Although moderate exercise can benefit health, acute and rigorous exercise regime can be sometimes hazardous to health. Regular exercise will reduce the risk of chronic diseases such as cancer, diabetes, cardiovascular diseases. However the amount of exercise required to achieve beneficial effects has not been clearly defined but to gain maximum health benefits, the frequency, intensity and the duration of exercise and pre-exercise fitness levels will be important determents. (McCutcheon et al, 1991)
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Strenuous exercise can induce alterations in the physiology and viability of circulating leucocytes which cause induced immune distress. Cumulating evidence has shown that intense exercise has adverse effects on adverse aspects of health. Rigorous physical activity can trigger an acute myocardial infarction and increase the occurrence of premature ventricular depolarisations which has been associated with long-term increase in the risk of cardiovascular deaths. Number of apoptosis of lymphocytes has been shown to be induced by intense treadmill exercise and this also induces cellular and oxidative stress. Study shows that Leucocyte mitochondrial transmembrane potential (MTP), a marker of the energy and redox status of the cells declined significantly after exhaustive aerobic exercise having a temporal relationship with intravascular oxidative stress. The changes in leucocyte MTP had declined significantly after the 1st exercise and it decreased even more after the 2nd and 3rd exercise sessions. The propensity of apoptosis of PMN, lymphocytes and monocytes increased gradually after each exercise session. (Kong, 2008)
In comparison with regular and intense exercise, several evidences showed the potential risks of acute and high intensity exercise. Exercise can elicit changes in the cellular and humoral immune systems and strenuous exercise can induce inflammatory reactions and immune disturbances. In addition to the immune disturbances, the energy needed for the increased metabolic demand during prolonged exercise is produced by oxidative metabolism, which may overwhelm endogenous antioxidative capacity and cause damage to cells and tissues. An example of exercise induced oxidative damage is DNA damage of leucocytes induced by high intensity aerobic exercise. (Kong, 2008) According to studies, strenuous exercise can induce the formation of reactive oxygen species, causing oxidative stress in areas where tissues are affected. The accentuated production of the reactive oxygen species may induce increased expression of death receptors and ligands and also disruption of leucocyte MTP. The variable correlation between the change of leucocyte MTP and apoptotic regulators implies that the leucocyte mitochondrial alterations are part of systematic immune disturbance induced by both short- term and high intensity exercise. The increased inflammatory cytokines and apoptotic regulators noticed after exhaustive physical activity will have deleterious effects on peripheral blood leucocytes. (Kong, 2008)
During intense exercise regimes for short durations, it has been shown that the body’s preferred energy substrate is glycogen. Glycogen is essentially a stored form of glucose in the liver and the skeletal muscle. During high intensity exercise regime, there is a reduction in the glycogen from 90mmol- kg-1 to 40 mmol-kg-1.This 50% reduction in glycogen may decrease the rate of glycolysis and this can bring in earlier onset of fatigue. (McCutcheon et al, 1991)
What is more not only glycogen level has been changed during exercise. Carbohydrate and fatty acid can be also use as a fuel. However, it depends on exercise intensity. George Brooks in ‘crossover concept’ explains this correlation. Input of carbohydrate oxidation to ATP formation rises while lipid oxidation decreases. Carbohydrate seems to be better source of energy for exercising muscles because it can creates greater rate of acetyl CoA for Krebs cycle. Moreover, carbohydrate can be also use in anaerobic glycolysis. (Houston, 2001)
High intensity exercise lead to several immune marker changes such as low level salivary immunoglobulin (antibodies), low serum complement levels, low lymphocyte count, depressed NK cell activity and decreased neutrophil phagocytic capacity. (Mackinnon 1992; Nieman; 1994; Pedersen &Ullum, 1994). (Gleeson, 2002) It is also associated with muscle cell damage. The immune system is involved in tissue repair and while this is being done, the host protection will suffer. A window of opportunity for the infection during recovery from high intensity exercise exists. Rest is recommended after rigorous exercise to allow the body to recover and moderate exercise may be better choice for enhancing good health and well being. The study shows that long-term high intensity exercise can lead to significant dysfunction of the mitochondrial energy status in peripheral blood immune cells accompanied by an increased propensity for apoptosis and an increase in pro apoptotic cytokines. The results support the potentially deleterious effects of excessive high density exercise on immune function and health. (Edelman et al, 2006)
Principle characteristic metabolic and biochemical alterations that take place during the “fed” state after a large meal containing high carbohydrate and fat content.
The food that we intake during a meal is digested by the body and this process is called ‘metabolism’. (Loeser, 2000) For several hours after a meal while the food is digested and absorbed there is an abundant supply of metabolic fuels. In fed state the regulatory mechanism such as the availability of substrates; allosteric regulation of enzymes; covalent modification of enzymes; induction repression of enzyme synthesis ensure that adequate nutrients are captured as glycogen. (Berg et al, 2002)
An allosteric effect usually involves rate determining reactions. For instance, glycolysis in the liver is stimulated following a meal by an increase in fructose. Many enzymes are regulated by the addition or removal of phosphate groups from specific serine. In the fed state, most the enzymes are regulated by these covalent modifications are in dephosphorylated form are active. Increased or decreased protein synthesis leads to changes in the total population of active sites. In the fed state elevated insulin levels result in increase in the synthesis of key enzymes such as acetyl coenzyme (CoA).
