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Exercise physiology is the physiology of physical exercise. It is one of the allied health professions that involves the study of the acute responses and chronic adaptations to exercise.

Understanding the effect of exercise involves studying specific changes in muscular, cardiovascular, and neurohumoral systems that lead to changes in functional capacity and strength due to endurance training or strength 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 of metabolism produced by exercise'.^[4]

Exercise physiologists study the effect of exercise on pathology, and the mechanisms by which exercise can reduce or reverse disease progression.

• 3Metabolic changes
• 4Brain
• 5Fatigue
• 10Education in exercise physiology

History[edit]

See also:Exercise § History; Aerobic exercise § History

British physiologist Archibald Hill introduced the concepts of maximal oxygen uptake and oxygen debt in 1922.^[5][6] Hill and German physician Otto Meyerhof shared the 1922 Nobel 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 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.^[8][9]

These days, 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 specific dose response prescriptions specific to each individual.

Energy expenditure[edit]

Humans have a high capacity to expend energy 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 182.5 W.^[10]

Skeletal muscle burns 90 mg (0.5 mmol) 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 a basal 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 as bonobos,^[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 a 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, and VO₂ max of an individual, during physical activity.^[19]

Metabolic changes[edit]

Rapid energy sources[edit]

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 (PCr) system, fast glycolysis, and adenylate kinase. All of these systems re-synthesize adenosine 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 enzyme creatine kinase. This enzyme catalyzes a reaction that combines phosphocreatine and adenosine diphosphate (ADP) 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 predominately 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. Lastly, adenylate kinase catalyzes a reaction by which 2 ADP are combined to form ATP and adenosine monophosphate (AMP). This reaction takes place during low energy situations such as intense exercise or conditions of hypoxia, but it is not a significant source of energy. The creation of AMP resulting from this reaction stimulates AMP-activated protein kinase (AMP kinase) which is the energy sensor of the cell. After sensing low energy conditions, AMP kinase stimulates various other intracellular enzymes geared towards increasing energy supply and decreasing all anabolic, or energy requiring, cell functions.^{[citation needed]}

Plasma glucose[edit]

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 stored glycogen (glycogenolysis) as well as synthesizing new glucose from specific reduced carbon molecules (glycerol, pyruvate, and lactate) 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 can not 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 uptake of glucose at the working skeletal muscles. During exercise, despite decreased insulin concentrations, muscle increases GLUT4 translocation of 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 (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.

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 (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 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.^[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.

Oxygen[edit]

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 in heart rate, breathing rate, and depth of breathing.

Oxygen consumption (VO₂) during exercise is best described by the Fick Equation: VO₂=Q x (a-vO₂diff), which states that the amount of oxygen consumed is equal to cardiac 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 through blood doping or the use of erythropoietin (EPO). 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.

Dehydration[edit]

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 by sweat-based thermoregulation. A male marathon 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]

Other[edit]

• Plasma catecholamine concentrations increase 10-fold in whole body exercise.^[25]
• Ammonia is produced by exercised skeletal muscles from ADP (the precursor of ATP) by purine nucleotide deamination and amino acidcatabolism of myofibrils.^[26]
• interleukin-6 (IL-6) increases in blood circulation due to its release from working skeletal muscles.^[27] This release is reduced if glucose is taken, suggesting it is related to energy depletion stresses.^[28]
• Sodium absorption is affected by the release of interleukin-6 as this can cause the secretion of arginine vasopressin which, in turn, can lead to exercise-associated dangerously low sodium levels (hyponatremia). This loss of sodium in blood plasma can result in swelling of the brain. This can be prevented by awareness of the risk of drinking excessive amounts of fluids during prolonged exercise.^[29][30]

Brain[edit]

At rest, the human 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 upon aerobic 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 its EEG 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 upon motor 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 Chord Injury, Cerebral Palsy and mental health conditions.

