The cumulative burden placed upon the HPA axis, the body’s central stress response system, resulting from chronic physiological, psychological, or inflammatory stressors. High load indicates sustained activation of this axis, leading to prolonged elevations in circulating cortisol and associated downstream endocrine disruption. Understanding this load is key to assessing chronic adaptive capacity.
Origin
This term is a direct descriptor from neuroendocrinology, referencing the anatomical components: Hypothalamus, Pituitary, and Adrenal glands. ‘Load’ quantifies the aggregate impact of stressors that demand sustained HPA axis engagement.
Mechanism
The mechanism involves sustained CRH release from the hypothalamus stimulating ACTH from the pituitary, which drives cortisol production by the adrenals. Chronic overstimulation can lead to glucocorticoid receptor desensitization or dysregulation of diurnal rhythmicity. This sustained signaling alters metabolic partitioning and immune function over time.
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