Stress, Cortisol and the HPA Axis

01What the measurements show

The Numbers Behind Cortisol in the Athlete

Eight findings that price the cost of adapting and locate where overtraining actually shows.

02The session as a dose

Cortisol Rises in Steps With Session Intensity

Cortisol in an athlete answers the intensity of the work, and it answers in steps rather than smoothly. Twelve moderately trained men completed 30 minutes of exercise at 40, 60 and 80 percent of maximal oxygen uptake on separate days Hill 2008. Time of day, prior diet, prior activity and psychological stress were all controlled.

Cortisol fell 6.6 percent across the resting control session. It rose 5.7 percent after the 40 percent session, 39.9 percent after the 60 percent session, and 83.1 percent after the 80 percent session. The 60 and 80 percent changes were significantly larger than the others and than each other. ACTH followed the same shape, and only the 80 percent session raised it significantly.

So the 40 percent session barely registered on the axis at all. Somewhere between 40 and 60 percent of maximal oxygen uptake, the hypothalamic-pituitary-adrenal axis starts answering, and above that the answer scales fast. A program that prescribes intensity is prescribing cortisol exposure, whether or not anyone writes that line into the plan.

Cortisol then does what hard training requires. It frees glucose and fatty acids for fuel, raises blood pressure and alertness, and dampens processes the body can postpone. A heavy squat session, a championship final, a red-eye flight, all of it flows through the same axis. The hormone itself is not the problem.

Where the circuit itself is taught

The relay behind those numbers is short. The hypothalamus releases corticotropin releasing hormone, the anterior pituitary answers with adrenocorticotropic hormone, and the adrenal cortex releases cortisol into the blood. The pulse architecture of that signal, its four daily phases and the shared steroid backbone it draws on belong to The HPA Axis and Cortisol in the neurology section.

What sport contributes is the dose and the record. The stress input here is written down in advance, delivered on a schedule, and measured in watts or in percentages of maximal oxygen uptake. It is then repeated for years against an outcome that is a race result rather than a questionnaire. No other population supplies that.

03The brake, measured in athletes

A Trained Axis Is Judged by How Cleanly It Stops

A healthy stress axis is defined less by how hard it fires than by how cleanly it stops. Cortisol acts back on the pituitary, the hypothalamus and higher centers including the hippocampus to shut its own release down, a self-limiting loop called negative feedback. When that brake works, a cortisol spike is a tool. When it does not, the spike becomes a state, and the athlete lives in low-grade alarm.

The hippocampus is dense with cortisol receptors and is the sensor most often named in accounts of hippocampal feedback failure. That circuitry is set out in The HPA Axis and Cortisol. The measurement made in athletes sits one station lower, and the paper reporting it is titled for the pituitary.

Endurance training by itself does not produce that state. Endurance-trained subjects show the same resting biological markers of axis activity as healthy untrained men, and training does not induce permanent hypercortisolism Duclos 2016. The difference appears when the axis is challenged, and that is where the athlete evidence has to be read.

Nine non-professional endurance-trained men were tested against eight age-matched sedentary men Duclos 2001. The trained group ran 50 to 70 km per week at a mean maximal oxygen uptake of 61 mL/kg/min. Morning plasma ACTH and cortisol matched the sedentary group, and so did 24 hour urinary free cortisol.

Then came the provocation. After a low dose dexamethasone suppression test followed by CRH, three of the nine trained men did not suppress. Their cortisol rose instead, to peaks of 88, 125 and 362 nanomoles per liter. No sedentary subject showed any increase at all.

Nothing in the resting bloodwork announced those three men. The interesting variable is the size of the answer the axis can still give, and a resting sample does not report it.

The receptor is half of the brake

Sensitivity to cortisol moves as well, and it moves on a clock. In endurance-trained men, monocytes became more sensitive to glucocorticoids during and just after a two hour run. Eight and 24 hours after the last training session, the same cells were less sensitive than untrained cells Duclos 2003.

The authors read the acute rise as a way to shut off the muscle inflammatory reaction after work, and the delayed fall as desensitization that protects the body from prolonged exposure. The inflammatory half of that argument belongs to Inflammation and Healing.

For anyone reading a cortisol value in an athlete, this is the practical consequence. The number reports what the adrenal cortex released. It does not report what the tissue did with it. Two athletes with the same morning value can be running different programs at the receptor. The brake, not the throttle, separates resilience from burnout.

04Overtraining and the axis

Overtraining Shows as a Smaller Answer, Not a Higher Level

Overtraining is a stress axis that has lost its rhythm, and the direction of the loss surprises most people. The Endocrine and Metabolic Responses on Overtraining Syndrome study compared 14 athletes with overtraining syndrome, 25 healthy athletes and 12 healthy non-active subjects, using provocation tests that do not depend on exercise Cadegiani 2017.

