In my book Muscle Up, I gave a host of reasons why strength training — which most people accomplish through lifting weights — is a uniquely healthful exercise and much better than aerobic or endurance exercise. Among these reasons are lower risk of heart disease and cancer, and a far better record at fat loss than endurance exercise. And weightlifting is anti-aging.
As an anti-aging intervention, weightlifting fights the loss of muscle (sarcopenia) that starts early in life, in the thirties, and maintains high insulin sensitivity, the loss of which is a main cause of the maladies of age.
Telomeres are the caps on the ends of chromosomes, and they shorten with age. Dr. Michael Fossel, one of the world’s foremost scientists in the field of aging research (whom I interviewed), believes that telomere shortening is the key process in aging: prevent telomere shortening, and you prevent aging.
Interventions that promote good health, such as exercise and fasting, lead to slower telomere shortening, and those that promote poor health, such as obesity and smoking, lead to faster telomere shortening.
Endurance athletes who are suffering from fatigue and overtraining have shorter telomeres.(1) These people have arguably passed to the wrong side of the hormetic U-shaped curve, and got to the point where too much exercise was harming them, just as Ryan Hall did, formerly America’s fastest runner, who retired due to chronic fatigue and low testosterone.
Endurance athletes who do not overtrain appear to have normal telomeres.
What about weightlifters?
An analysis was done using a group of power lifters with an average of 8 years of training behind them, and comparing them to a group of “healthy, active subjects with no history of strength training.”(2)
The authors of the study say that wanted to understand “whether long-term practice of sports might have deleterious effects on muscle telomeres.”
Result: not only did power lifting not have deleterious effects on telomeres, but the power lifters’ telomeres were longer than the non-strength-trainers.
Even more interesting, telomere length in the power lifters was strongly correlated with maximum lifts in the deadlift and squat.
The more weight the power lifters were able to lift, i.e. the stronger they were, the longer their telomere lengths.
Correction: Commenter Tom pointed out that I got some of this this wrong, and indeed I did.
The article I linked says, “There was no abnormal shortening of telomeres in PL. On the contrary, the mean (P = 0.07) and the minimum (P = 0.09) TRF lengths in PL tended to be higher than in C.” OK, so far so good, telomere lengths tended to be higher in the power lifters than in healthy, active controls.
But, “In PL, the minimum TRF length was inversely correlated to the individual records in squat (r = -0.86; P = 0.01) and deadlift (r = -0.88; P = 0.01).” In the measurement of telomere lengths, distinctions must be made, because they’re not all the same length in different cells in the same person. So, minimum telomere length is of interest, and these significantly correlated to max lifts in the power lifters, i.e. the more they could lift, the shorter the minimum telomere lengths.
Since power lifters tended to have longer telomeres overall, it’s not clear to me how the minimum telomere length bears on their health and longevity. The article states, “These results show for the first time that long-term training is not associated with an abnormal shortening of skeletal muscle telomere length. Although the minimum telomere length in PL remains within normal physiological ranges, a heavier load put on the muscles means a shorter minimum TRF length in skeletal muscle.”
An animal experiment (in mice) found that overexpression of a certain gene that leads to more muscle hypertrophy (growth) “can regress obesity and resolve metabolic disorders in obese mice”.(3)
The results included
All of this occurred with no changes in food intake.
In Muscle Up, I cited many studies in humans that showed that weightlifting produced far better results in terms of fat loss than endurance training. In essence, weightlifting works, endurance training doesn’t.
The cited study above on mice gives us a biochemical and physiological rationale for how more muscle means less fat. By changing the hormonal milieu, the body sheds its fat, and strength training produces the desired hormonal changes.
Weightlifting leads to less shortening of telomeres, and more muscle leads to hormonal changes that conduce to less fat tissue and better insulin sensitivity.
All of these are important to any anti-aging program.
Weightlifting is a unique component of such a program, since its benefits are not matched by endurance training, and it confers benefits that even the best dietary program won’t give you.
Of course you need to eat right to slow aging, but if weight training is not in your anti-aging rotation, you’re missing a major aspect of slowing aging.