Exercise Physiology Essays and Research Papers

Instructions for Exercise Physiology College Essay Examples

Title: Atkins diet Metabolic or not

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Essay Instructions: I am going to give you the writing specifications as well as the information to be used. This is a disscussion section only for a scientific writing class. I have turned in my rough draft and recieved considerable comments on how to improve. I am not actually asking you to write a paper from scratch, but actually taking what ?i have written and fixing the problem areas but adding to or deleting parts you think dont need to be there. The two points I have chosen are
1) Answer the question of whether weight loss occurs as a result of a metabolic advantage or a negative energy balance. 2)low-carbohydrate/ high fat diets on endurance athletes we see a trend in the studies that found the diet to be beneficial. How does it affect or improve performance?

I will give you specifications first and then provide you with my paper as is.
Effects of Low-carbohydrate Diets and Exercise on Body Weight and Composition:
1. How does diet affect weight and fat loss?
2. What's the rationale behind popular low-carbohydrate diets, like the Atkins diet?
3. Does any research support the Atkins diet?
4. Are low-carbohydrate/high-fat diets maintainable?
5. How does exercise affect weight and fat loss?
6. What energy sources fuel exercise?
7. What's the optimal diet for exercise and athletic performance?
8. What are the mechanisms of fatigue during exercise?

