UMLS:C0015672 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

Query: UMLS:C0015672 (fatigue)
51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Manganese superoxide dismutase (SOD2) converts superoxide to oxygen plus hydrogen peroxide and serves as the primary defense against mitochondrial superoxide. Impaired SOD2 activity in humans has been associated with several chronic diseases, including ovarian cancer and type I diabetes, and SOD2 overexpression appears to suppress malignancy in cultured cells. We have produced a line of SOD2 knockout mice (SOD2m1BCM/SOD2m1BCM) that survive up to 3 weeks of age and exhibit several novel pathologic phenotypes including severe anemia, degeneration of neurons in the basal ganglia and brainstem, and progressive motor disturbances characterized by weakness, rapid fatigue, and circling behavior. In addition, SOD2m1BCM/SOD2m1BCM mice older than 7 days exhibit extensive mitochondrial injury within degenerating neurons and cardiac myocytes. Approximately 10% of SOD2m1BCM/SOD2m1BCM mice exhibit markedly enlarged and dilated hearts. These observations indicate that SOD2 deficiency causes increased susceptibility to oxidative mitochondrial injury in central nervous system neurons, cardiac myocytes, and other metabolically active tissues after postnatal exposure to ambient oxygen concentrations. Our SOD2-deficient mice differ from a recently described model in which homozygotes die within the first 5 days of life with severe cardiomyopathy and do not exhibit motor disturbances, central nervous system injury, or ultrastructural evidence of mitochondrial injury.
...
PMID:Neurodegeneration, myocardial injury, and perinatal death in mitochondrial superoxide dismutase-deficient mice. 879 Apr 8

High-intensity contractile activity causes a rapid fall in peak tension or force, a reduced shortening velocity, decline in power, prolonged twitch duration, a sarcolemma action potential with a prolonged duration, reduced amplitude, and a conduction velocity that may result in conduction block. The calcium transient is characterized by a reduced amplitude and prolonged duration. What is the role of hydrogen in high-intensity exercise? It may affect E-C coupling but we do not think so. It definitely inhibits the rate of force development and calcium binding to TN-C. It also definitely inhibits the cross-bridge transition from the low to high force state. It inhibits velocity or the cross-bridge cycle rate and, therefore, decreases power and, importantly, prolongs the rate of calcium reuptake by inhibiting the sarcoplasmic reticulum calcium ATPase pump. Phosphate inhibits tension by reversing the cross-bridge transition from the low to the high force state, but it does not affect cycle rate; therefore, it does not have an effect on velocity. It may be involved in decreasing the free energy of ATP hydrolysis, which would provide less energy and, most importantly, play a role in inhibiting the sarcoplasmic reticulum calcium reuptake. Finally, what does all this mean to the athlete and how can fatigue be prevented? Basically, we do not have answers to these questions, but it is clear that the athlete is going to have to have a varied training program. If an athlete trains with one particular type of exercise, fatigue will result from other factors. Thus, a heterogeneous training program is essential. Diet is very important, and warm-up and fluid replacement are all factors that are going to be important in triggering peak performance.
...
PMID:Muscle fatigue: the cellular aspects. 894 17

The manifestations of fatigue, as observed by reductions in the ability to produce a given force or power, are readily apparent soon after the initiation of intense activity. Moreover, following the activity, a sustained weakness may persist for days or even weeks. The mechanisms responsible for the impairment in performance are various, given the severe strain imposed on the multiple organ systems, tissues and cells by the activity. At the level of the muscle cell, ATP utilization is dramatically accelerated in an attempt to satisfy the energy requirements of the major processes involved in excitation and contraction namely sarcolemmal Na+/K+ exchange, sarcoplasmic reticulum Ca2+ sequestration and actomyosin cycling. In an attempt to maintain ATP levels, high-energy phosphate transfer, glycolysis and oxidative phosphorylation are recruited. With intense activity, ATP production rates are unable to match ATP utilization rates, and reductions in ATP occur accompanied by accumulation of a range of metabolic by-products such as hydrogen ions, inorganic phosphate, AMP, ADP and IMP. Selective by-products are believed to disturb Na+/K+ balance, Ca2+ cycling and actomyosin interaction, resulting in fatigue. Cessation of the activity and normalization of cellular energy potential results in a rapid recovery of force. This type of fatigue is often referred to as metabolic. Repeated bouts of high-intensity activity can also result in depletion of the intracellular substrate, glycogen. Since glycogen is the fundamental fuel used to sustain both glycolysis and oxidative phosphorylation, fatigue is readily apparent as cellular resources are exhausted. Intense activity can also result in non-metabolic fatigue and weakness as a consequence of disruption in internal structures, mediated by the high force levels. This type of impairment is most conspicuous following eccentric muscle activity; it is characterized by myofibrillar disorientation and damage to the cytoskeletal framework in the absence of any metabolic disturbance. The specific mechanisms by which the high force levels promote muscle damage and the degree to which the damage can be exacerbated by the metabolic effects of the exercise remain uncertain. Given the intense nature of the activity and the need for extensive, high-frequency recruitment of muscle fibres and motor units in a range of synergistic muscles, there is limited opportunity for compensatory strategies to enable performance to be sustained. Increased fatigue resistance would appear to depend on carefully planned programmes designed to adapt the excitation and contraction processes, the cytoskeleton and the metabolic systems, not only to tolerate but also to minimize the changes in the intracellular environment that are caused by the intense activity.
...
PMID:Mechanisms of muscle fatigue in intense exercise. 923 50

