Skeletal Muscle Metabolism in Heart Failure: A 31P Nuclear Magnetic Resonance Spectroscopy Study of Leg Muscle

1990 ◽  
Vol 79 (6) ◽  
pp. 583-589 ◽  
Author(s):  
Leonard Arnolda ◽  
Michael Conway ◽  
Michael Dolecki ◽  
Hasanat Sharif ◽  
Bheeshma Rajagopalan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Nuclear Magnetic Resonance ◽  
Blood Flow ◽  
Magnetic Resonance ◽  
Inorganic Phosphate ◽  
Gastrocnemius Muscle ◽  
Resonance Spectroscopy ◽  
Control Subjects ◽  
Patients With Heart Failure

1. The gastrocnemius muscle of seven patients with mild to moderate chronic heart failure and of five healthy control subjects was studied using 31P nuclear magnetic resonance spectroscopy. Spectra were collected at rest and during an incremental, symptom-limited, exercise protocol. Blood flow was measured in the same study during brief interruptions to exercise. 2. The phosphocreatine/(phosphocreatine plus inorganic phosphate) ratio was lower in patients with heart failure than in control subjects at an exercise rate of 1.5 W, although intracellular pH and blood flow were similar. 3. The cytosolic free adenosine 5′-diphosphate concentration was markedly increased in patients with heart failure exercising at 1.5 W compared with control subjects exercising at the same workload. 4. Although the maximum workload achieved by patients with heart failure was less than half of that reached by control subjects, the pH and the phospho-creatine/(phosphocreatine plus inorganic phosphate) ratio were lower in patients with heart failure at maximal load. Blood flow was less at maximal exercise in patients with heart failure than in control subjects in keeping with the reduced work load. 5. The phosphocreatine depletion induced in the gastrocnemius muscle by exercise was more severe than previously described in the forearm of patients with heart failure. 6. Metabolic abnormalities in skeletal muscle may contribute to exercise intolerance in heart failure, particularly during submaximal exercise.

Muscular blood flow response to submaximal leg exercise in normal subjects and in patients with heart failure

1996 ◽  
Vol 81 (6) ◽  
pp. 2571-2579 ◽  
Author(s):  
Richard Isnard ◽  
Philippe Lechat ◽  
Hanna Kalotka ◽  
Hafida Chikr ◽  
Serge Fitoussi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Normal Subjects ◽  
Submaximal Exercise ◽  
Control Subjects ◽  
Flow Response ◽  
Patients With Heart Failure ◽  
Leg Exercise

Isnard, Richard, Philippe Lechat, Hanna Kalotka, Hafida Chikr, Serge Fitoussi, Joseph Salloum, Jean-Louis Golmard, Daniel Thomas, and Michel Komajda. Muscular blood flow response to submaximal leg exercise in normal subjects and in patients with heart failure. J. Appl. Physiol. 81(6): 2571–2579, 1996.—Blood flow to working skeletal muscle is usually reduced during exercise in patients with congestive heart failure. An intrinsic impairment of skeletal muscle vasodilatory capacity has been suspected as a mechanism of this muscle underperfusion during maximal exercise, but its role during submaximal exercise remains unclear. Therefore, we studied by transcutaneous Doppler ultrasonography the arterial blood flow in the common femoral artery at rest and during a submaximal bicycle exercise in 12 normal subjects and in 30 patients with heart failure. Leg blood flow was lower in patients than in control subjects at rest [0.29 ± 0.14 (SD) vs. 0.45 ± 0.14 l/min, P < 0.01], at absolute powers and at the same relative power (2.17 ± 1.06 vs. 4.39 ± 1.4 l/min, P< 0.001). Because mean arterial pressure was maintained, leg vascular resistance was higher in patients than in control subjects at rest (407 ± 187 vs. 247 ± 71 mmHg ⋅ l−1 ⋅ min, P < 0.01) and at the same relative power (73 ± 49 vs. 31 ± 13 mmHg ⋅ l−1 ⋅ min, P < 0.01) but not at absolute powers. Although the magnitude of increase in leg blood flow corrected for power was similar in both groups (31 ± 10 vs. 34 ± 10 ml ⋅ min−1 ⋅ W−1), the magnitude of decrease of leg vascular resistance corrected for power was higher in patients than in control subjects (5.9 ± 3.3 vs. 1.9 ± 0.94 mmHg ⋅ l−1 ⋅ min ⋅ W−1, P < 0.001). These results suggest that the ability of skeletal muscle vascular resistance to decrease is not impaired and that intrinsic vascular abnormalities do not limit vasodilator response to submaximal exercise in patients with heart failure.

Metabolic Adaptations to Endurance Training in Older Individuals

1993 ◽  
Vol 18 (4) ◽  
pp. 366-378 ◽  
Author(s):  
Gregory D. Marsh ◽  
Donald H. Paterson ◽  
R. Terry Thompson ◽  
Po Kee Cheung ◽  
J. Malcolm O. Arnold ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Blood Flow ◽  
Magnetic Resonance ◽  
Exercise Training ◽  
Magnetic Resonance Spectroscopy ◽  
Power Output ◽  
Resonance Spectroscopy ◽  
Older Individuals ◽  
Intracellular Acidosis ◽  
Progressive Exercise

The purpose of this study was to describe the effects of moderate intensity exercise training on the muscle energy utilization, blood flow, and exercise performance of four sedentary older individuals (58 ± 4 yrs). Subjects trained the dominant forearm each day for 12 weeks. The nondominant arm was not trained and served as a within-subject control. 31P nuclear magnetic resonance spectroscopy (31P NMRS) was used to identify the power output in watts (W) at the onset, or threshold, of intracellular acidosis (IT) in the exercising muscle during progressive exercise tests to fatigue. After 6 weeks of training, power output at the IT increased by 14% (p < 0.05) in the dominant arm; however, an additional 6 weeks of the same exercise program failed to produce a further increase in IT power. IT power of the nondominant forearm was not changed. In the dominant forearm, endurance time for a submaximal wrist flexion test was increased 34% and 58% at 6 and 12 weeks, respectively. Maximal voluntary strength was not affected by training, nor was resting or exercising blood flow. The training program delayed the onset of intracellular acidosis during progressive exercise and increased the capacity for submaximal work. These effects did not appear to depend on an increase in muscle blood flow. Key words: 31P nuclear magnetic resonance spectroscopy, muscle metabolism, exercise training

scholarly journals Sarcopaenia complicating heart failure

2019 ◽  
Vol 21 (Supplement_L) ◽  
pp. L20-L23 ◽  
Author(s):  
Guilherme Wesley Peixoto da Fonseca ◽  
Stephan von Haehling
Keyword(s):  
Quality Of Life ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Strength ◽  
Protein Intake ◽  
Skeletal Muscle Mass ◽  
Muscle Blood Flow ◽  
Patients With Heart Failure

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.

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