HLTH 4360 Week 2 Stress Response Mechanism Brief Example

From a Speech Before Judges to Cortisol Forty Minutes Later: The Stress Response in Order, a Fast Pathway Kept Apart From a Slow One and Every Timing Credited to Its Source

Student Name

Walden University

HLTH 4360: Stress Management and Wellness

Instructor Name

Month Day, Year

From a Speech Before Judges to Cortisol Forty Minutes Later: The Stress Response in Order, a Fast Pathway Kept Apart From a Slow One and Every Timing Credited to Its Source

Where the Sequence Starts

A mechanism has to begin somewhere, so this brief starts at a defined laboratory stressor rather than at "stress" in general. In the Trier Social Stress Test, a participant prepares a short job-interview speech and then delivers it, followed by a mental arithmetic task, in front of a panel that gives no encouragement (Kirschbaum et al., 1993). The task combines social evaluation with low control. Pooling 208 laboratory studies, Dickerson and Kemeny (2004) found that tasks containing both elements produced the largest cortisol and ACTH changes and the longest recovery times. Starting here gives the sequence a known trigger and a known time course.

Step 1: Detection and Appraisal

The first stage happens in the brain before any hormone is released. Sensory information about the panel and the task is processed in cortical and limbic regions, including the prefrontal cortex, amygdala and hippocampus. Ulrich-Lai and Herman (2009) describe these regions as shaping whether and how strongly the downstream systems are activated: the amygdala tends to drive the response, while the hippocampus and parts of the prefrontal cortex tend to restrain it. The output converges on the hypothalamus and the brainstem, which start the two pathways described next.

Step 2: The Fast Pathway, Sympathetic and Adrenal Medulla

Within seconds, brainstem and hypothalamic neurons activate the sympathetic nervous system. Sympathetic nerves act directly on the heart and blood vessels, and preganglionic fibers stimulate the adrenal medulla, which releases epinephrine, and some norepinephrine, into the blood (Ulrich-Lai & Herman, 2009). Heart rate and blood pressure rise, airways widen and glucose is released from stores. Because this pathway runs through nerves, its effects begin almost at once and also fade quickly when the stimulus ends. This is the sympathetic-adrenal-medullary pathway.

Step 3: The Slow Pathway, the HPA Axis

The second pathway is hormonal and slower. Neurons in the paraventricular nucleus of the hypothalamus release corticotropin-releasing hormone into the portal blood supply of the anterior pituitary. The pituitary responds by releasing adrenocorticotropic hormone (ACTH) into the general circulation. ACTH reaches the adrenal cortex, which synthesizes and releases cortisol (Ulrich-Lai & Herman, 2009). Each step requires a hormone to travel and a gland to respond, so cortisol rises minutes after the stressor begins, not seconds.

Dickerson and Kemeny (2004) report the timing from their meta-analysis: cortisol responses peaked 21 to 40 minutes after the onset of the stressor, and levels returned toward baseline 41 to 60 minutes after the stressor ended. In a speech-and-arithmetic task lasting about 10 minutes, the peak therefore arrives after the participant has left the room.

Step 4: What Cortisol Does

Cortisol acts on many tissues. It raises blood glucose by promoting gluconeogenesis, and it modulates immune and inflammatory activity. McEwen (1998) describes these actions as protective in the short term, because they mobilize energy and help the body cope with a challenge. The same mediators can cause damage when they are produced too often or are not shut off efficiently, a burden he termed allostatic load. That longer-term story is outside this brief.

Step 5: Shutting the Response Off

The HPA axis regulates itself through negative feedback. Cortisol binds receptors in the hypothalamus and pituitary, and in limbic regions such as the hippocampus, reducing further release of corticotropin-releasing hormone and ACTH (Ulrich-Lai & Herman, 2009). The fast pathway stops largely because sympathetic firing falls once the threat has passed. Recovery is therefore a stage of the sequence, not merely its absence.

Summary of Timing

The brief describes a typical response to one kind of stressor in healthy adults. Dickerson and Kemeny (2004) found that responses varied widely across tasks, and that tasks without social evaluation or uncontrollability often produced little cortisol change, which contradicts the belief that cortisol responds to every stressor.

Table 1

The Two Pathways After a Laboratory Social-Evaluative Stressor

Timing for the HPA axis from Dickerson and Kemeny (2004); pathway structure from Ulrich-Lai and Herman (2009).

References

Dickerson, S. S., & Kemeny, M. E. (2004). Acute stressors and cortisol responses: A theoretical integration and synthesis of laboratory research. Psychological Bulletin, 130(3), 355-391. https://doi.org/10.1037/0033-2909.130.3.355

Kirschbaum, C., Pirke, K.-M., & Hellhammer, D. H. (1993). The "Trier Social Stress Test": A tool for investigating psychobiological stress responses in a laboratory setting. Neuropsychobiology, 28(1-2), 76-81. https://doi.org/10.1159/000119004

McEwen, B. S. (1998). Protective and damaging effects of stress mediators. New England Journal of Medicine, 338(3), 171-179. https://doi.org/10.1056/NEJM199801153380307

Ulrich-Lai, Y. M., & Herman, J. P. (2009). Neural regulation of endocrine and autonomic stress responses. Nature Reviews Neuroscience, 10(6), 397-409. https://doi.org/10.1038/nrn2647