1. How does diet affect weight and fat loss?
As you've likely learned, the conventional view of weight control simply involves energy (calorie) intake and expenditure:
? Weight maintenance: energy intake = energy expended
? Weight gain: energy intake > energy expended (positive energy balance)
? Weight loss: energy intake < energy expended (negative energy balance)
In light of these equations, nutrition scientists who subscribe to conventional dietary approaches argue for the "calorie theory": regardless of the diet plan or exercise program, weight loss occurs only when caloric expenditure exceeds caloric intake.
In contrast to the conventional view, supporters of low-carbohydrate diets contend that the calorie theory is a myth. Instead, they argue for a "metabolic advantage" associated with the effects of carbohydrate restriction on energy metabolism. The key to this so-called advantage involves a metabolic shift, in which the body markedly reduces its use of carbohydrate and relies heavily on fatty acids and a fat-derived compound called ketones.
The two sides of this nutrition debate could not be more directly opposed. For example, the American Dietetic Association (ADA) recommends that for obese individuals dietary fat intake should not exceed 30 % of the total caloric intake. On such a diet, carbohydrate contributes over 50% of the total number of calories. In addition, the ADA advises eating mostly unsaturated fats. In contrast, the fat and carbohydrate content in Dr. Atkins' diet can be greater than 60 % and less than 10%, respectively; in addition, Atkins does not limit total calorie intake and saturated fats.
With regard to scientific support for the "optimal diet" for weight/fat loss, the only thing we know for certain is that this issue is unresolved due to inconsistent research approaches and findings. Below, we discuss this research and the conceptual arguments for low-carbohydrate diets.
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2. What's the rationale behind popular low-carbohydrate diets, like the Atkins diet?
Here we summarize the main conceptual premises of Dr. Atkins' view, along with common responses that characterize the conventional approach.
Premise 1: Obesity results from a metabolic disorder involving excessive insulin levels?a condition called hyperinsulinism; the key to losing fat is reversing hyperinsulinism by restricting dietary carbohydrates.
According to the late Dr. Atkins, the main culprit in obesity is insulin. This hormone, which is produced by the pancreas, is primarily responsible for maintaining blood glucose levels. When glucose levels are high, insulin is released to move glucose from the blood to the liver and muscles, where it is stored as glycogen. However, if glycogen stores in the liver and muscles are full, insulin converts glucose into fat for storage. Through various mechanisms, insulin promotes fat storage and inhibits fat breakdown. Thus, supporters of Atkins argue that high levels of insulin (hyperinsulinism) account for weight gain through the accumulation of adipose tissue.
What causes hyperinsulinism? Atkins' answer is dietary carbohydrates. Insulin is released from the pancreas in response to increases in blood glucose, which occur after you eat a high-carbohydrate meal. In contrast, only small amounts of insulin are released after you eat a high-protein or high-fat meal (i.e., with little carbohydrate). So Atkins reasons that if obese individuals severely restrict carbohydrate intake, and thereby reverse hyperinsulinism, their bodies won't store fat; instead, their bodies will burn fat. The first phase of the Atkins Diet requires restricting carbohydrate to approximately 20-40 grams a day, which would be a few ounces of orange juice or a few cups of lettuce. In contrast, professional organizations such as the ADA advise eating around 300 grams of carbohydrates a day.
Nutrition scientists and health professionals who oppose low-carbohydrate diets argue that Atkins has confused cause and effect. Atkins says that eating a lot of carbohydrates causes hyperinsulinism, which leads to obesity because insulin is a fat-storing hormone. In contrast, the conventional view is that obesity causes hyperinsulinism and that overeating causes obesity, regardless of whether people are overeating carbohydrates, fats, or protein. This last point is extremely important for you to understand, so let's make sure to discuss it in class.
Premise 2: The "calorie theory" is a myth; low-carbohydrate diets promote a "metabolic advantage" through the effects of ketosis.
The calorie theory is based on the conventional idea that weight gain and loss are governed simply by imbalances between energy intake and energy expenditure. People gain weight if they take in more calories than they expend, and people lose weight if they take in fewer calories than they expend. According to this concept, "a calorie is a calorie." It doesn't matter, with respect to weight loss, whether calories come from carbohydrates, fats, or proteins (see Golay et al., 1996 for support of the calorie theory).
Atkins argues that the calorie theory is a myth. Accordingly, people on his diet can eat as much food as they want, as long as they restrict carbohydrates. Atkins bases his argument on the effects of low-carbohydrate diets on physiological mechanisms associated with insulin reduction and ketone production/excretion. In the paragraphs below, we very briefly introduce the mechanisms. To better understand them you should read the chapters on the physiology of ketosis by McDonald (Larry will assign these chapters sometime during the first few weeks of the semester).
In theory, the Atkins diet works by shifting the source of primary source energy metabolism from carbohydrates to fat. Under "normal" dietary conditions (i.e., a balanced diet with relatively high levels of carbohydrate), the body uses glycogen/glucose, fatty acids, and protein for energy; normally, the brain uses only glucose for energy. However, dietary carbohydrate restriction, which occurs in individuals on the Atkins diet, reduces the body's levels of glycogen and glucose. Thus, the body must rely on other energy substrates for making ATP. Of course, the immediate choices are protein and fat. Unless the individual is starving the body tries to conserve protein because it is essential for producing key enzymes and for maintaining muscle mass. Also, the brain cannot use protein for energy. Thus, fat (in the form of free fatty acid) becomes the primary energy source for individuals on the Atkins diet within a day or so after they begin restricting carbohydrates. By approximately three days after an individual begins the Atkins diet, the body begins to produce large amounts of ketones, as a result of the incomplete breakdown of free fatty acids in the liver. The muscles and brain can use ketones for energy.
Atkins argues that the state of ketosis (i.e., producing ketones for energy) underlies the metabolic advantage of his diet. He has contended that ketones accumulate in the body and that they are eventually eliminated, in the urine, in an unused form. Considering that ketones are derived from fat, supporters of the Atkins diet argue that ketone excretion reflects fat leaving the body without going through normal metabolic pathways. Some supporters refer to this mechanism in terms of fat "melting off the body."
However, supporters of the conventional diet contend that the Atkins diet offers no metabolic advantage. Opponents of Atkins argue that weight loss in individuals on low-carbohydrate diets comes from sources other than fat. For example, one argument is that these diets cause weight loss through dehydration. When carbohydrate intake is restricted, glycogen stores in the muscle and liver are reduced through the process of glycogenolysis. One gram of glycogen is typically stored with 3-4 grams of water; therefore, as glycogenolysis occurs during the early phases of a low-carbohydrate diet, this water is consequently released from the cells and ultimately from the body.
Opponents also argue that muscle mass is reduced in individuals on low-carbohydrate diets. Because liver glycogen stores are quickly depleted in individuals who severely restrict carbohydrate intake, a process known as gluconeogenesis is initiated by the liver to continue the maintenance of plasma glucose. Gluconeogenesis is the process by which glucose is formed from non-carbohydrate substances, mainly lactate, glycerol and amino acids (proteins). Opponents of low-carbohydrate diets argue that this process leads to considerable loss of muscle mass, because proteins (which constitute muscle) are being used for energy. However, considerable controversy surrounds this issue (see Vazquez & Adibi, 1992).
Premise 3: Low-carbohydrate/high-fat diets reduce hunger.
Atkins argues that people on his diet can eat as much as they want because weight and fat loss will occur through the so-called metabolic advantage. However, he also says that the diet eliminates hunger. Although considerable debate surrounds this issue, some research indicates that fat and protein are indeed more satiating than carbohydrate (see Cecil et al., 1999 for evidence supporting the satiating effects of high-fat diets, but also see Holt et al., 1999 for an opposing argument). Thus, according to Atkins, people on his diet gain a greater advantage?even beyond the metabolic advantage?because they take in fewer calories. Actually, that point has been emphasized by those who oppose the Atkins Diet because it supports the calorie theory and suggests that the only way to lose weight is to create a negative energy balance.
