84: Relationship between Skeletal Muscle Function, Peak Oxygen Consumption and Cardiac Output in Patients with Chronic Heart Failure

Cardiac power output is a direct measure of overall cardiac function that integrates both flow- and pressure-generating capacities of the heart. The present study assessed the reproducibility of cardiac power output and other more commonly reported cardiopulmonary exercise variables in patients with chronic heart failure. Metabolic, ventilatory and non-invasive (inert gas re-breathing) central haemodynamic measurements were undertaken at rest and near-maximal exercise of the modified Bruce protocol in 19 patients with stable chronic heart failure. The same procedure was repeated 7 days later to assess reproducibility. Cardiac power output was calculated as the product of cardiac output and mean arterial pressure. Resting central haemodynamic variables demonstrate low CV (coefficient of variation) (ranging from 3.4% for cardiac output and 5.6% for heart rate). The CV for resting metabolic and ventilatory measurements ranged from 8.2% for respiratory exchange ratio and 14.2% for absolute values of oxygen consumption. The CV of anaerobic threshold, peak oxygen consumption, carbon dioxide production and respiratory exchange ratio ranged from 3.8% (for anaerobic threshold) to 6.4% (for relative peak oxygen consumption), with minute ventilation having a CV of 11.1%. Near-maximal exercise cardiac power output and cardiac output had CVs of 4.1 and 2.2%, respectively. Cardiac power output demonstrates good reproducibility suggesting that there is no need for performing more than one cardiopulmonary exercise test. As a direct measure of cardiac function (dysfunction) and an excellent prognostic marker, it is strongly advised in the assessment of patients with chronic heart failure undergoing cardiopulmonary exercise testing.

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Enhancing Calstabin Binding to Ryanodine Receptors Improves Both Cardiac and Skeletal Muscle Function in Heart Failure

Journal of Cardiac Failure ◽

10.1016/j.cardfail.2005.08.008 ◽

2005 ◽

Vol 11 (9) ◽

pp. S231

Author(s):

Andrew R. Marks

Keyword(s):

Heart Failure ◽

Skeletal Muscle ◽

Muscle Function ◽

Ryanodine Receptors ◽

Skeletal Muscle Function

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.00308.2003 ◽

2003 ◽

Vol 95 (3) ◽

pp. 1055-1062 ◽

Cited By ~ 88

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.

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