Introduction
Cancer continues to be a significant global health issue, with traditional genetic-based approaches to understanding and treating cancer having limited success. Researchers are increasingly exploring the impact of the environment, specifically inflammation and metabolism, on cancer development. This article reviews the literature on the role of mitochondria in metabolic health, physical activity, and cancer.
Mitochondria and Metabolic Health
Mitochondria are essential organelles that perform a wide range of functions within cells, such as producing ATP and metabolic intermediates, as well as assisting in cellular stress responses. They are intricately interconnected with other cellular components and are vital for energy metabolism in eukaryotic cells. Mitochondria generate the majority of the usable energy in cells through the breakdown of carbohydrates and fatty acids through a process called oxidative phosphorylation.
Mitochondria regulate cellular processes, such as metabolic adaptation, calcium homeostasis, and cell proliferation or death. They also participate in reactions, such as the tricarboxylic acid cycle (TCA), fatty acid oxidation (FAO), and oxidative phosphorylation (OXPHOS), which play a role in processes, such as ketogenesis, gluconeogenesis, heme biosynthesis, and Fe/S cluster formation. Given the many roles of mitochondria, their potential dysfunction or alteration is closely linked to a wide range of diseases, including cancer.
Mitochondrial Fitness and Cancer
The concept of “mitochondrial fitness” refers to the biological efficiency and adequacy of the mitochondria. This mitochondrial fitness can be divided into function and quality, both of which can be improved through physical exercise and nutrition. Mitochondrial fitness includes mitochondrial biogenesis, mitochondrial respiration, mitochondrial protein synthesis, increased reliance on fatty acid substrates by mitochondria, and better handling of oxidative stress. These processes result in the creation of new mitochondria, increased energy, vitality, and stamina, replacement of damaged mitochondria, prevention of associated diseases, and slower aging.
The development of cancer is linked to metabolic and mitochondrial alterations, which are closely related to epigenetics, which are largely modifiable factors that can act as triggers for the activation and expression of certain proteins that regulate metabolic pathways related to cancer. In other words, the presence of certain genes does not necessarily cause cancer, but rather external conditioning factors, such as epigenetics, determine whether a gene related to cancer is activated or not.
Metabolism and Cancer
One of the hallmark characteristics of tumor cells is their ability to undergo metabolic reprogramming, which allows them to fulfill their high biosynthetic demands and sustain unchecked growth. In contrast, normal differentiated cells utilize mechanisms, such as oxidative phosphorylation, to generate the energy and biomass necessary for cellular processes. However, unlike normal tissues, most cancer cells alter their metabolism to primarily rely on aerobic glycolysis after the energy regulation and reprogramming process. This phenomenon is known as the Warburg effect.
Tumor cells can bypass metabolic constraints by acquiring genetic mutations, such as tumor suppressors and oncogenes. These genetic changes can occur in cells throughout an individual’s lifespan and can alter the signaling pathways that control metabolic programming. Abnormal changes in these signaling pathways lead to increased nutrient uptake and metabolism, which are necessary for producing the energy required for survival and cell proliferation.
Oxidative Stress
Numerous substances are produced during oxidative metabolism, which generates energy in the mitochondria through aerobic respiration. While most of these compounds are beneficial, less than 5% of them may be harmful to cells if their concentration increases. These low-concentration products of oxidative metabolism are essential for subcellular processes, such as signal transduction, enzyme activation, gene expression, and disulfide bondformation during protein folding in the endoplasmic reticulum.
Reactive oxygen species (ROS), such as the superoxide anion (O2−), hydrogen peroxide (H2O2), hydroxyl radical (OH−), singlet oxygen (1O2), and ozone (O3), can cause oxidative stress when the balance between pro-oxidants and antioxidants is disrupted, leading to the alteration and damage of intracellular molecules, such as DNA, RNA, lipids, and proteins.
Physical Activity and Cancer
Engaging in high-energy-demanding movement, such as exercise, is a powerful intervention for improving mitochondrial function and increasing resistance to environmental stressors. Physical exercise and nutrition are among the epigenetic protectors that can be implemented and modified to improve metabolic and mitochondrial health.
Exercise appears to offer protection against the disease, reducing the risk of cancer by 10 to 25%. This is because exercise improves mitochondrial function, which includes mitochondrial biogenesis, mitochondrial respiration, mitochondrial protein synthesis, increased reliance on fatty acid substrates by mitochondria, and better handling of oxidative stress. These processes result in the creation of new mitochondria, increased energy, vitality, and stamina, replacement of damaged mitochondria, prevention of associated diseases, and slower aging.
Conclusion
The role of mitochondria in metabolic health, physical activity, and cancer is significant. Mitochondrial fitness, which can be improved through physical exercise and nutrition, plays a crucial role in cell metabolism, particularly their oxidative functions, and how proper function can prevent replication errors and regulate apoptosis.
Further research is required to fully understand the mechanisms by which physical activity improves mitochondrial function and potentially reduces the risk of cancer. This understanding can contribute to a better comprehension of this intricate illness and guide the development of new research methods and clinical interventions.
In conclusion, considering the role of the environment, specifically inflammation and metabolism, in cancer development and treatment is of utmost importance. The findings of this study support the significance of this consideration and highlight the importance of physical activity in improving mitochondrial function and potentially reducing the risk of cancer.
