Preserved muscle protein metabolism in obese patients with chronic heart failure

We hypothesized that obese chronic heart failure (CHF) patients, who are known to have less cardiac dysfunction, could show preserved muscle protein balance. The aim of this study was to relate muscle protein balance and cardiac function to body mass index (BMI) in order to provide further insight to the obesity paradox in CHF patients.

Thirty stable CHF patients were categorized by BMI (n=6, normal; n=14, overweight; n=10, obese) and underwent post-absorptive: (i) right heart catheterization to determine cardiac hemodynamics and (ii) arterial and venous blood sampling to measure arterial and venous levels of essential amino acids (EAAs) and to calculate arterovenous differences (positive = uptake; negative = release). Muscle protein over-degradation was assessed by muscle release of the EAA phenylalanine. Plasma N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) was also determined. Twenty healthy subjects, matched for age, served as controls and underwent radial artery and vein sampling only.

Obese CHF patients had normal muscle protein balance, muscle EAA release, and arterial EAA concentration. Among the non-obese patients, normally weighted ones had more pronounced muscle protein over-degradation and greater reduction of arterial EAAs (p<0.01 for both) and EAA release (p<0.06) than overweight ones. Arterial leucine levels correlated negatively with NT-pro-BNP (r=-0.75; p<0.0001) and positively with LVEF (r=+0.68; p<0.0001). Within EAAs, branched chain amino acids were positively associated with stroke volume index (r=+0.51; p=0.004).

Only obese patients with CHF have balanced muscle protein metabolism. This may contribute to explain the obesity paradox.