Figure 1.

Adaptive homeostasis in exercise training. Reactive oxygen and nitrogen species such as ${\text{O}}_2^{•-}$, H₂O₂, and NO^• activate cytoplasmic signaling proteins such as Nrf2, NFκB, TFAM, and PGC1α to translocate to the cell nucleus where they bind to upstream promoter regions of hundreds of target genes to initiate transcription and (ultimately) translation. The protein products of these target genes include mitochondrial proteins encoded in the nucleus, leading to mitochondria biogenesis, and numerous other adaptive and protective proteins. These changes in gene expression and increased mitochondrial biogenesis (in addition to other metabolic alterations) lead to increased exercise endurance capacity. The training effect is a transient process of expanding the range of adaptive homeostasis and it only lasts as long as the training stimulus is maintained. If training is discontinued then detraining results in adaptive homeostasis returning the range of endurance capacity to pre-training levels.