Vertebrate performance and welfare easily becomes compromised.

Vertebrates faced with stressful stimuli launch an endocrine stress response

In a matter of minutes after the catecholamine ((nor)-adrenaline) release, glucocorticoids, cortisol or corticosterone in particular depending on the species, are released through activation of the hypothalamic-pituitary-interrenal (HPI) axis in fish or hypothalamic-pituitary-adrenal (HPA) axis in other vertebrates.

These plasma glucocorticoids elicit a suite of physiological and behavioral changes that allow the vertebrate to cope with altered situations, and are subsequently generally accepted as biomarker for stress.

Failure to regain homeostasis will lead to chronic stress and maladaptation and eventually to pathologies.

So when an organism cannot fully recover and becomes prone to detrimental effects of glucocorticoid mediated actions (e.g. immune suppression, decreased growth, decreased reproduction, increased mortality), an organism experiences the transition from allostatic load (when the stress can be overcome, ‘eustress’) to allostatic overload (when the stress cannot be overcome and tips over to ‘distress’). Both terms come from the concept of allostasis (constancy through change, i.e. resetting the set-points for homeostasis relative to environmental cues).

The adaptive value of short-term cortisol actions is widely recognized.

Far less is known about persistent stress and its mostly detrimental consequences for health, growth and reproduction.



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