Leucine augments specific skeletal muscle mitochondrial respiratory pathways during recovery following 7 days of physical inactivity in older adults

Leucine supplementation attenuates the loss of skeletal muscle mass and function in older adults during bed rest. We sought to determine whether leucine could also preserve and/or restore mitochondrial function and muscle oxidative capacity during periods of disuse and rehabilitation. Healthy, older adults (69.1 +/- 1.1 yr) consumed a structured diet with supplemental leucine (LEU: 0.06 g/kg body weight/meal; n = 8) or alanine (CON: 0.06 g/kg body weight/meal; n = 8) during 7 days of bed rest and 5 days of inpatient rehabilitation. A 75-g oral glucose tolerance test (OGTT) was performed at baseline (PreBR), after bed rest (PostBR), and rehabilitation (PostRehab) and used to calculate an indicator of insulin sensitivity and metabolic clearance rate (MCR). Tissue samples from the m. vastus lateralis were collected at PreBR, PostBR, and PostRehab to assess mitochondrial respiratory capacity and protein markers of the oxidative phosphorylation and a marker of the antioxidant defense systems. During bed rest, leucine tended to preserve insulin sensitivity (change in MCR, CON vs. LEU: -3.5 +/- 0.82 vs. LEU: -0.98 +/- 0.88, P = 0.054), but had no effect on mitochondrial respiratory capacity (change in state 3(+succinate) CON vs. LEU -8.7 +/- 6.1 vs. 7.3 +/- 4.1 pmol O-2/s/mg tissue, P = 0.10). Following rehabilitation, leucine increased ATP-linked respiration (CON vs. LEU: -8.9 +/- 6.2 vs. 15.5 +/- 4.4 pmol O-2/s/mg tissue, P = 0.0042). Although the expression of mitochondrial respiratory and antioxidant proteins was not impacted, leucine supplementation preserved specific pathways of mitochondrial respiration, insulin sensitivity, and a marker of oxidative stress during bed rest and rehabilitation. NEW & NOTEWORTHY In older adults, leucine mitigated the loss of insulin sensitivity associated with muscular disuse. Leucine supplementation increased mitochondrial respiration and reduced a marker of oxidative stress following periods of disuse and rehabilitation.