Physical activity has long been associated with a reduced risk of cancer and improved survival rates among cancer patients. While these links are widely acknowledged, the precise biological mechanisms driving these benefits are not fully understood. Some explanations point to exercise’s influence on the gut microbiome and its effects on the immune system.
Researchers at Yale School of Medicine, led by Rachel Perry, explored an additional pathway by investigating exercise’s direct metabolic effects on tumors. In their study, breast cancer cells were introduced into 18 mice. Twelve of these mice were fed a diet designed to induce obesity, a condition known to exacerbate numerous cancer types. The researchers then provided half of the mice, irrespective of their diet, with an exercise wheel, allowing them to engage in physical activity voluntarily.
The findings after four weeks revealed a significant difference. Tumors in obese mice that utilized the exercise wheel were 60 percent smaller compared to those in obese mice that were denied access to a functioning wheel. Furthermore, these exercisers’ tumors were slightly smaller than those observed in sedentary mice on a standard diet. A single 30-minute exercise session correlated with increased oxygen and glucose uptake by skeletal and cardiac muscles, while simultaneously decreasing glucose uptake by the tumors.
“This research demonstrates that aerobic fitness fundamentally alters the metabolic competition between muscle tissue and tumors,” stated Perry. “It’s crucial to note that the exercise intervention was voluntary; we are not discussing strenuous marathon-level training, but rather the activity the mice chose to undertake.”
Further analysis of gene activity highlighted that exercise influenced 417 genes within key metabolic pathways in the mice. This genetic shift effectively meant that muscle tissues became more efficient at metabolizing glucose, while tumor tissues became less so. Specifically, the researchers noted a downregulation in cancer cells of mTOR, a protein integral to cell growth, which may be contributing to the restriction of tumor progression.
Potential Implications for Human Health
Perry suggests that the observed metabolic pathways are highly conserved across mammalian species, leading her to anticipate a similar effect in humans, even those who are not obese. Evidence supporting this includes reports of comparable gene activity changes in human cancer patients who exercise.
Rob Newton, from Edith Cowan University, commented on these findings, stating, “This presents another mechanism illustrating how exercise cultivates a more cancer-suppressive environment. While a clinical trial in humans is necessary, I see no reason why a similar outcome wouldn’t occur.”
Perry elaborated that metabolism occurs in all tissues and is influenced by both the microbiome and the immune system. She posits that these metabolic alterations could serve as the connecting factor between exercise, the microbiome, the immune system, and tumor growth. However, she also acknowledged the likelihood of exercise’s beneficial effects stemming from multiple mechanisms.
Exercise as a Proactive Cancer Strategy
The study also offers insight into why reduced muscle mass might increase the risk of cancer mortality, according to Newton. “If muscles preferentially absorb glucose, then having more muscle mass and activating it regularly will result in a greater positive effect,” he explained.
Newton advocates for considering exercise not merely as a healthy lifestyle choice but as a form of cancer medicine, to be integrated with other treatments. “It’s about identifying the primary drivers of a pro-cancer environment and targeting them directly,” Newton said. “This might involve improving cardiorespiratory fitness, but if a patient has particularly low muscle mass, resistance training would likely be the initial priority.”