Estrogen upregulates OT and OT receptor (OTR) production
testosterone promotes both OTR binding in the hypothalamus (Johnson et al., 1991) as well as production of AVP (Delville et al., 1996), which has many opponent actions to OT
men and women show differences in plasma OT levels
Alterations in the HPA and hypothalamic-pituitary-gonadal axes with a resultant decrease in testosterone:cortisol ratios have been implicated in OTS. Proinflammatory cytokines are potent activators of the HPA system, which cause release of corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol. These cytokines suppress testosterone through central inhibition
Some have suggested that a decreased testosterone:cortisol ratio can be diagnostic of NFO and/or OTS. However, the ratio represents the physiologic strain of training rather than the athlete’s maladaption to that stress
Cortisol (catabolic and anti-inflammatory) is converted to inactive cortisone by 11β-HSD2
A prospective study found a clinically significant increase in overnight urinary cortisol:cortisone ratio during a high training load period in triathletes, who subsequently underperformed and reported fatigue
It is proposed that cytokines may inhibit 11β-HSD2 activity and result in relative increases in cortisol and, hence, catabolism
Review of the evidence of OTS versus overreaching. Academic points about the difference really. This are both dysfunctional physiologies and they need to be approached the same.
Older article, but good one still on hormones and overtraining. Look to the Testosterone/Cortisol ratio. OTS will lead to decreased Testosterone and increased cortisol resulting in chronic catabolic state.
Over training syndrome and its effects on cortisol, SHBG, and IGF-1; or as they authors call it overreaching. The study contrasted OR versus basic training.