Cerebral oxygen[edit]

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]

Glucose[edit]

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 with lactate. Research suggests that this can be raised, when a person rests in a brain scanner, to about 17%,^[40] with a higher percentage of 25% occurring during hypoglycemia.^[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]

Hyperthermia[edit]

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 also can lower cerebral blood flow,^[47][48] and raise brain temperature.^[34]

Fatigue[edit]

Intense activity[edit]

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 factor determining exercise performance, at least during brief very intense exercise.

Each muscle contraction involves an action potential that activates voltage sensors, and so releases Ca²⁺ ions from the muscle fibre’s sarcoplasmic reticulum. The action potentials that cause this also require ion changes: Na influxes during the depolarization phase and K effluxes for the repolarization 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 1 ryanodine receptor) channels has also been identified with fatigue.^[54]

Endurance failure[edit]

After intense prolonged exercise, there can be a collapse in body homeostasis. Some famous examples include:

• Dorando Pietri in the 1908 Summer Olympicmen’s marathon ran the wrong way and collapsed several times.
• Jim Peters in the marathon of the 1954 Commonwealth Games staggered and collapsed several times, and though he had a five-kilometre (three-mile) lead, failed to finish. Though it was formerly believed that this was due to severe dehydration, more recent research suggests it was the combined effects upon the brain of hyperthermia, hypertonic hypernatraemia associated with dehydration, and possibly hypoglycaemia.^[55]
• Gabriela Andersen-Schiess in the woman’s marathon at the Los Angeles 1984 Summer Olympics in the race’s final 400 meters, stopping occasionally and shown signs of heat exhaustion. Though she fell across the finish line, she was released from medical care only two hours later.

Central governor[edit]

Tim Noakes, based on an earlier idea by the 1922 Nobel Prize in Physiology or Medicine winner Archibald Hill^[56] has proposed the existence of a central 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 as fatigue 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 as Dorando Pietri, Jim Peters and Gabriela Andersen-Schiess) can override it.^[62]

Other factors[edit]

Exercise fatigue has also been suggested to be effected by:

• brain hyperthermia^[63]
• glycogen depletion in brain cells^[42][64]
• reactive oxygen species impairing skeletal muscle function^[65]
• reduced level of glutamate secondary to uptake of ammonia in the brain^[26]
• Fatigue in diaphragm and abdominal respiratory muscles limiting breathing^[66]
• Impaired oxygen supply to muscles^[67]
• Ammonia effects upon the brain^[26]
• Serotonin pathways in the brain^[68]

Cardiac biomarkers[edit]

Prolonged exercise such as marathons can increase cardiac biomarkers such as troponin, B-type natriuretic peptide (BNP), and ischemia-modified (aka MI) albumin. This can be misinterpreted by medical personnel as signs of myocardial infarction, or cardiac 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).^[69][70][71]

Human adaptations[edit]

Humans are specifically adapted to engage in prolonged strenuous muscular activity (such as efficient long distance bipedal running).^[72] This capacity for endurance running may have evolved to allow the running down of game animals by persistent slow but constant chase over many hours.^[73]

Central to the success of this is the ability of the human body, unlike that of the animals they hunt, 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 specialized thermoregulation based on sweat evaporation. One gram of sweat can remove 2,598 J of heat energy.^[74] 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 of sweat glands, combined with a lack of body fur that would otherwise stop air circulation and efficient evaporation.^[75] 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.^[76]

Selective breeding experiments with rodents[edit]

Rodents have been specifically bred for exercise behavior or performance in several different studies.^[77] For example, laboratory rats have been bred for high or low performance on a motorized treadmill with electrical stimulation as motivation.^[78] The high-performance line of rats also exhibits increased voluntary wheel-running behavior as compared with the low-capacity line.^[79] In an experimental evolution approach, four replicate lines of laboratory mice have been bred for high levels of voluntary exercise on wheels, while four additional control lines are maintained by breeding without regard to the amount of wheel running.^[80] These selected lines of mice also show increased endurance capacity in tests of forced endurance capacity on a motorized treadmill.^[81] However, in neither selection experiment have the precise causes of fatigue during either forced or voluntary exercise been determined.