The crucial role of muscle glycogen as a fuel during prolonged exercise is well established, and the effects of acute changes in dietary carbohydrate intake on muscle glycogen content and on endurance capacity are equally well known. More recently, it has been recognized that diet can also affect the performance of high-intensity exercise of short (2-7 min) duration. If the muscle glycogen content is lowered by prolonged (1-1.5 h) exhausting cycle exercise, and is subsequently kept low for 3-4 days by consumption of a diet deficient in carbohydrate (< 5% of total energy intake), there is a dramatic (approximately 10-30%) reduction in exercise capacity during cycling sustainable for about 5 min. The same effect is observed if exercise is preceded by 3-4 days on a carbohydrate-restricted diet or by a 24 h total fast without prior depletion of the muscle glycogen. Consumption of a diet high in carbohydrate (70% of total energy intake from carbohydrate) for 3-4 days before exercise improves exercise capacity during high-intensity exercise, although this effect is less consistent. The blood lactate concentration is always lower at the point of fatigue after a diet low in carbohydrate and higher after a diet high in carbohydrate than after a normal diet. Even when the duration of the exercise task is kept constant, the blood lactate concentration is higher after exercise on a diet high in carbohydrate than on a diet low in carbohydrate. Consumption of a low-carbohydrate isoenergetic diet is achieved by an increased intake of protein and fat. A high-protein diet, particularly when combined with a low carbohydrate intake, results in metabolic acidosis, which ensues within 24 h and persists for at least 4 days. This appears to be the result of an increase in the circulating concentrations of strong organic acids, particularly free fatty acids and 3-hydroxybutyrate, together with an increase in the total plasma protein concentration. This acidosis, rather than any decrease in the muscle glycogen content, may be responsible for the reduced exercise capacity in high-intensity exercise; this may be due to a reduced rate of efflux of lactate and hydrogen ions from the working muscles. Alternatively, the accumulation of acetyl groups in the carbohydrate-deprived state may reduce substrate flux through the pyruvate dehydrogenase complex, thus reducing aerobic energy supply and accelerating the onset of fatigue.
...
PMID:Diet composition and the performance of high-intensity exercise. 923 52

Acidosis during exercise has long been associated with skeletal muscle fatigue. Recent evidence also has linked reactive oxygen species (ROS) with fatigue in skeletal muscle, including the diaphragm. We hypothesized that acidosis (designed to mimic blood pH during maximal exercise) would worsen ROS-induced depression of diaphragm contractility. The xanthine oxidase (XO) reaction in solution (0.01 U/ml) allows direct assessment of the effects of oxidant stress by ROS. Costal diaphragm fiber bundles from 24 Sprague-Dawley rats (200-250 g) were divided into four treatment groups: 1) pH 7.4, no XO (H); 2) pH 7.4 + XO (HXO); 3) pH 7.0, no XO (L); and 4) pH 7.0 + XO (LXO). Baseline twitch mechanics and force-frequency relationships (Pre) were determined in control Krebs solution (pH 7.4, no XO) before treatment. Treatment solutions were introduced, and the diaphragm underwent 2 min of contractions at 25 Hz (250 ms) at a rate of 1/s. After 10 min of recovery, the control solution was reintroduced into the bath and postcontractile function (Post) was measured. Significant reductions in twitch tension and low-frequency tetanic tension were greater in HXO and LXO compared with H, without an effect on maximal tetanic tension. One-half relaxation time was prolonged only by the combination of acidosis and oxidative stress. Addition of superoxide dismutase (50 U/ml) worsened and catalase (1,800 U/ml) attenuated XO-induced depression of diaphragm contractility. We concluded that XO induced a reduction of low-frequency tension in the fatigued diaphragm, which was mediated directly or indirectly through hydrogen peroxide and was exacerbated to a modest extent with acidosis.
...
PMID:Effect of oxidative stress and acidosis on diaphragm contractile function. 927 48

