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 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.

Impaired capillary hemodynamics in skeletal muscle of rats in chronic heart failure

1999 ◽  
Vol 87 (2) ◽  
pp. 652-660 ◽  
Author(s):  
Casey A. Kindig ◽  
Timothy I. Musch ◽  
Randall J. Basaraba ◽  
David C. Poole
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Capillary Tube ◽  
Muscle Blood Flow ◽  
Flow Distribution ◽  
Skeletal Muscle Blood Flow ◽  
Fiber Atrophy ◽  
Microscopy Techniques

Skeletal muscle blood flow is reduced and O2 extraction is increased at rest in chronic heart failure (CHF). Knowledge of red blood cell (RBC) flow distribution within the capillary network is necessary for modeling O2 delivery and exchange in this disease. Intravital microscopy techniques were used to study the in vivo spinotrapezius muscle microcirculation in rats with CHF 7 wk after myocardial infarction and in sham-operated controls (sham). A decrease in mean muscle fiber width from 51.3 ± 1.9 μm in sham to 42.6 ± 1.4 μm in CHF rats ( P < 0.01) resulted in an increased lineal density of capillaries in CHF rats ( P < 0.05). CHF reduced ( P < 0.05) the percentage of capillaries supporting continuous RBC flow from 87 ± 5 to 66 ± 5%, such that the lineal density of capillaries supporting continuous RBC flow remained unchanged. The percentage of capillaries supporting intermittent RBC flow was increased in CHF rats (8 and 27% in sham and CHF, respectively, P < 0.01); however, these capillaries contributed only 2.3 and 3.3% of the total RBC flux in sham and CHF rats, respectively. In continuously RBC-perfused capillaries, RBC velocity (252 ± 20 and 144 ± 9 μm/s in sham and CHF, respectively, P < 0.001) and flux (21.4 ± 2.4 and 9.4 ± 1.1 cells/s in sham and CHF, respectively, P < 0.01) were markedly reduced in CHF compared with sham rats. Capillary “tube” hematocrit remained unchanged (0.22 ± 0.02 and 0.19 ± 0.02 in sham and CHF, respectively, P > 0.05). We conclude that CHF causes spinotrapezius fiber atrophy and reduces the number of capillaries supporting continuous RBC flow per fiber. Within these capillaries supporting continuous RBC flow, RBC velocity and flux are reduced 45–55%. This decreases the potential for O2 delivery but enhances fractional O2 extraction by elevating RBC capillary residence time. The unchanged capillary tube hematocrit suggests that any alterations in muscle O2 diffusing properties in CHF are mediated distal to the RBC.

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

scholarly journals Skeletal muscle function at low work level as a model for daily activities in patients with chronic heart failure

1997 ◽  
Vol 18 (10) ◽  
pp. 1626-1631 ◽  
Author(s):  
C. Opasich ◽  
E. Pasini ◽  
R. Aquilani ◽  
F. Coelli ◽  
R. Solfrini ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Muscle Function ◽  
Daily Activities ◽  
Skeletal Muscle Function ◽  
Work Level

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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