Basal and Stimulated Cortisol Secretion
Under normal physiological conditions, cortisol secretion exhibits a robust circadian rhythm, with peak concentrations occurring in the early morning hours and declining progressively throughout the day. This basal secretion is tightly regulated by the negative feedback mechanisms of the HPA axis.
In response to acute stressors, cortisol secretion can increase rapidly—within minutes—from basal levels to several times the resting concentration. This acute surge provides the metabolic mobilisation necessary for immediate threat response. Once the stressor is removed, cortisol typically returns to basal levels within one to two hours, a process driven by negative feedback.
Chronic Stress and Altered Cortisol Patterns
When stress becomes chronic—persisting for weeks, months, or longer—the pattern of cortisol secretion can deviate substantially from the normal diurnal rhythm. Rather than a simple sustained elevation, chronic stress often produces more complex alterations:
- Flattened Circadian Rhythms: Some individuals show reduced day-to-night variations, with elevated cortisol throughout the 24-hour cycle or loss of the normal morning peak.
- Dysregulated Pulsatile Secretion: The normal episodic, pulsatile release pattern of cortisol may become irregular or suppressed.
- Altered Negative Feedback: The sensitivity of the HPA axis to negative feedback from cortisol itself may change, resulting in either over- or under-suppression of cortisol secretion.
- Sensitisation to Novel Stressors: Previously modest stressors may elicit exaggerated cortisol responses.
Circadian Disruption Under Chronic Stress
One of the most consistent findings in chronic stress research is disruption of the circadian rhythm of cortisol secretion. This disruption reflects altered signalling from the suprachiasmatic nucleus (the brain's "master clock") to the HPA axis, as well as potential direct effects of chronic stress on adrenal sensitivity to ACTH stimulation.
Flattened or inverted cortisol rhythms—where evening/night cortisol levels remain elevated rather than declining—are associated with metabolic dysregulation, impaired glucose tolerance, and increased visceral adiposity in population studies.
Metabolic Consequences of Altered Cortisol Dynamics
Sustained or dysregulated cortisol elevation influences energy metabolism through multiple mechanisms:
- Visceral Adiposity Accumulation: Glucocorticoids preferentially promote accumulation of visceral (intra-abdominal) fat, partly through increased expression of glucocorticoid receptors in visceral adipose tissue.
- Hepatic Glucose Production: Sustained cortisol elevation maintains elevated gluconeogenesis, contributing to higher fasting glucose and potential development of insulin resistance.
- Protein Catabolism: Chronic glucocorticoid elevation promotes muscle protein breakdown, leading to reduced lean mass and altered body composition.
- Lipid Metabolism: Changes in cortisol patterns influence circulating triglycerides and lipid distribution, contributing to dyslipidaemia.
Individual Variability in Cortisol Responses
Importantly, not all individuals exposed to chronic stress show identical patterns of cortisol dysregulation. Individual differences in HPA axis reactivity, genetic factors influencing glucocorticoid receptor sensitivity, and variations in coping mechanisms lead to substantial heterogeneity in cortisol responses to chronic stress.
Some individuals may show elevated basal cortisol throughout the day; others may show a blunted cortisol awakening response; still others may maintain relatively normal diurnal patterns despite exposure to chronic stress. These differences may partially explain why chronic stress exposure is associated with variable changes in body composition across individuals.
Adaptation and Allostatic Load
The concept of allostatic load refers to the cumulative physiological wear and tear resulting from prolonged activation of stress response systems. Whilst acute HPA axis activation is adaptive, the chronic activation and dysregulation associated with sustained stress exposure contributes to metabolic dysfunction, tissue damage, and increased risk of various chronic diseases.
The specific pattern of cortisol dysregulation—whether elevated, blunted, or flattened—appears to contribute differentially to metabolic and body composition changes, though the mechanisms remain incompletely understood.
Measurement and Assessment
In research settings, cortisol is typically measured in blood plasma, saliva, or 24-hour urine collections. Salivary cortisol sampling allows non-invasive assessment of the diurnal cortisol rhythm and cortisol awakening response. Plasma cortisol measured at specific times reflects instantaneous circulating levels. These different assessment methods capture complementary aspects of HPA axis function.
Summary
Cortisol dynamics under chronic stress deviate from the normal circadian pattern, producing altered secretion rates, flattened rhythms, and dysregulated feedback. These changes contribute to metabolic reshuffling—particularly visceral fat accumulation, altered glucose homeostasis, and lean mass loss. Individual variability in these responses is substantial and likely accounts for differences in stress-related body composition changes across populations.