Exercise physiology is thephysiology ofphysical exercise. It is one of theallied 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 inmuscular,cardiovascular, andneurohormonalsystems that lead to changes in functional capacity andstrength due toendurance training orstrength training.[2] The effect of training on the body has been defined as the reaction to the adaptive responses of the body arising from exercise[3] or as "an elevation ofmetabolism produced by exercise".[4]
Exercise physiologists study the effect of exercise onpathology, and the mechanisms by which exercise can reduce or reverse disease progression.
British physiologistArchibald Hill introduced the concepts ofmaximal oxygen uptake and oxygen debt in 1922.[5][6] Hill and German physicianOtto Meyerhof shared the 1922Nobel Prize in Physiology or Medicine for their independent work related to muscle energy metabolism.[7] Building on this work, scientists began measuring oxygen consumption during exercise. Notable contributions were made by Henry Taylor at theUniversity of Minnesota, Scandinavian scientistsPer-Olof Åstrand andBengt Saltin in the 1950s and 60s, the Harvard Fatigue Laboratory, German universities, and the Copenhagen Muscle Research Centre among others.[8][9]
In some countries it is a Primary Health Care Provider. Accredited Exercise Physiologists (AEP's) are university-trained professionals who prescribe exercise-based interventions to treat various conditions using dose response prescriptions specific to each individual.[citation needed]
Humans have a high capacity to expendenergy for many hours during sustained exertion. For example, one individual cycling at a speed of 26.4 km/h (16.4 mph) through 8,204 km (5,098 mi) over 50 consecutive days expended a total of 1,145 MJ (273,850 kcal; 273,850 dieter calories) with an average power output of 173.8 W.[10]
Skeletal muscle burns 90 mg (0.5mmol) of glucose each minute during continuous activity (such as when repetitively extending the human knee),[11] generating ≈24 W of mechanical energy, and since muscle energy conversion is only 22–26% efficient,[12] ≈76 W of heat energy. Resting skeletal muscle has abasal metabolic rate (resting energy consumption) of 0.63 W/kg[13] 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 asbonobos,[14] and in some small lizards.[15]
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.[16][17] Total energy expenditure (TEE) due to muscular expended energy is much higher and depends upon the average level of physical work and exercise done during the day.[18] 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, andVO2 max of an individual, during physical activity.[19]
Energy needed to perform short lasting, high intensity bursts of activity is derived fromanaerobic metabolism within thecytosol of muscle cells, as opposed toaerobic respiration which utilizes oxygen, is sustainable, and occurs in themitochondria. The quick energy sources consist of thephosphocreatine (PCr) system, fastglycolysis, andadenylate kinase. All of these systems re-synthesizeadenosine triphosphate (ATP), 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 enzymecreatine kinase. This enzyme catalyzes a reaction that combinesphosphocreatine and adenosine diphosphate (ADP) into ATP andcreatine. 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 viaglycogen 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.[citation needed]
Plasma glucose is said to be maintained when there is an equal rate of glucose appearance (entry into the blood) and glucose disposal (removal from the blood). 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 (hepatic) glucose output. Although glucose absorption from the gut is not typically a source of glucose appearance during exercise, the liver is capable of catabolizing storedglycogen (glycogenolysis) as well as synthesizing new glucose from specific reduced carbon molecules (glycerol, pyruvate, and lactate) in a process calledgluconeogenesis. 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 enzymeglycogen 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 decreasedinsulin concentrations, muscle increasesGLUT4 translocation and glucose uptake. The mechanism for increased GLUT4 translocation is an area of ongoing research.[citation needed]
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 areglucagon,epinephrine, andgrowth hormone. All of these hormones stimulate liver (hepatic) glucose output, among other functions. For instance, both epinephrine and growth hormone also stimulate adipocyte lipase, which increases non-esterified fatty acid (NEFA) release. By oxidizing fatty acids, this spares glucose utilization and helps to maintain blood sugar level during exercise.[citation needed]
Exercise for diabetes:Exercise is a particularly potent tool for glucose control in those who havediabetes mellitus. In a situation of elevated blood glucose (hyperglycemia), 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 withketoacidosis. Exercise could exacerbate ketoacidosis by increasing ketone synthesis in response to increased circulating NEFA's.[citation needed]