Under these conditions, glucose is a major fuel for oxidation in tissues, after we consume and digest a large meal containing high protein fat and carbohydrate content, glucose and amino acids are transported from the intestine to the blood. Glucose uptake into the muscle and adipose tissue is controlled by insulin which is secreted by cells of pancreas because of increased concentration of glucose in the blood. The liver is placed uniquely to process and distribute dietary nutrients and after a meal the liver is bathed in blood containing absorbed nutrients and elevated levels of insulin secreted in pancreas. The absorptive state is the 2 to 4 hour period after ingestion of the normal meal. During the interval, transient increases in plasma glucose, amino acids and triacylglycerols occur. (Loeser, 2000)
During absorptive period, the liver takes up carbohydrates, lipids, and amino acids. These nutrients are then metabolized stored and routed to other tissues. Thus, the liver smoothes out the availability of nutrients for the peripheral tissues. Liver is usually a glucose producing rather than glucose giving tissue and thus usually after a meal containing carbohydrate, the liver consumes glucose retaining 60% of every 100g present. This increased usage of glucose is not a result of stimulated glucose transport into hepatocyte but because this process is rapid. (Champe et al, 2000)
The insulin sensitive tissues will only take up glucose from the blood stream to any significant extent in the presence of hormones. The uptake of insulin into the liver is independent of insulin but liver has an isoenzyme of hexokinase so that the concentration of glucose entering the liver increases, so does the rate of synthesis of glucose. This is in excess of liver’s requirement for energy and this is used for synthesis of glycogen. Insulin signals the fed state and it stimulates the storage of fuel and synthesis of proteins in several ways. For instance, insulin initiates protein which stimulates glycogen synthesis in both muscle and the liver. Insulin also accelerates glycolysis in the liver which in turn increases the synthesis of fatty acid. In adipose tissue, insulin stimulates glucose uptake, its conversion to fatty acids and inhibits intracellular lipolysis and the release of fatty acids. (Champe et al, 2000)
The energy metabolism of the skeletal muscle is unique in being able to respond to substantial changes in the demand for ATP that accompanies muscle contraction. The transient increase in plasma glucose and insulin after a high carbohydrate rich meal leads to an increase in glucose transport into the muscle cells. Glucose is phosphorylated to glucose 6-phosphate and metabolized to provide energy for the cells. This contrasts with the postabsorptive state where the ketone bodies and fatty acids are the major fuels of resting muscles. Fatty acids are released from chylomicrons by the action of lipoprotein lipase. However, fatty acids are secondary importance as a fuel to muscle during well fed state in which glucose is the primary source of energy and fuel. A spurt in amino acid intake and protein synthesis occurs in absorptive state after ingestion meal containing carbohydrates and rich protein. The brain is vital to the proper functioning of the body and hence more priority will be given to its fuel needs. (Champe et al, 2000) To provide energy substrates must be able to cross the endothelial cells that line the blood vessels in the brain. Normally glucose will be the major contributor in providing the energy to the brain in fed state as concentration of ketone bodies in the fed state is too low to serve as an alternate source of energy to the brain. In the well fed state, the brain uses glucose exclusively as fuel completely oxidizing 140g /day to carbon dioxide and water. The brain contains no significant stores of glycogen and is completely dependent on the availability of blood glucose. (Berg et al, 2002)
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Under normal feeding patterns the rate of tissue protein catabolism is more or less constant throughout the day and it is only cachexia that there is an increased rate of protein catabolism. There is net protein catabolism in the postabsorptive phase of the feeding cycle and net protein synthesis in the absorptive phase when the rate of synthesis increases by 20 to 25%.The increased rate of protein synthesis is a response to insulin action. Protein synthesis is an energy expensive process which accounts almost to 20% of the energy expenditure in the fed state where there is abundance of amino acids from the diet but only 9% under starved state. (Murray et al, 2003)
Principle characteristic metabolic and biochemical alterations that take place during food starvation
Fasting may result from inability to obtain food from the desire to lose weight rapidly or in any clinical situations. In the absence of food, plasma levels of glucose, amino acids and TAG fall, triggering a decline in insulin secretion and an increase in glucagon release. (Elia, 1991) The decrease insulin to glucagon ration and the decreased availability of circulating substrates makes the period of nutrient deprivation. (Champe et al, 2000) This instigates an exchange of substrates between liver, adipose tissue, muscle and the brain that is guided by 2 priorities which are:
- The need to maintain adequate plasma levels of glucose to sustain adequate energy of the brain, red blood cells and glucose requiring tissues.
- The need to mobilize fatty acids from adipose tissues and the synthesis and release of ketone bodies from the liver, to supply energy to all other issues.
