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

Effects of reactive oxygen species (ROS), especially hydrogen peroxide (H(2)O(2)), on recovery of action potential by resting for 30 min after high-frequency fatigue were studied using frog skeletal muscle fibers. After stimulation at a frequency of 50 HZ for 2 min, the action potential amplitude was decreased by 14.5 mV from controls, and resting membrane was depolarized by 15.4 mV. Action potential duration was also prolonged by high-frequency stimulation (1.5 ms in controls to 2.6 ms). The high-frequency stimulation used here caused no muscle damage. The action potential was partially improved after a 30-min rest. Addition of catalase at 500 units/ml or H(2)O(2) at 0.5 mM to sartorius muscle did not alter any of the parameters of the action potential after high-frequency stimulation. Treatment with catalase accelerated post-fatigue recovery of the action potential. Application of H(2)O(2) delayed post-fatigue recovery of resting and action potentials. When added to detubulated toe muscle fibers, catalase no longer improved the attenuation of action potential induced by high-frequency stimulation, even after a 30-min rest. These findings suggest that removal of H(2)O(2) from transverse tubules is effective for post-fatigue recovery of action potential in skeletal muscle.
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PMID:Hydrogen peroxide decelerates recovery of action potential after high-frequency fatigue in skeletal muscle. 1100 86

Reactive oxygen species contribute to diaphragm dysfunction in certain pathophysiological conditions (i.e., sepsis and fatigue). However, the precise alterations induced by reactive oxygen species or the specific species that are responsible for the derangements in skeletal muscle function are incompletely understood. In this study, we evaluated the effect of the superoxide anion radical (O(2)(-).), hydroxyl radical (.OH), and hydrogen peroxide (H(2)O(2)) on maximum calcium-activated force (F(max)) and calcium sensitivity of the contractile apparatus in chemically skinned (Triton X-100) single rat diaphragm fibers. O(2)(-). was generated using the xanthine/xanthine oxidase system;.OH was generated using 1 mM FeCl(2), 1 mM ascorbate, and 1 mM H(2)O(2); and H(2)O(2) was added directly to the bathing medium. Exposure to O(2)(-). or.OH significantly decreased F(max) by 14.5% (P < 0.05) and 43.9% (P < 0. 005), respectively.OH had no effect on Ca(2+) sensitivity. Neither 10 nor 1,000 microM H(2)O(2) significantly altered F(max) or Ca(2+) sensitivity. We conclude that the diaphragm is susceptible to alterations induced by a direct effect of.OH and O(2)(-)., but not H(2)O(2), on the contractile proteins, which could, in part, be responsible for prolonged depression in contractility associated with respiratory muscle dysfunction in certain pathophysiological conditions.
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PMID:Superoxide, hydroxyl radical, and hydrogen peroxide effects on single-diaphragm fiber contractile apparatus. 1113 92

Muscle fatigue is frequently defined as a temporary loss in force- or torque-generating ability because of recent, repetitive muscle contraction (1). The development of this temporary loss of force is a complex process and results from the failure of a number of processes, including motor unit recruitment and firing rate, chemical transmission across the neuromuscular junction, propagation of the action potential along the muscle membrane and T tubules, Ca2+ release from the sarcoplasmic reticulum (SR), Ca2+ binding to troponin C, and cross-bridge cycling (for detailed reviews, see Bigland-Ritchie and Woods(1), McLester(2), and Favero(3)). Muscle fatigue may limit the time a person can stand, the distance a person can ambulate, or the number of stairs a person can ascend or descend. In practical terms, however, we cannot know what actually leads to a decline in function for a given patient. For a phenomenon that may have profound clinical implications, muscle fatigue often receives inadequate attention in physiology textbooks, many of which contain a page or less of information on the entire topic (4-8). In addition, many textbooks report that muscle fatigue is mainly the result of a decrease in pH within the muscle cell due to a rise in hydrogen ion concentration ([H+]) resulting from anaerobic metabolism and the accumulation of lactic acid (6-8). Recent literature, however, contradicts this assertion (9-10). The purpose of this update, therefore, is to provide a brief review of the role of pH in the development of muscle fatigue.
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PMID:Challenging the role of pH in skeletal muscle fatigue. 1173 24

