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.

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.

Baroreflex regulation of regional blood flow in congestive heart failure

1990 ◽  
Vol 258 (5) ◽  
pp. H1409-H1414 ◽  
Author(s):  
M. A. Creager ◽  
A. T. Hirsch ◽  
V. J. Dzau ◽  
E. G. Nabel ◽  
S. S. Cutler ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Lower Body Negative Pressure ◽  
Regional Blood Flow ◽  
Venous Pressure ◽  
Normal Subjects ◽  
Splanchnic Blood Flow ◽  
Patients With Heart Failure

In patients with congestive heart failure (CHF), the distribution of the cardiac output is altered. Cardiopulmonary and arterial baroreceptors normally can regulate regional blood flow, but their contribution in heart failure is not known. To examine the role of baroreceptors in the regulation of regional blood flow in CHF, the effect of lower body negative pressure (LBNP) on forearm, renal, and splanchnic blood flow was evaluated in 12 patients with heart failure. Incremental LBNP at -10 and -40 mmHg decreased central venous pressure but had not effect on systolic blood pressure or pulse pressure. Renal blood flow decreased from 505 +/- 63 to 468 +/- 66 ml/min during LBNP -10 mmHg (P less than 0.05) and to 376 +/- 74 ml/min during LBNP -40 mmHg (P less than 0.01). Splanchnic blood flow decreased from 564 +/- 76 to 480 +/- 62 ml/min during LBNP -10 mmHg (P less than 0.01) and to 303 +/- 45 ml/min during LBNP -40 mmHg (P less than 0.01). Forearm blood flow did not decrease during LBNP -10 mmHg or -40 mmHg. To determine whether the absence of limb vasoconstriction during LBNP was confined to abnormalities in the baroreflex arc or was secondary to impaired end-organ responsiveness, six patients with heart failure and six normal subjects received an intrabrachial artery infusion of phenylephrine. Phenylephrine increased forearm vascular resistance comparably in each group. These data demonstrate that baroreceptors can regulate splanchnic and renal but not limb vascular resistance in patients with congestive heart failure and may contribute to the redistribution of blood flow that occurs in this disorder.

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.

Prostaglandin production contributes to exercise-induced vasodilation in heart failure

1997 ◽  
Vol 83 (6) ◽  
pp. 1933-1940 ◽  
Author(s):  
Chim C. Lang ◽  
Don B. Chomsky ◽  
Javed Butler ◽  
Shiv Kapoor ◽  
John R. Wilson
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Peak Exercise ◽  
Prostaglandin Production ◽  
Leg Blood Flow ◽  
Patients With Heart Failure ◽  
Prostaglandin F ◽  
Exercise Induced ◽  
Arteriolar Vasodilation

Lang, Chim C., Don B. Chomsky, Javed Butler, Shiv Kapoor, and John R. Wilson. Prostaglandin production contributes to exercise-induced vasodilation in heart failure. J. Appl. Physiol. 83(6): 1933–1940, 1997.—Endothelial release of prostaglandins may contribute to exercise-induced skeletal muscle arteriolar vasodilation in patients with heart failure. To test this hypothesis, we examined the effect of indomethacin on leg circulation and metabolism in eight chronic heart failure patients, aged 55 ± 4 yr. Central hemodynamics and leg blood flow, determined by thermodilution, and leg metabolic parameters were measured during maximum treadmill exercise before and 2 h after oral administration of indomethacin (75 mg). Leg release of 6-ketoprostaglandin F1α was also measured. During control exercise, leg blood flow increased from 0.34 ± 0.03 to 1.99 ± 0.19 l/min ( P < 0.001), leg O2 consumption from 13.6 ± 1.8 to 164.5 ± 16.2 ml/min ( P < 0.001), and leg prostanoid release from 54.1 ± 8.5 to 267.4 ± 35.8 pg/min ( P < 0.001). Indomethacin suppressed release of prostaglandin F1α( P < 0.001) throughout exercise and decreased leg blood flow during exercise ( P < 0.05). This was associated with a corresponding decrease in leg O2 consumption ( P < 0.05) and a higher level of femoral venous lactate at peak exercise ( P < 0.01). These data suggest that release of vasodilatory prostaglandins contributes to skeletal muscle arteriolar vasodilation in patients with heart failure.

