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

5-Aminolevulinic acid (ALA), a heme precursor that accumulates in acute intermittent porphyria patients and lead-exposed individuals, has previously been shown to autoxidize with generation of reactive oxygen species and to cause in vitro oxidative damage to rat liver mitochondria. We now demonstrate that chronically ALA-treated rats (40 mg/kg body wt every 2 days for 15 days) exhibit decreased mitochondrial enzymatic activities (superoxide dismutase, citrate synthase) in liver and soleus (type I, red) and gastrocnemius (type IIb, white) muscle fibers. Previous adaptation of rats to endurance exercise, indicated by augmented (cytosolic) CuZn-superoxide dismutase (SOD) and (mitochondrial) Mn-SOD activities in several organs, does not protect the animals against liver and soleus mitochondrial damage promoted by intraperitoneal injections of ALA. This is suggested by loss of citrate synthase and Mn-SOD activities and elevation of serum lactate levels, concomitant to decreased glycogen content in soleus and the red portion of gastrocnemius (type IIa) fibers of both sedentary and swimming-trained ALA-treated rats. In parallel, the type IIb gastrocnemius fibers, which are known to obtain energy mainly by glycolysis, do not undergo these biochemical changes. Consistently, ALA-treated rats under swimming training reach fatigue significantly earlier than the control group. These results indicate that ALA may be an important prooxidant in vivo.
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PMID:5-aminolevulinic acid-induced alterations of oxidative metabolism in sedentary and exercise-trained rats. 153 18

Impairment of exercise tolerance is a common problem in patients with severe chronic obstructive pulmonary disease. The cause of exercise intolerance in patients with severe chronic obstructive pulmonary disease is multifactorial and includes impaired lung mechanics, fatigue of inspiratory muscles, impaired gas exchange, right ventricular dysfunction, malnutrition, occult cardiac disease, deconditioning, and psychologic problems; however, impaired lung mechanics and gas exchange abnormalities seem to be the major limiting factors. Recently, the approach to management of pulmonary rehabilitation in patients with chronic obstructive pulmonary disease has changed because improvement in exercise tolerance has been demonstrated after pulmonary rehabilitation. Other adjunctive measures that have been shown to contribute to the observed improvement in exercise tolerance include administration of oxygen, nutritional support, cessation of smoking, and psychosocial support. The roles of ventilatory muscle endurance training, respiratory muscle rest therapy, nasally administered continuous positive airway pressure, and training of the muscles of the upper extremities are less clearly defined.
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PMID:Exercise limitation and pulmonary rehabilitation in chronic obstructive pulmonary disease. 154 79

Respiratory muscle fatigue is induced experimentally by adding high external resistances to breathing. The role played by respiratory muscle fatigue in exercise limitation and in acute respiratory failure is still unclear. The electromyogram often reflects contractions beyond the fatigue threshold, but overt force failure has been only rarely demonstrated under these circumstances. Hypercapnic ventilatory failure may possibly not result from fatigue, but rather from an adaptation of the respiratory system for avoiding fatigue. The treatment of fatigue comprises respiratory muscle support by adequate nutrition and oxygen delivery, and if needed respiratory muscle rest by mechanical ventilation.
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PMID:[Fatigue of the respiratory muscles]. 154 80

During heavy exercise horses can increase oxygen uptake compared to resting conditions considerably more than man. Processes involved like respiration, heart size, cardiac output, oxygen transport capacity of the blood and oxygen release in the capillaries are discussed. Besides these advantages in the aerobic metabolism conditions for the anaerobic metabolism are also more advantageous in horses than in man. The portion of fast contracting muscle fibers with little fatigue-resistance and also some of the enzymes required for the anaerobic metabolism are higher in horses.
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PMID:[Physical performance--a comparison between horses and men]. 155 12

