In his excellent article series on anti-aging, anti-aging fitness expert Clarence Bass highlights this study showing that six months of progressive resistance training made the gene expression pattern of aging mitochondria appear significantly younger.
Muscles can become smaller and weaker with age (a process known as sarcopenia), and evidence suggests that a key part of the decline occurs in a component of muscle cells called the mitochondria, the primary engine of energy production.
From the study, which was done on men at an average age of 70 years old, researchers reported that “…the older individuals were able to improve strength by approximately 50%, to levels that were only 38% less than that of young individuals…”. This means that seniors engaged in weight training closed the strength gap between themselves and their counterparts who were nearly 40 years younger from 59% to 38%, which is an improvement of almost 36% in a mere six months of the study.
Muscle biopsies from the study showed “a remarkable reversal of the expression profile of 179 genes associated with age and exercise training…Genes that were down-regulated with age were correspondingly up-regulated with exercise, while genes that were up-regulated with age, were down-regulated with exercise.”
The researchers summed things up by reporting that “healthy older adults show a gene expression profile in skeletal muscle consistent with mitochondrial dysfunction and associated processes such as cell death, as compared with young individuals. Moreover, following a period of resistance exercise training in older adults, we found that age-associated transcriptome expression changes were reversed, implying a restoration of a youthful expression profile.”
So when it comes to mitochondria, weight training reversed nearly 40 years of aging!
But exercise doesn’t only affect mitochondria. Two more studies show how exercise protects DNA from the wear and tear of aging, and how the addition of fast-twitch muscle fibers precipitate fat loss and improve metabolic function – primarily by acting on telomeres.
Telomeres cap the DNA chromosomes in your cells and protect these chromosomes from damage. As you age, telomeres progressively wear and shorten from repeated cell division, oxidative stress, inflammation, and other metabolic processes, eventually leaving the cell’s chromosomes unprotected. When the caps are completely eroded or disappear, the wear and tear begins to cut into your genes, causing cells to become damaged and discarded as you grow older.
In this next study, scientists measured telomeres in twins to gauge the effect of exercise on aging, hypothesizing that “telomere dynamics might chronicle the cumulative burden of oxidative stress and inflammation and, as such, serve as an index of biological age” and that “physical activity level may have an [independent] effect on telomere attrition”.
They studied 2401 twins (2152 women and 249 men, aged 18 to 81), used questionnaires on physical activity level, smoking status, disease status, and socioeconomic status, and extracted DNA from blood samples.
So what did they find in this study on twins?
Telomere length decreased with age. No surprises there. But both the women and men who were physically active had longer telomeres than those who were sedentary, even after adjusting for the influence of age, weight, disease, socioeconomic status, and smoking.
In addition, the study participants who spent more than 3 hours each week engaged in vigorous physical activity (such as lifting weights) had longer telomeres than subjects 10 years younger, suggesting that individuals who eschew placing a vigorous load on their body may wind up biologically older by 10 years.
Obviously, since they were studying twins, these differences weren’t due to genes, but rather due to the lifestyle factor of exercise. When one twin exercised significantly more than the other, they had longer, more durable telomeres.
In the next study, researchers found that replacing slow-twitch type I muscle fibers with stronger and faster type II muscle fibers produced a significant reduction of fat mass and insulin resistance. Endurance training develops slow-twitch fibers, but strength training builds fast-twitch fibers.
For this study, researchers used a genetically engineered mouse that contained a muscle-growth regulating gene called Akt1 that could be turned on and off by the researchers. Activating Akt1 caused the mice to grow type II fibers, without exercise (important to note, since mice don’t really lift weights that well, even when commanded to by scientists in white lab coats). When the Akt1 gene was turned on, the mice took on the characteristics of a lean and powerful sprinter or weight lifter, and when the gene was turned off, the mice reverted to a predominance of type I muscle fibers, along with becoming more obese and insulin resistant (notably, this was without an actual change in diet!).
The researchers reported that “remarkably, type II muscle growth was associated with an overall reduction in body mass, due to a large decrease in fat mass. In addition, blood tests showed that these mice became metabolically normal [with no insulin resistance]. This work shows that type 2 muscle just doesn’t allow you to pick up heavy objects, it is also important in controlling whole body metabolism. It appears that the increase in type 2 muscle fiber orchestrates changes in the body through its ability to communicate with other tissues”.
Beyond the age of 30, we lose approximately six pounds of muscle mass per decade, and these findings indicate that interventions designed to increase skeletal muscle mass (such as weight training) may prove to be critical weapons in the fight against obesity and obesity-related ailments, including diabetes, heart disease, stroke, hypertension, and cancer.
The key point here of course is that weight training, due to it’s recruitment of type II muscle fibers, appears to be more effective than cardio, endurance and aerobics for fat loss, weight control, essentially converting the cells into a fat-burning machine.
Finally, yet another study on strength training effects on telomere length in human skeletal muscle looked into reports of a phenomenon of abnormally short telomeres in skeletal muscle of athletes who had overtraining and exercise-associated fatigue. This important study looked into the question of whether long-term hard exercise might have deleterious effects on muscle telomeres. So, using muscle biopsies, the researchers compared telomere length of a group of power lifters who had trained for an average of eight years against that of a group of healthy, active subjects who had no history of strength training.
There was absolutely no abnormal shortening of telomeres in the power lifters. As a matter of fact, telomere lengths in the power lifters were significantly higher than those of the control group, and telomere length was positively correlated to the power lifters’ individual records in the squat and deadlift!
These results show for the first time that long-term weight training is not associated with an abnormal shortening of skeletal muscle telomere length, and that the heavier the load you put on your muscles, the longer your telomeres will tend to be.
Written by: Ben Greenfield
Article Source: https://bengreenfieldfitness.com/2016/05/the-fittest-old-people/
“The Greatest Health of Your Life”℠
Boston Testosterone Partners
National Testosterone Restoration for Men
Wellness & Preventative Medicine