Premise 4: Low-carbohydrate/high-fat diets are "heart healthy."
Atkins claims that a low-carbohydrate/high-fat diet can reverse heart disease. He reasons that, because the body is burning so much fat for energy, fat does not accumulate in the bloodstream and coronary arteries in the form of triglycerides and LDL cholesterol. Atkins cites evidence from recent studies showing that cholesterol levels responded favorably in subjects who ate low-carbohydrate/high-fat diets (see Sharman et al., 2002 and Westman et al., 2002). Specifically, he argues that his diet reduces LDL cholesterol and triglycerides, and that it increases HDL cholesterol. This area raises perhaps the greatest controversy regarding low-carbohydrate/high-fat diets. The conventional wisdom has been that high-fat diets promote heart disease through increasing total and LDL cholesterol, while reducing HDL cholesterol (see Vidon et al., 2001 and Grundy, 1999 for support of the conventional view).
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3. Does any research support the Atkins diet?
Yes, since the 1950s, many studies have been published with results that can be interpreted to support the Atkins diet (see Freedman et al., 2001 for a review). In these studies, subjects ate diets that had identical numbers calories ("isocaloric" diets) but different percentages of carbohydrate and fat. The rationale behind this design is that if the calorie theory is correct, weight and fat loss should be the same across different diet groups (i.e., as long as the subjects were reducing their calorie intake by the same amount and expending the same number of calories). In a study supporting the calorie theory, Golay et al. (1996) found no differences in weight fat loss between subjects who ate a 1,000 calorie per day diet that consisted of either 15% carbohydrate or 45% carbohydrate.
In contrast, one early study supporting a metabolic advantage for low-carbohydrate/high-fat diets was conducted by Young et al. (1971). They assigned obese subjects to a 1,800 kcal per day diet that had either 104 grams (23.1% of total carbohydrate intake), 60 grams (13.3% of total carbohydrate intake), or 30 grams (13.3% of total carbohydrate intake) of carbohydrate per day; protein composition was identical in all three diets. Subjects on the 30 gram diet lost significantly more weight (16.18 kg) than subjects on the 60 gram diet (12.78 kg) and subjects on the 104 gram diet (11.85). Analyses of changes in body composition showed that subjects on the lowest carbohydrate diet lost mostly fat, rather than water or protein.
More recently, Volek et al. (2002) presented evidence that supports the Atkins diet for promoting greater weight and fat loss than the conventional diet. In addition, Volek et al. reported high correlations between insulin reduction and weight/fat loss, which supports Atkins' view that insulin is the culprit in obesity. Samaha et al. (2003) reported that subjects on the Atkins diet lost more weight and fat than subjects on a conventional diet; these researchers argued that subjects on the Atkins diet restricted their caloric intake to a greater degree than did subjects on the conventional diet. Foster et al. (2003) found that subjects on the Atkins diet lost more weight and fat than subjects on a conventional diet after 6 months; after 1 year, however, the amount of weight and fat loss did not differ across the two groups.
Also, as we mentioned above, recent studies have supported Atkins' argument that his diet improves cardiovascular health (Sharman et al., 2002; Westman et al., 2002).
Of course, for every study that supports the Atkins diet, a study refutes it, which makes this issue especially interesting and important. For a critical review of research comparing low- and high-carbohydrate diets, see Freedman et al. (2001).
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4. Are low-carbohydrate/high-fat diets maintainable?
Whereas many studies have shown that low-carbohydrate diets promote greater weight loss than high-carbohydrate diets, these studies have been conducted over relatively short periods, usually no longer than a month or two. However, a diet will be effective only if people can maintain it safely over relatively long periods. Opponents of low-carbohydrate diets argue that they are difficult to maintain over long periods because they lack variety, restrict essential vitamins and minerals, and cause unhealthy side effects. Whereas some studies show that people maintain high-carbohydrate/low-fat diets more successfully than low-carbohydrate/high-fat diets (Carmichael et al., 1998; Shick et al., 1998), others show that people can maintain and tolerate the latter without any problems (Phinney et al., 1983). Thus, this issue is currently unresolved.
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5. How does exercise affect weight and fat loss?
In order to describe the role of exercise in weight loss, we'll revisit the calorie theory (see tutorial question 1). Accordingly, exercise induces weight loss primarily through increasing energy expenditure. Daily energy expenditure results from three major factors: (a) resting metabolic rate (RMR), (b) the thermic effect of feeding (TEF), and (c) the thermic effect of activity (TEA). RMR includes the calories that are burned at rest in order for the body to maintain homeostasis and proper functioning. It represents the largest component of total daily energy expenditure (60-75%) and is influenced by such factors as sex, age, and body weight and composition. TEF represents the energy cost of ingesting, absorbing, metabolizing and storing food intake. TEF constitutes approximately 10% of total daily energy expenditure. TEA refers to the calories that are expended beyond both RMR and TEF, including involuntary activities such as fidgeting and shivering, as well as voluntary physical activity. TEA represents the most variable component of total daily energy expenditure. In sedentary individuals it may constitute approximately 15% of energy expended throughout the day, whereas in elite athletes it may contribute 30% of total daily energy expenditure.
The most obvious way that exercise increases total daily energy expenditure is through the direct energy cost of the exercise bout. During exercise, the body meets its demands for ATP by breaking down energy substrates (glucose, glycogen, fat, and protein). As we discuss in the following tutorial question, the degree to which specific energy substrates contribute to ATP production depends on the intensity and duration of the exercise bout. Regardless of the energy substrate used to make ATP, exercise greatly increases caloric expenditure.
Some of the increase in daily energy expenditure resulting from exercise occurs independent of the direct cost of the exercise bout. For instance, numerous studies have shown that exercise increases RMR. A question surrounding this issue is whether the exercise-induced increase in RMR results from a chronic adaptation to exercise training, or whether it is simply a prolonged elevation in energy expenditure following a single exercise bout. This phenomenon of an elevation in metabolism following the cessation of an exercise session is known as the excess post-exercise oxygen consumption (EPOC), and represents another method by which exercise may increase total daily energy expenditure.
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6. What energy sources fuel exercise?
Energy for exercise comes from the breakdown of the chemical building blocks of food?carbohydrates, proteins, and fats. As you know, the body uses these energy sources to produce ATP, which is necessary to generate muscle contractions. During exercise, the extent to which your muscles use each energy source depends on its availability and on the demands of the exercise bout, or its intensity and duration. Because the muscles typically use a relatively small and constant amount of protein, we'll focus our discussion on how fat and carbohydrate contribute to muscle contraction during exercise.
Fat is the major storage form of energy in the body. For most practical purposes, fat stores are inexhaustible, even in nonobese individuals. In a 70 kg man with 22% body fat approximately 135,000 calories are stored as fat, which would fuel approximately 45 back-to-back marathons, or approximately 1,200 miles of running. In contrast, this individual would store only 500 calories as carbohydrate in the form of muscle glycogen, which would fuel a maximum of approximately 18 miles of running. When you consider interactions between low-carbohydrate diets (like the Atkins diet) and exercise, stored glycogen levels are very important for two primary reasons. First, individuals on low-carbohydrate diets might come very close to depleting their glycogen because they are not replacing it through diet. Second, glycogen depletion is strongly associated with muscular fatigue during exercise (see tutorial question #8 below).
Because glycogen depletion causes muscle fatigue, ideally the body would spare glycogen and rely on fat as its primary energy source. At low intensities of exercise, when oxygen supply to the muscles meets their demands for oxygen (i.e., under aerobic conditions), the body does indeed rely primarily on fat to make ATP. However, as exercise intensity increases, and oxygen supply cannot meet the muscles' demands for oxygen (i.e., under anaerobic conditions), the contribution of glycogen must increase. At high intensities of exercise, the muscles cannot use fat to make ATP. The "crossover" from fat to carbohydrate metabolism is illustrated in the figure below (figure adapted from Brooks' exercise physiology textbook).

