What is Muscle Differentiation?

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Studies on muscle typing and its potential to differentiate were widely conducted throughout the last 50 years. It began with publications by Buller et al in 1960 which suggested evidence that the central nervous system controls muscle differentiation. This resulted from the inability of slow muscle differentiation in a cat limb after being operated from the spinal cord. They further postulated that the division and cross-unit of nerves of fast and slow muscles would move the motoneurones that was formerly innervating fast muscle to innervate slow muscle. They then applied this cross-innervation technique to investigate the possible effects in reverse contractile characteristics[1]. It has been documented that chronic electrical stimulation, muscle ablation, hindlimb suspension and hormone manipulation have been used to cause changes in metabolic enzymes, Ca2+ handling proteins , myosin isoforms and regulatory proteins of skeletal muscle and muscle fiber type and size. John Holloszy’s classic paper (1967) provides evidence on the malleability of rat muscles and the adaptation of their energy metabolism to chronic exercise training through simple physiological stimulus. This comes to the two classic papers on hand by Gollnick et al in 1972 and 1973, where they address the idea of fibre type plasticity in human skeletal muscle by using fiber typing and needle biopsy of muscle. The initial interest stemmed from the early work of Reggie Edgerton et al, which provided critical data on the development of fiber type classification systems. Furthermore, Edgerton’s investigation introduced other researchers to the idea of exercise-induced fiber type transformation in rodent muscle.[2] This lead Gollnick and his colle...

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...ghest in type I muscle fibers, average in type IIa and lowest in type IIb. It was also observed that there was significant difference between groups, where lipid content was ~25-50% higher in muscle from type 2 diabetes and obesity than normal subject, Lipid content intensity in muscle was ~40-50% higher in obese and type 2 diabetes than 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 an average value in type IIa. The ratios were comparatively smaller in normal subjects than obese and type 2 diabetes.

Ratios for oxidative enzyme activity-lipid content in Figure 3B determined that the values were lower in obesity and type 2 diabetes regardless of fiber type. These values were also similar across three fiber types in normal subjects.

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