Creatine is the most popular supplement proposed to be an ergogenic aid. There is some evidence in the literature that creatine supplementation increases lean body mass, muscular strength, and sprint power. However, the efficacy of creatine has not been consistent, and the potential mechanisms are unresolved. While limited evidence that suggests that creatine could possess an antioxidant effect this has not been tested directly. Because oxidants such as free radicals can affect muscle fatigue and protein turnover, it is important to know whether creatine can neutralize free radicals and other reactive oxygen species. We tested the hypothesis that creatine would remove superoxide anions (O(*-)(2)), peroxynitrite (OONO-), hydrogen peroxide, and lipid peroxides (t-butyl hydroperoxide). We also determined whether creatine displayed a significant antioxidant scavenging capacity (ASC) using 2,2'-azino-bis(3-ethylbenzothiazolamine-6-sulfonic acid) (ABTS+) quenching as a marker. Creatine did not significantly reduce levels of hydrogen peroxide or lipid peroxidation. In contrast, creatine displayed a significant ability to remove ABTS+, O(*-)(2), and OONO- when compared with controls. Creatine quenching of ABTS+ was less than physiological levels of reduced glutathione (0.375 mM). To our knowledge, this is the first evidence that creatine has the potential to act as a direct antioxidant against aqueous radical and reactive species ions.
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PMID:Direct antioxidant properties of creatine. 1177 31

Titanium and its alloy are increasingly attracting attention for use as biomaterials. However, delayed fracture of titanium dental implants has been reported, and factors affecting the acceleration of corrosion and fatigue have to be determined. The fractured surface of a retrieved titanium screw and metallurgical structures of a dental implant system were analyzed. The outer surface of the retrieved screw had a structure different from that of the as-received screw. It was confirmed that a shear crack initiated at the root of the thread and propagated into the inner section of the screw. Gas chromatography revealed that the retrieved screw had absorbed a higher amount of hydrogen than the as-received sample. The grain structure of a titanium screw, immersed in a solution known to induce hydrogen absorption, showed features similar to those of the retrieved screw. It was concluded that titanium in a biological environment absorbs hydrogen and this may be the reason for delayed fracture of a titanium implant.
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PMID:Fracture mechanisms of retrieved titanium screw thread in dental implant. 1203 93

We studied whether hydrogen peroxide (H(2)O(2)) at </=10 microM activates the ryanodine receptor and decreases releasable Ca(2+) content in the sarcoplasmic reticulum after fatigue. Exposure of rabbit or frog skeletal muscle ryanodine receptors to 10 microM H(2)O(2) enhanced channel activity in lipid bilayers when the redox potential was defined at cis = -220 mV and trans = -180 mV. Channel activation by 10 microM H(2)O(2) was also observed when cis potential was set at -220 mV without defining trans potential, but the effect was less. Reduction of trans redox potential from -180 to -220 mV did not alter channel activity. H(2)O(2) at 500 microM failed to activate the channel when the redox potential was not controlled. Stimulation of the frog muscle fiber for 2 min (50 Hz, a duty cycle of 200 ms/s) decreased tetanus tension by approximately 50%. After 1 min, tetanus recovered rapidly to approximately 70% of control and thereafter slowly approached the control level. Amplitudes of caffeine- and 4-chloro-m-cresol-induced contractures were decreased after a 60-min rest. The decrease is not enhanced by exposure to 10 microM H(2)O(2). These results suggest that H(2)O(2) markedly activates the ryanodine receptor under the redox control in vitro, but externally applied H(2)O(2) may not play an important role in the postfatigue recovery process.
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PMID:H2O2 activates ryanodine receptor but has little effect on recovery of releasable Ca2+ content after fatigue. 1239 Nov 5

