The effect of Tubocurare was quickly seen on Figure 3 along the raw data. A sharp fall in tension was correlated with the injection of the Tubocurare. The data represents the moment the injection stopped, and the first two minutes saw the greatest decrease. The muscle tension average was 21.43 grams during the first 15 seconds once the injection stopped. Although the preconceived expectations before starting the experiment involved a sharper decline of muscle tension that fall between 5 to 0 grams, there was still a sufficient and concrete decline emphasized on Figure 3. In a molecular level, this fall is attributed to the tubocurare ions occupying the receptor site of acetylcholine, thus the muscle contraction process ceased to exist. Furthermore, this was the point in time when tubocurare had the greatest presence in the gastrocnemius muscle of the frog, which correlated with the fast tension decline. In a study where researchers injected tubocurare into the physiological system of rabbits, no depolarization occurred in the non-myelinated fibers that otherwise needed acetylcholine (Bianchi et al, 1964, 181). Therefore, the explanation for Figure 3 is justified since depolarization on the postsynaptic terminal is critical for the generation of contraction through the release of calcium ions. Following the remaining 8 minutes of the trial, the tension average continued to fluctuate between 21.5 grams and 20.9 grams, so contraction did not flat line.
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A possible biochemical reasoning for this baseline average was that not all the acetylcholine receptors were occupied by the tubocurare. Therefore, the 0.25 ml of tubocurare injection was insufficient to completely inhibit acetylcholine in binding with the Nicotine Acetylcholine receptors. With that being said, the data had the possibility of reflecting a lower average if more tubocorare dosage was injected into the gastrocnemius muscle. Regardless, the experiment succeeded in demonstrating the significance of acetylcholine in muscle contraction, along with the cause and effect relationship of competitive inhibitors to the production of muscle contractions. The last experiment elicited muscle contractions without stimulating the neuronal pathway. The method involved two electrical needle rods attached on both ends of the gastrocnemius muscle, thus bypassing the sciatic nerve. In regards to the tubocurine from the previous experiment, at this point in the experiment a majority of the ions would have dissipated. Furthermore, muscle contraction via nerve stimulation requires acetylcholine, but under direct muscle stimulation the Ringers solution provided sufficient amount of calcium to generate contractions. Figure 4 is a graphical, side-by-side, comparison of tension strength produced using direct muscle stimulation versus nerve stimulation. It can be seen that nerve stimulation produced high magnitudes of tension using minor voltage stimulation. This was the opposite scenario for direct muscle stimulation. Direct stimulation required high levels of voltage input in order to generate miniscule semi-moderate tensions. Deviation of tension production indicates two different processes occurring in the gastrocnemius muscle under these two settings. Going back to the first two experiments, the sciatic nerve produced strong contractions by taking advantage of the muscle fiber arrangement. …show more content…
Depending on the settings of the stimulator, sizable muscle contractions were produced either by temporal summation or spatial summation. However, under direct muscle stimulation only a limited number of muscle fibers received the electrical stimulus. Meaning, only the muscle fibers that directly touch the electric needle will receive the stimulus to produce a contraction. Therefore, direct stimulation has a limiting factor of the number of fibers they are able to stimulate. With insufficient muscle fiber excitation, only weak to moderate tensions can be generated. Besides the need for direct contact to a stimulator, muscle fibers have limited efficiency to propagate a stimulus across one another by themselves. Previously stated, muscle fibers maintain conduction resistance to electric stimulus based on their diameter size. Therefore, the stimulus strength gets weaker and weaker as it gets passed onto its neighboring fiber (Widmaier et al, 2015, 270). From what can be inferred from the concepts in this laboratory, calcium is still needed to allow cross-bridges to form. In this case, the source of calcium did not come from the muscle fiber, but rather from Ringers solution. This mixture of ions provided calcium and moisture to the frog. With that being said, this lab experiment was a fitting end
A possible biochemical reasoning for this baseline average was that not all the acetylcholine receptors were occupied by the tubocurare. Therefore, the 0.25 ml of tubocurare injection was insufficient to completely inhibit acetylcholine in binding with the Nicotine Acetylcholine receptors. With that being said, the data had the possibility of reflecting a lower average if more tubocorare dosage was injected into the gastrocnemius muscle. Regardless, the experiment succeeded in demonstrating the significance of acetylcholine in muscle contraction, along with the cause and effect relationship of competitive inhibitors to the production of muscle contractions. The last experiment elicited muscle contractions without stimulating the neuronal pathway. The method involved two electrical needle rods attached on both ends of the gastrocnemius muscle, thus bypassing the sciatic nerve. In regards to the tubocurine from the previous experiment, at this point in the experiment a majority of the ions would have dissipated. Furthermore, muscle contraction via nerve stimulation requires acetylcholine, but under direct muscle stimulation the Ringers solution provided sufficient amount of calcium to generate contractions. Figure 4 is a graphical, side-by-side, comparison of tension strength produced using direct muscle stimulation versus nerve stimulation. It can be seen that nerve stimulation produced high magnitudes of tension using minor voltage stimulation. This was the opposite scenario for direct muscle stimulation. Direct stimulation required high levels of voltage input in order to generate miniscule semi-moderate tensions. Deviation of tension production indicates two different processes occurring in the gastrocnemius muscle under these two settings. Going back to the first two experiments, the sciatic nerve produced strong contractions by taking advantage of the muscle fiber arrangement. …show more content…
Depending on the settings of the stimulator, sizable muscle contractions were produced either by temporal summation or spatial summation. However, under direct muscle stimulation only a limited number of muscle fibers received the electrical stimulus. Meaning, only the muscle fibers that directly touch the electric needle will receive the stimulus to produce a contraction. Therefore, direct stimulation has a limiting factor of the number of fibers they are able to stimulate. With insufficient muscle fiber excitation, only weak to moderate tensions can be generated. Besides the need for direct contact to a stimulator, muscle fibers have limited efficiency to propagate a stimulus across one another by themselves. Previously stated, muscle fibers maintain conduction resistance to electric stimulus based on their diameter size. Therefore, the stimulus strength gets weaker and weaker as it gets passed onto its neighboring fiber (Widmaier et al, 2015, 270). From what can be inferred from the concepts in this laboratory, calcium is still needed to allow cross-bridges to form. In this case, the source of calcium did not come from the muscle fiber, but rather from Ringers solution. This mixture of ions provided calcium and moisture to the frog. With that being said, this lab experiment was a fitting end