means ◽  
Indirect Evidence ◽  
Atp Synthesis ◽  
Exercise Duration ◽  
Resonance Spectroscopy ◽  
Skeletal Muscle Insulin Resistance ◽  
Exercise In Humans ◽  
Substrate Source

Fat and carbohydrate are the principal substrates that fuel aerobic ATP synthesis in skeletal muscle. Most endogenous fat is stored as triacylglycerol in subcutaneous and deep visceral adipose tissue. Smaller quantities of triacylglycerol are deposited as lipid droplets inside skeletal muscle fibers. The potential role of intramyocellular triacylglycerol (IMTG) as a substrate source during exercise in humans has recently regained much of its interest because of the proposed functional relationship between IMTG accumulation and the development of skeletal muscle insulin resistance. Exercise likely represents an effective means to prevent excess IMTG accretion by stimulating its rate of oxidation. However, there is much controversy on the actual contribution of the IMTG pool as a substrate source during exercise. The apparent discrepancy in the literature likely stems from methodological difficulties that have been associated with the methods used to estimate IMTG oxidation during exercise. However, recent studies using stable isotope methodology,1H-magnetic resonance spectroscopy, and electron and/or immunofluorescence microscopy all support the contention that the IMTG pool can function as an important substrate source during exercise. Although more research is warranted, IMTG mobilization and/or oxidation during exercise seem to be largely determined by exercise intensity, exercise duration, macronutrient composition of the diet, training status, gender, and/or age. In addition, indirect evidence suggests that the capacity to mobilize and/or oxidize IMTG is substantially impaired in an obese and/or Type 2 diabetic state. As we now become aware that skeletal muscle has an enormous capacity to oxidize IMTG stores during exercise, more research is warranted to develop combined exercise, nutritional, and/or pharmacological interventions to effectively stimulate IMTG oxidation in sedentary, obese, and/or Type 2 diabetes patients.

Noninvasive measurement of phosphocreatine recovery kinetics in single human muscles

1997 ◽  
Vol 272 (2) ◽  
pp. C525-C534 ◽  
Author(s):  
G. Walter ◽  
K. Vandenborne ◽  
K. K. McCully ◽  
J. S. Leigh
Keyword(s):  
Intracellular Ph ◽  
Muscle Activation ◽  
Atp Synthesis ◽  
Oxidative Capacity ◽  
Medial Gastrocnemius ◽  
Hydrolysis Rate ◽  
Resonance Spectroscopy ◽  
Maximal Rate ◽  
Intracellular Acidosis ◽  
Human Muscles

The rate at which phosphocreatine (PCr) is resynthesized after exercise is related to muscle oxidative capacity (Vmax). With the use of a one-dimensional image-guided, localized nuclear magnetic resonance spectroscopy technique, PCr kinetics were monitored in the medial gastrocnemius of eight healthy subjects after voluntary, short duration, maximal rate exercise. Localized spectra were obtained every 6 s with <5% contamination from nonselected regions. Maximal rate exercise elicited near-maximal to maximal muscle activation, as indicated by the high-PCr hydrolysis rate (2.26 +/- 0.07 mM/s) and extensive PCr depletion. At the end of 9 s of maximal rate exercise, PCr was depleted by 61.4 +/- 2.4% and intracellular pH was 7.04 +/- 0.03. After 9 s of maximal rate exercise, PCr recovered with a rate constant (kPCr) of 1.87 +/- 0.15 min(-1) and a Vmax of 67.2 +/- 6.0 mM/min. Independent of prior activity, aerobic ATP synthesis rates reached 48.6 +/- 4.9 mM/min within 9 s. Extending maximal rate exercise to 30 s resulted in 92.0 +/- 1.2% PCr depletion and an intracellular pH of 6.45 +/- 0.07. The intracellular acidosis separated the direct relationship between kPCr and muscle Vmax but did not affect the initial PCr resynthesis rate.

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

scholarly journals Systemic oxidative stress is associated with lower aerobic capacity and impaired skeletal muscle energy metabolism in heart failure patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Yokota ◽  
Shintaro Kinugawa ◽  
Kagami Hirabayashi ◽  
Mayumi Yamato ◽  
Shingo Takada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Aerobic Capacity ◽  
Plantar Flexion ◽  
Exercise Intolerance ◽  
Whole Body ◽  
Resonance Spectroscopy ◽  
Systemic Oxidative Stress

AbstractOxidative stress plays a role in the progression of chronic heart failure (CHF). We investigated whether systemic oxidative stress is linked to exercise intolerance and skeletal muscle abnormalities in patients with CHF. We recruited 30 males: 17 CHF patients, 13 healthy controls. All participants underwent blood testing, cardiopulmonary exercise testing, and magnetic resonance spectroscopy (MRS). The serum thiobarbituric acid reactive substances (TBARS; lipid peroxides) were significantly higher (5.1 ± 1.1 vs. 3.4 ± 0.7 μmol/L, p < 0.01) and the serum activities of superoxide dismutase (SOD), an antioxidant, were significantly lower (9.2 ± 7.1 vs. 29.4 ± 9.7 units/L, p < 0.01) in the CHF cohort versus the controls. The oxygen uptake (VO2) at both peak exercise and anaerobic threshold was significantly depressed in the CHF patients; the parameters of aerobic capacity were inversely correlated with serum TBARS and positively correlated with serum SOD activity. The phosphocreatine loss during plantar-flexion exercise and intramyocellular lipid content in the participants' leg muscle measured by 31phosphorus- and 1proton-MRS, respectively, were significantly elevated in the CHF patients, indicating abnormal intramuscular energy metabolism. Notably, the skeletal muscle abnormalities were related to the enhanced systemic oxidative stress. Our analyses revealed that systemic oxidative stress is related to lowered whole-body aerobic capacity and skeletal muscle dysfunction in CHF patients.

