According to scientists, intense aerobic exercise increases the consumption of glucose (sugar) by the internal organs, thereby reducing the availability of energy for the tumor's internal organs, thereby reducing the availability of energy for the tumor.
Studies have shown that physical exercise reduces the risk of some types of cancer 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 add new insight, showing that high-intensity aerobic exercise that gets its energy from sugar can reduce the risk of metastatic cancer by up to 72%.
If until now the general message to the public has been "be active, be healthy", now we can 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 in a rigorous exercise regimen with data from healthy human volunteers examined before and after running. Human data, obtained from an epidemiological study that followed 3,000 individuals for about 20 years, indicated 72% less metastatic cancer in participants who reported regular high-intensity aerobic activity compared to those who did not engage in physical exercise.
An animal model showed a similar result, which also allowed researchers to identify its underlying mechanism. Taking samples from 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, lungs and liver.
The researchers hypothesized that, in both humans and animal models, this beneficial outcome was related to the increased rate of glucose consumption induced by exercise.
The study is the first to examine the impact of exercise on internal organs where metastases typically develop, such as the lungs, liver, and lymph nodes.
In examining the cells of these organs, we found an increase in the number of glucose receptors during high-intensity aerobic activity - increasing glucose uptake and turning the organs into efficient energy-consuming machines, very similar to muscles.
We hypothesize that this occurs because organs have to compete for sugar sources with muscles, which are known to burn large amounts of glucose during physical exercise.
Consequently, if cancer develops, fierce competition for glucose reduces the availability of energy, which is critical for metastasis. Moreover, 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 activity are good for our health.
Our internal organ study found that exercise changes the whole body so that cancer cannot spread and the primary tumor also shrinks.
Our results show that unlike fat-burning exercise, which is relatively mild, it is a high-intensity aerobic activity that helps prevent cancer. If the optimal intensity range for burning fat is 65-70% of your maximum heart rate, burning sugar requires 80-85% - even if only for short intervals.
For example, a one-minute sprint followed by a walk, then another sprint. In the past, such intervals were mostly typical of athletes' training regimens, but today we 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 future studies will enable personalized medicine to prevent specific cancers, with doctors reviewing family history and recommending 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 medication or medical intervention to date. An exercise-induced metabolic shield in distant organs blocks cancer progression and metastatic spread. Exercise prevents cancer incidence and recurrence, but the underlying mechanism of this relationship remains largely unknown.
Here, we report that exercise induces metabolic reprogramming of internal organs that increases nutrient requirements and protects against metastatic colonization by limiting nutrient availability to the tumor, creating an exercise-induced metabolic shield.
Proteomics and ex viva metabolic capacity analyzes of mouse internal organs revealed that exercise induced catabolic processes, glucose uptake, mitochondrial activity and GLUT expression. Proteomics analysis of routinely active human subject plasma demonstrated increased utilization of carbohydrates after exercise.
Epidemiological data from a 20-year prospective study of a large human cohort of initially cancer-free participants revealed that exercise before the onset of cancer had a modest impact on the incidence of low-metastatic cancer, but significantly reduced the likelihood of highly metastatic cancer.
In three melanoma mouse models, exercise before cancer injection significantly protected against metastasis in distant organs.
The protective effects of exercise were dependent on m TOR activity, and inhibition of the m TOR pathway by ex viva rapamycin treatment reversed the exercise-induced metabolic shield. Under glucose-limited conditions, active stroma consumed significantly more glucose at the expense of the tumor.
Collectively, these data suggest a clash between cancer metabolic plasticity and stress-induced stromal metabolic reprogramming, providing an opportunity to block metastasis by challenging the tumor's metabolic needs.
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