What is the physiological basis of fatigue during prolonged physical exertion? The physiological mechanisms responsible for fatigue during prolonged physical exertion (PEI) are discussed. By increasing the concentration of gastric acid, energy is released from the stomach and cause fatigue. Metabolism of gastric acid is accelerated leading to reduced oxygen consumption and deactivation of gastric acid. The body tries to compensate by converting the increase in gastric acid seen from PEI into increased oxygen consumption. As the body attempts to get faster and more oxygen, it is stimulated to take in more mechanical energy so it can generate more analgesic medullary innervation, blood flow, and produce muscle contractions. In the case of PEI, the circulation of blood allows increased oxygen consumption to compensate the reduction in oxygen consumption. The activation of neuromuscular neurons with a similar mechanism (i.e. increase the concentration of neuromuscular hormones, osmotic shock, and pH) have been studied using small interfering RNA in vitro, which increases the level of muscle action potentials [@b1]–[@b5]. These studies show that muscle relaxation, increased resistance, and reduced sensitivity to mechanical stimulation show no structural difference, indicating that muscle serotonin is not involved in the regulation and response to pain. Some other studies which use adeno-associated viral vectors for transactivation by non-nervous tissue cells (e.g. human neurovascular endothelial cells or human pancreatic acinar cells) also show that serotonin and its associated peptide have similar effects on muscle function [@b6]–[@b8]. The sympathetic nervous system (SNS) is involved in cardiovascular physiology and metabolism. It is the main CNS sympathetic system in heart and skeletal muscle, and maintains energy expenditure and ventilation. Recent studies have shown that increased plasma concentrations of serotonin in patients suffering from pain and depression show anti-necrotic response and are independent factors in the development of chronic pain and depression [@b9]–[@b13]. These findings indicate that the SNS potentially play an important role in long-lasting pain. Adverse hemodynamics and blood pressure are possible direct factors that interfere with the neurohormone response. Studies showing that the blood serotonin concentration is increased after stimulation of neurons can be explained look at here now involvement of the sympathetic nervous system. In addition to serotonin, the sympathetic nervous system also plays an important role in the renin-angiotensin-aldosterone system (RAAS) [@b14].
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In the context of the cardiovascular system, these receptors are responsible for sympathomimetic symptoms, such as acute heart failure and stroke, hypertension, and, primarily, in the diabetic patient. In this context, the metabolic pathways involved during this chronic process may be important for the control of these clinical signs. This is because the sympathetic nervous system is involved in the increased metabolic processes and its response to pain is in part related to the increased sympathomimetic effect of pain states. Conclusion ========== Pregnant women suffering from a chronic pain state can experience significant adverse physiological consequences following exercise (diurnal attacks), prolonged physical exertion (moderate or chronic), and associated illnesses such as arthritis, tuberculosis, liver disease, diabetes, or smoking. The frequency of such episodes is considered important but it is not apparent whether such disturbances occur with extreme numbers, namely during the majority of pain weeks. In order to examine the physiological basis of these adverse physiological effects post-exercise as they may be determined at the cardiovascular level, in this study we tested early and late regulation after vigorous physical exertion. We observed marked an increase of oxytocin peptide secretion and muscle lactate production during moderate and short bouts of exercise. To verify the specific effects of long-term exercise on these physiological processes, there may be other degrees of physical stress, in particular a change of muscle performance or fatigue. Further work will be necessary to clarify whether such stress are the manifestations of the anti-hypertensiveness, anti-carcinogenic milieu, or that they are the consequences of the anti-cardiac stress since such stress may affect the heart, the lungs, the muscles, and, perhaps, the whole autonomic nervous system. No potential conflicts of interest relevant to this article were reported. 






