Exercise physiology
Exercise physiology is the physiology of physical exercise. It is one of the allied health professions, and involves the study of the acute responses and chronic adaptations to exercise. Exercise physiologists are the highest qualified exercise professionals and utilise education, lifestyle intervention and specific forms of exercise to rehabilitate and manage acute and chronic injuries and conditions.
Understanding the effect of exercise involves studying specific changes in muscular, cardiovascular, and neurohormonal systems that lead to changes in functional capacity and strength due to endurance training or strength training. The effect of training on the body has been defined as the reaction to the adaptive responses of the body arising from exercise or as "an elevation of metabolism produced by exercise".
Exercise physiologists study the effect of exercise on pathology, and the mechanisms by which exercise can reduce or reverse disease progression.
History
British physiologist Archibald Hill introduced the concepts of maximal oxygen uptake and oxygen debt in 1922. Hill and German physician Otto Meyerhof shared the 1922 Nobel Prize in Physiology or Medicine for their independent work related to muscle energy metabolism. Building on this work, scientists began measuring oxygen consumption during exercise. Notable contributions were made by Henry Taylor at the University of Minnesota, Scandinavian scientists Per-Olof Åstrand and Bengt Saltin in the 1950s and 60s, the Harvard Fatigue Laboratory, German universities, and the Copenhagen Muscle Research Centre among others.In some countries it is a Primary Health Care Provider. Accredited Exercise Physiologists are university-trained professionals who prescribe exercise-based interventions to treat various conditions using dose response prescriptions specific to each individual.
Energy expenditure
Humans have a high capacity to expend energy for many hours during sustained exertion. For example, one individual cycling at a speed of through over 50 consecutive days expended a total of 1,145 MJ with an average power output of 173.8 W.Skeletal muscle burns 90 mg of glucose each minute during continuous activity, generating ≈24 W of mechanical energy, and since muscle energy conversion is only 22–26% efficient, ≈76 W of heat energy. Resting skeletal muscle has a basal metabolic rate of 0.63 W/kg making a 160 fold difference between the energy consumption of inactive and active muscles. For short duration muscular exertion, energy expenditure can be far greater: an adult human male when jumping up from a squat can mechanically generate 314 W/kg. Such rapid movement can generate twice this amount in nonhuman animals such as bonobos, and in some small lizards.
This energy expenditure is very large compared to the basal resting metabolic rate of the adult human body. This rate varies somewhat with size, gender and age but is typically between 45 W and 85 W.
Total energy expenditure due to muscular expended energy is much higher and depends upon the average level of physical work and exercise done during the day. Thus exercise, particularly if sustained for very long periods, dominates the energy metabolism of the body. Physical activity energy expenditure correlates strongly with the gender, age, weight, heart rate, and VO2 max of an individual, during physical activity.
Metabolic changes
Rapid energy sources
Energy needed to perform short lasting, high intensity bursts of activity is derived from anaerobic metabolism within the cytosol of muscle cells, as opposed to aerobic respiration which utilizes oxygen, is sustainable, and occurs in the mitochondria. The quick energy sources consist of the phosphocreatine system, fast glycolysis, and adenylate kinase. All of these systems re-synthesize adenosine triphosphate, which is the universal energy source in all cells. The most rapid source, but the most readily depleted of the above sources is the PCr system which utilizes the enzyme creatine kinase. This enzyme catalyzes a reaction that combines phosphocreatine and adenosine diphosphate into ATP and creatine. This resource is short lasting because oxygen is required for the resynthesis of phosphocreatine via mitochondrial creatine kinase. Therefore, under anaerobic conditions, this substrate is finite and only lasts between approximately 10 to 30 seconds of high intensity work. Fast glycolysis, however, can function for approximately 2 minutes prior to fatigue, and predominantly uses intracellular glycogen as a substrate. Glycogen is broken down rapidly via glycogen phosphorylase into individual glucose units during intense exercise. Glucose is then oxidized to pyruvate and under anaerobic conditions is reduced to lactic acid. This reaction oxidizes NADH to NAD, thereby releasing a hydrogen ion, promoting acidosis. For this reason, fast glycolysis can not be sustained for long periods of time.Plasma glucose
