Overview: Aerobic exercise reduces the risk of metastatic cancer by increasing glucose consumption.
sauce: Tel Aviv University
A new study from Tel Aviv University found that aerobic exercise reduces the risk of metastatic cancer by 72%.
According to researchers, intense aerobic exercise increases visceral glucose (sugar) consumption, thereby reducing the availability of energy to tumors.
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 Sports Institute. Professor Levy emphasizes that the combined scientific know-how of TAU’s various schools has led the new research to very important discoveries that may help prevent metastatic cancer. It is the leading cause of death in Israel.
A paper was published in a prominent journal cancer research Selected for the cover of the November 2022 issue.
Professor Levy and Dr. Gepner: “Studies have demonstrated that exercise reduces the risk of certain types of cancer by up to 35%. Similar effects: This study adds new insights showing that high-intensity aerobic exercise, powered by sugar, can reduce the risk of metastatic cancer by as much as 72%.
“So far, if the general message to the general public has been ‘stay active and be healthy,’ how does aerobic exercise prevent the most aggressive and metastatic types of cancer?” We can now explain how we can maximize it.”
The study combined data from an animal model in which mice were trained under a rigorous exercise regimen with healthy human volunteers tested before and after running.
Human data from an epidemiological study that monitored 3,000 people for approximately 20 years showed that participants who reported regularly engaging in vigorous-intensity aerobic showed 72% less metastatic cancer.
Animal models have shown similar results, and researchers have also been able to identify the underlying mechanisms. A sampling showed that aerobic exercise significantly reduced the incidence of lymph node, lung, and liver metastatic tumors.
The researchers hypothesized that this favorable outcome was related to an exercise-induced increase in the rate of glucose consumption in both humans and model animals.
Professor Levy: “Our study is the first to investigate the effects of exercise on internal organs where metastasis usually occurs, such as lungs, liver and lymph nodes.
“When we looked at the cells in these organs, we found that the number of glucose receptors increased during high-intensity aerobic exercise. It turns into an energy-consuming machine.
“We believe this happens because the muscles and organs, which are known to burn large amounts of glucose during exercise, have to compete for sugar resources.
“As a result, when cancer does occur, intense competition for glucose reduces the availability of energy, which is essential for metastasis. Moreover, if a person exercises regularly, this condition becomes permanent.” The tissue of the internal organs changes and becomes similar to muscle tissue.We all know that sports and exercise are good for our health.
“In our study looking at the internal organs, we found that exercise changed the whole body, preventing cancer from spreading and also reducing the size of primary tumors.”
Dr. Gepner adds: If the optimal intensity range for fat burning is 65-70% of maximum pulse rate, he needs 80-85% for sugar burning – even for short intervals.
“For example, one minute of sprinting followed by walking, then another sprinting. , is also found in other exercise routines.
“Our results suggest that healthy people should also include a high-intensity component in their fitness program. We believe that this will enable personalized medicine to prevent specific cancers.
“It must be emphasized that exercise, due to its unique metabolic and physiological effects, exhibits a higher level of cancer prevention than any previous medication or medical intervention.”
About this cancer and exercise research news
author: Noga Shahar
sauce: Tel Aviv University
contact: Noga Shahar – Tel Aviv University
image: image is public domain
See also
Original research: closed access.
“Exercise-induced Metabolic Shielding of Remote Organs Blocks Cancer Progression and Metastatic Dissemination” by Carmit Levy et al. cancer research
Overview
Exercise-induced metabolic shielding of distant organs blocks cancer progression and metastatic dissemination
Exercise prevents cancer initiation and recurrence, but the underlying mechanisms behind this relationship are poorly understood.
Here, we show that exercise induces metabolic reprogramming of internal organs, increases nutrient demand, prevents metastatic colonization by limiting nutrient availability to tumors, and generates an exercise-induced metabolic shield. report to
Proteomic and ex vivo metabolic capacity analyzes of mouse internal organs revealed that exercise induced catabolic processes, glucose uptake, mitochondrial activity and GLUT expression. Proteomic analysis of plasma from routinely active human subjects showed 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 pre-cancer exercise is associated with less metastatic stage cancer development. It was found to have a small impact on rates, but a significant reduction in the likelihood of metastatic cancer.
In three models of melanoma in mice, exercise prior to cancer injection significantly prevented metastasis to distant organs.
The protective effects of exercise depended on mTOR activity, and inhibition of the mTOR pathway by ex vivo rapamycin treatment reversed exercise-induced metabolic shielding. Under glucose-limited conditions, active stroma consumed more glucose at the expense of tumor.
Taken together, these data suggest a conflict between metabolic plasticity in cancer and exercise-induced metabolic reprogramming of the stroma, enhancing the chances of blocking metastasis by challenging the metabolic needs of tumors. increase.
