Rachel Perry, PhD, has spent most of her scientific life thinking about how the body moves energy around—how glucose rises and falls, how tissues compete for fuel, and how metabolism shifts during illness.
That curiosity began early. Growing up with type 1 diabetes meant she learned to track biological changes with almost clinical precision, forming what she now recognizes as the beginnings of a career in metabolic research.
Today, as an associate professor of medicine (endocrinology and metabolism) and of cellular and molecular physiology at Yale School of Medicine, Perry investigates how those same metabolic forces influence cancer. Her newest study, published in Proceedings of the National Academy of Sciences, reveals one of the clearest mechanisms to date behind a question patients often ask: Why does exercise seem to protect people against cancer?
In the study, Perry’s team used metabolic tracers in mouse models of breast cancer and melanoma to learn how glucose—a nutrient that tumors use to fuel rapid cell division—is distributed when the body is active.
The answer, they found, is that working muscles effectively outcompete tumors for the glucose supply. Because muscle contraction increases glucose uptake, exercise shifts metabolism, causing tumors to receive less of the fuel they need to grow.
That shift happened even when the mice exercised modestly. Even low levels of activity were enough to produce metabolic changes in certain tumor models.
“What this means is that any amount of activity a person can manage may be beneficial,” Perry says. “If someone is completely sedentary, simply starting to go for walks a couple of times a week may have a beneficial effect.”
Another layer emerged when the team measured VO₂ peak, a standard assessment of aerobic fitness. Fitness level sometimes predicted metabolic changes more clearly than exercise alone, suggesting that maintaining or improving fitness, even slightly, may be a key factor in how the body responds to tumors.
For many patients, vigorous physical activity isn’t realistic during treatment. Perry hopes the findings help shift expectations toward something more attainable. The study offers a biological explanation for why movement—even gentle or intermittent movement—may help slow tumor growth.
“A little bit of an improvement in fitness is advantageous,” Perry says. “The type and amount of exercise required to have a beneficial effect may be quite doable for many patients.”
Perry’s lab is now working to identify blood biomarkers that reflect the metabolic changes seen in muscle and tumor tissue. That work could pave the way for studies in people. But for now, her study underscores a simple, empowering idea: Movement, in any amount a patient can manage, may change the body’s internal landscape in ways that make it harder for tumors to thrive.
Other Yale authors include Brooks Leitner, Andim Fosam, Kaylee Zilinger, Susana Nakandakari, Xinyi Zhang, Rafael Gaspar, Wanling Zhu, and Curtis Perry.
Endocrinology and Metabolism is one of 10 sections in the Yale Department of Internal Medicine, and works to improve the health of individuals with endocrine and metabolic diseases by advancing scientific knowledge, applying new information to patient care, and training the next generation of physicians and scientists.
Avi Patel is a communications intern, Internal Medicine, Yale School of Medicine.
Editor’s note: This story is used in cooperation with Yale School of Medicine. The research reported in this news article was supported by the National Institutes of Health (awards R21CA275978 and R37CA258261) and Yale University. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.