Dynamic regulation of leg vasomotor tone in patients with chronic heart failure

1991 ◽  
Vol 71 (3) ◽  
pp. 1070-1075 ◽  
Author(s):  
M. J. Sullivan ◽  
F. R. Cobb
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Work Rate ◽  
Vasomotor Tone ◽  
Leg Blood Flow ◽  
Leg Exercise

We examined the central hemodynamic (n = 5) and leg blood flow (n = 9) responses to one- and two-leg bicycle exercise in nine ambulatory patients with chronic heart failure due to left ventricular systolic dysfunction (ejection fraction 17 +/- 9%). During peak one- vs. two-leg exercise, leg blood flow (thermodilution) tended to be higher (1.99 +/- 0.91 vs. 1.67 +/- 0.91 l/min, P = 0.07), whereas femoral arteriovenous oxygen difference was lower (13.6 +/- 3.1 vs. 15.0 +/- 2.9 ml/dl, P less than 0.01). Comparison of data from exercise stages matched for single-leg work rate during one- vs. two-leg exercise demonstrated that cardiac output was similar while both oxygen consumption and central arteriovenous oxygen differences were lower, indicating relative improvement in the cardiac output response at a given single-leg work rate during one-leg exercise. This was accompanied by higher leg blood flow (1.56 +/- 0.76 vs. 1.83 +/- 0.72 l/min, P = 0.02) and a tendency for leg vascular resistance to be lower (92 +/- 54 vs. 80 +/- 48 Torr.l-1.min, P = 0.08) without any change in blood lactate. These data indicate that, in patients with chronic heart failure, leg vasomotor tone is dynamically regulated, independent of skeletal muscle metabolism, and is not determined solely by intrinsic abnormalities in skeletal muscle vasodilator capacity. Our results suggest that relative improvements in central cardiac function may lead to a reflex release of skeletal muscle vasoconstrictor tone in this disorder.

scholarly journals Disturbed Blood Flow Acutely Increases Endothelial Microparticles and Decreases Flow Mediated Dilation in Patients With Heart Failure With Reduced Ejection Fraction

2021 ◽  
Vol 12 ◽  
Author(s):  
Thiago O. C. Silva ◽  
Allan R. K. Sales ◽  
Gustavo S. M. Araujo ◽  
Guilherme W. P. Fonseca ◽  
Pedro G. S. Braga ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Ejection Fraction ◽  
Brachial Artery ◽  
Left Ventricular Ejection ◽  
Flow Mediated Dilation ◽  
Endothelial Microparticles ◽  
Reduced Ejection Fraction ◽  
Control Subjects ◽  
Patients With Heart Failure

IntroductionDisturbed blood flow, characterized by high retrograde and oscillatory shear rate (SR), is associated with a proatherogenic phenotype. The impact of disturbed blood flow in patients with heart failure with reduced ejection fraction (HFrEF) remains unknown. We tested the hypothesis that acute elevation to retrograde and oscillatory SR provoked by local circulatory occlusion would increase endothelial microparticles (EMPs) and decrease brachial artery flow-mediated dilation (FMD) in patients with HFrEF.MethodsEighteen patients with HFrEF aged 55 ± 2 years, with left ventricular ejection fraction (LVEF) 26 ± 1%, and 14 control subjects aged 49 ± 2 years with LVEF 65 ± 1 randomly underwent experimental and control sessions. Brachial artery FMD (Doppler) was evaluated before and after 30 min of disturbed forearm blood flow provoked by pneumatic cuff (Hokanson) inflation to 75 mm Hg. Venous blood samples were collected at rest, after 15 and 30 min of disturbed blood flow to assess circulating EMP levels (CD42b−/CD31+; flow cytometry).ResultsAt rest, FMD was lower in patients with HFrEF compared with control subjects (P &lt; 0.001), but blood flow patterns and EMPs had no differences (P &gt; 0.05). The cuff inflation provoked a greater retrograde SR both groups (P &lt; 0.0001). EMPs responses to disturbed blood flow significantly increased in patients with HFrEF (P = 0.03). No changes in EMPs were found in control subjects (P &gt; 0.05). Disturbed blood flow decreased FMD both groups. No changes occurred in control condition.ConclusionCollectively, our findings suggest that disturbed blood flow acutely decreases FMD and increases EMP levels in patients with HFrEF, which may indicate that this set of patients are vulnerable to blood flow disturbances.

Blood flow and skeletal muscle in patients with heart failure

CHEST Journal ◽  
1992 ◽  
Vol 101 (5) ◽  
pp. 330S-332S ◽  
Author(s):  
P. A. Poole-Wilson ◽  
N. P. Buller ◽  
D. C. Lindsay
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Patients With Heart Failure
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