After an extended period of maximum contraction, the nerve’s signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the muscle appears to simply ‘stop listening’ and gradually cease to move, often lengthening. As there is insufficient stress on the muscles and tendons, there will often be no delayed onset muscle soreness following the workout. Part of the process of strength training is increasing the nerves ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force. It is this "neural training" that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force. Central fatigue
Central fatigue is a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output. It has been suggested that the reduced neural drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity. There has been a great deal of interest in the role of serotonergic pathways for several years because its concentration in the brain increases with motor activity. During motor activity, serotonin released in synapses that contact motoneurons promotes muscle contraction.
Centrilobular necrosis occurs.Macroscopically, the liver has a pale and spotty appearance in affected areas, as stasis of the blood causes pericentral hepatocytes (liver cells surrounding the central venule of the liver) to become deoxygenated compared to the relatively better-oxygenated periportal hepatocytes adjacent to the hepatic arterioles. This retardation of the blood also occurs in lung lesions, such as chronic interstitial pneumonia, pleural effusions, and intrathoracic tumors. Diagnosis
It is diagnosed with laboratory testing, including liver function tests, and radiology imaging, including ultrasounds. Treatment
Treatment is directed largely to removing the cause, or, where that is impossible, to modifying effects of the heart failure. Thus, therapy aimed at improving right heart function will also improve congestive hepatopathy. True nutmeg liver is usually secondary to left-sided heart failure, causing congestive right heart failure, so treatment options are limited.Treatments for heart failure include medications, an intra-aortic balloon pump, a ventricular assist device, heart valve replacements, extracorporeal membrane oxygenation (if the heart failure worsens suddenly and especially if an infection was the cause), an artificial heart, or a heart transplant (from a deceased human donor, or from a pig). Some patients may need a liver transplant; an artificial liver can be used for a short period of time (about two weeks or so) as a bridge to a transplant, or until the liver recovers. See also
Ischemic hepatitis

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