Boushel 2014 Pro Can Soc Exercise Physiol
|Boushel RC, Hattel H, Saltin B (2014) Lifelong endurance training keeps mitochondria young. Pro Can Soc Exercise Physiol S6.|
Abstract: Aging is associated with diminished cardiovascular function and sarcopenia, and loss of muscle oxidative capacity is considered a salient feature of aging. While moderate-to-high intensity training evokes mitochondrial biogenesis in skeletal muscle, it remains unclear to what extent aging in itself or rather a lower training stimulus that accompanies aging contributes to loss of skeletal muscle mitochondrial function. To address this question leg muscle mitochondrial respiratory capacity in 8 older men (65±2 yrs) who had maintained road cycling training 200 km/week for 50 years was compared to that of 8 age-matched sedentary (UT) controls (67±1 yrs).V˙ O2 max was measured on a bicycle ergometer and a biopsy obtained from vastus lateralis muscle was permeabilized and prepared for high resolution respirometry (Oxygraph, Oroboros, AT). V˙ O2 max was substantially higher (p<0.05) in lifelong trained (45±2 ml/kg/min) compared to UT (27±2 ml/kg/min). Mitochondrial LEAK respiration was higher in ET, and Vmax of mitochondrial respiration (OXPHOS) with mixed substrates was 2-fold higher in the ET (132±6 pmol/sec/mg) compared to UT (72±4 pmol/sec/mg, p<0.01). Higher fatty acid oxidation and substrate control ratios in ET indicate regulatory changes in mitochondria in addition to a larger mitochondrial volume. The findings indicate that skeletal muscle mitochondrial respiratory capacity of ‘lifelong trained’ older males is retained at a level comparable to young athletic individuals, and suggest that decrements in aerobic performance with age are primarily attributed to diminished cardiovascular function.
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Organism: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS Pathway: NS HRR: Oxygraph-2k