Fight Aging!

Exercise is good for you, the evidence is overwhelmingly in support of that conclusion, and most people should probably undertake more activity than they do. One of the interesting outcomes produced by advances in biotechnology is an increased ability to quantify the results of different types of exercise where they differ. Personally, I'm a firm believer in the idea that optimization of diet, activity, and other lifestyle choices beyond the 80/20 point is largely a waste of time at present, as you'll never know whether or not your attempts at optimization are actually producing further improvements in life expectancy. That may not be true in the future, however, given much more knowledge and better and more widely available tools. That said, in the future we'll have also have access to rejuvenation and enhancement therapies that will produce such profound effects on health as to make optimization of everyday health practices such as exercise pointless for other reasons.

It's oft-repeated but true: exercise keeps you healthy. It boosts your immune system, keeps the mind sharp, helps you sleep, maintains your muscle tone, and extends your healthy lifespan. Researchers have long suspected that the benefits of exercise extend down to the cellular level, but know relatively little about which exercises help cells rebuild key organelles that deteriorate with aging. A study has found that exercise - in particular high-intensity interval training in aerobic exercises such as biking and walking - caused cells to make more proteins for their energy-producing mitochondria and their protein-building ribosomes. "Based on everything we know, there's no substitute for these exercise programs when it comes to delaying the aging process. These things we are seeing cannot be done by any medicine."

The study enrolled 36 men and 36 women from two age groups - "young" volunteers who were 18-30 years old and "older" volunteers who were 65-80 years old - into three different exercise programs: one where the volunteers did high-intensity interval biking, one where the volunteers did strength training with weights, and one that combined strength training and interval training. Then the researchers took biopsies from the volunteers' thigh muscles and compared the molecular makeup of their muscle cells to samples from sedentary volunteers. The researchers also assessed the volunteers' amount of lean muscle mass and insulin sensitivity. They found that while strength training was effective at building muscle mass, high-intensity interval training yielded the biggest benefits at the cellular level. The younger volunteers in the interval training group saw a 49% increase in mitochondrial capacity, and the older volunteers saw an even more dramatic 69% increase. Interval training also improved volunteers' insulin sensitivity. However, interval training was less effective at improving muscle strength, which typically declines with aging.

As we age, the energy-generating capacity of our cells' mitochondria slowly decreases. By comparing proteomic and RNA-sequencing data from people on different exercise programs, the researchers found evidence that exercise encourages the cell to make more RNA copies of genes coding for mitochondrial proteins and proteins responsible for muscle growth. Exercise also appeared to boost the ribosomes' ability to build mitochondrial proteins. The most impressive finding was the increase in muscle protein content. In some cases, the high-intensity biking regimen actually seemed to reverse the age-related decline in mitochondrial function and proteins needed for muscle building. The high-intensity biking regimen also rejuvenated the volunteers' ribosomes, which are responsible for producing our cells' protein building blocks. The researchers also found a robust increase in mitochondrial protein synthesis. Increase in protein content explains enhanced mitochondrial function and muscle hypertrophy. Exercise's ability to transform these key organelles could explain why exercise benefits our health in so many different ways.

Link: https://www.eurekalert.org/pub_releases/2017-03/cp-het030217.php