"Excess post-exercise oxygen consumption Excess post-exercise oxygen consumption (EPOC, informally called afterburn) is a measurably increased rate of oxygen intake following strenuous activity. In historical contexts the term ""oxygen debt"" was popularized to explain or perhaps attempt to quantify anaerobic energy expenditure, particularly as regards lactic acid/lactate metabolism; in fact, the term ""oxygen debt"" is still widely used to this day. However, direct and indirect calorimeter experiments have definitively disproven any association of lactate metabolism as causal to an elevated oxygen uptake. In recovery, oxygen (EPOC) is used in the processes that restore the body to a resting state and"
"is produced more quickly than it is being removed and it serves to regenerate NAD cells on where it's needed. During intense exercise when oxygen is not being used, a high amount of ATP is produced and pH levels fall causing acidosis or more specifically lactic acidosis. Lactic acid build up can be treated by staying well-hydrated throughout and especially after the workout, having an efficient cool down routine and good post-workout stretching. Intense activity can cause significant and permanent damage to bodily tissues. In order to repair, vitamin E and other antioxidants are needed to protect muscle damage. Oxidation"
"Substrates are depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions. In essence, the muscle stops contracting because it lacks the energy to do so. Metabolites are the substances (generally waste products) produced as a result of muscular contraction. They include chloride, potassium, lactic acid, ADP, magnesium (Mg), reactive oxygen species, and inorganic phosphate. Accumulation of metabolites can directly or indirectly produce metabolic fatigue within muscle fibers through interference with the release of calcium (Ca) from the sarcoplasmic reticulum or reduction of the sensitivity of contractile molecules actin and myosin to calcium. Intracellular chloride partially"
"though not producing fatigue, it can inhibit or even stop performance if the intracellular concentration becomes too high. However, long-term training causes neovascularization within the muscle, increasing the ability to move waste products out of the muscles and maintain contraction. Once moved out of muscles with high concentrations within the sarcomere, lactic acid can be used by other muscles or body tissues as a source of energy, or transported to the liver where it is converted back to pyruvate. In addition to increasing the level of lactic acid, strenuous exercise causes the loss of potassium ions in muscle and causing"
"match the cells' demand for ATP, and lactic acidosis results. Also, muscle types that have few mitochondria and preferentially use glycolysis for ATP production (fast-twitch or type II fibers) are naturally prone to lactic acidosis. Lactic acidosis is also a consequence of the processes causing ""rigor mortis"". In the absence of oxygen, tissue in the muscles of the deceased carry out anaerobic metabolism using muscle glycogen as the energy source, causing acidification. With depletion of muscle glycogen, the loss of ATP causes the muscles to grow stiff, as the actin-myosin bonds cannot be released. (Rigor is later resolved by enzymatic"
"within the muscle cells themselves. New research from scientists at Columbia University suggests that muscle fatigue is caused by calcium leaking out of the muscle cell. This makes less calcium available for the muscle cell. In addition, the Columbia researchers propose that an enzyme activated by this released calcium eats away at muscle fibers. Substrates within the muscle generally serve to power muscular contractions. They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate. ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model. Creatine phosphate stores energy"
"contractions that last between 5–7 seconds. Glycogen is the intramuscular storage form of glucose, used to generate energy quickly once intramuscular creatine stores are exhausted, producing lactic acid as a metabolic byproduct. Contrary to common belief, lactic acid accumulation doesn't actually cause the burning sensation we feel when we exhaust our oxygen and oxidative metabolism, but in actuality, lactic acid in presence of oxygen recycles to produce pyruvate in the liver which is known as the Cori cycle. Substrates produce metabolic fatigue by being depleted during exercise, resulting in a lack of intracellular energy sources to fuel contractions. In essence,"
"and plasmalemma and its epimysium, perimysium, and/or endomysium. The mysium damage disrupts calcium homeostasis in injured fibers and fiber bundles, resulting in necrosis that peaks about 48 hours after exercise. The products of macrophage activity and intracellular contents (such as histamines, kinins, and K) accumulate outside cells. These substances then stimulate free nerve endings in the muscle; a process that appears accentuated by eccentric exercise, in which large forces are distributed over a relatively small cross-sectional area of the muscle . There is a known relationship between inflammation and muscle growth. For instance, high doses of anti-inflammatory medicines (e.g., NSAIDs)"
"They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate. ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model. Creatine phosphate stores energy so ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5–7 seconds. Glycogen is the intramuscular storage form of glucose, used to generate energy quickly once intramuscular creatine stores are exhausted, producing lactic acid as a metabolic byproduct. Substrate shortage is one of the causes of metabolic fatigue."
