Muscle contraction dynamics during chronic alcoholization

O. Podpalova
Taras Shevchenko National University of Kyiv, Kyiv


Alcoholic myopathy is considered a multifactorial disease. The mechanisms leading to the development of muscle pathology in the case of excessive alcohol consumption have several implementation options. Chronic alcohol intake and acute alcohol intoxication can reduce the rate of protein synthesis, including myofibrillar proteins, leading to at least 2 functional changes in contractile processes: increased relaxation time and inadequate, incorrect muscle contraction. Chronic alcohol abuse contributes to the impairment of muscle contraction, including the reduction of the force and mechanokinetic parameters of contraction, which may be the result of the ultrastructural organization disruption of myocytes and their atrophy, because ethanol is able to interact directly on membrane structures. Impaired membrane structures and increased Ca2+ -ATPase activity lead to changes in calcium homeostasis and impaired muscle contractile function.Alcohol myopathy is also represents by skeletal muscles weakness, which is caused by a decreasement of the relative weight of myosin, desmin, actin and troponin, titin and nebulin, as ethanol and acetaldehyde act like as potent inhibitors of synthesis of myofibilar and sarcoplasmic proteins. The purpose of the study was to compare the dynamics of the parameters of skeletal muscle contraction of alcoholic rats using electrical stimulation with different relaxation times. In the first series of the experiment, we performed stimulation of m.tibialis rats with electrical pulses of seconds. With a relaxation period of 30 s. In the next series of experiments, we increased the relaxation time to 1 min. in these stimulating conditions, myopathic muscles tend to increase the relaxation time rather than qualitatively or quantitatively change the dynamics of its contractile processes.


ethanol; alcohol; myopathy; contraction; relaxation; dynamics

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Received: 07.10.2019

Revised: 08.11.2019

Signed for the press: 08.11.2019



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