Final answer:
Blocking Ache activity leads to an accumulation of acetylcholine, causing prolonged muscle contractions and potentially severe physiological effects, including muscle spasms and respiratory failure.
Step-by-step explanation:
If a drug blocks the activity of Acetylcholinesterase (Ache), it will prevent the breakdown of the neurotransmitter acetylcholine in the synapses. This disruption can lead to an accumulation of acetylcholine, resulting in prolonged muscle contractions and a range of muscarinic and nicotinic effects, potentially including severe muscle spasms, excessive secretions, bradycardia, and respiratory failure. Such effects are seen in cases of poisoning with nerve agents like Sarin, or in medical situations where Ache inhibitors are used to treat conditions such as Alzheimer's and myasthenia gravis.
Anti-Ache drugs and insecticides like physostigmine and malathion impact nerve transmission by allowing acetylcholine to persist longer at the neuromuscular junction, thus enhancing cholinergic neurotransmission. Drugs like Botox, on the other hand, lead to flaccid paralysis by inhibiting the release of acetylcholine from motor neurons. The net effect of blocking Ache activity would be overly stimulated muscles that cannot relax, leading to potentially severe physiological consequences, including respiratory distress if the muscles involved in breathing become overstimulated and unable to relax.