Concept and types of the adaptation process
Adaptation process is a set of body reactions aimed at increasing resistance to an extreme factor and adapting to changing environmental conditions. Depending on prevalence, two forms are distinguished:
- Generalized (systemic) adaptation — involves the majority of the body's physiological systems;
- Local adaptation — develops at the level of damaged cells and tissues (inflammation, allergic reactions).
Causes of the adaptation process are divided into exogenous and endogenous. Exogenous causes are subdivided into infectious and non-infectious; the latter include physical factors (changes in temperature, atmospheric pressure, physical exertion), chemical exposures, and fluctuations in oxygen concentration.
Components of the adaptation mechanism
The development of the adaptation process requires the mandatory combination of three components:
- Extreme factor — the triggering stimulus (hypoxia, extreme conditions, etc.);
- Specific component — hyperfunction of dominant organs and systems that provide direct adaptation (e.g., an increase in the number of mitochondria and activation of cytochrome c oxidase in skeletal muscle during physical exertion);
- Nonspecific component — stress response: increased heart rate, immune activation, redistribution of blood flow.
The general scheme includes the deviation of homeostasis parameters, activation of the nervous and endocrine systems, exploratory behavior, and an attempt to avoid the factor. If the stimulus cannot be eliminated, specific (hyperfunction, hypertrophy, hyperplasia) and nonspecific (stress response) mechanisms are activated.
Stages of the adaptation process
- Urgent (acute) adaptation — an energetically "expensive" stage. The neuroendocrine system is activated, and the levels of catecholamines, mineralocorticoids, and glucocorticoids rise. Concentrations of intracellular messengers (calcium ions, cytokines) increase, phospholipases are activated, lipid peroxidation is intensified, and the breakdown of organic substrates is accelerated. The goal is to survive the acute period until stable adaptation is formed.
- Long-term adaptation (stage of stable resistance) — signs of the acute reaction are eliminated, the cellular genetic apparatus is activated, the energy supply of hyperfunctioning structures is increased, and hypertrophy and hyperplasia develop. An example is the increase in the number of myofibrils under systematic exercise.
- Stage of exhaustion (dysadaptation) — an optional stage. Occurs when the factor is excessively prolonged or intense. Manifests as pathology: hypertension, peptic ulcer disease, endocrinopathies.
Stress as a nonspecific component of adaptation
Stress — a generalized nonspecific reaction of the body to the action of various factors, accompanied by the activation of defense processes and an increase in general resistance with a possible subsequent decrease. Adaptation without stress is impossible, whereas stress can occur without full adaptation.
The stages of stress correspond to the general adaptation syndrome:
- Alarm stage — homeostasis deviation enhances afferent signaling to the central nervous system, activating the cortex and subcortical structures. Consequence — activation of the sympathoadrenal system and release of stress hormones (catecholamines, corticosteroids). Homeostasis maintenance at this stage is unstable.
- Resistance stage — prolonged action of the factor. Hyperfunction leads to hypertrophy and hyperplasia of effector systems, and the new "shifted" homeostasis parameters become the norm for the body (e.g., chronically high blood pressure or heart rate in chronic conditions).
- Stage of exhaustion — disorder of neurohumoral regulation, imbalance of biologically active substances, alteration of receptor sensitivity, substrate depletion. Excess intracellular calcium and activation of free radical reactions lead to calcium-dependent cell damage, dystrophies, dysplasias, and pathological processes, including oncological diseases against the background of chronic stress.
Antistress mechanisms
Most stress reactions terminate at the alarm stage due to the action of antistress systems. By their level of implementation, they are divided into:
- Central — GABAergic and opioid systems of the brain, limiting the activation of higher regulatory centers;
- Peripheral — prostaglandin, adenosine, antioxidant, and cholinergic mechanisms at the level of effector organs.
Action of adenosine in the heart
Excess catecholamines cause constriction of the coronary arteries and calcium overload of cardiomyocytes, which threatens ischemia and myocardial damage. During intense cell work, AMP accumulates, which is acted upon by 5'-nucleotidase to form adenosine. Adenosine inhibits calcium transport into coronary myocytes and cardiomyocytes, causing pronounced coronary vasodilation and limiting the calcium-dependent effects of catecholamines, protecting the myocardium from excessive work.
Action of group E prostaglandins
Prostaglandin E inhibits the release of norepinephrine from sympathetic axons and reduces the efficiency of adenylate cyclase signaling. Activation of phosphodiesterase converts cAMP to AMP, resulting in decreased protein kinase activity and attenuated effects of sympathetic stimulation.
Key points
- Adaptation can be generalized and local; it necessarily includes an extreme factor, specific and nonspecific components.
- The specific component is hyperfunction of dominant organs; the nonspecific is the stress response.
- Stages of adaptation: urgent (acute), long-term (stable resistance), exhaustion (dysadaptation).
- Stress is a generalized nonspecific reaction; adaptation is impossible without stress, but stress is possible without adaptation.
- Stages of stress: alarm, resistance, exhaustion; at the final stage, dystrophies and pathologies develop.
- Calcium-dependent damage and activation of lipid peroxidation are key mechanisms of cellular damage during exhaustion.
- Antistress mechanisms are divided into central (GABA, opioids) and peripheral (adenosine, prostaglandins, antioxidants).
- Adenosine provides coronary vasodilation and limits the calcium effects of catecholamines; PGE2 reduces norepinephrine release and cAMP-dependent cascade activity.