The purpose of this investigation was to test whether the concept of critical power used in previous studies could be applied to the field of competitive swimming as critical swimming velocity (vcrit). The vcrit, defined as the swimming velocity over a very long period of time without exhaustion, was expressed as the slope of a straight line between swimming distance (dlim) at each speed (with six predetermined speeds) and the duration (tlim). Nine trained college swimmers underwent tests in a swimming flume to measure vcrit at those velocities until the onset of fatigue. A regression analysis of dlim on tlim calculated for each swimmer showed linear relationships (r2 greater than 0.998, P less than 0.01), and the slope coefficient signifying vcrit ranged from 1.062 to 1.262 m.s-1 with a mean of 1.166 (SD 0.052) m.s-1. Maximal oxygen consumption (VO2max), oxygen consumption (VO2) at anaerobic threshold, and the swimming also velocity at the onset of blood lactate accumulation (vOBLA) were also determined during the incremental swimming test. The vcrit showed significant positive correlations with VO2 at anaerobic threshold (r = 0.818, P less than 0.01), vOBLA (r = 0.949, P less than 0.01) and mean velocity of 400 m freestyle (r = 0.864, P less than 0.01). These data suggested that vcrit could be adopted as an index of endurance performance in competitive swimmers.
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PMID:Determination and validity of critical velocity as an index of swimming performance in the competitive swimmer. 155 62

Free radical activation and lipid peroxidation have been described in skeletal muscle during strenuous exercise. We hypothesized that oxygen radicals could also be formed in the diaphragm muscle during strenuous resistive breathing and that these radicals might affect diaphragm function. Seven control and 12 experimental male Sprague-Dawley rats were studied. Six experimental animals were subjected to resistive breathing (RB) alone and six animals received 15 min of mechanical ventilatory support (MV) after the resistive breathing period. Inspiratory resistance was adjusted to maintain airway opening pressure at 70% maximum in both groups until exhaustion. Diaphragm samples were obtained for analysis of thiobarbituric acid-reactive substances (TBAR), reduced glutathione (GSH), and glutathione disulfide (GSSG). In vitro isometric contraction times, twitch (Pt) tension and maximum tetanic (Po) tension, force-frequency curves, fatigue index, and recovery index were measured. In RB and MV compared with controls, there were significant decreases in Pt and Po. Diaphragm TBAR concentrations were increased in MV compared with controls or RB. GSSG-to-total glutathione ratio was increased in RB and MV compared with controls. Production of free radicals during RB and MV may represent an important mechanism of diaphragmatic injury that could contribute to the decline in contractility.
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PMID:Resistive breathing activates the glutathione redox cycle and impairs performance of rat diaphragm. 155 28

Fatigue as a functional sign and muscle damage as a structural sign can be observed after prolonged exercise like marathon running or after strenuous exercise, especially with the involvement of eccentric contractions. For fatigue due to prolonged exercise, hypoxic conditions and the formation of free oxygen radicals seem to be of aetiological importance, resulting in an elevated lysosomal activity. Eccentric exercise of high intensity rather results in a mechanical stress to the fibres. Although these different mechanisms can be discerned experimentally, both result in similar impairments of muscle function. A good training status may attenuate the clinical signs of fatigue and muscle damage. The symptoms and events occurring during delayed onset of muscle soreness (DOMS) can be explained by a cascade of events following structural damage to muscle proteins.
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PMID:Exercise, muscle damage and fatigue. 156 6