Exercise-induced muscle pain[edit]

Physical exercise may cause pain both as an immediate effect that may result from stimulation of free nerve endings by low pH, as well as a delayed onset muscle soreness. The delayed soreness is fundamentally the result of ruptures within the muscle, although apparently not involving the rupture of whole muscle fibers.^[82]

Muscle pain can range from a mild soreness to a debilitating injury depending on intensity of exercise, level of training, and other factors.^[83]

There is some preliminary evidence to suggest that moderate intensity continuous training has the ability to increase someones pain threshold.^[84]

Education in exercise physiology[edit]

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 body Exercise 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 the American College of Sports Medicine.

An exercise physiologist's area of study may include but is not limited to biochemistry, bioenergetics, cardiopulmonary function, hematology, biomechanics, skeletal muscle physiology, neuroendocrine function, and central and peripheral nervous system function. Furthermore, exercise physiologists range from basic scientists, to clinical researchers, to clinicians, to sports trainers.

Colleges and universities offer exercise physiology as a program of study on various different levels, including undergraduate, graduate, and doctoral programs. The basis of Exercise Physiology as a major is to prepare students for a career in 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.^[85]

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:

• Health and risk assessment: In order to safely work with a client on the job, you must first be able to know the benefits and risks associated with physical activity. Examples of this include knowing specific injuries the body can experience during exercise, how to properly screen a client before their training begins, and what factors to look for that may inhibit their performance.
• Exercise testing: Coordinating exercise tests in order to measure body compositions, cardiorespiratory fitness, muscular strength/endurance, and flexibility. Functional tests are also used in order to gain understanding on a more specific part of the body. Once the information is gathered about a client, exercise physiologists must also be able to interpret the test data and decide what health-related outcomes have been discovered.
• Exercise prescription: Forming training programs that best meet an individuals health and fitness goals. Must be able to take into account different types of exercises, the reasons/goal for a clients workout, and pre-screened assessments. Knowing how to prescribe exercises for special considerations and populations is also required. These may include age differences, pregnancy, joint diseases, obesity, pulmonary disease, etc.^[86]

Curriculum[edit]

The curriculum for exercise physiology includes biology, chemistry, and applied 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.^[87]

See also[edit]

• Excess post-exercise oxygen consumption (EPOC)

References[edit]

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Abstract

The presumption that physical activity, i.e. exercise, as an independent and separated factor influences different aspects of cognitive mechanisms is substantially supported by the literature. The investigations of the influence of physical activity on cognitive functioning have offered several mechanisms which could explain this relationship. Physiological mechanisms including increased cerebral blood flow, changes in neurotransmitter release, structural changes in central nervous system and altered arousal levels are based on physical changes that occur in the body as a consequence of the physical activity. There is evidence that physical training selectively increases angiogenesis, synaptogenesis and neurogenesis. The role of central (BDNF) and peripheral (estrogens, corticosteroids, growth hormone, IGF-1) factors in mediation of the effects of physical exercise on brain functions, has been promoted. Also, there is convergent data on molecular and cellular level, as well as on behavioral and systemic level which support the presumption that physical activity is beneficial to cognition. These data emphasizes the importance of promotion of physical activity during the life span for the prevention of contemporary (obesity, diabetes and cardiovascular) diseases and cognitive decline in humans.

1. INTRODUCTION

There is a bulk of information obtained from studies, performed on humans, as well as on experimental animals, regarding the presumption that physical activity, especially aerobic training could demonstrate positive effect on many aspects of brain functions and cognition. The evidence from studies on animals have identified molecular and cellular changes that have occurred under the influence of physical training and could be related to the exerted effects of fitness on cognition. It has been proven that physical training selectively increases angiogenesis, synaptogenesis and neurogenesis (especially in gyrus dentatus in the hippocampus), as well as it initiates the up regulation of numerous neurothrophic factors in rat brain (, ). Nevertheless, there are numerous unanswered questions left regarding this issue. From a practical point of view there is little information on the subject of the design of an intervention which will enable an optimal effect of physical exercise on cognition and mental health. Future studies should answer questions such as when it is the best time to start the physical training, which types and which intensity of physical training are the most efficient.

