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

In their previous study, the authors carried out a fatigue test for AISI 316, 316L stainless steels and COP1 alloy in a living animal body and observed a remarkable deterioration in the fatigue durability of these metals. In that study, it was concluded that the reason the corrosion resistance of the metals was reduced in the living body was that the low concentration of dissolved oxygen gas in the body fluid (the partial pressure pO2; 28-78 mmHg) was insufficient to form the chromium oxide passivation film on the metal surface, and the base metal (iron) was released into the environmental fluid in ionic form. In this paper, with the concentration of dissolved oxygen gas in a physiological normal saline solution being set equivalent to that of living body fluid, fatigue tests on AISI 316 were made to simulate the stress corrosion behavior of the metal in the living body. As a result, remarkable deterioration of fatigue strength was observed in the low O2 concentrated normal saline solution, which was the same as that in the living animal body.
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PMID:Influence of low dissolved oxygen concentration in body fluid on corrosion fatigue behaviors of implant metals. 141 88

Markers of a heavy increase in training were examined in ten highly trained distance runners (mean(s.d.) age 29.8(1.7) years, maximal oxygen intake 65.3 ml kg-1 min-1, personal best 10-km time 31 min 4 s) who undertook a deliberate 38% increment of training over a 3-week period. Their running performance did not improve, and six of the ten subjects developed sustained fatigue, suggesting that training was excessive, although the full clinical picture of overtraining did not develop. The Profile of Mood States was the best single marker of disturbed function, indicating increased fatigue and decreased vigour. There were no useful changes of resting heart rate or perceived exertion during submaximal running, sleep was undisturbed, and there were no orthopaedic injuries. Two subjects developed rhinoviral infections following the heavy training, and a third complained of symptoms that were diagnosed 2 weeks later as exercise-induced asthma. The increase of serum cortisol normally induced by 30 min of submaximal exercise was no longer seen when the same acute exercise was performed after heavy training. Resting lymphocyte proliferation tended to increase in response to phytohaematoglutinin (PHA) and concanavalin A (Con A), the ratio of helper to suppressor cells (H/S) decreased, and pokeweed mitogen induced smaller increases in IgG and IgM synthesis. Whereas before heavy training, PHA-stimulated lymphocyte proliferation was unchanged by 30 min of acute submaximal exercise, after 3 weeks of heavy training the same bout of exercise caused an 18% suppression of proliferation. Likewise, heavy training brought about a decrease of T-lymphocytes in response to acute submaximal exercise, but an abolition of the acute exercise-induced decrease in the H/S ratio. The previously observed exercise-induced decrease of IgG synthesis did not occur when the same acute bout of exercise was performed after heavy training. We conclude that such minor and transient changes of immune function may possibly be a warning that training is becoming excessive, but they have only a limited significance for overall immune function.
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PMID:Potential markers of heavy training in highly trained distance runners. 142 53

Recently, we have shown that an untrained respiratory system does limit the endurance of submaximal exercise (64% peak oxygen consumption) in normal sedentary subjects. These subjects were able to increase breathing endurance by almost 300% and cycle endurance by 50% after isolated respiratory training. The aim of the present study was to find out if normal, endurance trained subjects would also benefit from respiratory training. Breathing and cycle endurance as well as maximal oxygen consumption (VO2max) and anaerobic threshold were measured in eight subjects. Subsequently, the subjects trained their respiratory muscles for 4 weeks by breathing 85-160 l.min-1 for 30 min daily. Otherwise they continued their habitual endurance training. After respiratory training, the performance tests made at the beginning of the study were repeated. Respiratory training increased breathing endurance from 6.1 (SD 1.8) min to about 40 min. Cycle endurance at the anaerobic threshold [77 (SD 6) %VO2max] was improved from 22.8 (SD 8.3) min to 31.5 (SD 12.6) min while VO2max and the anaerobic threshold remained essentially the same. Therefore, the endurance of respiratory muscles can be improved remarkably even in trained subjects. Respiratory muscle fatigue induced hyperventilation which limited cycle performance at the anaerobic threshold. After respiratory training, minute ventilation for a given exercise intensity was reduced and cycle performance at the anaerobic threshold was prolonged. These results would indicate the respiratory system to be an exercise limiting factor in normal, endurance trained subjects.
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PMID:The respiratory system as an exercise limiting factor in normal trained subjects. 142 35