Several factors can influence the crossover effect by essentially shifting the intensity at which carbohydrate metabolism predominates. These factors include training/fitness level, gender, body composition, and diet:
? Endurance training has the effect of shifting, to the right, the point at which the crossover to carbohydrate metabolism occurs. That is, at any relative work rate, trained individuals burn more fat and less carbohydrate than their sedentary peers. As a result, glycogen depletion and fatigue are delayed. These adaptations also allow trained individuals to more rapidly replete their glycogen stores during recovery.
? Concerning gender differences, a considerable amount of research has shown that women burn relatively more fat and less carbohydrate than men during sub-maximal exercise at the same relative intensity (Braun & Horton, 2001).
? In obese individuals at rest and during exercise, studies have shown that fat mobilization and utilization are impaired (Horowitz, 2001).
? In highly trained individuals, like elite cyclists and runners, a high-fat diet can increase total fat utilization during exercise (Helge, 2000; Muoio et al., 1994).
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7. What's the optimal diet for exercise and athletic performance?
Since the earliest research on sport and exercise nutrition, the conventional view has been that high-carbohydrate diets are optimal for performance. This view is largely based on the argument that a major cause of muscle fatigue during exercise is glycogen depletion (Costill & Hargreaves, 1992). Because glycogen stores in the body are extremely limited, and dietary carbohydrate restores muscle glycogen, researchers have recommended high-carbohydrate diets for individuals who exercise and compete in sports. Most sport nutrition experts have claimed that low-carbohydrate diets contribute to fatigue because they fail to restore glycogen. In addition, the conventional view is that low-carbohydrate diets decrease pH, which might impair muscle contraction and thereby limit exercise capacity (Langfort et al., 1997; Maughan et al., 1997).
However, beginning in the early 1990s several studies produced data that support a high-fat diet for optimal performance in endurance athletes (see Helge, 2000 for a review). For example, Muoio et al. (1994) found that six college distance runners had significantly longer running times to exhaustion when they were on a high-fat diet (91 minutes) compared to a high-carbohydrate diet (75 minutes). In addition, Phinney et al. (1980) reported that exercise capacity was not impaired in obese subjects on a low-carbohydrate diet.
In contrast to the studies summarized above, Pogliaghi and Veicsteinas (1998) found that the composition of dietary carbohydrate did not affect exercise capacity at all in untrained nonobese subjects. Thus, this issue involving the optimal diet for physical performance is clearly unresolved.
Two key determinants of the effects of low-carbohydrate/high-fat diets on exercise performance are (a) the individual's fitness level and (b) the physiological demands of the activity. We discussed these factors in detail in the previous tutorial question.
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8. What are the mechanisms of fatigue during exercise?
Fatigue can be defined as the loss of power output, or the inability to maintain a given exercise intensity. Despite the fact that fatigue has been the topic of considerable research in recent decades, the primary determinants of fatigue are still largely unknown. The difficulty in elucidating the mechanisms responsible for fatigue is that no single cause exists. Fatigue is dependent upon numerous factors, including gender, training status, environmental issues and exercise type and intensity. Generally, however, many exercise scientists contend that the following mechanisms likely cause fatigue during exercise: creatine phosphate depletion, hydrogen ion accumulation (associated with lactic acid production), glycogen depletion, hypoglycemia, and serotonin accumulation in the brain. Below, we very briefly introduce these mechanisms. To learn more about them, and how they might interact with the metabolic effects of low-carbohydrate diets, refer to Maughan et al. (1997) and Langfort et al. (1997).
Creatine phosphate depletion: An immediate pathway for generating ATP involves creatine phosphate (CP), which is stored in muscle in very low amounts. This compound is broken down to donate its high-energy phosphate to ADP, thereby forming ATP. Because CP is stored in muscle tissue, it can be used instantly to fuel muscle contraction. CP is responsible for fueling high-intensity, short-duration bursts of muscle activity, such as an all-out sprint. However, the small quantity of CP in muscle can fuel only about 5 seconds of muscle contraction before the CP is exhausted. Thus, CP depletion causes muscle fatigue. To sustain high-intensity exercise, particularly anaerobic glycolysis must "kick in."
Glycogen depletion:Especially in high-intensity exercise (i.e., greater than 85% of VO2 max), glycogen is the major source of ATP production. Glycogen is broken down through the process of glycolysis. As we discussed above, because glycogen stores in body are so limited, they can be depleted in people who exercise at high intensities and fail to replenish glycogen stores through dietary carbohydrates. If glycogen stores are depleted, fatigue ensues and exercise capacity is severely limited.
It is very important to note that even under aerobic conditions glycogen depletion can limit exercise capacity. This might seem puzzling in light of the abundance of stored body fat that can be utilized for energy. However, fats cannot be properly broken down and converted to usable energy when carbohydrates are not readily available. Fatty acids are normally broken down to form acetyl Co-A through a process known as Beta-oxidation. Under normal conditions, acetyl Co-A continues down the metabolic pathways in order to create usable energy. Specifically, acetyl Co-A enters the Krebs cycle and forms the molecule citrate by combining with another molecule, oxaloacetate, which is readily converted to pyruvate. However, when glycogen levels are depleted, the liver initiates gluconeogenesis in order to maintain blood glucose levels. In order to do so, the body must create the necessary gluconeogenic precursors: pyruvate, glycerol, and certain amino acids. One way that the body achieves this is by forming pyruvate from oxaloacetate. If the need for gluconeogenesis is high, then there is an insufficient amount of oxaloacetate left to bind with acetyl Co-A, and acetyl Co-A is thus unable to enter the Krebs cycle and complete the oxidation of fats (see figure below). Therefore, because carbohydrates are essential for proper oxidation of fats, exercise physiologists often say that "fats burn in a carbohydrate flame."