2. PHYSIOLOGICAL MECHANISMS WHICH EXPLAIN THE EFFECT OF PHYSICAL TRAINING ON COGNITION

The investigations of the influence of physical activity on cognitive functioning have proposed several mechanisms which could explain this relationship (3, 4, , 6). Physiological mechanisms including increased cerebral blood flow, changes in neurotransmitter release, structural changes in central nervous system and altered arousal levels are based on physical changes that occur in the body as a consequence of the physical activity.

One of the fundamental physiological mechanisms that explains the influence of physical activity on cognition is the increased blood flow through the brain. Studies using contemporary imaging techniques, have confirmed that medium and high intensity physical training significantly increases the blood flow through the brain, providing increased supply of necessary nutrients. The stimulation of brain neurotransmitter release after acute bout of exercise has also been suggested by several authors. Increased levels of norepinephrine and its precursors (, ), epinephrine (adrenaline A) () and serotonin (, ) have been documented. Another physiological explanation of the effects of physical activity on brain functions includes structural changes in the brain as a result of exercise. Studies on animals have shown that rats exposed to increased physical activity showed increased cerebral cortex vascularization and had shorter vascular diffusion distance compared to non-exercise rats (12).

3. THE ROLE OF BDNF ON COGNITION

Numerous investigations of brain functions on molecular level have revealed an important mechanism of the effect of physical exercise on cognition. The latest studies of the physiology of cognitive processes have discovered that BDNF (Brain Derived Neurotrophic Factor) is the key molecule engaged in learning and memory. The finding that physical exercise increases the production of this molecule seems to be very important. It has been suggested that this neurotrophic factor is responsible for neuron genesis, their survival and resistance to stress, which all together facilitate the learning process. Some researches call the BDNF, “Miracle Gro” (miracle growth factor for the brain). It has also been discovered in the hippocampus, the brain region which is directly involved in learning (, ). For example, the learning capacity has been connected to the effect of BDNF on synaptic plasticity, which is a potential basis of cognitive processes (, ). This substance can increase the learning and memory capacity of rats for a short period of time, that is only one week of running on a wheel (). The effect of physical training on BDNF system is exerted through the functions of the intracellular signaling system, including calcium- calmodulin kinase II and mitogen activating protein kinase. They execute the final effects on the synthesis and on the function of CAMP response element binding protein (CREB). There is evidence suggesting that physical training significantly increases the levels of mitochondrial uncoupling protein 2, which is a factor of protection of the energy homeostasis exerted through the preservation of calcium homeostasis, the production of ATP and the control of free radicals.

Infusion of BDNF in humans enhances learning (18), while deficiency of BDNF causes disturbances in learning capacity. The fact that physical exercise rises BDNF suggests that physical exercise has a potential to enhance learning. In addition to the hypothesis that the increased BDNF caused by physical training is one of the key mechanisms of the positive effect of physical activity on learning, it is also possible that physical activity modulates some other factors that are involved in gaining new knowledge. Hyppocampal neurogenesis which is a result of physical exercise, or placement of animals in enlarged environment (, ) is related to enhanced performance on spatial memory tests.

Recent genetic studies have accentuated the importance of the role of BDNF in human brain functioning. They have discovered a series of BDNF gen polymorphisms, and have determined their possible essential role in human cognition. The substitution of an amino-acid in the coding region of the BDNF gene (val/meth) results in damaged processing and release of BDNF (). The genetic research has shown that carriers of meth-BDNF allele have weaker memory function and abnormal hippocampal activity. These cognitive effects were revealed in a sample of healthy young subjects who had not shown any noticeable signs of cognitive or neurological abnormalities (25-45 years, 641 subjects) (). Other studies additionally pointed out that meth-BDNF and separately BDNF polymorphism represent risk factors for Alzheimer disease (, ). These studies have clearly indicated that when there is a malfunction in BDNF, cognitive functions suffer long-term decline.

