Author(s): FERGUSON, E., NYMAN, D.L.E., BUREAU, J., PUFAHL, C.J., BRAHMBHATT, A.N., SIMPSON, C.A., GURD, B.J., BARDANA, D.D., PERRY, C.G.R., MCGLORY, C., Institution: QUEEN'S UNIVERSITY , Country: CANADA, Abstract-ID: 2371

INTRODUCTION:
Periods of muscle-disuse lead to substantial skeletal muscle loss that is linked with reduced mitochondrial respiration rates. Omega-3 fatty acid (n-3) supplementation may attenuate muscle-disuse atrophy and declines in mitochondrial respiration rates in healthy humans undergoing single-leg immobilization. The purpose of this investigation was to test the hypothesis that combined n-3 and essential amino acid (EAA) supplementation (n-3+EAA) would attenuate declines in rates of mitochondrial respiration in individuals convalescing from anterior cruciate ligament (ACL) reconstruction surgery (ACLR).
METHODS:
Adult ACLR outpatients were randomly assigned to an n-3+EAA supplementation group (n=11; age: 28 ± 8 yrs; body mass: 85.8 ± 27.0 kg; body mass index: 29.1 ± 6.9 kg/m2) or placebo group (n=11; age: 30 ± 14 yrs; body mass: 73.7 ± 16.2 kg; body mass index: 25.6 ± 4.7 kg/m2). Participants undergoing the n-3+EAA supplementation protocol consumed n-3 fatty acids (5 g/day; 3.75 g eicosapentaenoic acid + 1.25 g docosahexaenoic acid) for 4 weeks prior to, and for 2 weeks following ACLR, plus EAA (40 g/day) for 1 week prior to, and for 2 weeks following, ACLR. Participants in the placebo group consumed safflower oil (5 g/day) and non-essential amino acids (40 g/day) in lieu of n-3s and EAAs, respectively. Vastus lateralis biopsies were obtained from the surgical leg 1 day prior to, and 2 weeks following, ACLR. Mass-specific rates of pyruvate and malate-supported, adenosine diphosphate (ADP)-stimulated mitochondrial respiration were measured in permeabilized muscle fibers in the presence of 20 mM creatine via high-resolution respirometry at each biopsy timepoint.
RESULTS:
Statistically significant declines in maximal complex I- (P = 0.005) and complex I+II-supported (P = 0.0005), ADP-stimulated mitochondrial respiration were observed in the placebo group following ACLR. No statistically significant declines in maximal complex I- (P = 0.840) and complex I+II-supported ADP-stimulated respiration (P = 0.094) were observed in the n-3+EAA supplementation group following ACLR. In addition, rates of mitochondrial respiration were lower following ACLR across a range of submaximal and maximal ADP concentrations in the placebo group, but not the n-3+EAA supplementation group (500 µM ADP: P = 0.002; 1000 µM ADP: P = 0.0008; 5000 µM ADP: P = 0.0007; and 7000 µM ADP: P = 0.001).
CONCLUSION:
Overall, mass-specific rates of submaximal and maximal complex I-supported ADP-stimulated mitochondrial respiration, and maximal complex I+II-supported ADP-stimulated respiration, are reduced following ACLR. N-3+EAA supplementation mitigates declines in rates of submaximal and maximal complex I-supported ADP-stimulated mitochondrial respiration and maximal complex I+II-supported ADP-stimulated mitochondrial respiration in the post-surgical period.