Affiliation:
1. University Medical Center Groningen
2. Washington University School of Medicine
3. University of Palermo
4. “Mater Salutis” Hospital
5. San Camillo, Forlanini Hospital
6. University of Sydney
Abstract
AbstractRegular 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 cellular 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 that 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 well-accepted marker of colon adenoma risk and cardiometabolic dysfunctions. Our data suggest that chronic high-volume high-intensity endurance exercise can play a major role in preventing the accumulation of senescent cells in cancer prone tissues like colon mucosa with age. Future studies are warranted to elucidate which tissues are most affected, and what are the molecular and cellular mechanisms that mediate the senomorphic effects of different forms of exercise training.
Publisher
Research Square Platform LLC