Summary: Aerobic exercise reduces the risk of metastatic cancer by increasing glucose consumption.
resource: 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, high-intensity aerobic exercise increases the consumption of glucose (sugar) by the internal organs, thereby reducing the energy supply to the tumor.
The study was led by two researchers from TAU's Sackler School of Medicine: Professor Carmit Levy of the Department of Human Genetics and Biochemistry and Dr. Yftach Gepner of the School of Public Health and the Sylvan Adams Institute for Physical Education. Prof. Levy emphasized that by combining the scientific knowledge of the different faculties of TAU, the new study led to a very important discovery that may help prevent metastatic cancer – the leading cause of death in Israel.
Papers published in authoritative journals cancer research and was chosen to be on the cover of the November 2022 issue.
Prof. Levy and Dr. Gepner: “Studies have shown that physical activity can reduce the risk of certain types of cancer by up to 35%. This positive effect is similar to the effect of exercise on other diseases such as heart disease and diabetes.” In this study , we added new insights showing that high-intensity aerobic exercise that derives energy from sugar can reduce the risk of metastatic cancer by up to 72%.
“If the general message to the public so far has been ‘be active, be healthy', now we can explain how aerobic exercise can maximize protection against the most aggressive and metastatic forms of cancer.”
The study combined an animal model in which mice were trained under a rigorous exercise regimen with examination of data from healthy human volunteers before and after running.
Human data from an epidemiological study of 3,000 people over approximately 20 years showed that participants who reported regular high-intensity aerobic exercise had less metastatic cancer than those who did not engage in physical activity. 72% less.
Animal models showed similar results, also allowing the researchers to identify the underlying mechanism. They sampled the guts of healthy animals, before and after physical exercise, and after injecting cancer, and found that aerobic exercise significantly reduced the development of metastatic tumors in the lymph nodes, lungs, and liver.
The researchers hypothesize that this favorable outcome is related to an exercise-induced increase in the rate of glucose consumption in both humans and animal models.
Professor Levy: “Our study is the first to investigate the effects of exercise on internal organs where metastases commonly occur, such as the lungs, liver and lymph nodes.
“Examining the cells of these organs, we found that the number of glucose receptors increases during high-intensity aerobic exercise — increasing glucose intake and turning the organ into an efficient energy-expending machine, much like muscle.
“We hypothesize that this happens because the organ has to compete for sugar resources with the muscles, which are known to burn a lot of glucose during physical exercise.
“Thus, if a cancer develops, intense competition for glucose reduces the availability of energy that is vital for metastasis. Furthermore, when a person exercises regularly, this condition becomes permanent: the internal organs change and become Muscle tissue is similar.We all know that exercise and physical activity are good for our health.
“Our study, examining internal organs, found that exercise changes the entire body so that cancer cannot spread and the primary tumor shrinks in size.”
Dr. Gepner added: “Our results suggest that, unlike relatively mild fat-burning exercise, it is a form of high-intensity aerobic exercise that can help prevent cancer. If the optimal intensity range for fat-burning is 65 -70%, then 80-85% is needed for sugar burn – even if only for short intervals.
“Example: a minute of sprinting, followed by a walk, followed by another minute of sprinting. In the past, intervals like this were mostly typical of athlete training regimens, but today we see them in other workout routines too, such as CPR.
“Our results suggest that healthy people should also include high-intensity content in their fitness programs. We believe that future research will enable personalized medicine to prevent specific cancers, with doctors reviewing family history to recommend the right physical activity .
“It must be emphasized that physical activity has unique metabolic and physiological effects that lead to a higher level of cancer prevention than any drug or medical intervention to date.”
News about this cancer and exercise research
author: Noga Shahar
resource: Tel Aviv University
touch: Noga Shahar – Tel Aviv University
picture: This image is in the public domain
see also
Original research: closed access.
“Exercise-induced metabolic barriers in distant organs prevent cancer progression and metastatic dissemination” by Carmit Levy et al. cancer research
Abstract
Exercise-induced metabolic barriers in distant organs prevent cancer progression and metastatic dissemination
Exercise protects against cancer initiation and recurrence, but the mechanisms underlying this relationship remain poorly understood.
Here, we report that exercise induces metabolic reprogramming of internal organs to increase nutrient requirements and prevent metastatic colonization by limiting nutrient availability to tumors, resulting in an exercise-induced metabolic barrier.
Proteomic and ex vivo metabolic capacity analyzes of mouse guts revealed that exercise induces catabolic processes, glucose uptake, mitochondrial activity, and GLUT expression. Proteomic analysis of plasma from daily active human subjects reveals increased carbohydrate utilization after exercise.
Epidemiological data from a 20-year prospective study of a large human cohort of initially cancer-free participants show that exercise before cancer onset modestly affects cancer incidence in low-metastatic stages but significantly reduces the likelihood of highly metastatic cancers sex.
In three mouse models of melanoma, exercising before injecting cancer significantly prevented distant organ metastasis.
The protective effect of exercise depends on mTOR activity, and inhibition of the mTOR pathway by rapamycin treatment in vitro reversed exercise-induced metabolic barriers. Under glucose-limited conditions, the active stroma consumed significantly more glucose at the expense of the tumor.
Collectively, these data suggest a conflict between cancer metabolic plasticity and exercise-induced mesenchymal metabolic reprogramming, thereby increasing the chances of preventing metastasis by challenging the tumor's metabolic demands.