"high force production causes a high influx of calcium into the muscle fibers increasing calcium permeability. Calcium ions build up in the mitochondria, impairing cellular respiration. The mitochondria are unable to produce enough ATP to power the cell properly. Reduction in ATP production impairs the cells ability to extract calcium from the muscle cell. The ion imbalance causes calcium-dependent enzymes to activate which break down muscle proteins even further. A high concentration of calcium activates muscle cells, causing the muscle to contract while inhibiting its ability to relax. The increase of sustained muscle contraction leads to oxygen and ATP depletion"
"exercise as well as other cellular functions requires oxygen to produce ATP and properly function. This normal function is called aerobic metabolism and does not produce lactic acid if enough oxygen is present. During heavy exercise such as long distance running or any demanding exercise, the body's need for oxygen to produce energy is higher than the oxygen supplied in the blood from respiration. Anaerobic metabolism to some degree then takes place in the muscle and this less ideal energy production produces lactic acid as a waste metabolite. If the oxygen supply is not soon restored, this may lead to"
"there is a shortage of oxygen (anaerobic exercise, explosive movements), carbohydrate is consumed more rapidly because the pyruvate ferments into lactate. If the intensity of the exercise exceeds the rate with which the cardiovascular system can supply muscles with oxygen, it results in buildup of lactate and quickly makes it impossible to continue the exercise. Unpleasant effects of lactate buildup initially include the burning sensation in the muscles, and may eventually include nausea and even vomiting if the exercise is continued without allowing lactate to clear from the bloodstream. As glycogen levels in the muscle begin to fall, glucose is"
"Lactic acid is now used as a measure of endurance training effectiveness and VO2 max. Muscle weakness may be due to problems with the nerve supply, neuromuscular disease (such as myasthenia gravis) or problems with muscle itself. The latter category includes polymyositis and other muscle disorders. Muscle fatigue may be due to precise molecular changes that occur ""in vivo"" with sustained exercise. It has been found that the ryanodine receptor present in skeletal muscle undergoes a conformational change during exercise, resulting in ""leaky"" channels that are deficient in calcium release. These ""leaky"" channels may be a contributor to muscle fatigue"
"cell. This causes there to be less calcium available for the muscle cell. In addition an enzyme is proposed to be activated by this released calcium which eats away at muscle fibers. Substrates within the muscle generally serve to power muscular contractions. They include molecules such as adenosine triphosphate (ATP), glycogen and creatine phosphate. ATP binds to the myosin head and causes the ‘ratchetting’ that results in contraction according to the sliding filament model. Creatine phosphate stores energy so ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful"
"effect was first hypothesized by A.V. Hill and H. Lupton in 1922. They theorized that the body needs to replace the oxygen used by working muscles during mild to intense bouts of exercise. More recently, researchers have used the term 'excess post-exercise oxygen consumption' to describe the different events that occur as the body restores itself to homeostasis, or rest. The body’s metabolic rate will be raised for a longer period post- exercise from high intensity bouts of exercise. Depending on the level of stress and intensity of exercise, metabolic increase can be seen for up to 18–24 hours. Exercises"
"so ATP can be rapidly regenerated within the muscle cells from adenosine diphosphate (ADP) and inorganic phosphate ions, allowing for sustained powerful contractions that last between 5–7 seconds. Glycogen is the intramuscular storage form of glucose, used to generate energy quickly once intramuscular creatine stores are exhausted, producing lactic acid as a metabolic byproduct. Contrary to common belief, lactic acid accumulation doesn't actually cause the burning sensation we feel when we exhaust our oxygen and oxidative metabolism, but in actuality, lactic acid in presence of oxygen recycles to produce pyruvate in the liver, which is known as the Cori cycle."
