Can anyone get the paper?
Image from paper (I believe) showing that mitochondria activity (citrate synthase) does not move with exercise intensity suggesting that consistency of activity over time will build to similar levels of mitochondria over a wide range of intensities.
Reading the actual paper would be better.
Citrate synthase Citrate synthase - Google Search
Thanks. Unfortunately this does not include any charts. I don’t know why.
Any charts are I think in the supplementary material.
Very interesting. I’m not particularly familiar with “maximum work capacity” or Wmax
Could anyone educate me as to what level of intensity 45% of wMax would be? (That being the lowest end of the range)
Are we talking zone 2 walking for example?
Supplementary materials for paper
Highlights
• Physical activity helps protect against age-related decline in physical performance
• Physical activity boosts mitochondrial energetics while aging per se has no impact
• Mitochondrial ROS production is unaffected by aging in both active and inactive men
• Mitochondrial calcium handling declines with age and is linked to muscle performance
Summary
Aging-related muscle atrophy and weakness contribute to loss of mobility, falls, and disability. Mitochondrial dysfunction is widely considered a key contributing mechanism to muscle aging. However, mounting evidence positions physical activity as a confounding factor, making unclear whether muscle mitochondria accumulate bona fide defects with aging. To disentangle aging from physical activity-related mitochondrial adaptations, we functionally profiled skeletal muscle mitochondria in 51 inactive and 88 active men aged 20–93. Physical activity status confers partial protection against age-related decline in physical performance. Mitochondrial respiration remains unaltered in active participants, indicating that aging per se does not alter mitochondrial respiratory capacity. Mitochondrial reactive oxygen species (ROS) production is unaffected by aging and higher in active participants. In contrast, mitochondrial calcium retention capacity decreases with aging regardless of physical activity and correlates with muscle mass, performance, and the stress-responsive metabokine/mitokine growth differentiation factor 15 (GDF15). Targeting mitochondrial calcium handling may hold promise for treating aging-related muscle impairments
Read the full paper: Mitochondrial respiration remains unaltered with age in physically active men
Calcium influx is driven by mitochondrial membrane potential
