Final answer:
Blocking calcium pumps on the terminal cisternae would impair muscle contraction. A drug blocking the calcium pumps on the terminal cisternae would cause prolonged muscle contraction, as calcium would remain in the cytoplasm, continually activating the contraction cycle.
Step-by-step explanation:
A drug that blocks calcium pumps on the terminal cisternae would have a significant effect on muscle contraction. In muscle contraction, calcium ions play a crucial role in triggering the interaction between thick and thin filaments. When the drug blocks the calcium pumps, it prevents the release of calcium ions from the sarcoplasmic reticulum. As a result, the actin and myosin filaments wouldn't be able to bind properly, leading to impaired muscle contraction.
A drug blocking the calcium pumps on the terminal cisternae would cause prolonged muscle contraction, as calcium would remain in the cytoplasm, continually activating the contraction cycle.
If a drug blocks calcium pumps on the terminal cisternae of the sarcoplasmic reticulum in muscle cells, it would prevent the re-uptake of calcium ions (Ca2+) into the sarcoplasmic reticulum, resulting in prolonged muscle contraction or even tetany. This is because during muscle contraction, calcium ions are released from the sarcoplasmic reticulum and bind to troponin, causing a conformational change that moves tropomyosin off the binding sites on actin filaments. The blocked re-uptake due to the drug would mean calcium remains in the cytoplasm to continually bind to troponin, thereby continuing the contraction cycle.
Normally, after a contraction, calcium ions need to be pumped back into the sarcoplasmic reticulum for the muscle to relax. If this pumping mechanism is inhibited, the muscle cannot effectively return to its relaxed state, prolonging the contraction and potentially causing muscle fatigue or damage if sustained over a long period.