Exercise physiology is the study of the acute responses and chronic adaptations to a wide-range of
physical exercise conditions. In addition, many exercise physiologists study the effect of exercise on
pathology, and the mechanisms by which exercise can reduce or reverse disease progression. Accreditation programs exist with professional bodies in most developed countries, ensuring the quality and consistency of education.
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 perpheral
nervous system function. Furthermore, exercise physiologists range from basic scientists, to clinical researchers, to clinicians, to sports trainers.
EnergyJatasia have a high capacity to expend
energy for many hours doing sustained exercise. For example, one individual cycling at a speed of 26.4 km/h (16.4 mph) across 8,204 km (5,098 mi) on 50 consecutive days may expended a total of 1,145 MJ (273,850 kcal) with an average power output of 182.5 W.
[1]Skeletal muscle burns 90 mg (0.5
mmol) of glucose each minute in continuous activity (such as when repetitively extending the human knee),
[2] generating ≈24 W of mechanical energy, and since muscle energy conversion is only 22-26% efficient,
[3] ≈76 W of heat energy. Resting skeletal muscle has a
basal metabolic rate (resting energy consumption) of 0.63 W/kg
[4] making a 160 fold difference between the energy consumption of inactive and active muscles. For short muscular exertion, energy expenditure can be far greater: an adult human male when jumping up from a squat mechanically generates 314 W/kg, and such rapid movement can generate twice this power in nonhuman animals such as
bonobos,
[5] and in some small lizards.
[6]This energy expenditure is very large compared to the resting metabolism basal metabolic rate of the adult human body. This varies somewhat with size, gender and age but is typically between 45 W and 85 W.
[7] [8] Total energy expenditure (
TEE) due to muscular expended energy is very much higher and depends upon the average level of physical work and exercise done during a day.
[9] Thus exercise, particularly if sustained for very long periods, dominates the energy metabolism of the body.
[edit]Metabolic changes[edit]Rapid Energy SourcesEnergy needed to perform short lasting, high intensity bursts of activity is derived from
anaerobic sources 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 condition 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. This reaction takes place during low energy situations such as extreme exercise or conditions of hypoxia, but 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.
[edit]Plasma glucosePlasma glucose is maintained by an equal rate of glucose appearance (entry into the blood) and glucose disposal (removal from the blood). In the healthy individual, rate 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 along with the onset of fatigue. Rate of glucose appearance is dictated by the amount of glucose being absorbed at the gut as well as 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,
hepatocytes 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 and therefore glucose uptake. The mechanism for increased GLUT4 translocation is an area of ongoing research; however, the most well-studied mechanism involves activation of AMP activated protein kinase. Other possible mechanisms involve signaling via
nitric oxide,
reactive oxygen species, as well as a physical mechanism caused by the contraction itself.
glucose control: As mentioned above, insulin secretion is reduced during exercise, and does not play a major role in
euglycemia during exercise. Insulin's counter-regulatory hormones, however, appear in increasing concentrations during exercise. Principle among these are
glucagon,
epinephrine, and
growth hormone. All of these hormones stimulate 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 euglycemia 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 plasma glucose, or
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. 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.
[edit]OxygenOxygen 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
ergogenic aids used in endurance sports to increase
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.
[edit]DehydrationDehydration 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.
[10] 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).
[11] People doing heavy exercise may lose two and half times as much fluid in sweat as urine.
[12] 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.
[11][13] [edit]Other- Plasma catecholamine concentrations increase 10 fold in whole body exercise.[14]
- Ammonia is produced by exercised skeletal muscles from ADP (the precursor of ATP) by purine nucleotide deamination and amino acid catabolism of myofibrils.[15]
- interleukin-6 (IL-6) increases in blood circulation due to its release from working skeletal muscles.[16] This release is reduced if glucose is taken, suggesting it links to energy related stresses.[17]
- Sodium absorption is affected by the release of interleukin-6 as this can cause the secretion of arginine vasopressin which, in turn, can led to exercise-associated hyponatremia (dangerously low sodium levels). This loss of sodium in blood plasma can result in encephalopathy (caused by swelling of the brain). This can be prevented by awareness of the risk of drinking excessive amounts of fluids during prolonged exercise.[18][19]
[edit]BrainAt rest, the
human brain receives 15% of total cardiac output, and uses 20% of the body's energy consumption.
[20] 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,
[21] with its
EEG going flat in 23 seconds.
[22] If it affected the oxygen and glucose supply to the brain, the metabolic demands of exercise could therefore quickly disrupt its functioning.
Protecting the brain from even minor disruption is important since exercise depends upon
motor control, and particularly, because humans are bipeds, the motor control needed for keeping balance. Indeed, 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.
[23] [edit]Cerebral oxygenCerebral autoregulation usually ensures the brain has priority to cardiac output, though this is impaired slightly by exhaustive exercise.
[24] During submaximal exercise, cardiac output increases and cerebral blood flow increases beyond the brain’s oxygen needs.