A cosyntropin stimulation test found no difference between the three groups. Every adrenal cortex in the study could still make cortisol on command. So the failure is not in the gland.

The insulin tolerance test separated them. Mean cortisol response reached 21.7 micrograms per deciliter in the healthy athletes and 17.9 in the overtrained. Median ACTH reached 91.4 picograms per milliliter against 30.3. Cortisol 30 minutes after waking averaged 500 nanograms per deciliter in the healthy athletes and 323 in the overtrained.

Read the comparison group before drawing the moral. The healthy athletes sat above the non-active subjects on every one of those measures. Conditioning had enlarged the answer the axis could give. Overtraining took the enlargement away and left the athletes near or below untrained values.

Why a resting sample misses it

If the deficit lives in the response, the test has to ask for one. Ten underperforming athletes ran a two-bout maximal exercise protocol, with hormones measured before and after each bout Meeusen 2010. Resting cortisol, ACTH and prolactin ran higher in overtraining syndrome than in non-functional overreaching, and the sensitivity of those resting values was low.

The ACTH and prolactin reactions to the second bout were much higher in the overreached athletes than in the overtrained ones, and those reactions showed the highest sensitivity for telling the two apart. The axis reveals the difference on the second effort of the day rather than the first. Adaptation and Supercompensation draws the line between overreaching and overtraining in full.

What the testosterone to cortisol ratio actually reports

The ratio of testosterone to cortisol is used as an indication of anabolic and catabolic balance. It falls with the intensity and duration of exercise, during periods of intense training, and through repeated competition Urhausen 1995. Regenerative measures reverse it, and it has correlated with training-induced changes in strength.

The review that established its use in sport also settled what it means. The ratio indicates the actual physiological strain of training rather than the overtraining syndrome. It is a load gauge read in hormones, and reading it as a diagnosis asks a strain measure to do work it was never shown to do.

The morning rise carries a cleaner load signal. Fifteen recreational endurance runners sampled saliva on waking and 30 minutes later across two weeks of varied training. Both the cortisol awakening response and its percentage form fell as training load rose, at r squared values of 0.352 and 0.373 Anderson 2018.

05Allostatic load in sport

The Cost of Adapting Is Measurable, and It Lands in the Injury Column

Allostatic load is the running bill for staying ready, and in a physically demanding cohort it predicts who gets hurt. Sixty-nine United States Marine Corps officer candidates, 23 of them women, wore devices through a 10 week training course Feigel 2024. The devices recorded energy expenditure, daytime heart rate, sleeping heart rate and sleep architecture.

The investigators also computed flux, the difference between one day or night and the one before it. That variable matters, because it measures how much a body is being asked to swing rather than where it is sitting. Twenty-one candidates, eight of them women, sustained an overuse musculoskeletal injury.

In the men, injury was positively associated with daytime heart rate, sleeping heart rate, relative and absolute energy expenditure, and the absolute flux in both energy expenditure terms. In the women, injury tracked relative energy expenditure, deep sleep time and percent deep sleep, and tracked negatively with the flux in sleeping heart rate.

The women's result is the one worth sitting with, because more time in the deepest sleep stage went with more injury rather than less. A body spending longer in restorative sleep is a body with more to restore. Sleep duration and the extension trials belong to Sleep and the Athlete, and this figure is a load reading rather than a sleep recommendation.

What the questionnaire missed

Asking an athlete how hard the last block was does not reliably recover the load. Female university football players were measured in August and again in December, just before a national tournament Sato 2024. Self-reported training load correlated positively with hair cortisol concentration, which integrates cortisol output across months rather than minutes.

The same self-reported training load had no significant relationship with fatigue on the Profile of Mood States or with the Stressor Scale for College Students. Hair cortisol correlated negatively with reaction time on a spatial Stroop task, although the repeated correlation analysis found no significant relationship, and the authors report both results.

So the chemistry tracked the training and the mood questionnaires did not. That is a finding about instruments. A questionnaire samples what an athlete can currently notice, and a hormone integrated over months samples what the body has been paying.

A high value is first a training record

Hair cortisol carries a caution that belongs beside every one of these numbers. Acute exercise raises cortisol, that rise eventually shows in hair, and exercise intensity is related to hair cortisol level Gerber 2012. Only weak correlations exist between hair cortisol and perceived stress.

Elevated hair cortisol in a regular exerciser is therefore not necessarily pathological. Reading an athlete's high value as evidence of poor mental health mistakes a training record for a diagnosis. The number has to be read against that athlete's own training history before it is read against anything else.

06Reading readiness daily

The Autonomic Read and the Hormonal Read Answer Different Questions

Heart rate variability, written HRV, is the practical daily window into an athlete's stress state, and cortisol is the slower and more expensive one. The same brain centers that govern the HPA axis also govern the autonomic nervous system. So when cortisol drive runs high, parasympathetic recovery tone runs low and heart rate variability falls. The methodology of that reading belongs to Heart Rate Variability.

