Researchers from Mayo Clinic have uncovered a novel way in which exercise may contribute to healthy aging by suppressing an age-related phenomenon known as the senescence-associated secretory phenotype, or SASP.

In recent years, research has uncovered a number of factors that contribute to or are present in the pathology of aging; among them, the SASP has gained a good deal of attention as a causal and potentially treatable contributor to the diseases of aging. Cellular senescence was first observed by Leonard Hayflick in 1965 and is characterized as a condition wherein a viable cell is no longer able to divide. As a result, cellular senescence is thought to act as a potential anti-cancer mechanism. Further, cellular senescence can result from a number of aberrant processes, including oxidative damage, mitochondrial dysfunction, telomere dysfunction, DNA damage/mutation, transcriptional dysregulation, and epigenetic dysregulation. Senescent cells have been observed to secrete a number of inflammatory hormones, and have therefore been implicated in driving what has been described as “inflamm-aging”, whereby chronic and unchecked inflammation leads to disease. These insights have led to a number of potentially promising interventions designed to remove or suppress senescent cells, referred to as senolytic or senomorphic therapies, respectively.

Exercise has long been attributed to improvements in health and longevity, and it has been hypothesized that these beneficial outcomes are due to improvements in a multitude of factors, including adiposity, cardiovascular health, and mitochondrial function. In their recent Aging Cell paper, Englund et al., have provided evidence for an additional mechanism by which exercise, via suppression of the SASP, may lead to benefits in aging populations. In this study, individuals undertook a 12-week progressive strength and endurance training program. As expected, study participants saw improvements in both physical performance and body composition measurements post-intervention when compared to their pre-intervention values. Additionally, levels of circulating CD3+ T-cells (cells involved in the adaptive immune response, targeting foreign agents) derived from peripheral blood showed decreased expression of SASP-associated mRNAs. Moreover, plasma-derived proteins known to be elevated as part of the SASP showed a significant reduction post-intervention.

While the authors note that previous interventional studies suggest that exercise may influence senescent cell burden, this had yet to be assessed in older adults utilizing known biomarkers. While the scope of this study does not address the mechanism (senolytic or senomorphic) by which exercise leads to a reduction in the SASP, the researchers demonstrate that exercise is effective in reducing SASP-associated biomarkers in older adults. Usefully, these biomarkers could aid researchers in determining the efficacy of future therapeutic interventions.

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