It encourages cells to make more RNA copies of the genes that code for mitochondrial proteins and proteins responsible for muscle growth.
Regular exercise has been shown to boost the immune system, heighten cognitive abilities, improve sleep, increase lifespan, and maintain muscle tone. Its benefits are proven; the research is conclusive.
However, the mechanisms that lie beneath exercise’s positive effects remain in the shadows. How do physical activities translate into rebuilding organelles that degrade as we age? Which activities are best?
Mitochondria are commonly referred to as the powerhouses of the cell; their primary function is to produce adenosine triphosphate – the molecule that transports chemical energy within cells. As we age, the capacity of mitochondria to generate energy slowly decreases.
By comparing proteomic and RNA-sequencing data across the exercise groups, the team found that exercise encourages cells to make more RNA copies of the genes that code for mitochondrial proteins and proteins responsible for muscle growth.
Younger volunteers carrying out interval training showed a 49 percent increase in mitochondrial capacity and, even more impressively, the older group saw a 69 percent increase.
High-intensity biking effectively reversed age-related decline in mitochondrial function.
Ribosomes, vital players in the synthesis of proteins, also received a boost from exercise – it increased their ability to build mitochondrial proteins, which explains the rise in both mitochondrial function and muscle hypertrophy.
Physical activity’s ability to bolster protein production is important. Muscle cells, like brain and heart cells, do not divide frequently. This means that, as we age, function declines.
Dr Nair explains: “Unlike liver, muscle is not readily re-grown; the cells can accumulate a lot of damage”. If exercise can restore or minimise the deterioration of ribosomes and mitochondria in muscle cells, there is a good chance that it does the same in other tissues.
In addition to the increase in mitochondrial capacity, the interval training also improved the participant’s insulin sensitivity, lowering the risk of developing diabetes. However, this exercise type was less effective at improving muscle strength.
Dr Sreekumaran Nair said that “Based on everything we know, there’s no substitute for these exercise programmes when it comes to delaying the ageing process. These things we are seeing cannot be done by any medicine.”
Although this study was not focused on making recommendations about duration or exercise type, Dr Nair says: “If people have to pick one exercise, I would recommend high-intensity interval training, but I think it would be more beneficial if they could do 3-4 days of interval training and then a couple of days of strength training.”
The study clearly demonstrates how exercise can increase the output of specific organelles. This relationship is likely to play a key part in slowing cellular ageing.
Dr Nair and his team plan to extend their deep dive into the cellular benefits of exercise in other tissue types. In the future, these findings could potentially be used to target specific pathways and reduce the impact of ageing.
In time, perhaps these positive changes could be triggered artificially, but as Dr Nair says:
“There are substantial basic science data to support the idea that exercise is critically important to prevent or delay ageing. There’s no substitute for that.”