MY PAPER- Please keep ideas in tact

Atkins Diet, Metabolic or Not?

In our study we were looking at the effects of a low-carbohydrate diet on body weight and composition against a calorie-reduced, fat-restricted diet. We did this study in order to answer the question of whether weight loss occurs as a result of a metabolic advantage or a negative energy balance. The cause of weight loss by metabolic advantages would be due to the body shifting from carbohydrates as the main source of energy to fat. Because the body?s glycogen and glucose levels would be down the body must rely on another source of energy, free fatty acids and ketones. In order to achieve a negative energy balance, which complies with the calorie theory, the energy intake of the subjects needs to be less than the energy expended. With all of this in mind, the most important finding of our study is that weight loss appears to occur because of a negative energy balance.
When taking a look at the total daily calorie intake of our subjects on both the conventional and Atkins diets, it was found that the subjects on the Atkins diet had a greater reduction in calorie intake over the six month study than the subjects on the conventional diet (724 kcal/month Vs 496 kcal/month). Body weight and Body fat were also lower over a six month period on the Atkins diet, rather than the conventional diet (16.2 kg & 8.1 Vs 10.8 kg & 5.2). One of the reasons for these findings could be that subjects on the Atkins diet may have experienced greater satiety. Cecil et al. supports this idea that high-fat diets are more satiating than high ?carbohydrate meals. Their results suggested that the high-fat meal suppressed hunger, induced fullness, and slowed gastric emptying. Holt et al. suggests a study that contradicts the Cecil et al. study, claiming that a high-carbohydrate diet increases satiety. However, there was a flaw in the methods of Holt et al. After the subjects ate their provided meals, they were able to leave the test center continuing normal day activities and eating what they please. Though the subjects may have eaten the high-fat diet, while being away from the testing center they may have gone back to normal eating habits of higher carbohydrates , which may have affected their satiety.
Our study does not restrict a calorie intake for the subjects on the Atkins diet, which further suggests that the subjects felt greater satiety on the low-carbohydrate, high- fat diet. With that being said we can propose the idea that the subjects on the Atkins diet chose to eat less on their own, in turn reducing their own calorie intake and creating a negative energy balance. Furthermore, the subjects were isolated in a resort and were under strict observation ensuring that they followed their diets accordingly. We can also discount the idea that the subjects may have been exercising. This supports our answer to the study question by providing evidence for the claim that weight loss was simply due to a negative energy balance and not as a result of a metabolic advantage.
Many nutrition scientists urge the ?calorie theory? and claim that a low-carbohydrate diet should not be followed and is not a healthy solution to losing weight. However, if we delve into a different aspect of our study and take a look at how a low-carbohydrate diet affects individuals who exercise we may find interesting results. A few studies have been done to observe the effects of a low-carbohydrate diet on obese individuals who are exercising while on the diet and even further how a low-carbohydrate diet affects endurance athletes.
Our study involved obese subjects, 100 on the Atkins diet and 100 on the conventional diet, who followed their respected diet plans and led sedentary life styles. By taking a look at subjects that are exercising rather than being in sedentary lifestyle while on the low-carbohydrate diet, we find that the subjects still lose weight and that they are able to perform exercise regularly or better. Studies done by Pogliaghi and Veicsteinas found that a low-carbohydrate/high fat diet does not affect exercise performance in subjects who are untrained and non-obese. However, this doesn?t mean that the subjects were affected negatively. The reason for these subjects not exemplifying any benefit from a low-carbohydrate/high fat diet may be because they have not been training. Endurance training has the effect of shifting the crossover point of carbohydrate metabolism to the right (figure in Brooks? exercise physiology book). It is also noted that trained athletes tend to be more conservative of their glucose stores by burning more fat than an untrained individual. This might explain why the studies done by Pogliaghi and Veicsteinas yielded such results as did. Furthermore, Phinney?s study, which involved obese subjects engaging in moderate exercise while on a low-carbohydrate/high fat diet, found that prolonged exercise at 60% of the subjects VO2Max can be continued for a longer period of time.
As we look at studies done on low-carbohydrate/ high fat diets on endurance athletes we see a trend in the studies that found the diet to be beneficial. The intensity of the workload was 60-75%. VO2Max. In the studies that presented results that a fat-rich diet during an endurance training program is detrimental to improvement in endurance, the exercise intensity was about 81-85% of VO2Max and the subjects were untrained to begin. It appears that as the exercise intensity increases we see a decrease in performance on a high fat diet. The reason for this is because as you increase intensity the oxygen supply can?t meet the oxygen demands of the muscles, thus shifting to and passed the point of glucose metabolism. This means that the subject at this high of intensity is beginning to burn the small amount of glucose stores they have available, from being on a high fat diet. The main reason why this low-carbohydrate/ high fat diet works is because the body, at moderate intensity, is using the fat as energy first and saving the glycogen stores.
Another point that shouldn?t go unnoticed is that the studies that yielded the best results for endurance athletes on a high fat diet had a high intake of carbohydrates as well. In Muoio et al. the high fat diet consisted of 50% carbohydrates, 38% fat, and 12% protein. The high carbohydrate diet of this study consisted of 73% carbohydrates, 15% fat, and 12% protein. The athletes that followed the high fat diet of this study ran for 91.2 minutes at 75% intensity, where as the athletes on the high carbohydrate ran for 75.8 minutes. The performance by these subjects is much better than subjects of the other studies. Since the carbohydrate intake was much higher in the high fat diet of these subjects, they had plenty of glucose stores available once hitting the point of oxygen demand exceeding oxygen supply; when the body shifts from using free fatty acids for energy to using glucose. In conclusion, a low-carbohydrate/ high fat diet does improve performance in endurance athletes and doesn?t affect untrained subjects negatively if the intensity is at 75% or lower. Also if the carbohydrate intake is higher, 40-50% of intake, in a high fat diet it proves to be more beneficial than having a high fat diet where the fat intake is 62% and the carbohydrate consumption is only 21%.

1. Greene, L. & Gentile, C. (2002). Effects of low-carbohydrate diets and exercise on body weight and composition: A tutorial for IPHY 3700. University of Colorado-Boulder, unpublished manuscript.
2. McDonald, L. (1996). The ketogenic diet: A complete guide for the dieter and practitioner: Physiology of ketosis chapters. Kearney, Nebraska: Morris Publishing.
3. Samaha et al. (2003). A low-carbohydrate as compared with a low-fat diet in severe obesity. The New England Journal of Medicine, 348, 2074-2081.
4. Helge, J.W., Richter, E.A., & Kiens, B. (1996). Interaction of training and diet on metabolism and endurance during exercise in man. Journal of Physiology, 492, 293-306.
5. Lambert, E.V., Speechly, D.P., Dennis, S.C., & Noakes, T.D. (1994). Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet. European Journal of Applied Physiology, 69, 287-293.
6. Muoio, D.M., Leddy, J.J., Horvath, P.J., Awad, A.B., & Pendergast, D.R. (1994). Effect of dietary fat on metabolic adjustments to maximal VO2 and endurance in runners. Medicine and Science in Sports and Exercise, 26, 81-88.

