Hormonal

In human skeletal muscle, obesity is associated with a specific defect in insulin receptor kinase activity toward exogenous substrates, which contributes to insulin resistance, whereas the structural integrity and autophosphorylation of the receptor remain normal.

In obesity, your muscle cells' ability to respond to insulin is impaired not just because there are fewer receptors, but because the receptors' internal signaling engine (kinase activity) is less effective at processing the signal. This is a biological adaptation to excess energy, not a permanent structural break. Addressing the underlying obesity is key to restoring this signaling efficiency.