The Concept of Cellular Exercise
Researchers here coin a term, cellular exercise, to describe the benefits resulting from mild cellular stress and the consequent housekeeping responses. Increased cellular maintenance activities in response to mild stress lead to a net improvement in cell and tissue function. In short-lived laboratory species, interventions that provide chronic mild stress, such as calorie restriction, improve long term health and increase life span. Interventions based on this approach may be less interesting in long-lived species such as our own, however, given that, for example, calorie restriction provides up to 40% extension of life in mice, but at most a few years in humans.
"Cellular exercise" is a concept where low levels of cellular stress, induced by chronic calorie restriction or physical exercise, can lead to molecular adaptations on the cellular level that can protect the body from cancer and cardiovascular disease. An increase in reactive oxygen species induced by caloric restriction and physical exercise can produce improvements in redox equilibrium that can result in a more adaptive capable cell.
Insulin-like growth factor-1 has a dual effect wherein calorie restriction downregulates insulin-like growth factor-1 inhibiting pathways of carcinogenic proliferation and metastasis and physical exercise can upregulate insulin-like growth factor-1 to promote mitochondrial biogenesis and protein synthesis thereby strengthening healthy muscle against hypoxic ischemic damage and muscular regenerative properties. Transcription of Nrf2 is also upregulated to attenuate inflammation induced by nuclear factor-κB, AMPK upregulates genes through PGC-1α to prevent sarcopenia and induce lipolysis.
This molecular melody is the complex composition that explains the cellular adaption that occurs to strengthen the body from cognitive dysfunction, cardiometabolic failure and carcinogenic implantation and metastasis via mechanisms of redox equilibrium, oxidative protection, attenuation of inflammation, and attenuation of carcinogenic proliferation and growth.
In the recent debates between AdG and Charles Brenner and on Twitter, Charles has been claiming that CR doesn't significantly increase mouse lifespan, or perhaps at all. His claim is that the controls are allowed to eat as much as they want and that this is reducing their lifespan significantly. He seems to claim that the CR life extension is only seen due to the poor care of the controls. He shows a graphic of the Rapamycin controls living nearly as long as the CR mice and claims they are the same mice, genetically. So, if the controls in one experiment live nearly as long as the supposed beneficiaries of CR, CR must not be doing much. I realize CR isn't expected to do much for long-lived species lifespan, but it still seems a potentially important point. @Reason, what are your thoughts on this? Am I understanding correctly?
I like the term 'cellular exercise'