As both disorders reduce the speed at which nerve impulses are conducted, there will be fewer action potentials conducted at the neuromuscular junction (NMJ). With fewer action potentials reaching the NMJ, less acetylcholine will be released thus, less bind to the acetylcholine receptor on the sarcolemma. Fewer sodium ions will enter and depolarise the post-synaptic membrane and the T-tubules. Consequently, fewer calcium ions will be released from storage in the sarcoplasmic reticulum. Calcium ions are needed to initiate contractions by binding on to troponin and keeping the actin-binding sites unobstructed. With fewer calcium ions being available few will bind to troponin. Thus less cross-bridge cycling (the pulling of the actin strands by the myosin) will occur. Hence often patients experience muscle weakness.