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.[20] 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.[citation needed]
Vigorous physical activity (such as exercise or hard labor) increases the body's demand for oxygen. The first-line physiologic response to this demand is an increase inheart rate,breathing rate, anddepth of breathing.[citation needed]
Oxygen consumption (VO2) during exercise is best described by theFick Equation: VO2=Q x (a-vO2diff), which states that the amount of oxygen consumed is equal tocardiac output (Q) 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 (ergogenic aids) aids used in endurance sports to increase the volume percentage of red blood cells (hematocrit), such as throughblood doping or the use oferythropoietin (EPO). Furthermore, peripheral oxygen uptake is reliant on a rerouting of blood flow from relatively inactiveviscera to the working skeletal muscles, and within the skeletal muscle, capillary to muscle fiber ratio influences oxygen extraction.[citation needed]
Dehydration refers both to hypohydration (dehydration induced prior to exercise) and to exercise-induced dehydration (dehydration that develops during exercise). The latter reduces aerobic endurance performance and results in increased body temperature, heart rate, perceived exertion, and possibly increased reliance on carbohydrate as a fuel source. Although the negative effects of exercise-induced dehydration on exercise performance were clearly demonstrated in the 1940s, athletes continued to believe for years thereafter that fluid intake was not beneficial. More recently, negative effects on performance have been demonstrated with modest (<2%) dehydration, and these effects are exacerbated when the exercise is performed in a hot environment. The effects of hypohydration may vary, depending on whether it is induced through diuretics or sauna exposure, which substantially reduce plasma volume, or prior exercise, which has much less impact on plasma volume. Hypohydration reduces aerobic endurance, but its effects on muscle strength and endurance are not consistent and require further study.[21] Intense prolonged exercise produces metabolic waste heat, and this is removed bysweat-basedthermoregulation. A malemarathon runner loses each hour around 0.83 L in cool weather and 1.2 L in warm (losses in females are about 68 to 73% lower).[22] People doing heavy exercise may lose two and half times as much fluid in sweat as urine.[23] This can have profound physiological effects. Cycling for 2 hours in the heat (35 °C) with minimal fluid intake causes body mass decline by 3 to 5%, blood volume likewise by 3 to 6%, body temperature to rise constantly, and in comparison with proper fluid intake, higher heart rates, lower stroke volumes and cardiac outputs, reduced skin blood flow, and higher systemic vascular resistance. These effects are largely eliminated by replacing 50 to 80% of the fluid lost in sweat.[22][24]
At rest, thehuman brain receives 15% of total cardiac output, and uses 20% of the body's energy consumption.[31] The brain is normally dependent for its high energy expenditure uponaerobic metabolism. The brain as a result is highly sensitive to failure of its oxygen supply with loss of consciousness occurring within six to seven seconds,[32] with itsEEG going flat in 23 seconds.[33] Therefore, the brain's function would be disrupted if exercise affected its supply of oxygen and glucose.
Protecting the brain from even minor disruption is important since exercise depends uponmotor control. Because humans are bipeds, motor control is needed for keeping balance. For this reason, brain energy consumption is increased during intense physical exercise due to the demands in the motor cognition needed to control the body.[34]
Exercise Physiologists treat a range of neurological conditions including (but not limited to): Parkinson's, Alzheimer's, Traumatic Brain Injury, Spinal Cord Injury, Cerebral Palsy and mental health conditions.[citation needed]
Cerebral autoregulation usually ensures the brain has priority to cardiac output, though this is impaired slightly by exhaustive exercise.[35] During submaximal exercise, cardiac output increases and cerebral blood flow increases beyond the brain's oxygen needs.[36] However, this is not the case for continuous maximal exertion: "Maximal exercise is, despite the increase in capillary oxygenation [in the brain], associated with a reduced mitochondrial O2 content during whole body exercise"[37] The autoregulation of the brain's blood supply is impaired particularly in warm environments[38]
In adults, exercise depletes the plasma glucose available to the brain: short intense exercise (35 min ergometer cycling) can reduce brain glucose uptake by 32%.[39]
