Cortisol Awakening Response: The Morning Stress Hormone Surge
Cortisol rises 50–160% within 30 minutes of waking — the cortisol awakening response (CAR); it is HPA-axis driven, distinct from the circadian cortisol rhythm, and requires intact sleep quality to be robust.
| Measure | Value | Unit | Notes |
|---|---|---|---|
| CAR magnitude | 50–160 | % rise from waking baseline | Large inter-individual variability; heritability ~48% |
| Time to peak cortisol | 20–30 | minutes post-waking | Falls back to normal diurnal levels by 60 min |
| Waking cortisol level | ~10–20 | nmol/L serum | Baseline immediately at waking; peaks at ~25–40 nmol/L |
| Peak cortisol timing | 8–9am | clock time | In habitual morning wakers; shifts with chronotype |
| CAR blunting in burnout | 30–50 | % reduction vs healthy | Hypocortisolism marker; associated with chronic stress and fatigue |
What Is the Cortisol Awakening Response?
The cortisol awakening response (CAR) is the rapid, pronounced increase in cortisol that occurs within the first 30–45 minutes after waking. Cortisol — the primary glucocorticoid hormone produced by the adrenal cortex — rises 50–160% from its immediate post-waking level, typically reaching its daily maximum within 20–30 minutes of waking, then declining gradually over the following hour.
The CAR is distinct from the broader circadian cortisol rhythm (which reflects SCN regulation of the HPA axis) and is triggered specifically by the act of waking, not simply by the time of day. Evidence: shifting wake time by several hours shifts the CAR accordingly, while the broader circadian rhythm shifts more gradually.
Biological Function
The CAR serves several preparatory functions:
- Metabolic mobilization: cortisol promotes gluconeogenesis, raises blood glucose, and prepares the body for the metabolic demands of the day
- Immune modulation: cortisol suppresses overnight immune activation, providing anti-inflammatory downregulation
- Cognitive priming: cortisol enhances synaptic consolidation of waking state, supporting memory retrieval and anticipatory planning
- Sympathetic activation: potentiates adrenergic signaling, increasing alertness and cardiovascular tone
Measurement and Research Utility
The CAR is measured in research by collecting saliva samples immediately at waking (+0 min) and at +15, +30, and +60 minutes. The area under the curve (AUC) of these samples provides a reliable index of HPA axis reactivity. Key variables that influence CAR:
| Variable | Effect on CAR |
|---|---|
| Alarm clock waking | Higher CAR than natural waking |
| Sleep quality (poor) | Blunted CAR |
| Work day vs. rest day | Higher CAR on work days (anticipatory stress) |
| Chronic stress (burnout) | Blunted CAR (hypocortisolism) |
| Shift work | Dysregulated CAR |
| Depression | Variable; often altered timing |
CAR as a Stress Biomarker
The CAR has become widely used as a non-invasive biomarker of HPA axis function in stress research. Pruessner et al. (1997) established its reliability and demonstrated that it correlated with perceived stress, work demands, and psychological well-being.
Elevated CAR: associated with acute stress, anticipatory anxiety, first day of work, high-demand work periods Blunted CAR: associated with chronic fatigue, burnout, depressive hypocortisolism, PTSD, and hypothalamic dysfunction
The combination of elevated perceived stress with a blunted CAR — indicating chronically exhausted HPA axis responsiveness — is a hallmark pattern of clinical burnout. Sleep deprivation specifically blunts the CAR while increasing evening cortisol, contributing to the HPA dysregulation pattern seen in chronically sleep-restricted individuals.
Related Pages
Sources
- Pruessner JC et al. — Free cortisol levels after awakening: a reliable biological marker for the assessment of adrenocortical activity. Life Sci (1997)
- Clow A et al. — The cortisol awakening response: more than a measure of HPA axis function. Neurosci Biobehav Rev (2010)
- Wüst S et al. — The cortisol awakening response — normal values and confounds. Noise Health (2000)
- Fries E et al. — A new view on hypocortisolism. Psychoneuroendocrinology (2005)