What triggers the stress response?
Any exposure of a stressor on the body initiates two parallel yet closely interrelated processes:
- Mobilization of physiological mechanisms. They form new functional systems whose task is to ensure specific adaptation to a particular stimulus. This can be a sharp drop in temperature (cold), oxygen deficiency (hypoxia), heavy physical exertion, or toxins entering the body.
- Activation of non-specific reactions. These are standard processes that are universal and develop in response to absolutely any unusual exposure. It is this combination of non-specific changes that constitutes the true essence of the stress response.
The role of stress and possible outcomes
The stress response plays a fundamental role in survival. It acts as an obligatory and inevitable link in the process of urgent adaptation to any emergency factor. Without this stage, further adaptation is impossible: stress always precedes the formation of the stable resistance stage and serves as its primary trigger.
The further course of events depends on the success of adaptation and has two main outcomes:
- Favorable outcome: if the body manages to develop stable resistance, all arising homeostatic disorders are successfully eliminated. At this point, the biological goal is achieved, and the stress response completely ceases.
- Unfavorable outcome: if the formation of resistance does not occur for any reason, deviations in the internal environment not only persist but continue to grow. In this case, the stress state drags on.
Three stages of the adaptation syndrome
The development of the general adaptation syndrome is a strictly programmed sequence of events. Three regular stages are traditionally distinguished in the course of the stress response:
- Alarm stage (Alarm reaction) — the primary general response and mobilization of resources.
- Resistance stage — the period of maximum resistance to the damaging factor.
- Exhaustion stage — the breakdown of adaptation mechanisms under excessive exposure.
Alarm reaction in detail
The first phase of stress represents the stage of emergency adaptation. Its main essence lies in the lightning-fast mobilization of all the body's protective reserves to counter an emergency factor.
Triggering factors of the alarm stage:
- Direct impact of the extreme stimulus itself, which severely disrupts homeostasis (acute pain, critical cooling, hypoxia, changes in barometric pressure — hypobaria or hyperbaria).
- Secondary deviation of key homeostatic parameters from the physiological norm. This includes a drop or rise in oxygen partial pressure (pO2), acid-base balance shifts (pH), sharp fluctuations in blood pressure (BP), changes in circulating blood volume (CBV), and body temperature.
Mechanism of reaction development:
- The impact of the factor causes a sharp increase in the flow of afferent signals to the central nervous system.
- These signals radically alter the current activity of cortical and subcortical regulation centers.
- An emergency formation of a new efferent signal program, adequate to the emerged threat, occurs in the nerve centers.
- The ready-made program is immediately implemented on the periphery with the active involvement of both neural and humoral regulatory mechanisms.
Briefly: answers to topical questions
Which hormones provide humoral regulation mechanisms during the alarm stage?
Sources explicitly indicate the participation of neural and humoral regulatory mechanisms for the alarm stage. Among the hormonal and biologically active factors mentioned in connection with an excessive or prolonged alarm stage are:
- catecholamines (hypercatecholaminemia);
- glucocorticoids, including cortisol as the stress adaptation hormone specified in the sources;
- mineralocorticoids;
- thyroid hormones;
- other biologically active substances (BAS).
Which mechanisms ensure the body's maximum resistance during the resistance stage?
Maximum resistance of the body is ensured by the following mechanisms:
- Increase in the capacity and reliability of functional systems — achieved through hypertrophy and hyperplasia of the structural elements of tissues and organs (endocrine glands, visceral and hematopoietic organs).
- Formation of specific resistance — resistance to a specific agent, as well as the phenomenon of cross-adaptation (resistance to other factors).
- Specific and non-specific adaptation — through hyperfunction of dominant systems and the stress response.
What are the pathogenetic mechanisms of the transition of stress into the exhaustion stage?
The transition to the exhaustion stage occurs if the action of the stressor continues or its intensity increases. At the same time, adaptation and compensation mechanisms become insufficient, leading to a breakdown and depletion of the body's adaptive reactions. At this stage, the size of the adrenal cortex decreases and hormone production drops.
The three stages of stress are easy to remember by the acronym TRI: Talarm (Trevoga), Resistance, Inexhaustion (Istoshchenie).
Class and exam questions
How do specific and non-specific reactions differ during stress?
Specific reactions ensure adaptation to a particular factor (e.g., cold or hypoxia). Non-specific reactions are standard and develop upon any unusual exposure—they form the basis of the stress response.
What happens if the body cannot adapt to the stressor?
If the stage of stable resistance is not formed, deviations in homeostatic parameters persist or increase. As a result, the stress state does not cease and subsequently transitions into the exhaustion stage.
Which homeostatic parameters deviate during the alarm stage?
First and foremost, such vital indicators as oxygen partial pressure (pO2), acid-base balance (pH), blood pressure, circulating blood volume (CBV), and body temperature change.
What else to study on this topic
- Mechanisms of formation of specific functional systems during adaptation
- Pathophysiology of the stable resistance stage
- Mechanisms of the stress response transition to the exhaustion stage
- The role of neural and humoral factors in implementing the efferent program
- The effect of prolonged deviation of pO2 and pH on the development of stress
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