At rest, energy for the adult brain is normally provided by glucose but the brain has a compensatory capacity to replace some of this withlactate. Research suggests that this can be raised, when a person rests in abrain scanner, to about 17%,[40] with a higher percentage of 25% occurring duringhypoglycemia.[41] During intense exercise, lactate has been estimated to provide a third of the brain's energy needs.[39][42] There is evidence that the brain might, however, in spite of these alternative sources of energy, still suffer an energy crisis since IL-6 (a sign of metabolic stress) is released during exercise from the brain.[26][34]
Humans use sweat thermoregulation for body heat removal, particularly to remove the heat produced during exercise. Moderate dehydration as a consequence of exercise and heat is reported to impair cognition.[43][44] These impairments can start after body mass lost that is greater than 1%.[45] Cognitive impairment, particularly due to heat and exercise is likely to be due to loss of integrity to the blood brain barrier.[46] Hyperthermia can also lower cerebral blood flow,[47][48] and raise brain temperature.[34]
Researchers once attributed fatigue to a build-up of lactic acid in muscles.[49] However, this is no longer believed.[50][51] Rather, lactate may stop muscle fatigue by keeping muscles fully responding to nerve signals.[52] The available oxygen and energy supply, and disturbances of muscle ion homeostasis are the main factors determining exercise performance, at least during brief very intense exercise.[citation needed]
Eachmuscle contraction involves anaction potential that activates voltage sensors, and so releasesCa2+ ions from themuscle fibre'ssarcoplasmic reticulum. The action potentials that cause this also require ion changes:Na influxes during thedepolarization phase and K effluxes for therepolarization phase.Cl− ions also diffuse into the sarcoplasm to aid the repolarization phase. During intense muscle contraction, the ion pumps that maintain homeostasis of these ions are inactivated and this (with other ion related disruption) causes ionic disturbances. This causes cellular membrane depolarization, inexcitability, and so muscle weakness.[53] Ca2+ leakage from type 1ryanodine receptor) channels has also been identified with fatigue.[54]
After intense prolonged exercise, there can be a collapse in bodyhomeostasis. Some famous examples include:
Tim Noakes, based on an earlier idea by the 1922Nobel Prize in Physiology or Medicine winnerArchibald Hill[56] has proposed the existence of acentral governor. In this, the brain continuously adjusts the power output by muscles during exercise in regard to a safe level of exertion. These neural calculations factor in prior length of strenuous exercise, the planned duration of further exertion, and the present metabolic state of the body. This adjusts the number of activated skeletal muscle motor units, and is subjectively experienced asfatigue and exhaustion. The idea of a central governor rejects the earlier idea that fatigue is only caused by mechanical failure of the exercising muscles ("peripheral fatigue"). Instead, the brain models[57] the metabolic limits of the body to ensure that whole body homeostasis is protected, in particular that the heart is guarded from hypoxia, and an emergency reserve is always maintained.[58][59][60][61] The idea of the central governor has been questioned since 'physiological catastrophes' can and do occur suggesting that if it did exist, athletes (such asDorando Pietri,Jim Peters andGabriela Andersen-Schiess) can override it.[62]
Exercise fatigue has also been suggested to be affected by:
Prolonged exercise such as marathons can increasecardiac biomarkers such astroponin,B-type natriuretic peptide (BNP), and ischemia-modified (aka MI)albumin. This can be misinterpreted by medical personnel as signs ofmyocardial infarction, orcardiac dysfunction. In these clinical conditions, such cardiac biomarkers are produced by irreversible injury of muscles. In contrast, the processes that create them after strenuous exertion in endurance sports are reversible, with their levels returning to normal within 24-hours (further research, however, is still needed).[70][71][72]
Humans are specificallyadapted to engage in prolonged strenuous muscular activity (such as efficient long distancebipedal running).[73] This capacity for endurance running may have evolved to allow therunning down of game animals by persistent slow but constant chase over many hours.[74]
Central to the success of this is the ability of the human body to effectively remove muscle heat waste. In most animals, this is stored by allowing a temporary increase in body temperature. This allows them to escape from animals that quickly speed after them for a short duration (the way nearly all predators catch their prey). Humans, unlike other animals that catch prey, remove heat with a specializedthermoregulation based onsweat evaporation. One gram of sweat can remove 2,598 J of heat energy.[75] Another mechanism is increased skin blood flow during exercise that allows for greater convective heat loss that is aided by our upright posture. This skin based cooling has resulted in humans acquiring an increased number ofsweat glands, combined with a lack ofbody fur that would otherwise stop air circulation and efficient evaporation.[76] Because humans can remove exercise heat, they can avoid the fatigue from heat exhaustion that affects animals chased in a persistent manner, and so eventually catch them.[77]
