Proceedings of The Physiological Society

Physiology 2016 (Dublin, Ireland) (2016) Proc Physiol Soc 37, PCB184

Poster Communications

Effect of age and endurance training on mitochondrial function in sedentary volunteers

D. Constantin-Teodosiu1, B. Popat3, D. Constantin1, L. Latimer3, C. Bolton2, M. Steiner3, P. Greenhaff1

1. School of Life Sciences, Nottingham University Medical School, Nottingham, United Kingdom. 2. Nottingham Respiratory Research Unit, Nottingham, United Kingdom. 3. NIHR Leicester Respiratory Biomedical Research Unit & Centre for Exercise and Rehabilitation Sci, Leicester, United Kingdom.


  • Table 1. Peak VO2, intrinsic mitochondrial function and relative mtDNA copy number in young and older subjects before and after 8 wks training<\#13>

    Values are mean

Contrary to the opinion of some (Lanza & Nair, 2010), human exercise training studies suggest the decline in mitochondrial function with age is not related to ageing per se, but rather reflects a decrease in muscle mitochondrial content resulting from age-related deconditioning (Broskey et al. 2014). We therefore investigated the impact of age and endurance exercise training on intrinsic mitochondrial function and an index of mitochondrial proliferation (relative mitochondrial DNA copy number, mtDNA) in sedentary young and older volunteers. Ten young (mean±SEM, age 28.0±1.6 yrs and BMI 26.0±2.4 kg.m-2) and 10 older (age 70.7±1.6 yrs and BMI 28.5±1.0 kg.m-2) sedentary, healthy, volunteers underwent 8 wks of supervised cycle exercise training (30 min at 65% peak power, 3 x wk). Before and after training, peak VO2 was measured during incremental cycling exercise, and a muscle biopsy was obtained from the Vastus Lateralis. Maximal rates of mitochondrial ATP production (MAPR) were measured bio-luminometrically in freshly isolated mitochondria in the presence of glutamate with succinate or malate (Glut/Succ, Glut/Mal), and normalised to citrate synthase activity to give intrinsic mitochondrial function. Relative mtDNA copy number was assessed by quantifying hydroxymethylbilane synthase gene and NADH:ubiquinone oxidoreductase subunit 1 in isolated genomic and mitochondrial DNA, respectively. Peak VO2 was greater in young than in older subjects at baseline and increased with training in both groups. There was no difference in intrinsic MAPR or relative mtDNA copy number between groups at baseline. Training increased intrinsic MAPR in young, which was blunted in older subjects (in particular Glut/Mal). Training also increased relative mtDNA copy number in young, but not in older subjects. Intrinsic mitochondrial function is not impaired in muscle from sedentary, healthy older compared to young. However, the magnitude of increase in intrinsic MAPR after 8 wks of training is blunted in older subjects, and appears to be related at least partly to diminished mitochondrial proliferation with exercise.

Where applicable, experiments conform with Society ethical requirements