Summary: Aerobic exercise increases glucose utilization and reduces the risk of metastatic cancer.

Source: Tel Aviv University

A new study at Tel Aviv University found that aerobic exercise can reduce the risk of metastatic cancer by 72 percent.

According to the researchers, intense aerobic exercise increases glucose consumption by the internal organs, reducing the energy supply to the tumor.

The study was led by two researchers from TAU’s Sackler Faculty of Medicine: 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. Prof. Levy, combining scientific knowledge from different schools in TAU, emphasized that the new research has led to a very important discovery, which is metastatic cancer – the leading cause of death in Israel.

The paper was published in a famous journal Cancer research And was selected for the cover of the November 2022 issue.

Professor Levy and Dr. Geppner: “Studies show that exercise can reduce the risk of some types of cancer by 35 percent.” This positive effect is similar to the effect of exercise on other conditions such as heart disease and diabetes. We add new insight to this study, which shows that high-intensity aerobic exercise that gets its energy from sugar can reduce the risk of metastatic cancer by 72 percent.

If “the overall message to the public so far is be active, be healthy,” we can now explain how aerobic activity can prevent the most aggressive and metastatic forms of cancer.

The study combined an animal model in which rats were trained in rigorous exercise by examining data from healthy human volunteers before and after running.

Human data from an epidemiological study that followed 3,000 individuals for nearly 20 years indicated that participants who reported high levels of regular aerobic activity had a 72% lower risk of metastatic cancer compared to those who did not.

An animal model has shown similar results, and allows the researchers to identify the underlying mechanism. By sampling the viscera of exercising animals before and after exercise and following cancer injection, they found that aerobic exercise significantly reduced the growth of metastatic tumors in the lymph nodes, lungs, and liver.

The researchers hypothesized that this beneficial effect in both humans and animal models was related to the amount of glucose consumption produced by exercise.

Professor Levy: “Our study is the first to examine the effects of exercise on internal organs such as the lungs, liver and lymph nodes.

“When we analyzed the cells of these organs, we found that during high aerobic activity, the number of glucose receptors increased – increasing glucose levels and turning the organs into efficient energy-consuming machines, like muscles.

We hypothesize that organs known to burn large amounts of glucose during exercise must compete with muscles for glucose resources.

“Therefore, if a cancer develops, the intense competition for glucose reduces the energy supply that is essential for metastasis. Moreover, when a person exercises regularly, this condition becomes permanent. We know.

“Our study of the internal organs showed that exercise changes the whole body, so that the cancer does not spread and the original tumor shrinks in size,” he said.

This shows a person running.
The researchers hypothesized that this beneficial effect in both humans and animal models was related to the amount of glucose consumption produced by exercise. The image is in the public domain.

Dr. Geppner added, “Our results suggest that, in contrast to burning fat, exercise is a relatively moderate, high-intensity aerobic activity that can help prevent cancer.” If the ideal weight for burning fat is 65-70% of your maximum heart rate, burning sugar requires 80-85% – even for short periods of time.

“For example: a minute of jogging followed by walking, then another run. In the past, such intervals were common in most athletes’ training regimens, but today we see them in other forms of exercise such as cardio and lung rehabilitation.

“Our results suggest that healthy individuals should include a high-intensity component in their exercise programs. We believe that future studies will enable personalized treatment to prevent specific cancers. Physicians can evaluate family history to recommend the right exercise regimen.”

It should be emphasized that exercise, through its unique metabolic and physiological effects, shows a higher level of cancer prevention than any drug or medical intervention.

About cancer and exercise research news

Author: Noga city
Source: Tel Aviv University
Contact: Noga Shahar – Tel-Aviv University
Image: The image is in the public domain.

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Preliminary study: Closed access.
Exercise-induced metabolic shielding in distant organs inhibits cancer growth and metastatic spread.” by Carmit Levy et al. Cancer research


Exercise-induced metabolic shielding in distant organs inhibits cancer growth and metastatic spread.

Exercise can prevent the occurrence and recurrence of cancer, but the underlying mechanism behind this relationship is largely unknown.

Here we report that exercise induces visceral metabolism and induces an exercise-induced metabolic shield that increases appetite and limits the supply of nutrients from the metastatic tumor.

Proteomic and ex vivo metabolic capacity analysis of murine visceral exercise induces catabolic processes, glucose uptake, mitochondrial activity and GLUT expression. Proteomic analysis of plasma from normally active human subjects revealed increased carbohydrate utilization following exercise.

Epidemiological data from a large cohort of cancer-free people in a 20-year study showed that exercise before cancer had a modest effect on the incidence of low-metastatic cancers but significantly reduced the risk of high-stage metastatic cancers.

In three melanoma models in mice, exercise prior to cancer injection significantly protected tumor metastasis in distant organs.

The protective effects of exercise are dependent on mTOR activity, and inhibition of the mTOR pathway by rapamycin treatment ex vivo 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 indicate a conflict between cancer metabolic plasticity and the exercise-induced stromal metabolic program, which counteracts the tumor’s metabolic demands and creates an opportunity to inhibit metastasis.

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