In the last post, we looked at the sympathetic nervous system, the activation branch that mobilizes energy, sharpens attention, and prepares the body to meet a demand. Its neurochemicals move fast. Epinephrine surges quickly and, when the stressor passes, clears within minutes. The acute spike resolves. And under healthy conditions, the system returns to baseline.
But there’s a second stress system running alongside the sympathetic branch, one that operates on a slower timescale and has longer-lasting effects on virtually every system in the body. It doesn’t fire in seconds. It unfolds over minutes, hours, and in the case of chronic stress, years.
It’s called the HPA axis, and it’s one of the most important and most misunderstood systems in the biology of stress.
What the HPA Axis Actually Is
HPA stands for hypothalamic-pituitary-adrenal, three structures that form a hormonal relay system, each one triggering the next in a cascade.
It begins in the hypothalamus, that small master coordinator we met in the first post, nestled near the base of the brain just above the brainstem. When the hypothalamus perceives a stressor, it initiates the cascade. And it’s worth pausing here on the word perceives, because the hypothalamus does not distinguish between a real threat, an anticipated one, or an imagined one. If you vividly picture a stressful conversation you’re dreading, or replay an argument that happened three days ago, or lie awake catastrophizing about something that may never occur, the hypothalamus can read that as a live threat and trigger the same hormonal chain of events as if the danger were standing right in front of you. The nervous system, in this sense, does not always know the difference between what is happening and what you are thinking about.
From the hypothalamus, a signaling hormone is released that travels to the pituitary gland, a pea-sized structure at the base of the brain, often called the “master gland” for how many hormonal systems it governs. The pituitary responds by releasing its own hormone into the bloodstream, which then travels to the adrenal glands, the two small, triangular glands sitting atop each kidney, signaling them to release cortisol.
The whole cascade, from perception of a stressor to peak cortisol levels, unfolds over roughly 20–30 minutes. Which is why this system is slower than the immediate epinephrine spike of the sympathetic branch, but also why its effects are more sustained and why a stressful morning can still be chemically present in your student’s body when they arrive for an evening class if they’re still reliving that stressor.
Cortisol: Still Not the Villain
We touched on this in the last post, but it bears repeating here with more depth: cortisol is not a stress hormone in the pejorative sense. It is a survival hormone that also happens to be released under stress.
On a normal, unstressed day, cortisol follows a natural rhythm. It actually begins rising before you wake up, and that rising cortisol level is part of what causes you to wake up, providing the physiological readiness to meet the day. It peaks sharply in the first 30-45 minutes after waking, known as the cortisol awakening response, delivering energy, mental clarity, and alertness. It then gradually declines through the afternoon and evening, reaching its lowest point in the early hours of sleep. This rhythm, called the diurnal cortisol curve, is one of the markers clinicians use to assess overall stress system health.
Cortisol does essential work throughout this daily cycle. It regulates blood sugar by signaling the liver to release stored glucose for fuel, the same mechanism that kicks in during a challenging power yoga class or any sustained physical effort, giving your muscles the energy they need to keep going. It modulates immune function. Contrary to popular belief, cortisol doesn’t simply suppress immunity; it regulates it, preventing inflammatory responses from overshooting. It supports cardiovascular function, assists in memory consolidation, and plays a role in mood stability.
The issue, as always, is not the hormone itself. Like most things in the body, too much of it for too long stops being a resource and starts being a liability.
When the Cascade Doesn’t Turn Off
Under healthy conditions, the HPA axis has a built-in off switch. As cortisol rises in the bloodstream, it feeds back to the hypothalamus and pituitary, essentially signaling: message received, you can stand down. This negative feedback loop is what allows the stress response to be time-limited. Stressor arrives, cascade activates, cortisol rises, feedback signals resolution, and the system returns to baseline.
But this elegant mechanism has vulnerabilities.
When stressors are chronic, such as financial pressure, relationship conflict, caregiving demands, systemic inequity, trauma looping, or a nervous system that never fully learned to return to baseline, the feedback loop becomes dysregulated. The hypothalamus keeps signaling. The pituitary keeps responding. The adrenal glands keep producing. And the body stays in a prolonged state of cortisol elevation it was never designed to sustain.