Rodents have been specifically bred for exercise behavior or performance in several different studies.[78] For example, laboratory rats have been bred for high or low performance on a motorized treadmill with electrical stimulation asmotivation.[79] The high-performance line of rats also exhibits increased voluntary wheel-running behavior as compared with the low-capacity line.[80] In anexperimental evolution approach, four replicate lines of laboratory mice have been bred for high levels ofvoluntary exercise on wheels, while four additional control lines are maintained by breeding without regard to the amount of wheel running.[81] These selected lines of mice also show increased endurance capacity in tests of forced endurance capacity on a motorized treadmill.[82] However, in neither selection experiment have the precise causes of fatigue during either forced or voluntary exercise been determined.[citation needed]
Physical exercise may cause pain both as an immediate effect that may result from stimulation offree nerve endings by low pH, as well as adelayed onset muscle soreness. The delayed soreness is fundamentally the result of ruptures within the muscle, although apparently not involving the rupture of wholemuscle fibers.[83]
Muscle pain can range from a mild soreness to a debilitating injury depending on intensity of exercise, level of training, and other factors.[84]
There is some preliminary evidence to suggest that moderate intensity continuous training has the ability to increase someone's pain threshold.[85]
Accreditation programs exist with professional bodies in most developed countries, ensuring the quality and consistency of education. In Canada, one may obtain the professional certification title – Certified Exercise Physiologist for those working with clients (both clinical and non clinical) in the health and fitness industry. In Australia, one may obtain the professional certification title - Accredited Exercise Physiologist (AEP) through the professional bodyExercise and Sports Science Australia (ESSA). In Australia, it is common for an AEP to also have the qualification of an Accredited Exercise Scientist (AES). The premiere governing body is theAmerican College of Sports Medicine.[citation needed]
An exercise physiologist's area of study may include but is not limited tobiochemistry,bioenergetics,cardiopulmonary function,hematology,biomechanics,skeletal muscle physiology,neuroendocrine function, and central and peripheralnervous system function. Furthermore, exercise physiologists range from basic scientists, to clinical researchers, to clinicians, to sports trainers.[citation needed]
Colleges and universities offer exercise physiology as a program of study on various different levels, including undergraduate, graduate degrees and certificates, and doctoral programs. The basis of Exercise Physiology as a major is to prepare students for a career in the field of health sciences. A program that focuses on the scientific study of the physiological processes involved in physical or motor activity, including sensorimotor interactions, response mechanisms, and the effects of injury, disease, and disability. Includes instruction in muscular and skeletal anatomy; molecular and cellular basis of muscle contraction; fuel utilization; neurophysiology of motor mechanics; systemic physiological responses (respiration, blood flow, endocrine secretions, and others); fatigue and exhaustion; muscle and body training; physiology of specific exercises and activities; physiology of injury; and the effects of disabilities and disease. Careers available with a degree in Exercise Physiology can include: non-clinical, client-based work; strength and conditioning specialists; cardiopulmonary treatment; and clinical-based research.[86]
In order to gauge the multiple areas of study, students are taught processes in which to follow on a client-based level. Practical and lecture teachings are instructed in the classroom and in a laboratory setting. These include:
The curriculum for exercise physiology includesbiology,chemistry, andapplied sciences. The purpose of the classes selected for this major is to have a proficient understanding of human anatomy, human physiology, and exercise physiology. Includes instruction in muscular and skeletal anatomy; molecular and cellular basis of muscle contraction; fuel utilization;neurophysiology of motor mechanics; systemic physiological responses (respiration, blood flow, endocrine secretions, and others); fatigue and exhaustion; muscle and body training; physiology of specific exercises and activities; physiology of injury; and the effects of disabilities and disease. Not only is a full class schedule needed to complete a degree in Exercise Physiology, but a minimum amount of practicum experience is required and internships are recommended.[88]
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