Summary: Aerobic exercise reduces the risk of metastatic cancer by increasing glucose consumption.
Source: Tel Aviv University
A new study at Tel Aviv University has found that aerobic exercise can reduce the risk of metastatic cancer by 72%.
According to the researchers, high-intensity aerobic exercise increases the consumption of glucose (sugar) by internal organs, thereby reducing the availability of energy for the tumor.
The study was led by two researchers from the Sackler School of Medicine at TAU: Professor Carmit Levy from the Department of Human Genetics and Biochemistry and Dr. Yftach Gepner from the School of Public Health and the Sylvan Adams Sports Institute. Professor Levy points out that by combining scientific know-how from different TAU schools, the new study has led to a very important finding that could help prevent metastatic cancer – the leading cause of death in Israel.
The article was published in the prestigious journal Research against cancer and chosen for the cover of the November 2022 issue.
Pr Levy and Dr Gepner: “Studies have shown that physical exercise reduces the risk of certain 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 added new information, showing that high-intensity aerobic exercise, which derives its energy from sugar, can reduce the risk of metastatic cancer by up to 72%.
“If until now the general message to the public was ‘be active, be healthy’, we can now explain how aerobic activity can maximize the prevention of the most aggressive and metastatic types of cancer.”
The study combined an animal model in which mice were trained on 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 approximately 20 years, indicated 72% less metastatic cancer in participants who reported regular high-intensity aerobic activity, compared to those who have not engaged in physical exercise.
The animal model showed a similar result, also allowing researchers to identify its underlying mechanism. By sampling the internal organs of physically fit animals before and after exercise, as well as after cancer injection, they found that aerobic activity significantly reduced the development of metastatic tumors in the lymph nodes, the lungs and the liver.
The researchers hypothesized that in humans and animal models, this favorable outcome is related to the exercise-induced increase in the rate of glucose consumption.
Pr Levy: “Our study is the first to investigate the impact of exercise on the internal organs in which metastases usually develop, such as the lungs, liver and lymph nodes.
“Examining the cells of these organs, we found an increase in the number of glucose receptors during high-intensity aerobic activity – increasing glucose supply and turning the organs into efficient energy-consuming machines, while like muscles.
“We suspect this happens because the organs have to compete for sugar resources with the muscles, which are known to burn large amounts of glucose during exercise.
“Therefore, if cancer develops, fierce competition for glucose reduces the availability of essential energy for metastasis. Additionally, when a person exercises regularly, this condition becomes permanent: the tissues of the internal organs change and become similar to muscle tissue.We all know that sports and physical exercise are good for our health.
“Our study, looking at internal organs, found that exercise changes the whole body so cancer can’t spread, and the size of the primary tumor also decreases.”
Dr. Gepner adds, “Our results indicate that unlike fat-burning exercise, which is relatively mild, this is high-intensity aerobic activity that helps prevent cancer. While the optimal intensity range for fat burning is 65-70% of maximum heart rate, burning sugar requires 80-85%, even if only for brief intervals.
“For example: a one-minute sprint followed by a walk, then another sprint. In the past, these intervals were mostly typical of athlete training regimens, but today we also see them in other exercise programs, such as cardiac and pulmonary rehabilitation.
“Our results suggest that healthy individuals 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 looking at family history to recommend the right type of physical activity.
“It should be emphasized that exercise, with its unique metabolic and physiological effects, exhibits a higher level of cancer prevention than any drug or medical intervention to date.”
About this news about cancer research and exercise
Author: City of Noga
Source: Tel Aviv University
Contact: Noga Shahar – Tel Aviv University
Image: Image is in public domain
Original research: Access closed.
“An exercise-induced metabolic shield in distant organs blocks cancer progression and metastatic spread” by Carmit Levy et al. Research against cancer
Exercise-induced metabolic shield in distant organs blocks cancer progression and metastatic spread
Exercise prevents cancer incidence and recurrence, but the mechanism underlying this relationship remains mostly 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.
Proteomic and ex vivo metabolic capacity analyzes of murine internal organs revealed that exercise induces catabolic processes, glucose uptake, mitochondrial activity and GLUT expression. Proteomic analysis of plasma from regularly active human subjects has demonstrated increased carbohydrate utilization after exercise.
Epidemiological data from a 20-year prospective study of a large human cohort of initially cancer-free participants found that exercise before cancer initiation had a modest impact on cancer incidence at low metastatic stages, but significantly reduced the likelihood of highly metastatic cancer.
In three mouse models of melanoma, exercise before cancer injection significantly protected against metastasis to distant organs.
The protective effects of exercise depended on mTOR activity, and inhibition of the mTOR pathway with ex vivo rapamycin treatment reversed the exercise-induced metabolic shield. Under glucose-limited conditions, the active stroma consumed significantly more glucose at the expense of the tumor.
Together, these data suggest a conflict between cancer metabolic plasticity and exercise-induced metabolic reprogramming of the stroma, which opens up the possibility of blocking metastasis by challenging the metabolic needs of the tumor.
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