Frog Muscle Lab Report

In order for a muscle to contract requires a nerve impulse to arrive at the neurotransmitter junction. This then causes a release of acetylcholine (ACh) from the presynaptic terminal. By binding with its receptors on the membrane of the muscle fiber, which opens sodium channels generating an action potential that spreads through the length of the fiber, stimulating release of calcium from the sarcoplasmic reticulum. Calcium is what activates the contractile mechanism, causing the muscle fiber to shorten (Rodriguez, et al. 2913). Calcium (Ca2+) channel blockers are components of several drugs such as those for high blood pressure and migraines. Therefor it is important to understand what adverse effects calcium channel blockers can have on muscle contractions because it can be dangerous if someone is operating heavy machinery while under the effects of a calcium channel blocker drug.
The purpose of this experiment is to study the effects of Ca2+ channel blockers in muscle contraction by observing the effects of injecting it in frog legs. Since calcium channel blockers, block the Ca2+ channels, inhibiting the calcium from binding to troponin, which exposes the myosin binding site, we hypothesize that the muscle fibers will not be able to contract to the same extent and therefor contraction will be