Human Physiology Question - Assignment Example

Physiology 1 Excitation-contraction in skeletal muscle 3 2.0 Muscle contraction 4 2 Effects of calcium deficiency on muscle contraction 4 2.2 Effects of low ATP on muscle contraction 5 2.3 Inadequate oxygen supply to the muscles 5 3.0 Case Study: Consumption of Simple Carbohydrates 5 4.0 Case Study: Exercising at maximal capacity 6 Bibliographies 8 1.0 Excitation-contraction coupling Excitation-contraction coupling is term used in the description of physiological process involved in the conversion of electrical stimulus into mechanical response. This is a very essential process to the muscle physiology and this is because electrical stimulus is mainly a potential action and the contraction is the mechanical response. Excitation-contraction coupling is often deregulated in many diseases and conditions. Although it has been known for a number of decades now, it is still a highly researched area of biomedicine. The general assumption by the researchers is that a potential action depolarizes the cell membrane. When depolarization occur the calcium transient is increased and this is also known as the increase in cytosolic calcium. When calcium increases, contractile proteins that are calcium sensitive use the ATP and this result in the shortening of the cells (Knowles; 892; 1980). 1.1 Excitation-contraction in skeletal muscle In skeletal muscle, excitation-contraction coupling is dependent on a receptor known as ryanodine which is activated by a domain that extends the space that lies between the T tubules and the sarcoplasmic reticulum which is the producer of the calcium transient and this is why contraction occurs. After acetylcholine is produced by the motor neuron into the junction of neuromuscular through synaptic vesicles exocytosis the motor cortex responds to an action potential. This leads to the generation of an action potential and this is through the response to the acetylcholine binding to the receptors known as nicotinic receptors and is transmitted down to the T tubules of the cells of the muscle (Drake; 19; 1997). The receptor known as dihydrophyridine is activated by the action potential and this receptor senses voltage. The voltage signal is transmitted to the ryanodine receptors by the triadic foot which extends from cytoplasmic which exists between the sarcoplasmic reticulum and the T tubule and these results in conformational change and also the channel is opened. Ryanodine receptors are the channels of releasing calcium from sarcoplasmic reticulum and ends up in cytoplasm. The ions of calcium that are released from sarcoplasmic reticulum are bound to troponin C and eventually lead to tropomyosin through actin filaments. A cross bridge is formed by myosin on the actin filaments and are pulled towards the sarcomere center and this process derives its energy from ATP hydrolysis (Knowles; 892; 1980). The calcium ions bind with troponing is broken and this leads to tropomyosin slipping back to its position of blocking the acting sites of binding. This leads to contraction ending and the actin sliding back to their original position of resting (Drake; 19; 1997). 2.0 Muscle contraction 2.1 Effects of calcium deficiency on muscle contraction Calcium is popularly known as the trigger for muscle contraction. Calcium ions regulate muscle contraction and this is achieved by calcium binding thin filament to troponin hence activating the thin filament. With calcium deficiency, muscle contraction will be inhibited because the thin filament will not be bound to the troponin and hence the thin filament will be in a state that is not activated (Knowles; 892; 1980). 2.2 Effects of low ATP on muscle contraction ATP is confused by many people to convert sugar into energy. However, ATP acts as a molecule that stores the energy within the body. ATP is produced by the body as it breaks the sugar into energy and its purpose is to store the energy that is produced. Hence, ATP is used to provide energy to the protein known as actin and this makes the protein move. It is important to note that actin and myosin are the two proteins that enable muscle contraction. ATP deficiency would mean that the actin proteins do not have enough energy to enable muscle contraction (Knowles; 892; 1980). 2.3 Inadequate oxygen supply to the muscles Free Fatty Acids (FFA) from fats and glucose from carbohydrates alongside with enzymes and oxygen are used in a cell called the mitochondria to produce ATP which provides the actin proteins with energy to ensure that muscle contraction is achieved. With inadequate oxygen supply to the muscle fibers means that inadequate ATP will be produced in the mitochondria and this will inhibit the muscle contraction (Drake; 19; 1997). 3.0 Case Study: Consumption of Simple Carbohydrates When you consume a kit-kat, a sundae and a coke, there is a high intake of carbohydrates and sugars. These kinds of foods are transformed into blood glucose very fast and they are known as simple carbohydrates. They raise the blood glucose very fast and this can explain why diabetics who are experiencing low sugar levels consume these kinds of foods. While watching an exciting program like Lost, one tends to get excited and this ensures that bloods flows faster than usual. When eating simple carbohydrates and watching Lost at the same time, the blood glucose is circulated over various body parts very fast. The osmotic movement of water is inhibited and this would trigger the hormonal mechanisms to request more water and this means that one would feel thirsty over some time. This would be the body’s mechanism to restore homeostasis (Drake; 19; 1997). If the following morning one goes for morning exercise, since there was the consumption of simple carbohydrates which is transformed into glucose, the body would produce a lot of ATP which would be used to transmit the energy to the actin protein which together with myosin enables muscle contraction (Drake; 19; 1997). 4.0 Case Study: Exercising at maximal capacity When exercising at maximal capacity it means that the heart rate and the oxygen carrying capacity are stretched and this requires that an alternative source of energy within the body is found. This requires a metabolism pathway and the best way for such a scenario is the fatty acid metabolism pathway whereby the stored fatty acids are degraded through a process known as fatty acid degradation. The fatty acids are transported into the mitochondria where they are also activated. They are then B-oxidized after which they are subjected to an electron transport chain (Zechner; 337; 2005). Carnitine-palmitoyl transferase I (CPT–I) transport the fatty acid across the outer mitochondrial membrane and then transported through the inner mitochondrial membrane by the use of carnitine. The fatty acids when they reach the matrix of mitochondrial they are B-oxidized and acetyl-CoA are retrieved from the fatty acids. Hence there will be the increase of acetyl-CoA in the body muscles and they enter the TCA cycle where the coenzymes Nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FADH) which are used in the electron transport chain which results in the production of ATP (Zechner; 337; 2005). Bibliographies Drake H, Daniel S, Küsel K, Matthies C, Kuhner C, Braus-Stromeyer S (1997). "Acetogenic bacteria: what are the in situ consequences of their diverse metabolic versatilities?". Biofactors 6 (1): 13 – 24. Knowles JR (1980). "Enzyme-catalyzed phosphoryl transfer reactions". Annu. Rev. Biochem. 49: 877–919. Zechner, R., Strauss, J.G., Haemmerle, G., Lass, A., Zimmermann R. (2005) Lipolysis: pathway under construction. Curr. Opin. Lipidol. 16, 333-340. Read More