Using data from a prospective study, researchers found that participants who regularly engaged in high-intensity aerobic activity had a 72% lower risk of metastatic cancer.
The finding from this Tel Aviv University study stems from both epidemiological data in humans and mechanistic investigations in animals, suggesting a metabolic basis for the protective effect of high-intensity aerobic exercise against metastatic cancer.
In the human component, researchers analyzed 20-year follow-up data from nearly 3,000 initially cancer-free participants. Those who regularly performed high-intensity aerobic activities (efforts reaching 80-85% of maximum heart rate, such as vigorous running) showed a 72% lower incidence of metastatic cancer compared to sedentary individuals. This was linked to metabolic shifts observed in a smaller group of runners, where blood samples post-exercise revealed increased carbohydrate metabolism.
The proposed biological mechanism centers on how such exercise alters energy dynamics in the body, making it harder for cancer cells to establish metastases. During high-intensity aerobic activity, muscles and internal organs (like the lungs, liver, and lymph nodes) ramp up their glucose uptake and mitochondrial activity to meet elevated energy demands. This effectively "reprograms" these organs into highly efficient metabolic states, causing them to consume more nutrients and outcompete potential metastatic tumor cells for available glucose, a key energy source that cancer cells rely on for proliferation and spread. In essence, the exercise creates a nutrient-scarce environment in these organs, starving nascent metastases and reducing their ability to grow.
Supporting this, the animal model using mice demonstrated similar effects: those trained with progressive high-intensity treadmill sessions before melanoma cell injection had significantly fewer metastases in distant organs. Proteomic and metabolic analyses revealed enhanced glucose transporters (GLUT proteins) and catabolic processes in the organs of exercised mice, confirming the nutrient competition hypothesis. While the study focused on melanoma in mice, the human data encompassed various cancers, indicating broader applicability; however, it noted a more modest impact on primary (non-metastatic) tumors.
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