Plasma glucose is said to be maintained when there is an equal rate of glucose appearance and glucose disposal. In the healthy individual, the rates of appearance and disposal are essentially equal during exercise of moderate intensity and duration; however, prolonged exercise or sufficiently intense exercise can result in an imbalance leaning towards a higher rate of disposal than appearance, at which point glucose levels fall producing the onset of fatigue. Rate of glucose appearance is dictated by the amount of glucose being absorbed at the gut as well as liver glucose output. Although glucose absorption from the gut is not typically a source of glucose appearance during exercise, the liver is capable of catabolizing stored glycogen as well as synthesizing new glucose from specific reduced carbon molecules in a process called gluconeogenesis. The ability of the liver to release glucose into the blood from glycogenolysis is unique, since skeletal muscle, the other major glycogen reservoir, is incapable of doing so. Unlike skeletal muscle, liver cells contain the enzyme glycogen phosphatase, which removes a phosphate group from glucose-6-P to release free glucose. In order for glucose to exit a cell membrane, the removal of this phosphate group is essential. Although gluconeogenesis is an important component of hepatic glucose output, it alone cannot sustain exercise. For this reason, when glycogen stores are depleted during exercise, glucose levels fall and fatigue sets in. Glucose disposal, the other side of the equation, is controlled by the uptake of glucose by the working skeletal muscles. During exercise, despite decreased insulin concentrations, muscle increases GLUT4 translocation and glucose uptake. The mechanism for increased GLUT4 translocation is an area of ongoing research.glucose control:
As mentioned above, insulin secretion is reduced during exercise, and does not play a major role in maintaining normal blood glucose concentration during exercise, but its counter-regulatory hormones appear in increasing concentrations. Principle among these are glucagon, epinephrine, and growth hormone. All of these hormones stimulate liver glucose output, among other functions. For instance, both epinephrine and growth hormone also stimulate adipocyte lipase, which increases non-esterified fatty acid release. By oxidizing fatty acids, this spares glucose utilization and helps to maintain blood sugar level during exercise.
Exercise for diabetes:
Exercise is a particularly potent tool for glucose control in those who have diabetes mellitus. In a situation of elevated blood glucose, moderate exercise can induce greater glucose disposal than appearance, thereby decreasing total plasma glucose concentrations. As stated above, the mechanism for this glucose disposal is independent of insulin, which makes it particularly well-suited for people with diabetes. In addition, there appears to be an increase in sensitivity to insulin for approximately 12–24 hours post-exercise. This is particularly useful for those who have type II diabetes and are producing sufficient insulin but demonstrate peripheral resistance to insulin signaling. However, during extreme hyperglycemic episodes, people with diabetes should avoid exercise due to potential complications associated with ketoacidosis. Exercise could exacerbate ketoacidosis by increasing ketone synthesis in response to increased circulating NEFA's.
Type II diabetes is also intricately linked to obesity, and there may be a connection between type II diabetes and how fat is stored within pancreatic, muscle, and liver cells. Likely due to this connection, weight loss from both exercise and diet tends to increase insulin sensitivity in the majority of people. In some people, this effect can be particularly potent and can result in normal glucose control. Although nobody is technically cured of diabetes, individuals can live normal lives without the fear of diabetic complications; however, regain of weight would assuredly result in diabetes signs and symptoms.
Oxygen
Vigorous physical activity increases the body's demand for oxygen. The first-line physiologic response to this demand is an increase in heart rate, breathing rate, and depth of breathing.Oxygen consumption during exercise is best described by the Fick Equation: VO2=Q x, which states that the amount of oxygen consumed is equal to cardiac output multiplied by the difference between arterial and venous oxygen concentrations. More simply put, oxygen consumption is dictated by the quantity of blood distributed by the heart as well as the working muscle's ability to take up the oxygen within that blood; however, this is a bit of an oversimplification. Although cardiac output is thought to be the limiting factor of this relationship in healthy individuals, it is not the only determinant of VO2 max. That is, factors such as the ability of the lung to oxygenate the blood must also be considered. Various pathologies and anomalies cause conditions such as diffusion limitation, ventilation/perfusion mismatch, and pulmonary shunts that can limit oxygenation of the blood and therefore oxygen distribution. In addition, the oxygen carrying capacity of the blood is also an important determinant of the equation. Oxygen carrying capacity is often the target of exercise aids used in endurance sports to increase the volume percentage of red blood cells, such as through blood doping or the use of erythropoietin. Furthermore, peripheral oxygen uptake is reliant on a rerouting of blood flow from relatively inactive viscera to the working skeletal muscles, and within the skeletal muscle, capillary to muscle fiber ratio influences oxygen extraction.