Recent studies have noted BDNF as a simple non-pharmacological potential factor of brain function improvement. Most recent reports confirm that regulation of BDNF protein is controlled by the expression of the BDNF gene in neurons, and the level of gene expression is modulated by a sequence of neurotransmitter interactions. Peripheral factors like blood level of circulating hormones (for example: estrogen, corticosteroids and insulin like growth factor 1) also influence BDNF and its function in the brain (). The CNS (neurotransmitter) mechanism that is involved in the regulation of BDNF gene expression is the neuronal activity. In CNS, glutamate is the predominant excitatory neurotransmitter which promotes neuronal activity. The transmission of signals by glutamate is essential for mediation of up-regulation of BDNF levels in hippocampus. Gene regulation of BDNF is additionally sensitive to numerous other neurotransmitters which have converting effects on the modulation of glutamatergic neuronal function in hippocampus. The neurotransmitter systems: acetylcholine, GABA, serotonin and noradrenalin which act as mediators in regulation of BDNF in hippocampus related to physical activity have been investigated until now (, ).

4. PERIPHERAL REGULATORY MECHANISMS

In addition to the leading role of central factors in mediation of the effects of physical activity on brain function, it is necessary to point out the importance of peripheral influences. The peripheral control of the effects of physical activity on brain function involves estrogen, corticosteroids and IGF-1. These hormones control BDNF and also modulate the neurogenesis, which is an important element of the mechanism by which physical activity exerts its effect on brain function. Estrogen: there are several possible mechanisms which could be involved in the regulation of the effect of physical activity on BDNF expression by the estrogen. The estrogen could both have a direct molecular effect on BDNF gene expression and an indirect one through stimulation of physical activity. Some beneficial effects of estrogen on the brain could be mediated by regulation of the expression of BDNF gene, aiming to increase the availability of this trophic factor. In women the presence of estrogen has proved to be necessary for the regulation of BDNF by physical activity (). The physical activity has failed to increase the levels of BDNF mRNA in rat hippocampus, after two months of estrogen deprivation. Though, when physical activity is combined with estrogen substitution, the level of BDNF is significantly increased compared to solitary estrogen substitution. The presence of estrogen in women could be a permissive factor necessary for the regulation of BDNF with physical activity. It could be pointed out that the level of voluntary physical activity depends on estrogen status. In absence of estrogen, the women are less active, while estrogen substitution returns the physical activity on normal levels ().

5. CORTICOSTEROIDS/STRESS

Represent another neuro-endocrinological mechanism which could influence the level of BDNF and may modulate the effect of physical exercise on the brain. These hormones, which are released by the adrenal gland as an answer to stressful events, can enter the brain and can bind to specific glucocorticoid receptors in order to perform a modification of gene expression. The concentration of glucocorticoid receptors in hippocampus makes this brain region particularly sensitive to the effect of stress and to glucocorticoids. Physical exercise is considered to have protective features against the negative effects of stress exposure. One of the mechanisms by which this protective features could be mediated may be through the regulation of BDNF–increased levels of glucocorticoids reduce hippocampal BDNF mRNA and protein expression (). Physical activity may neutralize stress and may confront its negative effect on two levels: behavioral and neurochemical. BDNF has been considered to have a key role in this protective effect of exercise against the consequences of stress ().

6. GROWTH HORMONE (GH) AND INSULIN DERIVED GROWTH FACTOR (IGF-1)

Aanother peripheral mechanism which could mediate the effects of exercise on BDNF in the brain is the GH/IGF-1 axis. Exercise increases circulating GH which is the main stimulator of IGF-1 production. Major quantity of circulating IGF-1 is produced in the liver, but many other tissues, including the brain, can also produce IGF-1. IGF-1 may have multiple biological effects on processes like neurogenesis, learning, cognition, amyloidal processing and other systematic effects (,). IGF-1 and BDNF act through different signal pathways. It has been supposed that in order to promote the health of the brain and its plasticity these factors could act separately and also in a synergistic way.

