Lambert Eaton syndrome is another neuromuscular disease that has symptoms of progressive muscle weakness and fatigue. The syndrome is caused by circulating antibodies to presynaptic Ca²⁺ channels. The antibodies bind to the channels and prevent Ca²⁺ entry into motoneuron terminals, thus preventing depolarization and release of acetylcholine. In experimental models of myasthenia gravis and Lambert Eaton syndrome, one can repetitively stimulate the motoneurons and observe the action potentials produced in the skeletal muscle fibers that they innervate. Based on the pathophysiology of the two diseases, what effect on skeletal muscle action potentials would you expect with repetitive motoneuron stimulation? Given the difference that you predict, what role might repetitive nerve stimulation play in the treatment of the two diseases?