The Orbeli-Ginetzinsky Phenomenon
The classic proof of the adaptive-trophic influence of the sympathetic nervous system is demonstrated by an experiment on striated muscle known as the Orbeli-Ginetzinsky phenomenon.
The experiment consists of two key phases:
- Fatigue induction: The muscle is continuously and rhythmically stimulated via its motor nerve. As a result, fatigue predictably develops, leading to a decline in contractile amplitude.
- Sympathetic stimulation: While continuing motor nerve stimulation, electrical current is additionally applied to the postganglionic sympathetic fibers innervating the same muscle.
Result: The contractile amplitude of the fatigued muscle is restored.
The main conclusion of this experiment is that the restorative effect is caused by a direct metabolic action of the sympathetic system on muscle tissue. To prove that this recovery was not merely due to increased local blood flow (a vascular effect), the experimenters previously filled the vascular bed of the muscle with vaseline. Despite complete blockade of perfusion, sympathetic stimulation still restored muscular work capacity.
Mechanism of Action: Trophic Function and Trophogens
Although a trophic (nourishing) effect is characteristic of all nerves, it is most pronounced in the sympathetic nervous system. This process is mediated by the release of specific neuroactive substances—trophogens—from synaptic terminals.
Several groups of substances possess adaptive-trophic activity:
- Basic trophogens: Nucleotides, specific amino acids, prostaglandins, complex lipids, and gangliosides. This category also includes classic neurotransmitters (acetylcholine, serotonin, catecholamines), as well as substance P and calcitonin gene-related peptide (CGRP).
- Oligopeptides: Releasing and inhibiting hormones (liberins and statins), endorphins and enkephalins, bradykinin, cholecystokinin (CCK), neurotensin, oxytocin, and ACTH fragments.
- Growth factors (released upon stimulation of postganglionic fibers): Nerve growth factor (NGF), epidermal growth factor (EGF), insulin-like growth factor (IGF), and tumor necrosis factor (TNF).
Sympathoadrenal System and Metabolic Effects
The sympathetic nervous system is closely integrated with endocrine regulation. The sympathoadrenal system is a functional complex consisting of sympathetic preganglionic fibers and the chromaffin cells of the adrenal medulla that they innervate. Its primary physiological role is global mobilization of the organism, serving as a key stress-response system.
The adrenal medulla is functionally a modified sympathetic ganglion (chromaffin tissue). Preganglionic sympathetic neurons form excitatory cholinergic synapses on these cells. Upon activation, the adrenal medulla secretes approximately 90% epinephrine and 10% norepinephrine into the bloodstream.
Metabolic effects of catecholamines: Acting as metabolic hormones, catecholamines trigger energy-mobilizing pathways:
- Glycogenolysis: Acceleration of carbohydrate breakdown (glycogen breakdown).
- Lipolysis: Increased mobilization of free fatty acids from subcutaneous adipose tissue.
The binary cellular effect of epinephrine depends on the target receptor subtype:
- Interaction with $\alpha_2$-adrenergic receptors leads to inhibition of cellular processes.
- Interaction with $\beta$-adrenergic receptors activates adenylate cyclase, resulting in the intracellular accumulation of cAMP (cyclic adenosine monophosphate).