[25] 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”
[26] The autoregulation of the brain’s blood supply is impaired particularly in warm environments
[27] [edit]GlucoseIn adults, exercise depletes the plasma glucose available to the brain: short intense exercise (35 min ergometer cycling) can reduce brain glucose uptake by 32%.
[28]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%,
[29] with a higher percentage of 25% occurring during
hypoglycemia.
[30] In intense exercise, lactate has been estimated to provide a third of the brain’s energy needs.
[31][32] 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.
[15][23] [edit]HyperthermiaHumans use sweat thermoregulation for body heat clearance, particularly to remove the heat produced during exercise. Mild dehydration as a consequence of exercise and heat is reported to impair cognition.
[33][34] These impairments can start after body mass lost that is greater than 1%.
[35] Cognitive impairment, particularly due to heat and exercise is likely to be due to loss of integrity to the blood brain barrier.
[36] Hyperthermia also can lower cerebral blood flow,
[37][38] and raise brain temperature.
[23] [edit]AmmoniaExercised skeletal muscles produces ammonia. This ammonia is taken up by the brain in proportion to its arterial concentration. Since perceived effort links to such ammonia accumulation, this could be a factor in the sensation of fatigue.
[15] [edit]Combinational exacerbationThese metabolic consequences of exercise can exacerbate each other’s negative neurological effects. For example, the uptake of ammonia by the brain is greater with glucose depletion (
CSF ammonia levels: rest, below 2 μmol min−1detection level; following 3 hours exercise with glucose supplementation, 5.3 μmol min−1, without glucose supplementation, 16.1 μmol min−1).
[15] The effects of dehydration are greater and happen at a lower threshold in hot environments.
[36] [edit]Fatigue[edit]Intense activityResearchers once attributed fatigue to a build-up of lactic acid in muscles.
[39] However, this is no longer believed.
[40][41] Indeed, lactate may stop muscle fatigue by keeping muscles fully responding to nerve signals.
[42]Instead, providing 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.
[url=http://en.wikipedia.org/wiki/Fileorando_Pietri.jpg][/url][url=http://en.wikipedia.org/wiki/Fileorando_Pietri.jpg][/url]
Dorando Pietri about to collapse at the Marathon finish at the 1908 London Olympic Games
[edit]Endurance failureAfter intense prolonged exercise, there can be a collapse in body
homeostasis. Some famous examples include:
- Dorando Pietri in the 1908 Summer Olympic men’s marathon ran the wrong way and collapsed several times.
- Jim Peters in the marathon of the 1954 Commonwealth Gamesstaggered 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.[45]
- 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.
[edit]Central governorTim Noakes, based on an earlier idea by the 1922
Nobel Prize in Physiology or Medicine winner
Archibald Hill[46] 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
[47] the metabolic limits of the body to ensure that whole body homeostasis is protected, in particular that the heart is stopped from developing myocardial ischemia, and an emergency reserve is always maintained.
[48][49][50][51] The idea of the central governor has been questioned since ‘physiological catastrophes’ can and do occur suggesting athletes (such as
Dorando Pietri,
Jim Peters and
Gabriela Andersen-Schiess) can over-ride the ‘‘central governor’.
[52] [edit]Other factorsThe exercise fatigue has also been suggested to be effected by:
[edit]Cardiac biomarkersProlonged exercise such as marathons can increase
cardiac biomarkers such as
troponin,
B-type natriuretic peptide(BNP), and ischemia-modified
albumin. This can be misinterpreted by medical personnel as signs of
myocardial ischemia, 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).
[59][60][61] [edit]Human evolutionHumans are specifically
adapted to engage in prolonged strenuous muscular activity (such as efficient long distance
bipedal running).
[62] This capacity for endurance running evolved to allow the
running down of game animals by persistent slow but constant chase over many hours.
[63]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.
[64] Another mechanism is increased skin blood flow during exercise that allows for greater convective heat loss that is aided by the upright posture. This skin based cooling has involved humans in acquiring an increased number of
sweat glands, combined with a lack of
body fur that would otherwise stop air circulation and efficient evaporation.
[65] Because humans can remove exercise heat, they can avoid the fatigue from heat exhaustion that affects animals chased in persistence hunting, and so eventually catch them when they fatigue from heat exhaustion due to being forced to move constantly.
[66] [edit]Selective breeding experiments with rodentsRodents have been specifically bred for exercise behavior or performance in several different studies.
[67] For example, laboratory rats have been bred for high or low performance on a motorized treadmill with electrical stimulation as
motivation.
[68] The high-performance line of rats also exhibits increased voluntary wheel-running behavior as compared with the low-capacity line.
[69] 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.
[70] These selected lines of mice also show increased endurance capacity in tests of forced endurance capacity on a motorized treadmill.
[71] However, in neither selection experiment have the precise causes of fatigue during either forced or voluntary exercise been determined.
[edit]Exercise-induced muscle painPhysical exercise may cause pain both as an immediate pain 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.
[72]