"thick filament moves or slides along the thin filament, resulting in muscle contraction. This process is known as the sliding filament model. The binding of the myosin heads to the muscle actin is a highly regulated process. The thin filament is made of actin, tropomyosin, and troponin. The contraction of skeletal muscle is triggered by nerve impulses that in turn stimulate the release of Ca. The release of Ca from the sarcoplasmic reticulum causes an increase in the concentration of Ca in the cytosol. Calcium ions then bind to troponin, which is associated with tropomyosin. Binding causes changes in the"
"the effect of various techniques are therefore subject to heavy inquiry. Although static stretching (see image on the right for an example) is part of some warm-up routines, a study in 2013 indicated that it weakens muscles. For this reason, an active dynamic warm-up (movement of the muscle groups with lights weights for example) is recommended before exercise in place of static stretching. Studies have shed light on the function, in stretching, of a large protein within the myofibrils of skeletal muscles named titin. A study performed by Magid and Law demonstrated that the origin of passive muscle tension (which"
"by the UPR in response to the exercise-induced ER stress. Muscular contraction during exercise causes calcium to be released from the sarcoplasmic reticulum (SR), a specialized ER network in skeletal muscles. This calcium then interacts with calcineurin and calcium/calmodulin-dependent kinases that in turn activate transcription factors. These transcription factors then proceed to alter the expression of exercise-regulated muscle genes. PGC-1alpha, a transcriptional coactivator, is a key transcription factor involved in mediating the UPR in a tissue-specific manner in skeletal muscles by coactivating ATF6alpha. Therefore, PGC-1alpha gets expressed in muscles after acute and long-term exercise training. The function of this transcription"
"Delayed onset muscle soreness Delayed onset muscle soreness (DOMS) is the pain and stiffness felt in muscles several hours to days after unaccustomed or strenuous exercise. The soreness is felt most strongly 24 to 72 hours after the exercise. It is thought to be caused by eccentric (lengthening) exercise, which causes small-scale damage (microtrauma) to the muscle fibers. After such exercise, the muscle adapts rapidly to prevent muscle damage, and thereby soreness, if the exercise is repeated. Delayed onset muscle soreness is one symptom of exercise-induced muscle damage. The other is acute muscle soreness, which appears during and immediately after"
"action potentials that cause this require also 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. Ca leakage from type 1 ryanodine receptor) channels has also been identified with fatigue. After intense prolonged exercise, there can be a collapse in body homeostasis. Some famous examples include: Tim"
"normally stored in the sarcoplasmic reticulum accumulates in the damaged muscles. Cellular respiration is inhibited and ATP needed to actively transport calcium back into the sarcoplasmic reticulum is also slowed. This accumulation of calcium may activate proteases and phospholipases which in turn break down and degenerate muscle protein. This causes inflammation, and in turn pain due to the accumulation of histamines, prostaglandins, and potassium. An earlier theory posited that DOMS is connected to the build-up of lactic acid in the blood, which was thought to continue being produced following exercise. This build-up of lactic acid was thought to be a"
"common risk factor for exertional rhabdomyolsis because it causes a reduction of plasma volume during exertion. This leads to a reduction of blood flow through the vascular system which inhibits blood vessel constriction. Exertional rhabdomyolysis, the exercise-induced muscle breakdown that results in muscle pain/soreness, is commonly diagnosed using the urine myoglobin test accompanied by high levels of creatine kinase (CK). Myoglobin is the protein released into the bloodstream when skeletal muscle is broken down. The urine test simply examines whether myoglobin is present or absent. When results are positive the urine normally obtains a dark, brown color followed by serum"
"is due to the change in elastin stiffness. Elastin serves an important function in arteries as a medium for pressure wave propagation to help blood flow and is particularly abundant in large elastic blood vessels such as the aorta. Elastin is also very important in the lungs, elastic ligaments, elastic cartilage, the skin, and the bladder. It is present in all vertebrates above the jawless fish. Elastin is made by linking together many small soluble precursor tropoelastin protein molecules (50-70 kDa), to make the final massive insoluble, durable complex. The unlinked tropoelastin molecules are not normally available in the cell,"
"reported for skeletal muscle. Catalase is an enzyme that removes hydrogen peroxide, a reactive oxygen species, and thus limits oxidative DNA damage. In mice, when catalase expression is increased specifically in mitochondria, oxidative DNA damage (8-OHdG) in skeletal muscle is decreased and lifespan is increased by about 20%. These findings suggest that mitochondria are a significant source of the oxidative damages contributing to aging. Protein synthesis and protein degradation decline with age in skeletal and heart muscle, as would be expected, since DNA damage blocks gene transcription. In a recent study Piec et al. found numerous changes in protein expression"
