Muscle Fatigue: Causes, Mechanisms, and Consequences, Diapositivas de Fisiología

¡Descarga Muscle Fatigue: Causes, Mechanisms, and Consequences y más Diapositivas en PDF de Fisiología solo en Docsity! Muscle Fatigue DOMS (muscle soreness) Overtraining Rhabdomyolysis oa Muscle fatigue can be classified as:  Temporary: due to strenuous physical activities. The time to recover from muscle fatigue will depend on the extent of the intensity and length of the physical task. On average, the individual should be fully recovered within 3 to 5 days. The usual intervention to speed up muscle recovery involves massage, cold compression, and light analgesics’ intake. However, muscle fatigue lasting beyond 2 weeks should require medical attention.  Chronic: related to muscle wasting mediated by aging, immobilization, insulin resistance, diseases associated with systemic inflammation (arthritis, sepsis, infections, trauma, heart failure, chronic obstructive pulmonary disease (COPD)), chronic kidney failure, muscle dystrophies, muscle myopathies, multiple sclerosis, and, more recently, coronavirus disease 2019 (COVID-19). Muscle Fatigue: Inability to maintain a given exercise intensity or power output. Individual is rarely completely fatigued – He/She can maintain lower intensity output Contributions of PCr (light green), glycolysis (medium green) and oxidative phosphorylation (dark green) to ATP turnover during maximal exercise. Muscle samples were obtained before and during 30 s of all-out cycling exercise 1.- Déficit of ATP production. Energy Systems and Fatigue When we feel fatigued, we often express this by saying “I have no energy.” Can a deficit of substrates necessary for ATP synthesis cause fatigue during exercise? 1.1.- PCr depletion • Biopsy studies of human muscle have shown that during repeated maximal contractions, fatigue coincides with PCr depletion  • Causality or Chance? • Possibly, intracellular accumulation of Pi, which increases during intense short-term exercise because of the breakdown of ATP, is a potential cause of fatigue in this type of exercise. • Pi impairs myofibrillar performance altering the crossbridge turnover and reduces Ca2+ release from the Sarcoplasmic Reticulum 1.2.- Glycogen Depletion • Diverse studies have shown a correlation between muscle glycogen. depletion and fatigue during prolonged exercise. • As with PCr use, the rate of muscle glycogen depletion is controlled by the intensity of the activity. • Increasing the intensity results in a higher rate of muscle glycogen breakdown. • During sprint running, for example, muscle glycogen may be used 35 to 40 times faster than during walking. • The perception of severe fatigue does not occur until muscle glycogen levels are very low. • Marathon runners experience a sudden onset of fatigue at 29 to 35 km (“hitting the wall”). At least part of this sensation is due to muscle glycogen depletion. Carbohydrate loading can delay fatigue, thus improving performance, sparing muscle glycogen levels. The utilization of extramuscular and intramuscular carbohydrate and fat fuels, along with the major sites of regulation at key enzymes and transport proteins. Interactions between anaerobic and aerobic pathways, and between carbohydrate and fat, ensure the ATP supply for contracting skeletal muscle. FFA, free fatty acids; PM, plasma membrane; FABPPM, plasma membrane fatty acid–binding protein; FATP, fatty acid transport protein; ATG, adipose triglyceride; HS, hormone sensitive; MG, monoglyceride; TG, triglyceride; FABPc, cytoplasmic fatty acid binding protein; HK, hexokinase; PFK, phosphofructokinase; LDH, lactate dehydrogenase; Cr, creatine; mtCK, mitochondrial creatine kinase; mt OM and mt IM, outer and inner mitochondrial membrane; ACT, acyl-CoA transferase; MCT, monocarboxylase transporter; ANT, adenine transport; PDH, pyruvate dehydrogenase; ETC, electron-transport chain. Fig. 4: Key metabolic pathways in contracting skeletal muscle during exercise. 2.- Accumulation of metabolic by-products 2.1.- Pi  Commented previously regarding ATP-PCr depletion. 2.2.- Heat. • Energy expenditure results in heat production, causing core temperature to rise. • High muscle temperature could impair skeletal muscle function  • Time to exhaustion is affected by ambient temperature: • In a study, time to exhaustion was longest at 11º C and shorter at colder and warmer temperatures. • Precooling of muscles prolongs exercise, while preheating causes earlier fatigue. 2.3.- Lactic Acid and Hydrogen ions • Activities of short duration and high intensity, such as sprint running and sprint swimming, depend on anaerobic glycolysis and produce large amounts of lactate and H+ within the muscles. • Lactate by itself is not responsible for fatigue (in fact, it is a fuel source), but hydrogen ion is capable of decreasing pH both inside and outside of muscle cells. • Fortunately, the cells and body fluids possess buffers, such as proteins and bicarbonate (HCO3 ―), that minimize the disrupting influence of the H+. • Because of the body’s buffering capacity, the H+ concentration does not rise exponentially during the most severe exercise, allowing muscle pH to decrease from a resting value of 7.1 to no lower than 6.6 to 6.4 at exhaustion. • However, pH changes of this magnitude can already affect energy production and muscle contraction. • An intracellular pH below 6.9 starts to inhibit the action of phosphofructokinase, an important glycolytic enzyme, slowing the rate of glycolysis and ATP production. • At a pH of 6.4, glycogen breakdown is stopped, causing a rapid decrease in ATP and ultimately exhaustion. • H+ may displace calcium within the fiber, interfering with the coupling of the actin-myosin cross-bridges and decreasing the muscle’s contractile force. 