The effects of gamma radiation and low temperature hydrogen peroxide gas plasma (HPGP) sterilization on structure and cyclic mechanical properties were examined for orthopedic grade ultra-high-molecular-weight polyethylene (UHMWPE) and compared to each other as well as to no sterilization (control). Density was monitored with a density gradient column and was found to be directly influenced by the sterilization method employed: Gamma radiation led to an increase, while plasma did not. Oxidation of the polymer was studied by observing changes in the carbonyl peak with Fourier transform infrared spectrometry and was found to be strongly affected by both gamma radiation and subsequent aging, while plasma sterilization had little effect. Gamma radiation resulted in embrittlement of the polymer and a decreased resistance to fatigue crack propagation. This mechanical degradation was a direct consequence of postradiation oxidation and molecular evolution of the polymer and was not observed in the plasma-sterilized polymer. Both gamma radiation and plasma sterilization led to improved wear performance of the UHMWPE compared to the nonsterile control material.
...
PMID:Comparison of the effects of gamma radiation and low temperature hydrogen peroxide gas plasma sterilization on the molecular structure, fatigue resistance, and wear behavior of UHMWPE. 957 68

Physiological and kinematic data were collected from elite under-19 rugby union players to provide a greater understanding of the physical demands of rugby union. Heart rate, blood lactate and time-motion analysis data were collected from 24 players (mean +/- s(x): body mass 88.7 +/- 9.9 kg, height 185 +/- 7 cm, age 18.4 +/- 0.5 years) during six competitive premiership fixtures. Six players were chosen at random from each of four groups: props and locks, back row forwards, inside backs, outside backs. Heart rate records were classified based on percent time spent in four zones (>95%, 85-95%, 75-84%, <75% HRmax). Blood lactate concentration was measured periodically throughout each match, with movements being classified as standing, walking, jogging, cruising, sprinting, utility, rucking/mauling and scrummaging. The heart rate data indicated that props and locks (58.4%) and back row forwards (56.2%) spent significantly more time in high exertion (85-95% HRmax) than inside backs (40.5%) and outside backs (33.9%) (P < 0.001). Inside backs (36.5%) and outside backs (38.5%) spent significantly more time in moderate exertion (75-84% HRmax) than props and locks (22.6%) and back row forwards (19.8%) (P < 0.05). Outside backs (20.1%) spent significantly more time in low exertion (<75% HRmax) than props and locks (5.8%) and back row forwards (5.6%) (P < 0.05). Mean blood lactate concentration did not differ significantly between groups (range: 4.67 mmol x l(-1) for outside backs to 7.22 mmol x l(-1) for back row forwards; P < 0.05). The motion analysis data indicated that outside backs (5750 m) covered a significantly greater total distance than either props and locks or back row forwards (4400 and 4080 m, respectively; P < 0.05). Inside backs and outside backs covered significantly greater distances walking (1740 and 1780 m, respectively; P < 0.001), in utility movements (417 and 475 m, respectively; P < 0.001) and sprinting (208 and 340 m, respectively; P < 0.001) than either props and locks or back row forwards (walking: 1000 and 991 m; utility movements: 106 and 154 m; sprinting: 72 and 94 m, respectively). Outside backs covered a significantly greater distance sprinting than inside backs (208 and 340 m, respectively; P < 0.001). Forwards maintained a higher level of exertion than backs, due to more constant motion and a large involvement in static high-intensity activities. A mean blood lactate concentration of 4.8-7.2 mmol x l(-1) indicated a need for 'lactate tolerance' training to improve hydrogen ion buffering and facilitate removal following high-intensity efforts. Furthermore, the large distances (4.2-5.6 km) covered during, and intermittent nature of, match-play indicated a need for sound aerobic conditioning in all groups (particularly backs) to minimize fatigue and facilitate recovery between high-intensity efforts.
...
PMID:Heart rate, blood lactate and kinematic data of elite colts (under-19) rugby union players during competition. 975 60