Feedback from professor:

1. Much of the content in this first paragraph provides a general introduction to your discussion essay. If this assignment were to write a complete discussion section, the content in this paragraph would be very appropriate. But consider that I'm going to evaluate only the content that helps you accomplish your two power goals. Also consider that in your revision you may need space to develop your ideas and arguments for accomplishing your two power goals. So, I encourage you to evaluate the content here for whether all of it is essential.

2. Good point about how the difference in calorie restriction is a likely explanation for the greater weight loss in the Atkins subjects! But how do you know that the greater calorie restriction accounted completely for the difference in weight loss between the two groups? How would you respond to an alternative argument that the metabolic advantage could have contributed, in at least a small way, to the greater weight loss in the Atkins subjects? You can answer these questions by thinking critically about our data, to analyze the degree to which the calorie restriction might have accounted for the weight loss.

3. It's good that you are using the research on diet composition and satiety to support your claim for negative energy balance as the cause of greater weight loss in our Atkins subjects. But I'm wondering whether your readers will be convinced that the Cecil study strongly supports the claim that high-fat diets are more satiating than high-carbohydrate diets. You say that the study supports the claim. But will readers simply accept your statement that Cecil's results show that high-fat meals suppress hunger? How can you strengthen your argument based on the Cecil study? I hope that we get to discuss this comment!

Also, it's good that you're considering and trying to refute the alternative argument that is supported by the results of Holt. But I don't understand your explanation of the flaw in Holt's methods. I question whether your undergraduate readers will understand the flaw as well, because they haven't read the Holt study. To understand the flaw that you're discussing, readers will need to know more about the methods and results of the Holt study. Readers might ask these questions: What do you mean by "provided meals"? What do you mean by "the high-fat diet"?

Most important, readers may not understand the idea in the last sentence of this paragraph. It's unclear how the subjects' time and activities away from the testing center could have "affected their satiety"? Here and below, I see room for improvement in descriptions and explanations of the research that support your arguments.

4. I know that your power goal for this section is to expand our research into the area involving the Atkins diet for exercising individuals. I think that you're on the right track to successfully accomplishing that power goal in this whole section. But I'm wondering whether you're taking on too big a challenge by addressing both (1) the effects of the Atkins diet on weight loss in obese individuals who are exercising and (2) the effects of the Atkins diet on performance in trained endurance athletes. These are two fairly separate issues, which require two separate sets of ideas and arguments. So, below I got confused about whether you were arguing for how the Atkins diet affects obese, sedentary individuals who exercise or how it affects trained endurance athletes.

5. Here's a place where I got confused about whether your argument involves sedentary obese individuals or athletes. The paragraph starts with ideas that expand our study, on sedentary obese individuals. You raise a good point about some studies that support the claim that subjects on low-carbohydrate diets are able to exercise successfully, or at least without any negative effects. The Pogliaghi study supports that claim. But, here, I'm confused about why you're talking about endurance training and trained athletes. I don't understand the point that you're trying to make about "shifting the crossover point of carbohydrate metabolism to the right." I doubt that your undergraduate readers will understand that point either.

6. Here's a place to evaluate the content for whether it clearly explains the research methods and results. I know that you're trying to argue that the effects of low-carbohydrate diets on athletes depend on the intensity of the endurance test in which researchers measure time to exhaustion. But consider how your undergraduate readers might respond to the idea that "the intensity of the workload was 60-75%." They might interpret this intensity to be the athletes' regular training intensity rather than the intensity of the endurance test itself.

Also, check this section for whether readers will understand the goal that you're trying to accomplish. Why are you talking about the exercise intensity in these studies? How does the content here expand our research?

7. Here you're trying to explain why the high-fat diet can enhance endurance performance. That's a great strategy. But I question whether you're providing enough physiological knowledge to help readers deeply understand your explanation. Your main point is that the diet works because the body uses fat at a moderate exercise intensity. Does that idea really explain why low-carbohydrate diets can improve endurance performance? Does the idea explain how the diet actually affects physiological mechanisms underlying performance? I hope that we get to discuss this comment!
8. I don't follow how the content in this section helps you expand our research. Readers will expect you to make an argument about how the Atkins diet (which is very low in carbs!) affects exercise performance in sedentary, obese individuals and trained athletes. But here you're saying that a relatively high-carbohydrate diet is optimal. Do you see the problem here?

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Cecil, J.E., Francis, J., & Read, N.W. (1999, August). Comparison of the effects of a high-fat and high-carbohydrate soup delivered orally and intragastrically on gastric emptying, appetite, and eating behavior. Physiology and Behavior, 67(2), 299-306.

Freedman, M.R., King, J., & Kennedy, E. (2001, March). Popular diets: a scientific review. Obesity Research, 9(1), 40-47S.

Golay A, Allaz A-F, Morel Y, de Tonnac N, Tankova S, & Reaven G. (1996). Similar weight loss with low- or high-carbohydrate diets. American Journal of Clinical Nutrition, 63, 174-8.

Helge, J.W., Richter, E.A., & Kiens, B. (1996). Interaction of training and diet on metabolism and endurance during exercise in man. Journal of Physiology, 492, 293-306.

Holt, S.H., Delargy, H.J., Lawton, C.L., & Blundell, J.E. (1999, January). The effects of high carbohydrate vs. high fat breakfasts on feelings of fullness and alertness, and subsequent food intake. International Journal of Food Science Nutrition, 50(1), 12-28.

Phinney, S.D., Bristrian, B.R., Wolfe, R.R. & Blackburn, G.L. (1983, August). The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metabolism, 32(8), 757-768.