The purpose of this study was to evaluate the hypotheses that accumulation of hydrogen ions and/or inorganic phosphate (Pi) in skeletal muscle increases with repeated bouts of isotonic exercise. (31)P-Magnetic resonance spectroscopy was used to examine the gastrocnemius muscle of seven highly aerobically trained females during four bouts of isotonic plantar flexion. The exercise bouts (EX1-4) of 3 min and 18 s were separated by 3 min and 54 s of complete rest. Muscle ATP did not change during the four bouts. Phosphocreatine (PCr) degradation during EX1 (13.3 +/- 2.4 mmol/kg wet weight) was higher (P < 0.01) compared with EX3-4 (9.7 +/- 1.6 and 9.6 +/- 1.8 mmol/kg wet weight, respectively). The intramyocellular pH at the end of EX1 (6.87 +/- 0.05) was significantly lower (P < 0.001) than those of EX2 (6.97 +/- 0.02), EX3 (7.02 +/- 0.01), and EX4 (7.02 +/- 0.02). Total Pi and diprotonated Pi were significantly higher (P < 0.001) at the end of EX1 (17.3 +/- 2.7 and 7.8 +/- 1.6 mmol/kg wet weight, respectively) compared with the values at the end of EX3 and EX4. The monoprotonated Pi at the end of EX1 (9.5 +/- 1.2 mmol/kg wet weight) was also significantly higher (P < 0.001) than that after EX4 (7.5 +/- 1.1 mmol/kg wet weight). Subjects' rating of perceived exertion increased (P < 0.001) toward exhaustion as the number of exercises progressed (7.1 +/- 0.4, EX1; 8.0 +/- 0.3, EX2; 8.5 +/- 0.3, EX3; and 9.0 +/- 0.4, EX4; scale from 0 to 10). The present results indicate that human muscle fatigue during repeated intense isotonic exercise is not due to progressive depletion of high energy phosphates nor to intracellular accumulation of hydrogen ions, total, mono-, or diprotonated Pi.
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PMID:Progressive decrease of intramyocellular accumulation of H+ and Pi in human skeletal muscle during repeated isotonic exercise. 1257 Sep 84

Vastus lateralis muscle biopsies were obtained from six individuals with multiple sclerosis (MS) having an Expanded Disability Status Score of 4.75 +/- 0.28, and from six age- and gender-matched individuals without MS. Biopsies from the MS group showed fewer fibers (31 +/- 4 vs. 46 +/- 4%) containing the type IIa myosin heavy chain (MHC) isoform exclusively. However, the percentage of fibers coexpressing type IIa and IIx MHC increased in direct proportion with MS disability status. The average unloaded shortening velocity of skinned fibers containing type I or IIa MHC did not differ between subject groups. Peak Ca(2+)-activated force was 11-13% lower in fibers from the MS group due to atrophy (type I and IIa fibers) and reduced specific force (type I fibers). Increasing intracellular inorganic phosphate (0-30 mM) or hydrogen ion (pH 7.0-6.2) reduced Ca(2+)-activated force in a manner that was independent of MS status. Thus, fibers from the MS group showed a subtle shift in fast MHC isoform coexpression and a modest reduction in cross-bridge number, density, or average force, with no change in maximal cross-bridge cycling rate or susceptibility to intracellular metabolites. These changes explain part of the muscle weakness and fatigue experienced by individuals with MS.
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PMID:Cross-bridge mechanisms of muscle weakness in multiple sclerosis. 1266 Oct 47

