BackgroundStudies on muscle typing and its differentiation potential have been extensively conducted over the past 50 years. It all started with publications by Buller et al in 1960 suggesting evidence that the central nervous system controls muscle differentiation. This is due to the inability of slow differentiation of muscles in a cat's limb after being operated on from the spinal cord. They further postulated that the division and transverse unity of the nerves of the fast and slow muscles would move the motor neurons that previously innervated the fast muscles to innervate the slow muscles. They then applied this cross-innervation technique to study the possible effects on reverse contractile characteristics[1]. Chronic electrical stimulation, muscle ablation, hindlimb suspension, and hormonal manipulation have been documented to cause changes in metabolic enzymes, Ca2+-handling proteins, myosin isoforms, and proteins. regulators of skeletal muscle and the type and size of muscle fibers. John Holloszy's classic paper (1967) provides evidence for the malleability of rat muscles and the adaptation of their energy metabolism to chronic training through simple physiological stimuli. This gets to the two classic papers available from Gollnick et al in 1972 and 1973, in which they address the idea of ​​fiber type plasticity in human skeletal muscle using fiber typing and needle biopsy of the muscle. Initial interest arose from the early work of Reggie Edgerton et al., which provided critical data on the development of fiber type classification systems. Additionally, Edgerton's investigation introduced other researchers to the idea of ​​exercise-induced fiber type transformation in rodent muscle.[2] This leads Gollnick and his colleague...... center of paper ...... largest in type I muscle fibers, medium in type IIa, and smallest in type IIb. It was also observed that there was a significant difference between the groups, where the lipid content was approximately 25-50% higher in type 2 diabetic and obese muscles compared to normal subjects, while the intensity of the Muscle lipids were approximately 40-50% higher in obese subjects and those with type 2 diabetes. 2 diabetes compared to normal subjects. In Figure 3A, the ratio of glycolytic-oxidative enzyme activities was lowest in type 1 muscle fibers but highest for type IIb, with a medium value in type IIa. The ratios were relatively smaller in normal subjects compared to obese subjects and type 2 diabetes. The ratios for oxidative enzyme activity-lipid content in Figure 3B determined that the values ​​were lower in obesity and type 2 diabetes. 2 regardless of the fiber type. These values ​​were also similar for the three fiber types in normal subjects.