The introduction of this lab report discussed and elaborated how muscle contraction is an intricate and precise step-by-step process in the body. The concepts outlined at the introduction intertwine with the experiments performed in this laboratory. The experiments aimed to showcase the physiological cause and effect of skeletal muscle response towards various settings. For instance, the first experiment demonstrated spatial summation through the form of muscle recruitment. The cause of this reaction was due to the increased voltage stimuli on the sciatic nerve. Furthermore, the second case study exhibited temporal summation, where constant stimulus exposure lead to a fusion of twitches called a tetanic contraction. As for the third experiment,
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Consequently, the adductor pollicis of the hand only generated below 30% the maximum voluntary contraction when no muscle recruitment was integrated. Hence, a conclusion was established that recruitment played a critical role in the production of contractile force range (Clamann et al, 1981, 45-55). This study supports the data on Figure 1 because the upward trend reflected increments of motor recruitment. Additionally, the linear trend indicated an increase in tension, thus correlating with the results of the brachial bicep contraction. Following trial 3, the small motor units led the contraction to a mounted and sustained substantial tension. As the experiment came to an end, the last four trials led to a linear plateau where the tension remained to fluctuate between 117.8 to 118.5 grams. This signified that all small and large motor units of the gastrocnemius muscle have been recruited (Widmaier et al, …show more content…
The experiment was designed to witness the effect of competitive inhibition on acetylcholine and its relationship with the production of muscle contraction. In formality, tubocurare was the neurotoxin used in this lab exercise, and it is a form of a competitive inhibitor against acetylcholine. The tubocurare ions bind to the specific active site of acetylcholine receptors on the motor end plates called Nicotine Acetylcholine Receptors. Consequently, tubocurare diminishes the available outlets for acetylcholine to initiate depolarization reactions on the surface of the muscle fibers (Bianchi et al, 1964, 181). The introduction of this report emphasized the importance of acetylcholine in the excitation-contraction coupling. Previously mentioned, acetylcholine diffuses into the presynaptic cleft and bind to the Nicotine Acetylcholine Receptors on the postsynaptic membrane of the muscle fibers. Without acetylcholine, a cascade effect will happen and the essential step of calcium binding to troponin to induce a conformational change to tropomyosin ceases to occur. As a result, tropomyosin will continue to block the site where thin and thick filaments bind with each other (Widmaier et al, 2015, 264). Thus, tubocurare indirectly prevents thin and thick filaments to form cross-bridges. Overall, competitive inhibition for acetylcholine stops the step-by-step process of contraction
Consequently, the adductor pollicis of the hand only generated below 30% the maximum voluntary contraction when no muscle recruitment was integrated. Hence, a conclusion was established that recruitment played a critical role in the production of contractile force range (Clamann et al, 1981, 45-55). This study supports the data on Figure 1 because the upward trend reflected increments of motor recruitment. Additionally, the linear trend indicated an increase in tension, thus correlating with the results of the brachial bicep contraction. Following trial 3, the small motor units led the contraction to a mounted and sustained substantial tension. As the experiment came to an end, the last four trials led to a linear plateau where the tension remained to fluctuate between 117.8 to 118.5 grams. This signified that all small and large motor units of the gastrocnemius muscle have been recruited (Widmaier et al, …show more content…
The experiment was designed to witness the effect of competitive inhibition on acetylcholine and its relationship with the production of muscle contraction. In formality, tubocurare was the neurotoxin used in this lab exercise, and it is a form of a competitive inhibitor against acetylcholine. The tubocurare ions bind to the specific active site of acetylcholine receptors on the motor end plates called Nicotine Acetylcholine Receptors. Consequently, tubocurare diminishes the available outlets for acetylcholine to initiate depolarization reactions on the surface of the muscle fibers (Bianchi et al, 1964, 181). The introduction of this report emphasized the importance of acetylcholine in the excitation-contraction coupling. Previously mentioned, acetylcholine diffuses into the presynaptic cleft and bind to the Nicotine Acetylcholine Receptors on the postsynaptic membrane of the muscle fibers. Without acetylcholine, a cascade effect will happen and the essential step of calcium binding to troponin to induce a conformational change to tropomyosin ceases to occur. As a result, tropomyosin will continue to block the site where thin and thick filaments bind with each other (Widmaier et al, 2015, 264). Thus, tubocurare indirectly prevents thin and thick filaments to form cross-bridges. Overall, competitive inhibition for acetylcholine stops the step-by-step process of contraction