Human Physiological Systems - Coursework Example

Running Head: Human Physiological Systems Name: University: Course: Table of Contents Introduction 3 An overview of the processes that lead to skeletal muscle contraction 3 The flow chart for muscle contraction 4 The relaxation phase flow chart 5 How these processes are disturbed by muscular dystrophies 6 Duchenne muscular dystrophies 8 Conclusion 9 References 10 Introduction The process of skeletal muscle contraction is one of the most important processes in the body of human beings as well as animals. This is because of the fact that movement is vital for them and it depends upon the process. The process is a complicated one and it involves a numbers of steps as well as the utilizations of muscles and hormones. It has been documented that the whole process of relaxation and contraction is also facilitated by the energy ATP which is actually the main component of the contraction and relation process (Authur & John, 2000). Also the two other key components of muscle contraction are the myosin and the Actin. An overview of the processes that lead to skeletal muscle contraction The process of the muscle contraction is basically initiated in the central nervous system. The process can either be voluntary or initiated. This happens depending on whether it is initiated from the brain or from the spinal cord. The process initiated from the spinal cord as a result of a reflex activity while the process initiated from the brain is voluntary (Pascale, 2005). In the spinal cord specifically at the ventral horn is activated leading to the passing of an action potential outward in the root called ventral in the spinal cord. Then there is a branching of the axon for the purposes of supplying several nerves fibres called motor unit. Right at the end plate of the motor the potential action initiates release of quanta or packets of acetylcholine in synaptic cleft s which are located on muscle fibre surface. The electrical potential resting is caused by the Acetylcholine under the end plate of the motor to cause a change. This initiates a change in the action potential which is passed in both of the direction along the muscle fibre surface. At every transverse tubule where it touches sarcoplasmic reticulum part, there is an initiation of Ca++ release by the sarcoplasmic reticulum. The results caused by the calcium ions movement is the movement of the tropomyosin and troponin in the thin filaments (Tassinary, 2000). This then enables the molecules of the myosin heads to swivel and grab their own way usually along hose thin filaments. This in turn causes the muscle contraction. Basically there are a number of sequences of events that are responsible for turning off the process of contraction (Saladin, 2010). There is a brake down at the junction of the neuromuscular of the Acetylcholine by the acetyl cholinesterase. This process leads to the termination of the action potential stream along the surface of the muscle fibre. There is the ceasing of calcium release by the sarcoplasmic reticulum which ensures that there is an immediate resequester of all calcium ions released. When the Calcium ions are no longer being released, there is great change in the process of configuration of tropomyosin as well as troponin which leads to the process of blocking actions of myosin heads molecules hence the process of contraction ceases. It should be noted that in most cases, the external forces like gravitational force or the antagonistic muscle in living animals will pull back the muscles to its original length. The flow chart for muscle contraction State of rest Action potential motor nerve arrival at the end plate motor Release of the acetylcholine, membrane depolarization and sarcolemma Transmission of the action potential via the T-tubules to the SR Release of the Ca++ from the terminal of the SR cisternnae in the sarcoplasm The bounding of the Ca++ by the troponin Activation of the ATPase as well as the ATP hydrolyzation The shifting of the tropomyosin from the binding site of the Actin Cross bridge formation of the Actin-myosin The repetition of the breaking and formation of the cross bridges causes sliding of the filaments as well shortening of the sarcomere The relaxation phase flow chart The breakdown of acetylcholine and the release of cholinesterase Repolarization of the T-tubules and sarcolemma Activation of the SR Ca++ and Ca++ return to the SR cisternnae terminal Formation of the Actin-myosin cross bridge terminated The tropomyosin returned to the binding site of the Actin Formation of the Mg++ complex with ATP Filament passive sliding Return of the Sarcomere to the resting place It should be noted that there are basically three main events involved in the process of skeletal muscle contraction namely the electrical excitation of all the muscle fibres, coupling excitation- contraction and finally the contraction of the muscle fibres. The process of electrical excitation of all the muscle fibres is stimulated by the motor neuron in the body or by the voltage stimulator inside the laboratory (Tassinary, 2000). Whichever the method used for the stimulation, there is a resultant of depolarization in the sarcolemma. It is after the threshold reaches its threshold that an action potential is then initiated. The process of coupling excitation- contraction entails the transmission of the action potential along sarcolemma and the T tubule. This initiates the release of the calcium ions by the terminal cistern of all the sarcoplasmic reticulum. This ion couples some electrical excitation to the muscle fibre by binding to the troponin attached to the tropomyosin and filaments (Richard, 2000). This leads to the change in the shape of the troponin pulling tropomyosin away form the sites of myosin binding on Actin filament. Finally the process of the contraction of the muscle fibres entails the exposure of the myosin binding sites on the entire Actin filament. This initiates the four steps of the muscle fibre (Actin), sliding beyond the thick filaments called the myosin. This causes the shortening of the muscle fibre by 1% length (Michael, 1996). The four steps are ATP hydrolyzation, attachment process of the myosin to the actins so as to form the cross bridge, power stoke and finally the detachments of the myosin from the Actin. How these processes are disturbed by muscular dystrophies Muscular dystrophies refer to one of the inherited disorders of the muscles which cause inflammation and the disorder of the muscles is very progressive but it does not cause any abnormality of the peripheral nerve or central nerve. The disease affects all the muscles leading to a definite degeneration of the fibre but it does not leave any evidence of the aberrations of morphology. The illness mainly affects the males and nor the females. The problem is initiated by the weakening of the muscles. This happens in the direction of the proximal-to-distal direction. It should be noted