Repetitive static exercise (RSE) is a repetitive condition of partial ischaemia/reperfusion and may therefore be connected to the formation of oxygen-derived free radicals and tissue damage. Seven subjects performed two-legged intermittent knee extension exercise repeating at 10 s on and 10 s off at a target force corresponding to about 30% of the maximal voluntary contraction force. The RSE was continued for 80 min (n = 4) or to fatigue (n = 3). Four of the subjects also performed submaximal dynamic exercise (DE) at an intensity of about 60% maximal oxygen uptake (VO2max) for the same period. Whole body oxygen uptake (VO2) increased gradually with time during RSE (P less than 0.05), indicating a decreased mechanical efficiency. This was further supported by a slow increase in leg blood flow (P less than 0.05) and leg oxygen utilization (n.s.) during RSE. In contrast, prolonged RSE had no effect on VO2 during submaximal cycling. Maximal force (measured in six additional subjects) declined gradually during RSE and was not completely restored after 60 min of recovery. After 20 and 80 min (or at fatigue) RSE phosphocreatine (PC) dropped to 74% and 60% of the initial value, respectively. A similar decrease in PC occurred during DE. Muscle and arterial lactate concentrations remained low during both RSE and DE. The three subjects who were unable to continue RSE for 80 min showed no signs of a more severe energy imbalance than the other subjects. A continuous release of K+ occurred during both RSE and DE.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Repetitive static muscle contractions in humans--a trigger of metabolic and oxidative stress? 156 68

Recovery from muscle fatigue after exercise is known to have two beneficial effects: improved blood lactate elimination and a central nervous recuperation of the capacity for exercise. This study indicates circulatory mechanisms that might limit active recovery. Ten subjects were seated on a cycle ergometer and performed arm cranking exercise at an anaerobic intensity which was for each individual in three periods of 6 min, alternating with recovery intervals of 14 min. In two randomly assigned tests, recovery consisted either of passive sitting (control) or cycling at 80 W for 12 min. Both tests terminated with an identical final passive rest period of 25 min. In the cycling test arm cranking led to a heart rate increase which was further elevated with each repetition, while in the control test no differences were shown among the cranking periods. No corresponding difference was found for oxygen consumption. During the 25 min of final rest, the cycling test showed arterial hypotension and elevated heart rate both of which were absent in the control tests. Venous-occlusion-plethysmography revealed a postcranking forearm hyperaemia. In the cycling test hyperaemia was markedly reduced with the onset of cycling due to vasoconstriction; this effect was absent in the control test. A reduction in blood lactate occurred faster in the cycling test, mainly at the onset of cycling. Total plasma fluid loss combined with forearm fluid uptake was accentuated and prolonged by cycling recovery. Recovery exercise performed by muscles other than those that were fatigued could have led to arterial hypotension (shock-index about 1) through both plasma fluid loss and additional vasodilatation depending on the muscle mass involved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular limitations of active recovery from strenuous exercise. 156 71

The effect of preexercise muscle glycogen content on the metabolic responses to exercise has been investigated. Seven men cycled at a work load calculated to elicit 75% of maximal oxygen uptake [211 +/- 17 (SE) W] on two occasions: 1) to fatigue (37.2 +/- 5.3 min) and 2) at the same work load and for the same duration as the first. Biopsies were obtained from the quadriceps femoris muscle before and after exercise. Before the first experiment, muscle glycogen was lowered by exercise and diet, and before the second experiment, muscle glycogen was elevated. In the low-glycogen condition (LG), muscle glycogen decreased from 182 +/- 15 at rest to 7 +/- 4 mmol glucosyl units/kg dry wt at fatigue, while in the high-glycogen condition (HG), glycogen decreased from 725 +/- 31 at rest to 353 +/- 53 mmol glucosyl units/kg dry wt at the end of exercise. Hexose monophosphates were not increased after LG exercise but increased approximately fivefold after HG exercise. Lactate increased more during HG exercise (LG = 16 +/- 5, HG = 61 +/- 7 mmol/kg dry wt; P less than or equal to 0.001), whereas IMP increased more during LG (LG = 2.8 +/- 0.6, HG = 0.9 +/- 0.2 mmol/kg dry wt; P less than or equal to 0.05). The increases in the sum of tricarboxylic acid cycle intermediates (TCAI; citrate+malate+fumarate) and acetylcarnitine (which is in equilibrium with acetyl CoA) were significantly greater during HG exercise (P less than or equal to 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of low glycogen on carbohydrate and energy metabolism in human muscle during exercise. 156 23


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