Pogliaghi, S. & Veicsteinas, A. (1999, January). Influence of low and high dietary fat on physical performance in untrained males. Medicine & Science in Sports & Exercise, 31(1), 149-155.


1. Greene, L. & Gentile, C. (2002). Effects of low-carbohydrate diets and exercise on body weight and composition: A tutorial for IPHY 3700. University of Colorado-Boulder, unpublished manuscript.

2. McDonald, L. (1996). The ketogenic diet: A complete guide for the dieter and practitioner: Physiology of ketosis chapters. Kearney, Nebraska: Morris Publishing.

3. Samaha et al. (2003). A low-carbohydrate as compared with a low-fat diet in severe obesity. The New England Journal of Medicine, 348, 2074-2081.

4. Helge, J.W., Richter, E.A., & Kiens, B. (1996). Interaction of training and diet on metabolism and endurance during exercise in man. Journal of Physiology, 492, 293-306.

5. Lambert, E.V., Speechly, D.P., Dennis, S.C., & Noakes, T.D. (1994). Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet. European Journal of Applied Physiology, 69, 287-293.

6. Muoio, D.M., Leddy, J.J., Horvath, P.J., Awad, A.B., & Pendergast, D.R. (1994). Effect of dietary fat on metabolic adjustments to maximal VO2 and endurance in runners. Medicine and Science in Sports and Exercise, 26, 81-88.

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  • Total Pages: 15
  • Words: 4210
  • Works Cited:0
  • Citation Style: APA
  • Document Type: Research Paper
Essay Instructions: We will pay $250.00 for this order!!


Purpose: The purpose of this assignment is two fold

The first part reflects your learning regarding your performance during the self directed outdoor pursuits. This should refer to aspects of exercise physiology, skills acquisition, biomechanics, equipment, nutrition and psychology.

The second part of this assignment allows you to take a closer look at one outdoor pursuit, an aspect of it or contrast two pursuits, and apply a theoretical base to actual practice.

What do I have to do?
You are required write up your reflections regarding your levels of performance during the range of outdoor activities experienced throughout self directed learning. This must refer to aspects of human performance theory such as; exercise physiology, skills acquisition, biomechanics, equipment, nutrition and psychology.

For the second part you are required to prepare a detailed analysis of an outdoor activity and review this against available literature, comparing theory to actual practice you have personally observed.

It is permissible to study contrasting aspects of one activity (eg forward paddle strokes while kayaking on flat water and moving water), or to contrast the requirements of two activities (eg endurance for long-distance tramping compared with long-distance kayaking). The study of the energy requirement or physiological differences between carrying ones pack while tramping verses carrying your load while mountain biking or sea kayaking is also a suitable topic. The study should be based on students’ own performance.

Length of study: (part a) 2500 words min.
Length of study: (part b) 2000 words min. – 2500 max.

Criteria for assessment:
Part a (10 marks available) 2500 words
15 days (15 different outdoor activities) logged
Analysis of each day from human performance standpoint.

Part b (30 marks available) 2000 words
Clarity and coherence of objectives
Breadth and depth of literature review
Appropriateness of methodology
Consistent application of methodology
Clarity of presentation of results
Depth and clarity in discussion of results.
Appropriateness of conclusions
Standard of expression and presentation of study.

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Works Cited:


AOS. (2007). Shin Splints. American Academy of Orthopaedic Surgeons. Retrieved October 20, 2009, from: http://orthoinfo.aaos.org/topic.cfm?topic=A00407.

Braver, R. "How to Test and Treat Exertional Compartment Syndrome: Why the ECS

Diagnosis Is Often Missed" Podiatry Today; Vol. 15 (May 1, 2002). Retrieved

October 20, 2009, from: http://www.podiatrytoday.com/article/382

Howard JL, Mohtadi NG, Wiley JP. "Evaluation of outcomes in patients following surgical treatment of chronic exertional compartment syndrome in the leg."

Clinical Journal of Sport Medicine; Vol. 10, No. 3 (2000): 176-84.

Mohler IR, Styf JR, Pedowitz RA, Hargens AR, Gershuni DH. "Intramuscular deoxygenation during exercise in patients who have chronic anterior compartment syndrome of the leg." Journal of Bone and Joint Surgery; Vol. 79, No. 6 (1997):


NIH. (2009). Handout on health: Sports injuries. National Institute of Arthritis and Musculoskeletal and Skin Diseases. Retrieved October 20, 2009, from:


Schissel DJ, Godwin J. "Effort-related chronic compartment syndrome of the lower extremity." Military Medicine; Vol. 164, No. 11 (1999): 830-2.

Wilder RP, Sethi, S. "Overuse injuries: tendinopathies, stress fractures, compartment syndrome, and shin splints." Clinics in Sports Medicine; Vol. 23: 55-81 (2004).

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Title: Autobiography

  • Total Pages: 4
  • Words: 1338
  • Bibliography:0
  • Citation Style: APA
  • Document Type: Essay
Essay Instructions: Hi. I need you to write a Master's level autobiographical essay for Graduate school. I am an African-American female applying to Howard University, a historically black college. I need to talk about what I can do, in the field of Health, Human Performance and Leisure Studies; with a specialization in Exercise Physiology to help strengthen the African-American Community. What I can give back to the African-American community is important to Howard, since it's a black college. Below is a sketch of the major events in my personal and academic life. You can add whatever you need to to make my autobiography sound intelligent and interesting-life experiences, challenges-the stuff that an African-American Black Admissions Officer would find intriguing.
I can go through and add/re-add details. If at all possible, this could not be double-spaced (but 1.5)I'd greatly appreciate it. thanks a million.

