scholarly journals Abnormal skeletal muscle bioenergetics during exercise in patients with heart failure: role of reduced muscle blood flow.

Circulation ◽  
1986 ◽  
Vol 73 (6) ◽  
pp. 1127-1136 ◽  
Author(s):  
D H Wiener ◽  
L I Fink ◽  
J Maris ◽  
R A Jones ◽  
B Chance ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Patients With Heart Failure

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.

Effects of chronic heart failure on skeletal muscle capillary hemodynamics at rest and during contractions

2003 ◽  
Vol 95 (3) ◽  
pp. 1055-1062 ◽  
Author(s):  
Troy E. Richardson ◽  
Casey A. Kindig ◽  
Timothy I. Musch ◽  
David C. Poole
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Muscle Function ◽  
Muscle Blood Flow ◽  
Rat Skeletal Muscle ◽  
Exercise Onset ◽  
Final Response ◽  
Microscopy Techniques

Chronic heart failure (CHF) reduces muscle blood flow at rest and during exercise and impairs muscle function. Using intravital microscopy techniques, we tested the hypothesis that the speed and amplitude of the capillary red blood cell (RBC) velocity ( VRBC) and flux (FRBC) response to contractions would be reduced in CHF compared with control (C) spinotrapezius muscle. The proportion of capillaries supporting continuous RBC flow was less ( P < 0.05) in CHF (0.66 ± 0.04) compared with C (0.84 ± 0.01) muscle at rest and was not significantly altered with contractions. At rest, VRBC (C, 270 ± 62; CHF, 179 ± 14 μm/s) and FRBC (C, 22.4 ± 5.5 vs. CHF, 15.2 ± 1.2 RBCs/s) were reduced (both P < 0.05) in CHF vs. C muscle. Contractions significantly (both P < 0.05) elevated VRBC (C, 428 ± 47 vs. CHF, 222 ± 15 μm/s) and FRBC (C, 44.3 ± 5.5 vs. CHF, 24.0 ± 1.2 RBCs/s) in C and CHF muscle; however, both remained significantly lower in CHF than C. The time to 50% of the final response was slowed (both P < 0.05) in CHF compared with C for both VRBC (C, 8 ± 4; CHF, 56 ± 11 s) and FRBC (C, 11 ± 3; CHF, 65 ± 11 s). Capillary hematocrit increased with contractions in C and CHF muscle but was not different ( P > 0.05) between CHF and C. Thus CHF impairs diffusive and conductive O2 delivery across the rest-to-contractions transition in rat skeletal muscle, which may help explain the slowed O2 uptake on-kinetics manifested in CHF patients at exercise onset.

scholarly journals α-Adrenergic receptor regulation of skeletal muscle blood flow during exercise in heart failure patients with reduced ejection fraction

2019 ◽  
Vol 316 (5) ◽  
pp. R512-R524 ◽  
Author(s):  
Zachary Barrett-O’Keefe ◽  
Joshua F. Lee ◽  
Stephen J. Ives ◽  
Joel D. Trinity ◽  
Melissa A. H. Witman ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Ejection Fraction ◽  
Adrenergic Receptor ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Reduced Ejection Fraction ◽  
Leg Blood Flow ◽  
Related Increase

Patients suffering from heart failure with reduced ejection fraction (HFrEF) experience impaired limb blood flow during exercise, which may be due to a disease-related increase in α-adrenergic receptor vasoconstriction. Thus, in eight patients with HFrEF (63 ± 4 yr) and eight well-matched controls (63 ± 2 yr), we examined changes in leg blood flow (Doppler ultrasound) during intra-arterial infusion of phenylephrine (PE; an α1-adrenergic receptor agonist) and phentolamine (Phen; a nonspecific α-adrenergic receptor antagonist) at rest and during dynamic single-leg knee-extensor exercise (0, 5, and 10 W). At rest, the PE-induced reduction in blood flow was significantly attenuated in patients with HFrEF (−15 ± 7%) compared with controls (−36 ± 5%). During exercise, the controls exhibited a blunted reduction in blood flow induced by PE (−12 ± 4, −10 ± 4, and −9 ± 2% at 0, 5, and 10 W, respectively) compared with rest, while the PE-induced change in blood flow was unchanged compared with rest in the HFrEF group (−8 ± 5, −10 ± 3, and −14 ± 3%, respectively). Phen administration increased leg blood flow to a greater extent in the HFrEF group at rest (+178 ± 34% vs. +114 ± 28%, HFrEF vs. control) and during exercise (36 ± 6, 37 ± 7, and 39 ± 6% vs. 13 ± 3, 14 ± 1, and 8 ± 3% at 0, 5, and 10 W, respectively, in HFrEF vs. control). Together, these findings imply that a HFrEF-related increase in α-adrenergic vasoconstriction restrains exercising skeletal muscle blood flow, potentially contributing to diminished exercise capacity in this population.

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.

scholarly journals Beneficial haemodynamic effects of insulin in chronic heart failure

Heart ◽  
2001 ◽  
Vol 85 (5) ◽  
pp. 508-513
Author(s):  
W A Parsonage ◽  
D Hetmanski ◽  
A J Cowley
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Chronic Heart Failure ◽  
Insulin Infusion ◽  
Muscle Blood Flow ◽  
Haemodynamic Effects ◽  
High Dose ◽  
Skeletal Muscle Blood Flow

OBJECTIVETo characterise the central and regional haemodynamic effects of insulin in patients with chronic heart failure.DESIGNSingle blind, placebo controlled study.SETTINGUniversity teaching hospital.PATIENTSTen patients with stable chronic heart failure.INTERVENTIONSHyperinsulinaemic euglycaemic clamp and non-invasive haemodynamic measurements.MAIN OUTCOME MEASURESChange in resting heart rate, blood pressure, cardiac output, and regional splanchnic and skeletal muscle blood flow.RESULTSInsulin infusion led to a dose dependent increase in skeletal muscle blood flow of 0.36 (0.13) and 0.73 (0.14) ml/dl/min during low and high dose insulin infusions (p < 0.05 and p < 0.005 v placebo, respectively). Low and high dose insulin infusions led to a fall in heart rate of 4.6 (1.4) and 5.1 (1.3) beats/min (p < 0.05 and p < 0.005 v placebo, respectively) and a modest increase in cardiac output. There was no significant change in superior mesenteric artery blood flow.CONCLUSIONIn patients with chronic heart failure insulin is a selective skeletal muscle vasodilator that leads to increased muscle perfusion primarily through redistribution of regional blood flow rather than by increased cardiac output. These results provide a rational haemodynamic explanation for the apparent beneficial effects of insulin infusion in the setting of heart failure.

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