In this experiment, the mechanism examined was the contraction force of skeletal muscle in the gastrocnemius, which is a part of the calf muscle. Skeletal muscle is used for voluntary movement, such as walking, typing, and talking. For these contractions to occur, a signal must be sent from the neuron to the neuromuscular junction which stimulates the muscle fiber. For the signal to be sent, a change occurs to the electrical stimulus by an axon potential. The action potential causes an influx of calcium into the axon terminal, which then causes the neurotransmitter, acetylcholine, to release into the neuromuscular junction. In the neuromuscular junction, acetylcholine will bind to receptors, thus activating voltage-gated sodium channels, in the muscle fiber membrane, to reach a certain threshold. something about how we found the threshold in a part of the experiment. After this threshold is reached, the muscle fiber is excited by an action potential which continues down the transverse tubule causing calcium to be released from the sarcoplasmic reticulum into the muscle fiber (Greising et al.). The binding of the neurotransmitter is an important step for muscle contraction to occur. If the neurotransmitter does not bind to the receptors an action potential will not propagate and then calcium will not get released into the muscle fiber, which is vital for the contraction to occur. (Sherwood, 260). Tubocurare is a type of paralytic drug, which was used in this experiment, that binds to the same receptors that acetylcholine binds with, not allowing an action potential to propagate to the muscle fiber (Magleby, 109). When using the tubocurare, the gastrocnemius muscle contractions should be diminished. The muscle fiber is composed of sarcomeres, which is the contractile unit of skeletal muscle. The sarcomere contains a thick filament composed of myosin and a thin filament composed of actin, tropomyosin, and troponin. The formation of a cross-bridge between myosin (thick filament) and actin (thin filament) is the start of a contraction. When the muscle is relaxed, the tropomyosin is covering up the actin molecules so that the myosin cannot from a cross-bridge. When the muscle is going to contract, the calcium, released from the sarcoplasmic reticulum, will bind to troponin moving the troponin-tropomyosin out of the way. Now actin is exposed to bind with the myosin and shorten, which causes the muscle fiber to contract. It is key for calcium to be present in the muscle fiber for contraction to occur (Greising et al.). A muscle contraction can be caused by a single twitch or a summation of twitches to generate a stronger force. To increase the number of twitches, a process known as twitch summation, the muscle fiber must be stimulated repeatedly, before it has completely relaxed, this creates a greater tension. When a muscle fiber keeps firing rapidly with no time to relax at all, contraction of maximal strength occurs, this is known at tetanus. (Sherwood 267). The consequence of tetanus, or overstimulation of the muscle fiber is the decrease in calcium being released from the sarcoplasmic reticulum which causes fatigue in the muscle (Györke, 707). The purpose of this experiment was to analyze the effects of stimulus intensity, frequency response, acetylcholine receptor inhibition, and direct stimulation on muscle contraction (Bautista and Korber, 2009, 9). For stimulus intensity, the greater the voltage the neuron is receiving the greater the force produced. Second, frequency response will demonstrate the concept of twitch summation and tetany the extent of muscle contraction. As the frequency of the stimulus is increased the force of the contraction is greater, much more than a high voltage. Third, the consequence of inhibiting the acetylcholine receptor will reflect by a decrease in force of the contraction. Lastly, direct stimulus will. Together, these experiments will demonstrate the effect of each variable contributes to overall muscle contraction.