Natasha Kaleena Jones, 22 year old African-American female currently residing in St. Louis MO. I recieved my
Born in Little Rock AR, 6/8/1982
moved to St. Louis MO at 1 years old. My mom's job-Southwestern Bell telephone company-transfered to St. Louis so my mom, dad, and I moved. My mom was a billing manger at SouthWestern Bell
My dad had a variety of odd jobs-bus driver, chef at local resteraunts, and a driver for Health South, a rehabilitation facility. He did not graduate from high school.
My dad and I never got a long-he was moody, controlling. My mom was and is my inspiration, my best friend, my sister.
Neither of my parents graduated from college. My mom, finally got her degree in '93 in buisness. This degree helped her recieve a job promotion.
I grew up in a virtually white middle class surburbs. Racist things were said to us by Whites but I didn't reflect on the racist too much in my life.

I grew up as an only child, a self-proclaimed introvert who perferred academics, books, and movies to the company of others. I wasn't atheletic (grew up chubby)or part of any clubs or sports in my elementary years and home life wasn't so pleasant-my parents fought a lot. I wrote poetry and listened to music to escape. As a result, I am quite a good writer (except when it comes to writing about my self!) and I have a very ecletic musical taste: R&B, trip-hop, rap, classical-about everything except for country music I love)

In high school, I was part of the yearbook and newspaper committees had a decent amount of friends and was voted class psychologist-people always came to me to talk about their problems. I was also a tomboy and found the company of guys much more appealing than females-still do.

I did well in school. I was a mostly A student. I recieved my first C in College.I went to private school all my life except for two years in St. Louis MO (Andrews Academy in elementrary school, St. Elizabeth's Academy-an all Girl catholic school for high school[had to wear uniforms and all], Haverford College, Meramac College, University of Missouri at St. Louis for undergraduate college. Recieved my BA in Psychology in May 2004.

I've work in college as a tutor for Disability Access Services (I still work there) in mostly English and various Psychology courses.

I don't know what to talk about as far as inspiration or things that have changed me. I majored in psychology because I wanted to have a science background and help others: I want to into Human health performance with a specialization in exercise physiology because *I want to learn how to provide information and scientific expertise to enable athletes and coaches to benefit from training, dietary regimes, fitness, injury prevention and to optimize performance in sport. I am interested in devising and supervising health/fitness programs for patients, as well researching the recreational aspects of sport, exercise, and health promotion
*this piece is from my personal statement-please use this as a reference point because they already have this information.

I got into health and fitness after wanting to personally improve on this aspects in my life and after my parents' illnesses: my father had a heart attack in 1997 and a stroke in 2001. My mother had a heart attack and is left permanetly disabled 2 years ago. I wanted to apply my passion (health/exercise) with science: logically exercise science was the course I wanted to take.

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Title: Physical Activity increases Testosterone

  • Total Pages: 7
  • Words: 2418
  • Sources:10
  • Citation Style: MLA
  • Document Type: Research Paper
Essay Instructions: EXS 430 Research Methods : Guidelines for Final Paper/Presentation.

In order to display comprehension of the concepts of research methods, students will complete a final paper. Students will select a topic of interest in one of the primary disciplines of exercise science (i.e. exercise physiology, biomechanics, motor learning, strength and conditioning), and write a scholarly review on the topic. Your topic must be approved by the instructor! The review should explore the current literature and summarize current thinking based on available research. A minimum of 10 references from peer-reviewed journals are required for full credit. The paper should be no more than 10 pages in length (reference and appendixes in different paper excluded)--anything over ten pages will not be read!

The topic I?ve chosen and got approved by my instructor was:
?Physical Activity enhances Testosterone?

About 7 to 8 pages should do just fine, references should be relevant on database such as, PubMed, Google Scholar, and MEDLINE.

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Works cited

Ardis, L.I. Testosterone research trends. New York: Nova Biomedical Books, 2007.

Cumming, David C, Garry D. Wheeler and Ewen M. Mccoll. "The effects of exercise on reproductive function in men." Sports Medicine 7, no. 1 (1989): 1 -- 17.

HAakonsen, Linn Berger, Ane Marie Thulstrup, Anette SkAerbech Aggerholm, JOrn Olsen, Jens Peter Bonde, Claus Yding Andersen, Mona Bungum, Emil Hagen Ernst, Mette Lausten Hansen, Erik Hagen Ernst and Others. "Does weight loss improve semen quality and reproductive hormones? Results from a cohort of severely obese men." Reprod Health 8, no. 1 (2011): 24.

Hiruntrakul, Ashira, Ratanavadee Nanagara, Alongkot Emasithi and Katarina T. Borer. "Effect of endurance exercise on resting testosterone levels in sedentary subjects." Central European journal of public health 18, no. 3 (2010).

Liu, Te-Chi, Chia-Hua Kuo and Paulus S. Wang. "Exercise and testosterone." Adapt. Med 1, (2009): 24 -- 29.

Penedo, Frank J. And Jason R. Dahn. "Exercise and well-being: a review of mental and physical health benefits associated with physical activity." Current opinion in psychiatry 18, no. 2 (2005): 189 -- 193.

Saad, Farid, Antonio Aversa, Andrea M. Isidori and Louis J. Gooren. "Testosterone as potential effective therapy in treatment of obesity in men with testosterone deficiency: a review." Current diabetes reviews 8, no. 2 (2012): 131.

Saad, Farid. "The role of testosterone in type 2 diabetes and metabolic syndrome in men." Arquivos Brasileiros de Endocrinologia & Metabologia 53, no. 8 (2009): 901 -- 907.

Schmid, P, HH Pusch, W Wolf, E Pilger, H Pessenhofer, G Schwaberger, H Pristautz and P. Purstner. "Serum FSH, LH, and testosterone in humans after physical exercise." Int J. Sports Med 3, no. 2 (1982): 84 -- 9.

Shakeri, Nader, Hojjattolah Nikbakht, Mohammad Ali Azarbayjani and Ali Mohammad Amirtash. "The effect of different types of exercise on the testosterone/cortisol ratio in untrained young males.." Annals of Biological Research 3, no. 3 (2012).

Sutton, JR, MJ Coleman, J Casey and L. Lazarus. "Androgen responses during physical exercise." British Medical Journal 1, no. 5852 (1973): 520.

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