It is known that prolonged starvation and fasting leads to a reduction in resting metabolic rate (RMR) and induces immunodeficiency characterized by disproportionate loss of lymphoid tissue impaired cell mediated immunity and increased susceptibility to infectious diseases. This is both due to decrease in body mass and to a fall in the energy expenditure of the remaining body tissues. A typical well nourished man weighing 70 kg has fuel reserves totalling 161,000 kcal. The energy required for a day ranges from 1600 kcal to 6000kcal depending upon the extent of activity. Thus, stored fuel suffices to meet caloric needs of starvation for 1-3 months. However, the carbohydrate reserves are exhausted within a day. (Voet et al, 2006)
Fasting induces profound changes in the body in order to decrease the energy expenditure and to conserve energy. Even under starvation period, the blood glucose level must be maintained above 2.2 mm. The first priority of metabolism in starvation is to provide adequate glucose to the brain and other tissues, red blood cells which are adequately dependent on this fuel. Most energy is stored in the fatty acyl moieties of triacylglycerols. Fatty acids cannot be converted to glucose but the glycerol moiety of triacylglycerol can be converted to glucose but the availability is limited. The other source of glucose is amino acids derived from the breakdown of proteins. Since proteins are not stored in any form the second priority of metabolism in starvation is to preserve protein. (Berg et al, 2002)
The metabolic changes on the first day of starvation are like those after the overnight fast. The low blood sugar level leads to decreased secretion of glucagon. The intake of glucose by the muscle will be diminished because of low insulin level but fatty acids will enter freely. Consequently the muscle will shift for fuel from glucose to fatty acids. The oxidation of the fatty acids by muscles halts the conversion of pyruvate into acetyl CoA. (Berg et al, 2002)
During starvation, degraded proteins are not replenished and serve as carbon sources for glucose synthesis. Initial sources of protein are those that turn rapidly such as proteins of the intestinal epithelium and the secretion of the pancreas. Proteolysis of muscle protein provides some of 3 carbon precursors of glucose. However, survival of animals depends on being able to move rapidly which requires large muscle mass. During the first 3 days of starvation some muscle protein is degraded and this halt in protein breakdown and loss of muscle mass occurs because of large amount of acetoacetate and Ketone bodies are formed in the liver. This change in metabolism occurs because the citric acid cycle is unable to oxidize all the acetyl units generated by the degradation of the fatty acids. (Berg et al, 2002)
After 3 days of starvation, the liver forms large amounts of acetocetate and D-3- hydroxybutyate. Their synthesis from acetyl CoA increase because of the citric acid cycle is unable to oxidize the acetyl units generated by the degradation of fatty acids. Gluconeogenesis depletes the supply of oxaloacetate which is the entry of acetyl CoA into the citric acid cycle. Consequently, the liver produces large amount of ketone bodies which are released into the blood. In starvation, the body releases protein which is conserved in the part by generation of an alternate energy source namely ketone bodies which are derived from the breakdown of fat. At this time, the brain begins to consume more amount of acetoacetate in place of glucose. After 3 days of starvation, about a third of the energy needs of the brain are met by ketone bodies. The heart, kidney and liver also use ketone bodies as fuel. During the first days of starving, the brain continues to use glucose extensively as fuel. In prolonged fasting( greater than 2 or 3 weeks), plasma ketone bodies reach significantly elevated levels and replace glucose as the primary source of fuel for the brain. This reduces the need for protein catabolism for gluconeogenesis. The metabolic changes that occur during fasting ensure that all the tissues have an adequate supply of fuel molecules.
As fasting continues into early starvation and beyond, the kidney plays a very important role. Kidney expresses the enzymes of glucnepgenesis, including glucose 6- Phosphatase and in late fasting about 50% of gluconeogenesis occurs. The kidney also provides compensation for the acidosis that accompanies increased production of ketone bodies. The glutamine released from the muscle metabolism of branched chain amino acids is taken by the kidney and acted upon by renal glutaminase producing ketoglutarate that can enter the TCA cycle. In long term fasting there is a switch from nitrogen disposal in the form of urea to disposal in the form of ammonia. (Champe et al, 2000)
After several weeks of starvation, the brain uses ketone bodies as a major source of fuel. Acetoacetate is activated by the transfer of CoA from Succinyl CoA to give acetoacetyl CoA. Ketone bodies become an equivalent supplement of fatty acids that can pass through the blood brain barrier 40 g of glucose will be needed per day for the brain to function as compared to 120g of glucose on the first day of starvation. The effective conversion of fatty acids to ketone bodies by the liver which is used by the brain and other organs markedly diminishes the need for glucose and hence less muscle is degraded as compared to the first days of starvation. A person’s survival time depends upon the size of the triacylglycerol depot. Once the triacylglycerol stores deplete the only other source of fuel is from proteins in the body. Protein degradation accelerates in the body and this induces death inevitably by the loss of liver, kidney or heart function. The present study confirms that there has been a significant change in the cardiovascular, metabolic and hormonal changes accompanying acute starvation. (Champe et al, 2000)
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