Peripheral vascular disease (PVD) is generally accepted to result in the failure of skeletal muscle blood flow to increase adequately at the onset of muscular work. There are currently no routine pharmacological interventions towards the treatment of PVD, however, recent Phase III trials in the USA have demonstrated the clinical potential of the phosphodiesterase III inhibitor Cilostazol for pain-free and maximal walking distances in patients with intermittent claudication. PVD is characterized by a marked reliance on oxygen-independent routes of ATP regeneration (phosphocreatine hydrolysis and glycolysis) in skeletal muscle during contraction and the rapid onset of muscular pain and fatigue. The accumulation of metabolic by-products of oxygen-independent ATP production (hydrogen and lactate ions and inorganic phosphate) has long been associated with an inhibition in contractile function in both healthy volunteers and PVD patients. Therefore, any strategy that could reduce the reliance upon ATP re-synthesis from oxygen-independent routes, and increase the contribution of oxygen-dependent (mitochondrial) ATP re-synthesis, particularly at the onset of exercise, might be expected to improve functional capacity and be of considerable therapeutic value. Historically, the increased contribution of oxygen-independent ATP re-synthesis to total ATP generation at the onset of exercise has been attributed to a lag in muscle blood flow limiting oxygen delivery during this period. However, recent evidence suggests that limited inertia is present at the level of oxygen delivery, whilst considerable inertia exists at the level of mitochondrial enzyme activation and substrate supply. In support of this latter hypothesis, we have reported on a number of occasions that activation of the pyruvate dehydrogenase complex, using pharmacological interventions, can markedly reduce the dependence on ATP re-synthesis from oxygen-independent routes at the onset of muscle contraction. This review will focus on these findings and will highlight the pyruvate dehydrogenase complex as a novel therapeutic target towards the treatment of peripheral vascular disease, or any other disease state where premature muscular fatigue is prevalent due to metabolite accumulation.
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PMID:Metabolic inertia in contracting skeletal muscle: a novel approach for pharmacological intervention in peripheral vascular disease. 1499 19

The aim of this review is to provide greater insight and understanding regarding the scientific nature of cycling. Research findings are presented in a practical manner for their direct application to cycling. The two parts of this review provide information that is useful to athletes, coaches and exercise scientists in the prescription of training regimens, adoption of exercise protocols and creation of research designs. Here for the first time, we present rationale to dispute prevailing myths linked to erroneous concepts and terminology surrounding the sport of cycling. In some studies, a review of the cycling literature revealed incomplete characterisation of athletic performance, lack of appropriate controls and small subject numbers, thereby complicating the understanding of the cycling research. Moreover, a mixture of cycling testing equipment coupled with a multitude of exercise protocols stresses the reliability and validity of the findings. Our scrutiny of the literature revealed key cycling performance-determining variables and their training-induced metabolic responses. The review of training strategies provides guidelines that will assist in the design of aerobic and anaerobic training protocols. Paradoxically, while maximal oxygen uptake (V-O(2max)) is generally not considered a valid indicator of cycling performance when it is coupled with other markers of exercise performance (e.g. blood lactate, power output, metabolic thresholds and efficiency/economy), it is found to gain predictive credibility. The positive facets of lactate metabolism dispel the 'lactic acid myth'. Lactate is shown to lower hydrogen ion concentrations rather than raise them, thereby retarding acidosis. Every aspect of lactate production is shown to be advantageous to cycling performance. To minimise the effects of muscle fatigue, the efficacy of employing a combination of different high cycling cadences is evident. The subconscious fatigue avoidance mechanism 'teleoanticipation' system serves to set the tolerable upper limits of competitive effort in order to assure the athlete completion of the physical challenge. Physiological markers found to be predictive of cycling performance include: (i) power output at the lactate threshold (LT2); (ii) peak power output (W(peak)) indicating a power/weight ratio of > or =5.5 W/kg; (iii) the percentage of type I fibres in the vastus lateralis; (iv) maximal lactate steady-state, representing the highest exercise intensity at which blood lactate concentration remains stable; (v) W(peak) at LT2; and (vi) W(peak) during a maximal cycling test. Furthermore, the unique breathing pattern, characterised by a lack of tachypnoeic shift, found in professional cyclists may enhance the efficiency and metabolic cost of breathing. The training impulse is useful to characterise exercise intensity and load during training and competition. It serves to enable the cyclist or coach to evaluate the effects of training strategies and may well serve to predict the cyclist's performance. Findings indicate that peripheral adaptations in working muscles play a more important role for enhanced submaximal cycling capacity than central adaptations. Clearly, relatively brief but intense sprint training can enhance both glycolytic and oxidative enzyme activity, maximum short-term power output and V-O(2max). To that end, it is suggested to replace approximately 15% of normal training with one of the interval exercise protocols. Tapering, through reduction in duration of training sessions or the frequency of sessions per week while maintaining intensity, is extremely effective for improvement of cycling time-trial performance. Overuse and over-training disabilities common to the competitive cyclist, if untreated, can lead to delayed recovery.
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PMID:The science of cycling: physiology and training - part 1. 1583 Oct 59


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