In myasthenia gravis, what is the impact on muscle contractions due to ACh receptor attack?

In myasthenia gravis, the body's immune system mistakenly produces antibodies that attack nicotinic acetylcholine receptors (AChR) at the neuromuscular junction. This attack leads to a decrease in the number of functional ACh receptors available for binding acetylcholine, which is essential for muscle contraction.

As a result, the binding of acetylcholine to the receptor is reduced, leading to a diminished response from the muscle fibers. Consequently, this impairment causes ineffective muscle contractions, as the signals sent from motor neurons cannot result in proper muscle activation due to the lack of adequate receptor engagement. Over time, patients may experience muscle weakness that worsens with activity and improves with rest, underscoring the impact of the antibody-mediated attack on muscle contraction efficacy.

In contrast, options suggesting increased muscle strength, effective muscle contraction, or muscle hypertrophy do not align with the pathological basis of myasthenia gravis, as the disease fundamentally decreases muscle strength and coordination due to the compromised signaling at the neuromuscular junction.