Abstract
Background:
Disturbances in protein metabolism and impaired muscle health have been observed in chronic obstructive pulmonary disease (COPD). The ω-3 (n-3) PUFAs EPA and DHA are known for their anti-inflammatory and muscle health-enhancing properties.
Objectives:
We examined whether daily EPA + DHA supplementation can improve daily protein homeostasis in patients with COPD by reducing postabsorptive whole-body protein breakdown (PB) and enhancing the anabolic response to feeding in a dose-dependent way.
Methods:
Normal-weight participants with moderate to severe COPD (n = 32) received daily for 4 wk, according to a randomized double-blind placebo controlled 3-group design, a high dose (3.5 g, n = 10) of EPA + DHA, a low dose (2.0 g, n = 10) of EPA + DHA, or placebo (olive oil, n = 12) via gel capsules. At pre- and postintervention, stable isotope tracers were infused to assess postabsorptive netPB [postabsorptive PB - protein synthesis (PS)] and the anabolic response (prandial netPS = prandial PS-PB) to a protein meal. In addition, muscle mass and function were measured.
Results:
Plasma phosphatidylcholine EPA and DHA concentrations were higher after 4 wk of supplementation in both EPA + DHA groups (P < 0.004), and there was a trend toward higher values for plasma EPA after the high compared with the low dose of EPA + DHA (P = 0.065). Postabsorptive PB was lower after 4 wk of the high dose of EPA + DHA, whereas netPB was lower independent of the dose of EPA + DHA (low dose, P = 0.037; high dose, P = 0.026). Prandial netPS was increased only after the high dose of EPA + DHA (P = 0.03). Extremity lean mass but not muscle function was increased, independent of the EPA + DHA dose (P < 0.05).
Conclusions:
Daily n-3 PUFA supplementation for 4 wk induces a shift toward a positive daily protein homeostasis in patients with COPD in part in a dose-dependent way. Daily doses up to 3.5 g EPA and DHA are still well tolerated and lead to protein gain in these patients. This trial was registered at clinicaltrials.gov as NCT01624792.
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