Over time, this does measurable damage across multiple systems:
Sleep deteriorates. Cortisol and melatonin have an inverse relationship; as one rises, the other falls. Chronically elevated evening cortisol is associated with lower melatonin signaling and more fragmented sleep architecture, reducing the deep, restorative stages the nervous system most needs to recover.
Immune function is disrupted. Short-term cortisol elevation is anti-inflammatory. Chronic elevation does the opposite. It desensitizes immune cells to cortisol’s regulatory signal, which paradoxically leads to increased baseline inflammation. This is one of the mechanisms that can connect chronic stress to conditions like autoimmune disorders, cardiovascular disease, and accelerated cellular aging.
Memory and cognition are affected. The hippocampus, the brain region most central to memory formation and threat contextualization, is densely packed with cortisol receptors and highly sensitive to sustained cortisol exposure. Chronic stress can reduce hippocampal volume over time, which matters enormously for a very specific reason. A healthy hippocampus allows the nervous system to accurately assess whether something is actually a threat. It’s the part of the brain that looks at a stick on the ground and says that’s just a stick, after your amygdala, your threat-detection center, has already fired as if it were a snake. When the hippocampus is compromised by chronic stress load, that corrective signal weakens. The amygdala keeps firing. Threat responses become hair-trigger. The nervous system starts to lose its ability to distinguish between real danger and the memory or anticipation of it, which, as we noted earlier, the hypothalamus was never very good at distinguishing in the first place.
Mood dysregulation increases. Chronic HPA-axis disruption shows up frequently in depression research and anxiety-related conditions. The relationship is bidirectional. Stress dysregulates mood, and mood dysregulation sustains stress activation, creating feedback loops that can be genuinely difficult to interrupt through top-down means alone (more on this in a future post).
Over time, the stress response itself can become dysregulated. After sustained periods of high demand, cortisol rhythms may become altered, sometimes showing lower morning output or a flattened daily curve. This can show up as the flat, depleted, can’t-get-going feeling many people describe as burnout. Morning cortisol may fail to peak adequately, energy can feel low, and recovery may be slow. The diurnal rhythm that normally rises in the morning and falls through the day can lose its natural shape.
This cumulative toll is what we referred to in the first post as allostatic load, the physiological cost of sustained, unresolved adaptation. The HPA axis is one of its primary mechanisms.
What This Looks Like in Your Classroom
You cannot look at a student and know their HPA axis history. But you can develop an informed intuition for what chronic stress load looks like in a body.
The student who is perpetually exhausted but can’t relax. The one who moves through a vigorous practice without ever seeming to build heat, a nervous system so habituated to high activation that it barely registers the input. The one who bursts into tears in a hip opener, not because something dramatic happened, but because the body finally found enough safety to release what it had been holding. The one who falls asleep in every savasana, not from peace, but from a nervous system that collapses the moment vigilance is no longer required.
These can be outward patterns of chronic stress physiology. Not diagnoses; you are not your students’ clinician, but patterns worth recognizing and having compassion for.
What yoga offers these students is not a fix. Chronic HPA dysregulation is not resolved by a single class, a single workshop, or even a single year of consistent practice. But a well-held yoga class, one that builds activation and then guides genuine recovery, creates safety through consistency and predictability, and uses breath, movement, stillness, and consent-based touch as bottom-up regulatory tools, is a legitimate input into the system. Over time and with repetition, it can contribute to improving stress regulation, lowering baseline activation, and restoring some of the flexibility the system has lost.
This is not conjecture. There is a growing body of research suggesting that regular yoga practice can influence measurable markers of stress physiology, including cortisol levels, HPA axis reactivity, and inflammatory markers.
The Takeaway
The HPA axis is the body’s slow-burn stress system, powerful, essential, and vulnerable to the demands of modern life in ways the sympathetic nervous system alone doesn’t fully capture. Understanding it gives you a more complete picture of what chronic stress actually does to a human body and why so many of your students arrive carrying far more than their yoga mat.
In the next post, we turn to the other side of the autonomic nervous system, the parasympathetic branch, the vagus nerve, and the biology of genuine rest.
This is the third post in a foundational series on nervous system literacy for yoga teachers. Start from the beginning with post one, or subscribe to follow along as the series unfolds.
If this kind of science-meets-teaching thinking is useful to you, this is what I do. The Tissue Literacy for Yoga Teachers blog at rubberbandmethod.com goes deeper — same lens, applied directly to hands-on assists and adjustments.