that under some very rare cases there is distal myopathyies causing distal weakness. One of the most predominant symptoms is the potential ambulation of the patient hence cardiopulmonary malfunctioning (chulz & Schirmer, 1990). The disorder also causes the structural contractures of the soft-tissues as well as the deformity of the spinal cord. These may develop from poor posturing caused by the progressive muscle weakness and imbalance, all of which can further compromise function and longevity. Equinovarus contractures start as flexible dynamic deformities and advance to rigid contractures. This altered anatomy prevents normal ambulation, proper shoe wear, and transfers (how patients can be picked up to transfer out of their chair).Once wheelchair bound, patients with MDs tend to develop worsening contractures and rapidly progressive scoliosis. On average, for each 10° of thoracic scoliosis curvature, the forced vital capacity (FVC) decreases by 4%. In a patient with an already-weakened cardiopulmonary system, this decrease in FVC could rapidly become fatal. The goal of orthopedic management is, therefore, to preserve or prolong patients' ambulatory status for as long as possible (Robert, 1992). This goal can be achieved with soft-tissue releases for contractures and early stabilization of the spine. The problems mainly affect the proteins of the muscles. The etiology of MD is an abnormality in the genetic code for specific muscle proteins.They all are classified according to the clinical phenotype, the pathology, and the mode of inheritance (Louise & Katharine, 2001). The inheritance pattern includes the sex-linked, autosomal recessive, and autosomal dominant MDs. Within each group of heritable MDs (see below), several disorders exist. These are characterized by the clinical presentation and pathology. The group of the hereditary genes invades the muscles hence weakening them to a point of affecting their movement. Some of the main characteristics of the defects are the gradual weakening of the skeletal muscles, defects of proteins that make up the muscles, death of the cells as well as tissues (Peter, 2008). Some examples of the diseases classified as muscular dystrophy are emery-dreifuss, distal, facioscapulohumeral, myotonic, oculopharyngeal, congenital, Becker, limb girdle and Duchenne. Most of these diseases are disorders that affect multi-system and they mainly manifests in the following body systems; gastrointestinal, heart, nervous system, endocrine system, brain, eyes and skin. Some of the other defects include learning disorders and mood swings. The main symptoms includes poor balance, muscular wasting which is progressive, eyelids drooping, Gonadal, difficulty is respiratory, calf deformation, limited movement, frequent falls, inability to be able to walk, loss of control of the bladder, scoliosis and waddling gait (Costanzo, 2002). Duchenne muscular dystrophies This is one of the examples of the muscular dystrophies which may not be detected at birth because it does not arise any obvious suspicion because the manifestation of the muscle weakness begins only after the child begins to walk. This is because at this point a child will lose his or her ambulate ability. The child experiences a delay in his or her motor milestone due to the weakness of the muscles. Another very common effect is the delay in the mental development of the child. The defect is also defined as a X- linked severe recessive kind of muscular dystrophy (Lauralee, 2008). It is the most prevalent form of the muscular dystrophy. It mainly affects the males but can the females are the carriers. A female will also develop the defect if the father suffers from it and if the mother is a carrier as well. The main cause of the disease is the mutation of the dystrophin gene which is located in the × chromosome and it that gene which codes for dystrophin protein which one of the most important component of the muscle tissue. The dystrophin is responsible for providing the muscle tissue with the structural component (Gary, 2007). The dystrophin is also responsible for the provision of structural stability to dystroglycan complex which is located in the cell membrane. The symptoms of the disease usually begin in the male children at the age of five but in some rare cases it is also very much visible during the infancy age. The disease causes progressive weakness of the proximal muscles especially of the legs as well as the pelvic region. There is also a characteristic wasting of the muscles followed by the weakening of the arms as well as neck among other parts. Some of the early signs of the illness are pseudohypertrophy which involves the enlargement of deltoid muscles and calf, low endurance as well as difficulties of the child when standing up without any support and also the child is not able to climb up the stairs. The progression of the symptom causes muscle wasting such that at the age ten years the child can not walk unaided meaning they have to use a wheelchair. Conclusion The process of skeletal muscle contraction is one of the most important processes in the body of human beings as well as animals. This is because of the fact that movement is vital for them and it depends upon the process. However it should be noted that there are some disease which can greatly interfering with the skeletal muscle contraction and relaxation hence interfering with its process of movement. This means that when need be prevention is very important since some of the diseases have no known cure at the moment like the Duchenne (Clive, 1993). Physiotherapy is also very helpful to the children since they can at least regain their muscle strength. References Authur,C. & John, E. 2000. Textbook of medical physiology. Cambridge, MA: MIT Press. Clive, R. 1993. Muscle contraction. Cambridge, MA: MIT Press. Chulz, G. Schirmer, R. 1990. Principles of Protein Structure. In 'Springer Advanced Texts in Chemistry'. (Ed. C. R. Cantor), Springer-Verlag, London. Costanzo, S. 2002. Physiology (2nd ed.). Philadelphia: Saunders. Gary, A. 2007.structure and function of the body. California: Cengage Learning. Lauralee, S. 2008. Skeletal muscle: form and function. New York: Pearson Education. Louise, V.& Katharine M. 2001. Muscular Dystrophy: Methods and Protocols (Methods in Molecular Medicine). Totowa, NJ: Humana Press. Michael, B. 1996. Biochemistry of smooth muscle contraction. London: Tavistock. Pascale, C. 2005. Cellular Microbiology. Oxford: oxford university press Peter, M. 2008. Skeletal muscle damage and repair. England: Prentice hall Robert, M. 1992. Muscular contraction. California: Cengage Learning. Richard, H. 2000. Skeletal muscle contraction. Englewood Cliffs, NJ, USA: Prentice-Hall. scientific management of this story Saladin, S. 2010. Anatomy and Physiology (5nd ed.). New York: Watnick. Tassinary, C. 2000. "The Skeletomotor system: surface electromyography", Handbook of psychophysiology, oxford: oxford university press. Read More