Summary: Aerobic exercise reduces the risk of metastatic cancer by increasing glucose consumption.
source: Tel Aviv University
A new study at Tel Aviv University found that aerobic exercise can reduce the risk of developing metastatic cancer by 72%.
According to researchers, intense aerobic exercise increases glucose (sugar) consumption of internal organs, thus reducing energy availability to the tumor.
The study was led by two researchers from the University of Washington School of Medicine, Professor Carmit Levy from the Department of Human Genetics and Biochemistry and Dr. Yiftach Gebner from the School of Public Health and the Sylvan Adams Mathematical Institute. Professor Levy stresses that by combining scientific knowledge from different schools at TAU, the new study has led to a very important discovery that may help prevent metastatic cancer – the leading cause of death in Israel.
The paper was published in the prestigious journal cancer research She was chosen for the cover of the November 2022 issue.
Prof. Levy and Dr. Gebner: “Studies have shown that physical exercise reduces the risk of some cancers by up to 35%. This positive effect is similar to the effect of exercise on other conditions, such as heart disease and diabetes. In this study we added new insight, showing that High-intensity aerobic exercise, which derives its energy from sugar, can reduce the risk of developing metastatic cancer by up to 72%.
“If the general message to the public so far has been ‘Be active, be healthy,’ we can now explain how aerobic activity can increase the prevention of the most aggressive and common types of cancer.”
The study combined an animal model in which mice were trained according to a strict exercise regimen, with data from healthy human volunteers examined before and after the run.
Human data, obtained from an epidemiological study that monitored 3,000 individuals for approximately 20 years, indicated a 72% reduction in the incidence of metastatic cancer in participants who reported regular aerobic activity at a high intensity, compared to those who did not exercise.
The animal model showed a similar result, which also enabled the researchers to determine the mechanism behind it. By taking samples from the internal organs of healthy animals, before and after physical exercise, as well as after cancer injections, they found that aerobic activity significantly reduced the development of metastases in the lymph nodes, lungs and liver.
The researchers hypothesized that in both humans and model animals, this positive outcome correlates with the enhanced rate of glucose consumption induced by exercise.
Professor Levy: “Our study is the first to look at the effect of exercise on the internal organs where metastases usually develop, such as the lungs, liver and lymph nodes.
“In examining the cells of these organs, we found a rise in the number of glucose receptors during high-intensity aerobic activity – increased glucose intake and the transformation of organs into efficient energy-consuming machinery, much like 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.
As a consequence, if cancer develops, fierce competition for glucose reduces the availability of energy necessary for metastasis to spread. Moreover, when a person exercises regularly, this condition becomes permanent: the tissues of internal organs change and become similar to muscle tissue. We all know that sports and physical exercise are good for our health.
“Our study, which examined the internal organs, discovered that exercise changes the whole body, so that the cancer does not spread, and the size of the primary tumor shrinks.”
Dr. Gibner adds: “Our results indicate that, unlike fat-burning exercise, 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 your maximum pulse rate, sugar burns Requires 80-85% – even if only for short periods.
“For example: a one-minute sprint followed by a walk, then another sprint. In the past, such intervals were mostly typical of athlete training regimens, but today we also see them in other exercise routines, such as cardiopulmonary 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 clinicians 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 cancer and practice research news
author: Shahar Nougat
source: Tel Aviv University
Contact: Noga Shahar – Tel Aviv University
picture: The image is in the public domain
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“Exercise-induced metabolic shield in distant organs prevents cancer development and metastasisWritten by Carmit Levy et al. cancer research
Exercise-induced metabolic shield in distant organs prevents cancer development and metastasis
Exercise prevents cancer from occurring and recurring, yet the mechanism behind this relationship remains mostly unknown.
Here we report that exercise stimulates metabolic reprogramming of internal organs that increases nutrient demand and protects against metastatic colonization by reducing nutrient availability to the tumor, generating an exercise-induced metabolic shield.
Protein metabolic capacity and ex vivo analyzes of rat internal organs revealed that exercise induces catabolic processes, glucose uptake, mitochondrial activity, and GLUT expression. Proteomic analysis of routinely active human plasma showed an increase in carbohydrate utilization after exercise.
Epidemiological data from a 20-year prospective study of a large human group of initially cancer-free participants revealed that pre-cancerous exercise had a modest effect on cancer incidence in low metastatic stages, but significantly reduced the likelihood of highly metastatic cancer.
In three mouse melanoma models, exercise prior to cancer injection significantly protected against metastases 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 took up more glucose at the expense of the tumor.
Collectively, these data suggest a clash between cancer metabolic plasticity and exercise-induced metabolic reprogramming of the stroma, increasing the chance of preventing metastasis by challenging the metabolic needs of the tumor.