The purpose of respiratory muscle training for patients with chronic respiratory failure is to improve exercise performance during daily life. Firstly, to confirm the clinical effect on respiratory muscle training, the abdominal pad method for inspiratory muscle training and abdominal pad method with expiratory resistor for both inspiratory and expiratory muscle training were simultaneously performed. Both methods were clinically useful to increase respiratory muscle power and to subjectively decrease dyspnea. Ventilatory pattern analyzed by the Konno-Mead (K-M) diagram during exercise also showed their effectiveness. Secondly, the influence of hypoxemia and hypophosphatemia, which are important factors producing respiratory muscle fatigue, was investigated in a patient with respiratory failure. (1) O2 inhalation in patients receiving home oxygen therapy was effective in terms of the endurance time and ventilatory pattern analyzed by the K-M diagram during exercise. (2) A case of hypercapnea due to hypoventilation caused by respiratory muscle fatigue developed reduced PaCO2 following correction of serum phosphate level, suggesting that hypophosphatemia is an important clinical factor producing respiratory muscle fatigue.
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PMID:[Clinical study on respiratory muscle training for chronic respiratory failure]. 143 18

Output power and metabolic input power values were determined for unconditioned canine latissimus dorsi (two), gastrocnemius (seven), and triceps (three) muscles contracting linearly to cause compression of a doubly valved pouch in a hydraulic model of the circulation. The motor nerves to the muscles were stimulated tetanically with 450 msec trains of 0.1 msec pulses having a frequency of 50/sec. The muscles were contracted 10, 20, 30, and 40 times per minute and pouch output in milliliters per minute was measured directly for each muscle at each contraction (train) rate. The output power in milliwatts was determined by two methods: (1) by using the pouch output and the pressure rise imparted to the stroke volume (average power) and (2) by using the pressure-volume loop. Metabolic input power in milliwatts was determined from the oxygen consumption in milliliters per minute of the working muscle. It was found that as the pouch output was increased, the pouch output power and the metabolic input power both increased. The average power output was slightly less than that computed from the pressure-volume loop. The mean output power values, when pumping at L liters per minute, were 0.62 L (average) and 0.75 L mW/gm (pressure-volume loop) for the latissimus dorsi muscles; 0.83 L (average) and 1.16 L mW/gm (pressure-volume loop) for the gastrocnemius muscles; and 0.55 L (average) and 0.66 L mW/gm (pressure-volume loop) for the triceps muscles. The percent efficiency of energy conversion ranged from 9.2% to 17.8% for the latissimus dorsi muscles, from 5.1% to 19.5% for the gastrocnemius muscles, and from 10.5% to 27.3% for the triceps muscles. However, it should not be concluded that one muscle type is better than another on the basis of percent efficiency because efficiency does not take endurance into account. An important observation in this study relates to the large output obtained with the three linearly contracting muscle types. All were capable of pumping in excess of 1.5 L/min. A second observation relates to the absence of fatigue, although determination of endurance was not an objective in these studies.
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PMID:Output power and metabolic input power of skeletal muscle contracting linearly to compress a pouch in a mock circulatory system. 143 27

The present investigation was undertaken to examine the relationship between plasma potassium (K+) and ventilation (VE) during incremental exercise. Blood lactate (La-) was also measured, and its relationship with VE was similarly examined. Eight endurance-trained triathletes (ET) and eight active but untrained men (UT) performed an incremental cycling test to volitional fatigue. Maximal oxygen uptake (VO2max) and oxygen uptake (VO2) at lactate threshold (LT) were higher (P < 0.05) in ET (VO2max 4.60 +/- 0.10 l/min, LT 2.77 +/- 0.85 l/min) than in UT (VO2max 3.79 +/- 0.11 l/min, LT 1.94 +/- 0.60 l/min). There were significant (P < 0.05) correlations between VE and K+ (UT 0.87, ET 0.77) and between VE and La- (UT 0.88, ET 0.85). In ET compared with UT, VE was lower (P < 0.05) at 330 W, K+ was lower at 300 and 330 W, and La- was lower at all work loads > 90 W. These results suggest that K+ may make an important contribution to the regulation of ventilation during incremental exercise and that endurance training attenuates the K+ response to that exercise.
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PMID:Potassium and ventilation during incremental exercise in trained and untrained men. 144 71

If the failing left ventricle could be given an effective push, other approaches to the treatment of heart failure would not be needed. We have inotropes only for short-term parenteral use. We have no safe inotrope for chronic oral use. The effect of digitalis is only feeble and the phosphodiesterase inhibitors seem to increase mortality from sudden death. Diuretics are dramatic for acute pulmonary oedema and the mainstay for chronic fluid retention but do not improve the pump and by reducing blood volume stimulate the renin angiotensin system to vasoconstriction, further fluid retention and hypokalaemia. Nitrates drop pre-load without reducing blood volume but tolerance is a problem and stroke volume does not increase. Reduction of afterload helps the failing ventricle to empty, the pull and output increases. The angiotensin converting enzyme inhibitors (ACEI) are now the cornerstone of heart failure treatment, reducing mortality in severe heart failure (CONSENSUS) and superior to standard vasodilator therapy (V-HeFT-2) at improving the survival of patients with mild to moderate heart failure. ACEI can reduce the incidence of ventricular ectopy and probably do this through improving left ventricular function, from decreasing sympathetic tone, reducing myocardial oxygen demand or increasing serum potassium but ACEI did not diminish the incidence of sudden death in the SOLVD trial despite reducing mortality. Disappointingly little improvement in exercise tolerance and persistence of chronic fatigue in heart failure concentrated attention on the periphery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The push, the pull and the periphery. 144 45

