Muscle Respiration Lab Report

The initial burst of speed and subsequent 5 seconds in the 100m sprint, is fuelled by the Phosphagen ATP- PC system as there is 4-5 times more Phosphocreatine (PCr) readily available in the skeletal muscles compared to that of ATP (1). The initial ATP stored is used within 2 seconds of maximal activity by the Myosin ATPase enzyme to cleave energy, leaving Adenosine Diphosphate (ADP)

muscular rigidity. Explain why a lack of ATP would cause the sustained muscle contraction of rigor mortis.

Creatine phosphate has been heavily experimented upon to show that it is an important effector towards muscle activity. When creatine phosphate is present in a solution containing muscle fibers without the presence of ATP, it serves as the energy supplier due to the fact that it absorbs bound adenine nucleotide, which is firmly linked to the contractile elements on muscle fibers (Bozler, 1953). Even in low concentrations this nucleotide can be considered an energy transfer mechanism, for it takes full advantage of the creatine phosphates energy supply, thus acting as a substrate for the enzymatic activity of the contractile elements of a muscle group. Consumption of this nucleotide leads to an increase in the strength of contraction. Creatine phosphate also speeds up rate of relaxation of muscles, for it induces the relaxing effect of ATP (Bozler, 1953). Thus, this research suggests that creatine phosphate is directly linked to instigate muscle contractibility.

DEVINE CE, SOMLYO AV & SOMLYO AP 1972, ‘Sarcoplasmic reticulum and excitation –contraction coupling in mammalian smooth muscles’, Journal of Cell Biology, vol. 52, no. 8, pp. 690-718

The power stroke is responsible for the contraction of the muscle and force generation. ATP binding to the myosin head detaches the myosin head from the actin filament and allows the cycle to repeat. The coordinated contraction and relaxation of many muscles in an antagonistic fashion is the basis for the kinematics of any movement.

Martini, F. H., Nath, J. L., and Bartholomew, E. F. “Muscle Tissue.” Anatomy & Physiology. 9th

As discussed in paper one, readers can see the complexity that lies behind muscle fibers and the contractile units that make up each muscle cell. At the normal physiology level, muscle fibers exist as complex bundles of small muscle filaments. These filaments, known as actin and myosin bind in such a way that allows for sarcomere contraction. In assistance with calcium flowing into muscle cells, proteins known as tropomyosin and troponin ultimately allow “cross bridging” to occur. Throughout the body three types of muscle fibers exist, these types of fibers are slow oxidative, fast oxidative and fast glycolytic. Activation or recruitment of these fibers varies from person to person depending on the muscle specificity needed to perform a given contraction. In other words the innervation of each fiber depends solely on the muscle needed to engage in a specific exercise. By first knowing the anatomy behind a muscle cell one can then have a better understanding of the effects training has on muscle cell hypertrophy.

After each nerve impulse, the amount of ACh released by the presynaptic motor neuron decreases due to a temporary depletion of ACh stores. This is a normal phenomenon known as presynaptic rundown. MG results in a reduction of the available AChR at the postsynaptic membrane as well as a flattening of the postsynaptic folds. Therefore, even without the phenomenon of presynaptic rundown, MG can result in an inefficient neuromuscular transmission due to a reduction in the number of AChRs at the motor end plate. The inefficient neuromuscular transmission and presynaptic rundown phenomenon account for the fatigability seen in MG due to the progressive decrease in the amount of muscle fibers that are activated with each successive nerve impulse. Patients begin to exhibit symptoms of fatigue when there is a reduction of approximately 70% of the available AChRs.

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 lab. The experiments aimed to showcase the physiological cause and effect of skeletal muscle responses towards various situations. 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 input on the sciatic nerve. Furthermore, the second case study exhibited temporal summation, where constant stimulus exposure led to a fusion of twitches called a tetanic contraction. As for the third experiment, the

The findings of this experiment reinforced the hypothesis that the resting membrane potential is most influenced by the ion potassium. We were able to deduce this through the collection of a multitude of intracellular and extracellular recordings, such as the one shown below in Figure 1. This shows how this experiment was able to record every single resting membrane potential in all three different muscle groups under all six solutions.

For example; increases in 100 and 200m swimming performance (22) and increases in 2000m rowing performance (18) as well as increases in cycling capacity (17) have been demonstrated (for reviews see Refs. 10, 16). However, the precise mechanisms by which carnosine may elicit increases in exercise performance and capacity remain to be fully elucidated. During high intensity exercise, hydrogen cation (H+) accumulation is significantly increased, which results in significantly decreased intracellular pH (23). Furthermore, H+ accumulation is reported to disrupt the ability of the muscle’s contractile machinery to function (8, 12). Due to carnosine’s imidazole ring having a pKa of 6.83, it is well acknowledged that carnosine is a perfectly suited intracellular pH buffer across the entire physiological range (4). Therefore, during high intensity exercise where H+ accumulation is likely to be the biggest contributing factor that limits exercise performance, carnosine’s ability to increase intracellular buffering capacity and maintain muscular function, is suggested to be the most pertinent mechanism by which carnosine evokes an ergogenic effect (27). Hill et al., (17) suggested increased intracellular buffering capacity resulting from an increase in muscle carnosine concentrations explained a significant increase (TWD: +16.2%) in cycling capacity following 10 weeks of BA

The results of this experiment suggest that the Nernst equation is not an accurate measure of resting membrane potential. Table 1 lists the membrane voltage for each muscle group at each KCl concentration that was used to test voltage changes. It shows that the membrane potential changes when the cells are bathed in extracellular solutions of different concentrations. The Nernst equation predicted that the higher the concentration of KCl, the more the cell would depolarize, which did occur, but the degree to which the depolarization occurred was inaccurate. A one sample t-test was used for each muscle group at each concentration to determine if the Nernst value was a good predictor of that specific membrane potential. For all muscles and concentrations the p-value was less

Potassium is crucial to heart function and plays a key role in skeletal and smooth muscle contraction, making it important for normal digestive and muscular

In human body, ATP, adenosine triphosphate, is separated to make vitality for muscle withdrawal. The human body makes ATP vigorously and anaerobically. There is one oxygen consuming vitality framework and two anaerobic vitality frameworks. Most exercises of the body utilize an intricacy of each of the three vitality frameworks to produce the vitality required.

One of the functions of the calcium is to help control muscle contractions. Researchers at the