Muscle Contraction Lab Report

Introduction:
Skeletal muscle cells are specialized cells that contain multinucleated muscle fibers called myocytes. These myocytes contain thicker fibers that facilitate the release of calcium, the generation of an action potential within the sarcolemma, and the subsequent production of a muscle contraction. Muscle contractions are a direct byproduct of motor unit recruitment, and for this lab we can examine these effects with aid of a finger pulse transducer and a bar stimulus electrode. The finger pulse transducer generates a force peak amplitude that displays the extent to which a muscular twitch responds to a nerve stimulus, and nerve frequency. Therefore, the purpose of this lab was to observe how the motor unit recruitment in contractile
Acetylcholine binds to the nicotinic cholinergic receptors found on the chemically gated channels of the sarcolemma, and triggers the influx of Na+ ions. The influx of Na+ depolarizes the membrane as the action potential travels down the sarcolemma and t-tubules, and triggers voltage-gated DHP receptors to change shape and pull open the mechanical gated ryanodine Ca2+ channels on the SR. Ca2+ enters the sarcoplasm from the SR and binds with troponin to uncover actin-myosin binding sites and from cross-bridges that facilitate a muscle contraction. Ca2+ enters the sarcoplasm when DHP receptors on the t-tubules respond to an action potential and trigger the opening of ryanodine channels on the SR. Ca2+ gets cleared when calsequestrin triggers the Ca2+ channel to close, and the calcium is used up from a muscle contraction cycle. The role of Ca2+ is that it binds to troponin and removes tropomyosin from the binding sites for myosin on the actin myofilaments, and allows them bind and thus facilitate a muscle contraction. Muscle force is controlled by stimulus intensity and size principle, in that motor units are recruited in order of smallest to largest, and that the greater the stimulus, the lager the motor unit recruitment/muscle fibers activated. This belief was examined by Temesi, et. al (2014), when they evaluated lower-limb fatigue in responds to transcranial magnetic stimulation (TMS), and they concluded that high intensity stimuli triggers co-activation/recruitment of larger motor units. Lastly, the muscle force is controlled by stimulus frequency and summation, in that the CNS can sense and regulate the amount of force needed for a contraction. A small force will only require a small and less frequent signal to stimulate smaller motor units, while a large force would require a more frequent and greater stimulus for