Exercise-induced hormesis describes the phenomenon where a low-to-moderate dose of physiological stress from physical activity triggers an adaptive, beneficial response in the body that enhances cellular resilience and overall health. This beneficial stressor, or eustress, stimulates repair mechanisms and antioxidant defenses, ultimately leading to a net improvement in hormonal signaling and metabolic function. The principle highlights that the dose of exercise determines whether the outcome is therapeutic or detrimental.
Origin
The concept combines “exercise,” referring to physical exertion, with “hormesis,” a term from toxicology that describes a dose-response phenomenon where a low dose of an agent that is otherwise inhibitory or toxic stimulates a beneficial effect. Its application to exercise science recognizes that the transient oxidative stress and mild damage caused by physical activity initiate a robust overcompensation by the body’s repair systems, including the endocrine and immune systems.
Mechanism
The mechanism involves the acute stress of exercise stimulating the release of reactive oxygen species (ROS) and mild cellular damage, which in turn activates stress-response pathways like Nrf2 and AMPK. Activation of these pathways upregulates the production of endogenous antioxidants and chaperones, enhances mitochondrial biogenesis, and improves insulin receptor sensitivity. This cellular adaptation, driven by the transient hormonal changes of exercise, results in improved glucose control and increased resistance to chronic oxidative stress.
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