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Figure 1

Figure 1. From: Inflammatory modulation of exercise salience: using hormesis to return to a healthy lifestyle.

The theoretical relationship between the biphasic hormetic curve and exercise salience. Regular hormetic stressors result in better mitochondrial function and increased resistance to oxidative stress, which translates into reduced inflammatory tone, improved metabolic flexibility and higher exercise salience. Without regular hormetic stressors and/or with chronic inflammation (e.g. from an injury or infection), an animal may cross a tipping point and remain in an inflammatory state due to a feed forward loop (1 and 2). In times of plenty (but with some stressors), it may exist in zone 3, where optimal energy storage occurs (mild inflammation induces insulin resistance) - but it is still relatively metabolic flexible. Beyond this, regular hormetic stressors would act to induce further exercise salience (zones 4 and 5). However, as hormetic stressors increased, damage would result in a gradual decrease in function and reducing exercise salience (6 and 7) until the animal had to slow down to recover (8). If excessive stress continued, it might develop chronic inflammation, and eventually succumb (9 and 10). The ability to resist transiting zones may be associated with an epigenetic shifting of the tipping point. In effect, an animal may adapt over time (or be preprogrammed from the preceding generations). In a non-hormetic environment, this would reinforce the inflammatory cycle, while in a hormetic environment, the anti-inflammatory cycle will predominate. Much of the Western society appears to reside in zone 2 due to a lack of hormesis and an excess of calories. Key to zones: 1 = inflammatory induced sickness behaviour; 2 = subclinical inflammation; 3 = remain sedentary and store food; 4 = active and seek food; 5 = migratory; 6 = late migratory; 7 = stress induced damage; 8 = sedentary recovery zone; 9 = inflammatory induced sickness behaviour; 10 = failure of systems and death.

Alistair V Nunn, et al. Nutr Metab (Lond). 2010;7:87-87.

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