All exercise draws first on intramuscular stores of ATP and creatine phosphate; initially these are replenished by anaerobic glycolysis. The lactic acid produced contributes to the rapid development of fatigue in high intensity exercise. Aerobic metabolism (at first mainly of glycogen, later increasingly of fat) is the principal route of ATP resynthesis in activities lasting longer than 2 min, but can only maintain work-rates about 1/4 of those possible in very brief bursts. Blood lactate rises at the higher aerobic work rates. 'Lactate threshold' (LT: approximately 2 mmol/l) is almost exactly the speed at which endurance races are won, and close to those apparently providing optimal aerobic training. This training, predominantly of muscle aerobic capacity, elevates LT more than maximum oxygen consumption. LT is not now thought to indicate oxygen-deprivation, but intracellular adjustments driving oxidative phosphorylation faster. Ventilatory breakpoints, formerly considered to indicate LT, correlate more closely with the accumulation of potassium than lactate.
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PMID:Aerobic exercise, anaerobic exercise and the lactate threshold. 145 Aug 85

Clinical and metabolic responses to atropine plus pethidine and to scopolamine plus morphine premedication were studied in 45 ASA physical status III patients undergoing gynaecological procedures. Atropine 0.5 mg plus pethidine 50 mg intramuscularly (Group 1), scopolamine 0.24 mg plus morphine 8 mg (Group 2), or intramuscular placebo (Group 3) premedication were given in random, double-blind fashion. Scopolamine-morphine premedication caused a significant decrease in energy expenditure (EE) and oxygen consumption (VO2) (from 1229 +/- 193 to 1184 +/- 221 kcal/24 h, P = 0.004 and from 105 +/- 11 to 102 +/- 12 ml/min/m2, P = 0.006, respectively) simultaneously with a decrease in rate-pressure product (RPP) (P = 0.0001) and an increase in pressure-rate quotient (PRQ) (P = 0.034). Atropine-pethidine premedication induced a decrease in RPP but not in EE or VO2. In the placebo group both RPP and VO2 first increased and then slowly returned to the levels measured prior to premedication. The RPP was significantly lower in Group 2 than in Groups 1 and 3 at both 30 and 60 min. The degrees of subjective tiredness and anxiolysis were significantly greater in Groups 1 and 2 (showing good sedative and anxiolytic effect) than in Group 3. These results show that in ASA III patients, atropine-pethidine premedication does not decrease the sympathoadrenal reaction to the degree its anxiolytic and sedative effect would suggest. This may indicate neuroendocrine stress induced by atropine-pethidine.
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PMID:Clinical and metabolic responses to different kinds of premedication in ASA III patients. 146 14

The development of fatigue was investigated by electrical stimulation in 15 domestic pigs (1 yr old, 70-90 kg body weight) and seven adult dogs (3 yr old, 45 kg body weight). After anaesthesia, silver electrodes were implanted in the anterior and posterior parts of the right masseter muscles. The contralateral muscle was used as control. The bite force was measured. Muscle biopsies were obtained from the anterior, central and posterior parts, and were immediately frozen in liquid nitrogen. A fluorometrical analysis by enzymatic methods for glycogen, glucose, creatine phosphate, NAD, NADH, lactate and pyruvate was made. Blood flow was measured by 133Xe wash-out; oxygen consumption was monitored with an oxygen electrode. The porcine masseter was continuously stimulated for 60 min (100 V, 4 Hz and 2 ms). The canine masseter was intermittently stimulated (100 V, 20 Hz and 2 ms). The contraction was repeated four times, with a 10-min rest between. The porcine masseter could sustain longer endurance times than the canine masseter, which was easily fatigued. A marked substrate depletion was evident. The precontractional contents of glycogen, glucose and creatine phosphate were reduced. Lactate accumulation was evident (2-4 times more in the porcine and 4-8 times more in the canine masseter). The NADH concentration increased and the NAD content decreased. Blood-flow impairment (80% reduction in the dog, 60% in the pig) was observed. After the contraction phase, there was a hyperaemia (58% elevation of blood flow in the pig masseter, 45% in the canine). The oxygen tension followed in magnitude and time the blood-flow changes. These circulatory variables returned to normal after recovery. The high degree of substrate depletion, blood-flow impairment and a simultaneous decrease in oxygen transport to the contracted muscle, in combination with a prominent lactate accumulation, may induce a decrease in bite-force production.
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PMID:Bite-force development, metabolic and circulatory response to electrical stimulation in the canine and porcine masseter muscles. 147 60


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