Increases in the resistance to tendon during movement may lead to rupture or gapping of the repaired tendon. The relative contribution of these factors—tissue oedema, tendon oedema, and the intact A2 pulley—to resistance to tendon gliding is unclear. In in vitro chicken models, we created oedema in subcutaneous tissue or tendon. The work of digital flexion (WOF) increased significantly after creation of oedema in those tissues. WOF decreased significantly after division of the A2 pulley. Preservation of the integrity of the A2 pulley significantly increased WOF at post-operative weeks 1 and 2 in the in vivo chicken model; increases in WOF were greater than those due to the presence of oedematous subcutaneous tissue. Pulley division at the time of surgery reduced WOF more drastically than the removal of volar subcutaneous tissue. Presence of an intact A2 pulley adds greater resistance to the movement of the repaired flexor tendon than volar oedematous subcutaneous tissue.