Muscular exercise results in an increased production of radicals and other forms of reactive oxygen species. Further more, growing evidence implicates cytotoxic ROS as an underlying cause in exercise-induced disturbances in muscle redox status that could result in muscle fatigue or injury. Muscle cells contain complex cellular defense mechanisms to minimize the risk for oxidative injury. Two major classes of endogenous protective mechanisms work together to reduce the harmful effects of oxidants in the cell: (1) enzymatic and (2) nonenzymatic antioxidants. Key antioxidant enzymes include superoxide dismutase, glutathione peroxidase, and catalase. These enzymes are responsible for removing superoxide radicals, hydrogen peroxide or organic hydroperoxides, and hydrogen peroxide, respectively. Important nonenzymatic antioxidants include vitamins E and C, beta-carotene, GSH, uric acid, ubiquinone, and bilirubin. Vitamin E, beta-carotene, and ubiquinone are located in lipid regions of the cell, whereas uric acid, GSH, and bilirubin are in aqueous compartments of the cell. Although numerous animal experiments have demonstrated that the addition of antioxidants can improve muscular performance, to date, limited evidence shows that dietary supplementation with antioxidants improves human performance. This is an important area for future research.
...
PMID:Antioxidants and exercise. 1041 Aug 39

During the 7.1-MPa hydrogen-helium-oxygen record human dive, we tested the hypothesis that the increased ambient pressure would alter the maximal muscle performance, specifically that breathing dense gas would lead to fatigue of the respiratory muscle. A group of hand muscles (adductor pollicis, AP) and the inspiratory muscles (IM) were studied in three professional divers. Maximal voluntary contractions (MVC) of AP and maximal inspiratory pressure (P(i(max))) generated by IM were measured prior to the dive, during compression and decompression, and then 1 and 2 months after the dive. The decrease in MVC (-22%) was significant at 3.1 MPa, i.e. at the beginning of the introduction of hydrogen into the breathing mixture, whereas P(i(max)) fell progressively during the dive and decompression (maximal DeltaP(i(max)) = -55%), a significant reduction still being measured 1 month after the dive. The altered IM function was attributed to the consequences of long-term ventilatory loading, a condition associated with breathing a dense gas. The transient decrease in MVC of the skeletal muscle would indicate a possible effect of the hyperbaric environment, possibly the high partial pressure of hydrogen, on neuromuscular drive.
...
PMID:Changes in maximal performance of inspiratory and skeletal muscles during and after the 7.1-MPa Hydra 10 record human dive. 1066 92

Performance in endurance events is typically evaluated by the power or velocity that can be maintained for durations of 30 min. to four hours. The two main by-products of intense and prolonged oxidative metabolism that can limit performance are the accumulation of hydrogen ion (i.e. lactic acidosis) and heat (i.e. hyperthermia). A model for endurance performance is presented that revolves around identification of the lactate threshold velocity which is presented as a function of numerous morphological components as well as gross mechanical efficiency. When cycling at 80 RPM, gross mechanical efficiency is positively related to Type I muscle fiber composition, which has great potential to improve endurance performance. Endurance performance can also be influenced by altering the availability of oxygen and blood glucose during exercise. The latter need forms the basis for ingesting carbohydrate at 30-60 grams per hour during exercise. In laboratory simulations of performance, athletes fatigue due to hyperthermia when esophageal is approximately 40 degrees C, in association with near maximal heart rate and perceived exertion. It is likely that the central nervous system is involved in the aetiology of fatigue from hyperthermia. Dehydration during exercise promotes hyperthermia by reducing skin blood flow, sweating rate and thus heat dissipation. The combination of dehydration and hyperthermia during exercise causes large reductions in cardiac output and blood flow to the exercising musculature, and thus has a large potential to impair endurance performance. Endurance performance is optimized when training is aimed specifically at developing individual components of the model presented and nutritional supplementation prevents hypoglycemia and attenuates dehydration and hyperthermia. Indeed, the challenge at the transition to a new millennium is to synergistically integrate these physiological factors in training and competition.
...
PMID:Physiological determinants of endurance exercise performance. 1066 57

<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>