Metformin is a biguanide, its mechanisms of action are not completely understood, but rather than specifically targeting purely muscle tissue, its primary sites of action for insulin sensitizing effects (a somewhat minor mechanism besides its primary glucose disposal actions) are actually the liver & gut (primarily by AMPK activation). Metformin reduces hepatic lipid stores & increases intestinal GLP-1 activity.
Its effects on skeletal muscle are generally unfavorable, as AMPK activation inhibits mTORC1/P70S6K1 phophorylation, thereby preventing the adaptive preferential shift from type I to type IIA fibers (resulting in a tendency towards reduced strength gains) & abrogates the endurance training enhancement of insulin sensitivity.