"oxygen, fermentation prevents the buildup of NADH in the cytoplasm and provides NAD+ for glycolysis. This waste product varies depending on the organism. In skeletal muscles, the waste product is lactic acid. This type of fermentation is called lactic acid fermentation. In strenuous exercise, when energy demands exceed energy supply, the respiratory chain cannot process all of the hydrogen atoms joined by NADH. During anaerobic glycolysis, NAD+ regenerates when pairs of hydrogen combine with pyruvate to form lactate. Lactate formation is catalyzed by lactate dehydrogenase in a reversible reaction. Lactate can also be used as an indirect precursor for liver"
"exercise. The soreness is perceived as a dull, aching pain in the affected muscle, often combined with tenderness and stiffness. The pain is typically felt only when the muscle is stretched, contracted or put under pressure, not when it is at rest. This tenderness, a characteristic symptom of DOMS, is also referred to as ""muscular mechanical hyperalgesia"". Although there is variance among exercises and individuals, the soreness usually increases in intensity in the first 24 hours after exercise. It peaks from 24 to 72 hours, then subsides and disappears up to seven days after exercise. The muscle soreness is caused"
"made through continuous training. Another important issue is the regulation of blood flow during exercise. Blood flow must increase in order to provide the working muscle with more oxygenated blood which can be accomplished through neural and chemical regulation. Blood vessels are under sympathetic tone; therefore, the release of noradrenaline and adrenaline will cause vasoconstriction of non-essential tissues such as the liver, intestines, and kidneys, and decrease neurotransmitter release to the active muscles promoting vasodilatation. Also, chemical factors such as a decrease in oxygen concentration and an increase in carbon dioxide or lactic acid concentration in the blood promote vasodilatation"
"and other slowly digesting carbohydrates, which release energy in a more stable fashion than high-glycemic sugars and starches. This is important as high-glycemic carbohydrates cause a sharp insulin response, which places the body in a state where it is likely to store additional food energy as fat. However, bodybuilders frequently do ingest some quickly digesting sugars (often in form of pure dextrose or maltodextrin) after a workout. This may help to replenish glycogen stored within the muscle, and to stimulate muscle protein synthesis. The motor proteins actin and myosin generate the forces exerted by contracting muscles. Current advice says that"
"only molecule that can trigger the Bohr effect. If muscle cells aren't receiving enough oxygen for cellular respiration, they resort to lactic acid fermentation, which releases lactic acid as a byproduct. This increases the acidity of the blood far more than CO alone, which reflects the cells' even greater need for oxygen. In fact, under anaerobic conditions, muscles generate lactic acid so quickly that pH of the blood passing through the muscles will drop to around 7.2, which causes haemoglobin to begin releasing roughly 10% more oxygen. The magnitude of the Bohr effect is usually given by the formula formula_1."
"immune cells. Recent studies have shown the ability of exercise to control oxidative stress and inflammation in cardiovascular disease. A proinflammatory cytokine may be present in adipose tissues. Adipocytes generate TNF-α and other interleukins. Cytokines derived from adipose tissue serve as remote regulators such as hormones. Studies have shown that TNF-α and IL-6 concentrations are elevated in obesity. Obesity leaves an excess of nutrients for the body, thereby causing adipocytes to release more proinflammatory cytokines. Classically activated macrophages in the visceral fat accumulate in the fat tissues and continuously release proinflammatory cytokines, causing chronic inflammation in obese individuals. TNF-α, IL-1"
"This contrasts with composition of the dry outside air at sea level, where the partial pressure of oxygen is 21 kPa (or 160 mm Hg) and that of carbon dioxide 0.04 kPa (or 0.3 mmHg). During heavy breathing (hyperpnea), as, for instance, during exercise, inhalation is brought about by a more powerful and greater excursion of the contracting diaphragm than at rest (Fig. 8). In addition the ""accessory muscles of inhalation"" exaggerate the actions of the intercostal muscles (Fig. 8). These accessory muscles of inhalation are muscles that extend from the cervical vertebrae and base of the skull to the"
"soreness and muscle soreness not caused by lactate production during intense exercise. Some have shown a weak correlation: however, the majority of recent studies discount the relationship. One study has shown that athletes who perform an appropriate cool-down are less likely to become injured. Cool downs should involve the following important steps to ensure an effective cool down. After exercise, a gradual yet continuous decrease in exercise intensity (such as from a hard run to an easy jog to a brisk walk) should be the first step in cooling down the body. Duration can vary for different people, but 3–10"