4.- Central Nervous System (CNS) and Fatigue • The CNS plays a role in most types of fatigue, perhaps limiting performance as a protective mechanism. • Indeed, the perceived discomfort of fatigue (psychological fatigue) precedes the onset of muscular (physiological) fatigue. • Athletes who feel exhausted can often be encouraged to continue by various signals that stimulate the CNS, such as listening music or shouts of encouragement and support. • Unless they are highly motivated, most individuals terminate exercise before their muscles are physiologically exhausted. • The precise mechanisms by which the CNS exert these actions is at present unknown 5. Heart and Lung as sites of Fatigue • No evidence that heart and lungs are sites of fatigue. • Arterial PO2 and Cardiac Output are maintained during exercise. • Heart and respiratory muscles can utilize lactate or FFA as energy fuels as well as glycogen ECG  no signs of ischemia at maximal effort or fatigue. • If there were signs  heart disease • With severe dehydration due to prolonged exercise  Cardiac arrhythmias are possible Delayed-Onset Muscle Soreness (DOMS)  Dolor Muscular Tardío o Agujetas • Appears 24 - 48 hours after strenuous exercise. • Not due to lactic acid microcrystals!!!!!!!!!!!!!! • Due to microscopic tears in muscle fibers or connective tissue that results in cellular degradation and inflammatory response. • Eccentric exercise (running downhill) causes more damage than concentric exercise (cycling) • It is interesting to slowly begin a specific exercise to avoid DOMS • The symptoms of DOMS disappear in a couple of days as the injury is repaired. • Muscle damage appears to be a precipitating factor for muscle hypertrophy. Overreaching • An increased training volume without adequate recovery may propitiate the athlete to fall during a few days or weeks into a state of fatigue called overreaching. • This state is relatively common during the training process and runs parallel to a decreased performance. • Done correctly, this allows the body to adapt to the increased training stimulus, and this transitory decrement in performance lasting several days to several weeks is followed by an increase in performance (supercompensation). Overtraining • If recovery is inadequate and/or training loads are still too high, the athlete can experiment an unexplained decline in performance that extends over weeks, months or even years. • This condition is termed overtraining, and its precise causes are not fully understood. Research has pointed to both psychological and physiological causes. Common Symptoms of Overtraining Symptoms of Overtraining: • Elevated heart rate at rest • • Decreased Heart Rate Variability  Increased sympathetic tone. • Elevated heart rate and blood lactate levels during exercise. • Loss in body weight  Due to reduction in appetite. • Chronic fatigue, sleep disturbances. • Psychological staleness: irritability, restlessness, excitability, loss of motivation and vigor; lack of mental concentration; feelings of depression. • Frequent colds • Decrease in performance Excessive, prolonged or repetitive exercise may overstretch the sarcoplasmic reticulum Skeletal muscle! | LADA ) )a protein fibers ¡2 ] Sarcoplasmic 7 Reticulum $] Increase in E into muscle cell Activation of sarcolemma (cell membrane): release degrading enzymes Increase in sarcolemma permeability Release of harmful proteins in blood that may cause renal failure, blood clotting, heart arrhythmias Rhabdomyolysis becomes clinically relevant when the muscle damage is severe, which can lead to Acute Renal Failure Damaged muscle cells release into the bloodstream diverse intracellular products, such as potassium ions, Myoglobin, and Enzymes (CK, Transaminases, Lactate Dehydrogenase). • Myoglobin (Molecular Mass = 17800 daltons) is filtrated by the glomerulus and excreted by urine, giving it a dark color, like cola or tea. If serum myoglobin concentration is very high (as in severe muscle damage), it can precipitate into the renal tubules causing acute renal failure and even death. The most common signs and symptoms of rhabdomyolysis include • Severe muscle pain in the entire body, • Muscle weakness, • Dark urine: cola- or tea-colored urine. Diagnosis: • The patient`s medical history (anamnesis), including his/her signs and symptons: severe muscle pain, dark-color urine… • High serum levels of Creatinkinase (can also be observed in DOMS) • Hyperkalemia  Potassium from broken muscle fibers enters the bloodstream. • If acute renal failure: serum elevation of creatinine.