The two readings are not interchangeable. A morning RMSSD value costs nothing and can be taken every day. A cortisol curve costs a laboratory and cannot. What the hormone adds is a different question: how large an answer the axis is still able to give, which no resting autonomic value reports.

Thirty-two jockeys made the case in one occupation Landolt 2017. They completed computerized cognitive tasks in September and again in November, naturally lower and higher stress periods, on either side of an acute stress test. Work stress was scored with the effort reward imbalance model.

Higher effort reward imbalance correlated with the cortisol awakening response, at r of minus 0.37 in the high stress period and plus 0.36 in the low stress period. In the high stress period it also went with decision making decrements comparable to a blood alcohol concentration of 0.08. The low frequency to high frequency ratio of heart rate variability shaped that association.

Look at the sign flip before anything else. One questionnaire tracked the morning cortisol rise upward in one season and downward in the other. The relationship between a demand and its hormonal answer changed direction when the state receiving the demand changed.

Why competition is not training with a scoreboard

The same measured work does not cost the same in the two settings. Psychological stress during competitive events produces a higher ratio of catecholamines to lactate than training sessions do Urhausen 1995. Blood lactate reports the metabolic side of the effort, so a competition carrying more catecholamine per unit of lactate is an event the stress systems priced higher than the muscles did.

The same review describes overtraining as a disturbed autonomic regulation, whose parasympathetic form shows a diminished maximal secretion of catecholamines and an incomplete mobilization of anaerobic reserves. Reduced maximal blood lactate and reduced maximal performance follow from that. Once again the failure reads as a smaller available answer.

So readiness is a nervous-system question rather than a willpower one. A trending drop in morning RMSSD alongside a flattening cortisol curve is the body reporting that the stress axis has not reset. How parasympathetic drive comes back after work is the subject of The Vagus and Recovery.

07The sympathetic bias substrate

Stuck in Fight or Flight Has an Address in the Brainstem

The sympathetic half of a stress state is generated at a known place. Barosensitive bulbospinal neurons in the rostral ventrolateral medulla provide the major tonic excitatory drive to sympathetic vasomotor neurons, and they are prominently inhibited by GABA Schreihofer 2002. A major source of that inhibition is the caudal ventrolateral medulla, the area immediately behind them.

Some of those inhibitory neurons are driven by the arterial baroreceptors and some are not. The baroreceptor-independent half tonically restrains the presympathetic cells, and the authors propose that this restraint may set the long-term level of sympathetic vasomotor tone. Sympathetic drive is therefore a released quantity as much as a generated one.

The size of that drive has been measured directly, in anesthetized rats. Silencing about half the catecholaminergic C1 population of the rostral ventrolateral medulla cut renal sympathetic nerve activity by roughly 50 percent and dropped arterial blood pressure by about 25 millimeters of mercury Marina 2011. Half a small cell group carried half the traffic.

The Unified Model of Tone reads that anatomy as the neural substrate for what clinicians recognize as being stuck in fight or flight, and holds that the substrate is specific, measurable and anatomically localized. An athlete who cannot downshift is not weak-minded and is not imagining it. A drive generator is running with its inhibition reduced.

What care aims at when the axis will not stand down

Performance care for this system aims at the ability to downshift rather than at the cortisol value. The goal is not to suppress cortisol. It is to restore the brake. Suppressing the hormone would remove the response that makes a session productive. The evidence above says the overtrained athlete already gives too small an answer to a demand.

What a chiropractic neurologist examines is the central integrative state, the summed readiness a nervous system brings to whatever arrives next. That state is read through joint position sense, balance, eye movements, reaction time and the autonomic measures, and its cellular account sits in The Neuron and the Central Integrative State.

The autonomic balance that governs cortisol is set in the brainstem and modulated by the spine and its rich sensory input. How a joint moves changes how the brain reads and drives the body, and Cortical Drive and Force carries that experimental record. Care of this kind is drug free and anti-doping compliant, which decides whether a competitor under testing can use it at all.

An over-driven sympathetic system is not a temperament. It is tonic inhibition released at a known nucleus, and it can be read from the same instruments that read the rest of the athlete.

It works alongside the foundations that load the axis directly, which are sleep, fueling and intelligent training load. The markers a sports scientist records are the markers to record here: the morning cortisol rhythm and HRV, scored against the athlete's own baseline rather than a population range. Autonomic regulation is a trainable asset rather than a fixed trait, and an athlete who can switch the stress response on hard and off fast owns the recovery that makes the next adaptation possible.

08What we corrected

Five Claims Changed or Removed From This Page

An earlier version of this lesson said that overtraining flattens a chronically high cortisol curve and that cortisol then erodes muscle, immunity and bone. The erosion claim could not be traced to a source in the athlete literature and is gone. The direction is also corrected above: resting values in trained athletes match untrained values, and the deficit sits in the size of the response Duclos 2016.

