Biomechanical and biochemical characteristics of musculus soleus contraction in obese rats
Abstract
Background: Obesity is accompanied by complex metabolic disorders that significantly affect skeletal muscle physiology, including contractile activity and fatigue resistance. However, the mechanisms linking obesity to altered muscle function remain insufficiently characterized.
Objectives: The present study aimed to evaluate the impact of obesity on the biomechanical parameters of musculus soleus contraction in rats under fatigue conditions. In parallel, blood levels of creatinine, creatine phosphokinase (CPK), and lactate dehydrogenase (LDH) were measured to assess the relationship between metabolic alterations and neuromuscular dysfunction associated with obesity.
Materials and methods: Experiments were conducted on male white non-linear rats divided into control and high-calorie diet groups. The musculus soleus contraction force was recorded using strain gauges attached to the muscle tendons. Electrical stimulation of the L4-L5 efferents was performed with 2 ms impulses at 1 Hz, generated through platinum electrodes controlled by an ADC-DAC system. Muscle fatigue was induced by three stimulation series separated by 5 min rest intervals. The maximum contraction force, time to decrease muscle contraction force by 25% and 50% of the initial level and muscle force impulse were determined. Blood levels of creatinine, CPK, and LDH were measured by commercial kits.
Results: The findings have shown that obesity cause a significant suppression of the contractile activity of rat musculus soleus. The concentrations of creatinine, CPK, and LDH in the blood of obese rats increased, indicating impaired neuromuscular function and insufficient recovery during repeated stimulation. These alterations reflect obesity-induced dysfunction in muscle energy metabolism and contractile mechanisms.
Conclusions: Obesity causes pronounced suppression of the contractile activity of musculus soleus and disrupts neuromuscular homeostasis, as evidenced by both biomechanical and biochemical markers. The findings contribute to understanding the pathophysiological basis of muscle fatigue in obesity and may support diagnostics of obesity-related muscular dysfunction.
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