The Tired Swimmer Case Study Go to this Website: http://www.sciencecases.org/tired_swimmer/tired_swimmer.asp Answer the Following Questions for Parts IIV. Part I: 1. What vital signs or symptoms does Annie exhibit? Blurred vision and eye strain, hands ache and feel weak, gasping for air, weakness & Constant fatigue 2. Can you see any common features in Annie’s signs and symptoms? Blurred vision and eyestrain we must look at the optic nerve within the brain. Whenever you don’t see well other factors will play into it, like headaches, soreness, and fatigue. 3. Why is Annie having problems breathing? Because she has multiple sclerosis, Annie is having degeneration of this area since it is apart of the brain and spinal …show more content…
According to Annie’s EMG test, was Annie’s skeletal muscle function normal? Annie's skeletal muscle function was not normal in the EMG test. 3. Considering your answers to Questions 1 and 2, why did activity in Annie’s motor nerves produce a skeletal muscle response that fatigued during repetitive stimulation? Annie's muscles fatigued after repetitive stimulation because there might be a short in the nerve pathway. This would lead to a closer look at Annie's central nervous system for possible causes. 4. Create a table that replicates Figure 1 and fill it out completely. 5. Now take each stage in turn and discuss how sustained neural activity could create a dysfunction and result in a decrease in muscle response during repetitive motor nerve stimulation. If the nerve impulse is not released than it will not cause an action potential. If acetylcholine is not liberated than it would also not cause an action potential which would not cause a muscle contraction. If the calcium and sodium channels remain open, it would cause a uncontrolled muscle twitch. Part IV: 1. What is the role of the thymus in the body? It processes the white blood cells T-lymphocytes which add cells in finding and destroying bacteria, viruses, abnormal cell growth and non cell tissues. 2. What is an antigen? An antigen is anything in the body the is non self which could include bacteria, viruses, chemicals or abnormal cell growth.
2. Novocain blocks action potential production at the site of injection. How do you think Novocain works on the axon membrane, and how does it block the sensation of pain?
When a stimulus is applied to smooth muscle, it causes an action potential, depolarizing the plasma membrane. Voltage gated calcium channels open allowing calcium into the cell. This increases calcium levels in smooth muscle cells.
3. Increasing frequency of stimulation to the trigger zone: DOES NOT increase the production of action potentials.
Muscle contraction can be understood as the consequence of a process of transmission of action potentials from one neuron to another. A chemical called acetylcholine is the neurotransmitter released from the presynaptic neuron. As the postsynaptic cells on the muscle cell membrane receive the acetylcholine, the channels for the cations sodium and potassium are opened. These cations produce a net depolarization of the cell membrane and this electrical signal travels along the muscle fibers. Through the movement of calcium ions, the muscle action potential is taken into actual muscle contraction with the interaction of two types of proteins, actin and myosin.
Periodic Paralysis Syndrome is a blanket term for a couple of inherited muscular disorders. The most common types are hypokalemic periodic paralysis and hyperkalemic periodic paralysis. Both of these are inherited and generally present from childhood, tho it is possible for symptoms to start showing later in adolescence. In hyperkalemic periodic paralysis, high levels of potassium in the blood interact with genetically caused abnormalities in sodium channels (pores that allow the passage of sodium molecules) in muscle cells, resulting in temporary muscle weakness and, when severe, in temporary paralysis. This disease may be caused by genetic defects in either the calcium channel or the sodium channel. Hypokalemic disease may be caused by genetic defects in either the calcium channel or the sodium channel (Medline Plus).
friend’s muscles in a stretched position. How does this explain her seeming loss of strength?
Smooth muscle contraction occurs when calcium is present in the smooth muscle cell and binds onto calmodulin to activate myosin light chain kinase (Wilson et al., 2002). Phosphorylation of myosin light chains result in myosin ATPase activity thus cross-bridge cycling occurs causing the muscle to contract (Horowitz et al., 1996). There are two known models of excitation and contraction in smooth muscle, electromechanical coupling (EMC) and pharmomechanical coupling
2. Discuss the biological processes that explain why peak contractile force changes with different stimulus strengths.
As a result of the contractions in the Muscle- Skeletal Longitudinal Section cells and the Muscle- Skeletal Cross Section cells, it allows your muscle to be able to contract in response to nerve stimuli. This means that the movements of most of these muscles are not involuntary, you can control them. Therefore, once the stimulation stops, the muscles relax.
In this exercise, you examined the effect of increasing stimulus intensity on the nerve. What other stimulus parameter
-From my data, the conditions that a second action potential requires are a larger interval between stimuli and a smaller stimulus voltage. For example, there was a second action potential when the interval between stimuli was 250 and the stimulus voltage was 20. There wasn’t a second action potential when the interval between stimuli was 60 and the stimulus voltage was 20.
Muscle fatigue occurs when the muscle system experiences a reduction in its ability to produce force and accomplish a desired movement. Muscle Fatigue is caused by the limitation of a nerves ability to generate a sustained signal or known as a neural fatigue as well as the reduced ability of a muscle fibre to contact (metabolic fatigue).
Review Sheet Results 1. Describe how increasing the stimulus frequency affected the force developed by the isolated whole skeletal muscle in this activity. How well did the results compare with your prediction? Your answer: When the stimulus frequency was at the lowest the force was at its lowest level out of all of the experiments. As the stimulus frequency was increased to 130, s/s the force increased slightly but fused tetanus developed at the higher frequency. When the stimulus frequency was increased to the amounts of 146-150 s/s, the force reached a plateau and maximal tetanic tension occurred, where no further increases in force occur from additional stimulus frequency. 2. Indicate what type of force was developed by the isolated skeletal muscle in this activity at the following stimulus frequencies: at 50 stimuli/sec, at 140 stimuli/sec, and above 146 stimuli/sec. Your answer: At 50- Unfused
1. As you increase voltage to the muscle describe how it responds to the increased stimulus.
When acetylcholine reaches the muscles side of neuromuscular junction, it attaches and locks into receptors. If anything interferes with these steps, the nerve will not be able to control muscle contraction. When there is an interruption of normal communication between the nerves and the muscles at the neuromuscular junction, myasthenia gravis occur. This interruption is caused by antibodies that prevent acetylcholine from reaching muscle by destroying or blocking the receptors.