The page also said that a falling testosterone to cortisol ratio marks the broken axis. The review that put the ratio into sport concluded it reports the physiological strain of training rather than the overtraining syndrome Urhausen 1995. It stays on the page as a load gauge.

A third claim held that restoring spinal motion and quieting an over-driven sympathetic system can help an athlete return to parasympathetic recovery faster. That is an efficacy claim, no trial cited here supports it, and it has been removed. What remains is the mechanism claim the evidence does support: spinal input reaches the systems that set the central integrative state.

The page also listed dipping mood and motivation among the early warning signs of an axis that has not recovered. In female university footballers, self-reported training load tracked hair cortisol and had no significant relationship with fatigue on the Profile of Mood States Sato 2024. Mood questions stay on the list of things worth asking and come off the list of load measures.

A gold pull-quote on stress and information overload carried Dr. Jason Dulberg's name. Nothing he said or wrote is its source, so it has come off the page. Every claim that remains is either sourced to the literature or named explicitly as the model's.

09The model's claim

Overtraining Is a Narrowed Range, and the Range Is What Should Be Measured

Keep the measurements and the claim apart, because they are doing different jobs. The measurements are the intensity steps in cortisol, the three trained men who would not suppress, and the shrunken provocation responses in overtraining syndrome. They are also the receptor swing across 24 hours, the morning rise falling as load climbed, and the injury column in a 10 week course. Each belongs to the laboratory that recorded it.

The claim is the sentence that turns them into one finding. In the Unified Model of Tone, the master pathology is the loss of the adaptive range within which values should fluctuate. Point that sentence at the athlete's axis and it predicts the pattern the endocrine literature keeps producing.

Resting cortisol looks ordinary in trained athletes and looks ordinary again in overtrained ones Duclos 2016. What changed is how far the axis can travel when something asks it to. A cosyntropin test found no difference between overtrained athletes, healthy athletes and non-active subjects. An insulin tolerance test found a large one Cadegiani 2017. The gland was intact and the range was not.

The sympathetic side reads the same way. Presympathetic cells in the rostral ventrolateral medulla run under tonic inhibition, so releasing that inhibition raises drive with no structure changed anywhere Schreihofer 2002. A season can move an athlete's baseline and leave nothing for a scan to find.

The prediction this page makes

This is a claim about how the cost of adapting is organized rather than a claim about what treatment does, and it is specific enough to record. Take one squad through one season. Score every value against that athlete's own baseline rather than against a population range, and collect four things.

The morning cortisol increment, from the waking sample to the one 30 minutes later, is the response range read at the steadiest hour of the day. The percentage rise in cortisol across a standardized 30 minute step at a fixed share of maximal oxygen uptake is response capacity under load. The week to week spread of morning RMSSD is variability structure. The minutes salivary cortisol needs to come back to that athlete's own resting value after the step is recovery time.

The model predicts those four do not drift independently. It predicts the morning increment shrinks before mean session output falls, because a smaller answer arrives before a slower one. It predicts that two athletes matched on resting cortisol still separate on the shared factor behind the four, with compensation deciding which of the four shows the difference, which is what one underlying organization means in practice.

Nobody has recorded the hormonal response range and the autonomic response range in the same athletes across a season. Sport can do it with saliva kits, a chest strap and a bike. If the morning cortisol increment, the rise to a standardized load step, the weekly spread of morning RMSSD, and cortisol return time move together across a season, the unification claim is confirmed.

10The tone reading

The Stress Axis as a Range the Athlete Can Move Inside

Three foundations of tone carry the signature in an athlete under training load.

The remaining foundations run through the same axis. Time course: monocytes answered cortisol more strongly during a run and less strongly 8 and 24 hours after the last session, so the hour decides what a concentration means. Set-point: morning cortisol and 24 hour urinary free cortisol in endurance-trained men sit where untrained values sit, which is why the defended value is the weaker readout here. Oscillation: the daily curve is the carrier, and the morning rise from waking to 30 minutes later is the part that moved with training load. Coupling: the same central circuitry drives the axis and the autonomic outflow, so a flattened morning rise and a falling variability reading arrive together. Input quality: a competition and a training session of equal lactate are different events, and the competition carries the higher catecholamine ratio. Prediction: the axis answers an anticipated demand, which is why the jockeys' morning cortisol tracked their appraisal of the season rather than the rides. The full framework is set out in the Unified Model of Tone.

11Where this sits

How This Page Relates to the Rest of the Library

Seven places this argument continues, each with the claim that earns the link.

12Questions athletes ask

Questions Athletes Ask

13The sources

References

14 primary sources, each linked to its record. Figures quoted on this page were checked against the published abstract.