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.

scholarly journals Oxidative capacity of skeletal muscle in heart failure patients versus sedentary or active control subjects

2001 ◽  
Vol 38 (4) ◽  
pp. 947-954 ◽  
Author(s):  
Bertrand Mettauer ◽  
Joffrey Zoll ◽  
Hervé Sanchez ◽  
Eliane Lampert ◽  
Florence Ribera ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Active Control ◽  
Oxidative Capacity ◽  
Heart Failure Patients ◽  
Control Subjects

scholarly journals Metabolic abnormality of calf skeletal muscle is improved by localised muscle training without changes in blood flow in chronic heart failure

Heart ◽  
1997 ◽  
Vol 78 (5) ◽  
pp. 437-443 ◽  
Author(s):  
M. Ohtsubo ◽  
K. Yonezawa ◽  
H. Nishijima ◽  
K. Okita ◽  
A. Hanada ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Metabolic Abnormality ◽  
Muscle Training

Skeletal muscle phosphate metabolism abnormalities in volume-overload experimental heart failure

1994 ◽  
Vol 267 (6) ◽  
pp. H2186-H2192 ◽  
Author(s):  
Z. Chati ◽  
F. Zannad ◽  
C. Michel ◽  
B. Lherbier ◽  
P. M. Mertes ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Early Stage ◽  
Volume Overload ◽  
Significant Rise ◽  
Initial Slope ◽  
Heart Weight ◽  
Resonance Spectroscopy ◽  
Phosphate Metabolism

We studied skeletal muscle phosphate metabolism abnormalities to examine their contribution at an early stage of congestive heart failure (CHF) in rats with aortocaval fistula (ACF) 4 wk after the procedure. In a group of 26 rats (13 with ACF and 13 sham operated), we assessed the degree of CHF. The ACF produced a significant rise in heart weight and plasma atrial natriuretic peptide. In a second group of 26 rats (13 ACF and 13 sham operated), we performed 31P-magnetic resonance spectroscopy in the gastrocnemius muscle during motor activity produced by electrical stimulation. The rate of phosphocreatine depletion, expressed by its initial slope, was higher in the ACF rats compared with controls (0.078 +/- 0.01 vs. 0.041 +/- 0.007; P < 0.03). pH and ATP decreased and phosphodiesters increased in all rats during electrical stimulation, with no difference between ACF rats and controls. The kinetics of phosphocreatine recovery were not different between ACF rats and controls. Together with previous studies, our present results suggest that muscle metabolism abnormalities in CHF may vary according to the experimental model and may be observed early in the course of the disease.

scholarly journals Altered mechanisms of sympathetic activation during rhythmic forearm exercise in heart failure

1998 ◽  
Vol 84 (5) ◽  
pp. 1551-1559 ◽  
Author(s):  
David H. Silber ◽  
Greg Sutliff ◽  
Qing X. Yang ◽  
Michael B. Smith ◽  
Lawrence I. Sinoway ◽  
...  
Keyword(s):  
Heart Failure ◽  
Matched Control ◽  
Circulatory Arrest ◽  
Voluntary Contraction ◽  
Control Group ◽  
Resonance Spectroscopy ◽  
Muscle Metaboreflex ◽  
Separate Control ◽  
Forearm Exercise ◽  
Exercise Induced

In congestive heart failure (CHF), the mechanisms of exercise-induced sympathoexcitation are poorly defined. We compared the responses of sympathetic nerve activity directed to muscle (MSNA) and to skin (SSNA, peroneal microneurography) during rhythmic handgrip (RHG) at 25% of maximal voluntary contraction and during posthandgrip circulatory arrest (PHG-CA) in CHF patients with those of an age-matched control group. During RHG, the CHF patients fatigued prematurely. At end exercise, the increase in MSNA was similar in both groups (CHF patients, n = 12; controls, n = 10). However, during PHG-CA, in the controls MSNA returned to baseline, whereas it remained elevated in CHF patients ( P < 0.05). Similarly, at end exercise, the increase in SSNA was comparable in both groups (CHF patients, n = 11; controls, n = 12), whereas SSNA remained elevated during PHG-CA in CHF patients but not in the controls ( P < 0.05). In a separate control group ( n = 6), even high-intensity static handgrip was not accompanied by sustained elevation of SSNA during PHG-CA. 31P-nuclear magnetic resonance spectroscopy during RHG demonstrated significant muscle acidosis and accumulation of inorganic phosphate in CHF patients ( n = 7) but not in controls ( n = 9). We conclude that in CHF patients rhythmic forearm exercise leads to premature fatigue and accumulation of muscle metabolites. The prominent PHG-CA response of MSNA and SSNA in CHF patients suggests activation of the muscle metaboreflex. Because, in contrast to controls, in CHF patients both MSNA and SSNA appear to be under muscle metaboreflex control, the mechanisms and distribution of sympathetic outflow during exercise appear to be different from normal.

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