Omega-3 fatty acids and vitamin D in immobilisation: Part B- modulation of muscle functional, vascular and activation profiles

Abstract Objectives: This study set out to determine whether two potential protein-sparing modulators (eicosapentaenoic acid and vitamin D) would modulate the anticipated muscle functional and related blood vessels function deleterious effects of immobilisation. Design: The study used a randomised, double-blind, placebo-controlled design. Setting: The study took part in a laboratory setting. Participants: Twenty-four male and female healthy participants, aged 23.0±5.8 years. Intervention: The non-dominant arm was immobilised in a sling for a period of nine waking hours a day over two continuous weeks. Participants were randomly assigned to one of three groups: placebo (n=8, Lecithin, 2400 mg daily), omega-3 (-3) fatty acids (n=8, eicosapentaenoic acid (EPA); 1770 mg, and docosahexaenoic acid (DHA); 390 mg DHA, daily) or vitamin D (n=8, 1,000 IU daily). Measurements: Isometric and isokinetic torque, antagonist muscle co-contraction (activation profile), muscle fatigability indices, and arterial resting blood flow were measured before, at the end of the immobilisation period, and two weeks after re-mobilisation. Results: Muscle elbow flexion and extension isometric and isokinetic torque decreased significantly with limb immobilisation in the placebo group (P0.05) towards attenuating the decreases observed in the placebo group. There was no significant change in muscle fatigue parameters or co-contraction values with immobilisation and no effect of supplementation group (P>0.05). Similarly, this immobilisation model had no impact on the assessed blood flow kinetics. All parameters had returned to baseline values at the re-mobilisation phase of the study. Conclusion: Overall, at the current doses, neither -3 nor vitamin D supplementation significantly attenuated declines in torque associated with immobilisation. It would appear that muscle function (described here in Part B) might not be as useful a marker of the effectiveness of a supplement against the impact of immobilisation compared to tissue composition changes (described in Part A)

Oxidative capacity interacts with oxygen delivery to determine maximal O2 uptake in rat skeletal muscles in situ

Based on proportional changes in V̇O2,max with alterations in O2 delivery, it is widely held that O2 availability limits V̇O2,max. In contrast, reductions in V̇O2,max are also seen when mitochondrial oxidative capacity is reduced. Taken collectively, these prior results are consistent with the notion that there is not a single-step limitation to V̇O2,max. We used a pump-perfused rat hindlimb model to test the hypothesis that combining moderate reductions in O2 delivery and mitochondrial oxidative capacity would yield a greater reduction in V̇O2,max than seen when performing each intervention independently, demonstrating an interaction between O2 supply and mitochondrial oxidative capacity in determining V̇O2,max. Four groups of animals were studied: two in high O2 delivery conditions (hindlimb O2 delivery: 88 ± 1 μmol O2 min−1; mean ± s.e.m.) and two in moderately reduced O2 delivery conditions (66 ± 2 μmol O2 min−1). One group at each level of O2 delivery was treated with 0.1 μM myxothiazol to reduce mitochondrial oxidative capacity via competitive inhibition of NADH cytochrome c reductase. V̇O2,max in control animals (no myxothiazol) was 29 % lower in the moderately reduced O2 delivery group (592 ± 24 mmol O2 min−1 (100 g)−1); P < 0.05) than in the high O2 delivery group (833 ± 63 μmol O2 min−1 (100 g)−1). Similarly, V̇O2,max was reduced by 29 % (594 ± 22 μmol O2 min−1 (100 g)−1); P < 0.05) in myxothiazol-treated animals in high O2 delivery conditions compared to control animals in high O2 delivery conditions. When myxothiazol treatment was combined with moderately reduced O2 delivery, V̇O2,max was reduced by an additional 18 % (484 ± 21 μmol O2 min−1 (100 g)−1); P < 0.05) compared to either intervention performed independently. These results show that O2 supply and mitochondrial oxidative capacity interact to determine V̇O2,max