Long Term Exercise in Humans Reduces Markers of Cellular Senescence in Intestinal Tissue
Cells become senescent constantly throughout life, largely those that reach the Hayflick limit on cellular replication. Near all such cells rapidly self-destruct or are removed by the immune system. With age, the immune system becomes less efficient and senescent cells begin to linger in ever-increasing numbers, the balance between creation and destruction thrown off. These cells produce inflammatory signaling that, when sustained over the long term, causes cell and tissue dysfunction, contributing to age-related disease.
If interested in how lifestyle interventions might impact the process, a sensible place to look is tissues with rapid cell division and turnover of cells, such as the intestinal barrier, as effects should appear more rapidly. In this study, researchers show that long-term exercise does reduce signs of cellular senescence in this tissue, though this appears to be a matter of reducing the proportion of the study population exhibiting high biomarker values rather than moving the average for everyone. Whether this outcome is similar in other tissues is an open question. While exercise is beneficial, one can't exercise one's way out from under degenerative aging, only somewhat slow its progression.
Regular endurance exercise training is an effective intervention for the maintenance of metabolic health and the prevention of many age-associated chronic diseases. Several metabolic and inflammatory factors are involved in the health-promoting effects of exercise training, but regulatory mechanisms remain poorly understood. Cellular senescence - a state of irreversible growth arrest - is considered a basic mechanism of aging. Senescent cells accumulate over time and promote a variety of age-related pathologies from neurodegenerative disorders to cancer. Whether long-term intensive exercise training affect the accumulation of age-associated cellular senescence is still unclear.
Here, we show that the classical senescence markers p16 and IL-6 were markedly higher in the colon mucosa of middle-aged and older overweight adults than in young sedentary individuals, but this upregulation was significantly blunted in age-matched endurance runners. Interestingly, we observe a linear correlation between the level of p16 and the triglycerides to HDL ratio, a marker of colon adenoma risk and cardiometabolic dysfunction. Our data suggest that chronic high-volume high-intensity endurance exercise can play a role in preventing the accumulation of senescent cells in cancer-prone tissues like colon mucosa with age. Future studies are warranted to elucidate if other tissues are also affected, and what are the molecular and cellular mechanisms that mediate the senopreventative effects of different forms of exercise training.
I have read where the naked Mole rat has mitochondria that produce a molecular form of humanin that is like that found in humas, but is different than that found in other rats and mice. I have also read where humanin is 3X times higher in the children of centenarians, so there may be evidence that humanin benefits longevity in humans. There are apparently three different alleles that human mitochondria carry, including A, G, and C. I have allele A, which is protective of having too much calcium deposition in blood vessels, but allele G is does not have this protection. Allele C is found in Asia, and some have speculated it may be why there are higher rates of centenarians in Japan, for instance. Brian