Summary: Aerobic exercise reduces the risk of metastatic cancer by increasing glucose consumption.
Font: Tel Aviv University
A new study from Tel Aviv University found that aerobic exercise can reduce the risk of metastatic cancer by 72%.
According to the researchers, intense aerobic exercise increases glucose (sugar) consumption from internal organs, thereby reducing energy availability to the tumor.
The study was led by two researchers from TAU’s Sackler School of Medicine: Prof. Carmit Levy from the Department of Human Genetics and Biochemistry and Dr. Yftach Gepner from the Sylvan Adams School of Public Health and Sports Institute. Prof. Levy emphasizes that by combining scientific insights from different TAU schools, the new study has led to a very important discovery that can help prevent metastatic cancer, the leading cause of death in Israel.
The article was published in the prestigious magazine cancer research and chosen for the cover of the November 2022 issue.
Prof. Levy and Dr. Gepner: “Studies have shown that physical exercise reduces the risk of some types of cancer by up to 35%. This positive effect is similar to the impact of exercise on other conditions, such as heart disease and diabetes. In this study, we add new insights, showing that high-intensity aerobic exercise, which gets its energy from sugar, can reduce the risk of metastatic cancer by up to 72%.
“If until now the general message to the public has been ‘stay active, stay healthy,’ we can now explain how aerobic activity can maximize prevention of the most aggressive and metastatic cancers.”
The study combined an animal model in which mice were trained under a strict exercise regimen, with data from healthy human volunteers examined before and after running.
Human data, obtained from an epidemiological study that followed 3,000 people for about 20 years, indicated 72% fewer metastatic cancers in participants who reported regular high-intensity aerobic activity, compared with those who did not engage in physical exercise.
The animal model exhibited a similar result, which also allowed the researchers to identify its underlying mechanism. Taking samples from the internal organs of physically fit animals, before and after physical exercise, and also after cancer injection, they found that aerobic activity significantly reduced the development of metastatic tumors in the lymph nodes, lungs, and liver. .
The researchers hypothesized that in both human and animal models, this favorable outcome is related to the increased rate of exercise-induced glucose consumption.
Prof. Levy: “Our study is the first to investigate the impact of exercise on internal organs where metastases normally develop, such as the lungs, liver and lymph nodes.
“By examining the cells of these organs, we found an increase in the number of glucose receptors during high-intensity aerobic activity, which increases glucose intake and turns the organs into effective energy-consuming machines, much like the muscles.
“We hypothesize that this happens because the organs must compete for sugar resources with the muscles, which are known to burn large amounts of glucose during physical exercise.
“Consequently, if cancer develops, the fierce competition for glucose reduces the availability of energy that is critical for metastasis. Also, when a person exercises regularly, this condition becomes permanent – the tissues of internal organs change, becoming similar to muscle tissue. We all know that sport and physical exercise are good for our health.
“Our study, looking at the internal organs, found that exercise changes the whole body so that the cancer can’t spread and the primary tumor shrinks as well.”
Dr. Gepner adds: “Our results indicate that, unlike exercise to burn fat, which is relatively moderate, it is high-intensity aerobic activity that helps prevent cancer. If the optimal intensity range for fat burning is 65-70% of maximum pulse rate, burning sugar requires 80-85%, even if only for short bursts.
“For example: a minute sprint followed by walking, then another sprint. In the past, such intervals were mostly typical of athletes’ training regimens, but today we also see them in other exercise routines, such as cardiac and pulmonary rehabilitation.
“Our results suggest that healthy people should also include high-intensity components in their fitness programs. We believe that future studies will enable personalized medicine to prevent specific cancers, with doctors reviewing family history to recommend the right type of physical activity.
“It must be emphasized that physical exercise, with its unique metabolic and physiological effects, shows a higher level of cancer prevention than any drug or medical intervention to date.”
About this news about cancer research and exercise
Author: Noga Shahar
Font: Tel-Aviv University
Contact: Noga Shahar – Tel Aviv University
Image: The image is in the public domain.
See also
original research: closed access.
“An exercise-induced metabolic shield in distant organs blocks cancer progression and metastatic spread” by Carmit Levy et al. cancer research
Summary
An exercise-induced metabolic shield in distant organs blocks cancer progression and metastatic spread
Exercise prevents cancer incidence and recurrence, but the underlying mechanism behind this relationship remains largely unknown.
Here we report that exercise induces metabolic reprogramming of internal organs that increases nutrient demand and protects against metastatic colonization by limiting nutrient availability to the tumor, generating an exercise-induced metabolic shield.
Ex vivo metabolic capacity and proteomic analyzes of murine internal organs revealed that exercise induces catabolic processes, glucose uptake, mitochondrial activity, and GLUT expression. Plasma proteomic analysis of routinely active human subjects demonstrated increased carbohydrate utilization after exercise.
Epidemiologic data from a 20-year prospective study of a large human cohort of initially cancer-free participants revealed that exercise prior to cancer onset had a modest impact on the incidence of low-metastatic stage cancer but significantly reduced the likelihood of highly metastatic cancer.
In three mouse models of melanoma, exercise prior to cancer injection significantly protected against metastasis in distant organs.
The protective effects of exercise were dependent on mTOR activity, and inhibition of the mTOR pathway with ex vivo rapamycin treatment reversed exercise-induced metabolic shielding. Under glucose-limited conditions, the active stroma consumed significantly more glucose at the expense of the tumor.
Taken together, these data suggest a clash between cancer metabolic plasticity and exercise-induced stromal metabolic reprogramming, raising the opportunity to block metastasis by challenging the metabolic needs of the tumor.