Basic scientific research on animal models provide documented evidence of the positive effects of physical activity on brain health as well as its positive effects on cognition and learning which could lead to more efficient adaptation. Physical activity induces BDNF mRNA production in glutamate neurons in hippocampus and some other brain regions (). In current literature on research on humans it has been strongly suggested that BDNF influences cognitive functions, while BDNF polymorphism (related to protein processing and release) in animals has been related with reduced cognitive function. This has been a very important discovery which suggests that animal studies could be translated into human studies. In human research there has been a small number of clinical studies with placebo control related to BDNF and cognition. Most of the studies are descriptive, based on retrospective analyzes. Never the less, the existing literature suggests that physical exercise i.e. increased aerobic fitness is one of the variables that consistently appears as a predictor of higher cognitive functions as well as of lower depressiveness in humans (, ).

Long term physical exercise increases the expression of neurotrophic factors. It may also have a neurogenerative and neuroprotective effect in the brain, which could be exerted by stimulation of new cells growth and development and by the protection of neurons from ischemic damages ().

Influence of other lifestyle factors on cognition

Some interesting and intriguing studies have been conducted with an aim to determine whether physical activity interacts with other lifestyle factors during its influence on cognition and brain health. For example, Molten and all () have investigated the interaction between the effect of diet and exercise on molecular level, through their effects on BDNF and learning. They reported that physical exercise diminishes the negative effects of diet rich with lipids on BDNF and learning. In another study, the effects of physical activity on hippocampal neurogenesis have substantially been reduced and postponed in a group of socially isolated rodents, compared to those animals which were kept in group (). These results suggest that further research on the interaction between social factors and physical activity and their effect on brain function and cognition in humans should be conducted. In current literature, there are several epidemiological prospective studies on influence of different lifestyle factors and physical exercise on cognition and neurodegenerative disorders. Carp and al, have reported that cognitive, physical and social activities reduced the risk of dementia in 778 adult subjects during three year period. Subjects with highest scores on all three mentioned variables showed biggest benefit ().

Despite the research reviewed above, there are several gaps in our understanding of the relation of physical activity and cognitive functions. To date, the majority of research studies assessing this relationship have been cross-sectional in nature. Longitudinal randomized controlled trials are necessary to elucidate causal influence between physical activity, brain structure and brain processes. Research is needed to understand the optimal physical activity criteria that target cognitive and brain health: the frequency, the duration, the intensity and the mode of physical activity. While some understanding of the mechanisms supporting exercise-induced changes in cognition is provided through animals models, many molecular and cellular details in the human brain steel remain to be discovered.

7. CONCLUSION

The number of studies which indicate the beneficial effects of physical activity on different cognitive functions is constantly growing (). These studies suggest that physical activity improves executive functions (, , ), attention (, ), cognitive speed (, ) and episodic memory (). Cardiovascular training has been related to improvement of cognitive functions in aging people (43). Sedentary subjects who participated in a protocol with cardio aerobic exercise had significant benefit in the volume of both grey and white matter in several brain regions, such as prefrontal and temporal cortex (). It has been suggested that those brain regions undergo negative structural changes related to aging. These studies are compatible with reports of neuronal proliferation and survival, growth of capillary vessels and an increased number of dendrite extensions in certain brain structures, which could be related to beneficial effects of physical exercise on cognition in humans and animals (, , -).

It has been suggested that aerobic exercise is potentially important not only for stopping the neuronal decline caused by aging process, but also is a potentially efficient mechanism for roll-back of some normal functions that have been disturbed due to reductions in brain structure related to aging (-).

Physical activity has been suggested to be a useful tool for the reduction of the risk for cognitive impairment related to aging. Future randomized studies should investigate different levels of physical activity and its type, that could be recommended with an aim to prevent or postpone cognitive decline.

There is convergent evidence on molecular and cellular level, also on behavioral and systemic levels, which emphasizes the importance of promotion of physical activity during the life span for the prevention of contemporary (obesity, diabetes and cardiovascular) diseases and cognitive and neurologic decline in people. In addition to its role in health promotion, physical activity could also reduce the economic burden to society related to chronic degenerative diseases.

REFERENCES

Molecular And Cellular Exercise Physiology Pdf Notes Pdf

Molecular And Cellular Exercise Physiology Pdf Notes Online