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

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

Intensive exercise is associated with a pronounced increase in extracellular K+ ([K+]o). Because of the ensuing depolarization and loss of excitability, this contributes to muscle fatigue. Intensive exercise also increases the level of circulating catecholamines and lactic acid, which both have been shown to alleviate the depressing effect of hyperkalemia in slow-twitch muscles. Because of their larger exercise-induced loss of K+, fast-twitch muscles are more prone to fatigue caused by increased [K+]o than slow-twitch muscles. Fast-twitch muscles also produce more lactic acid. We therefore compared the effects of catecholamines and lactic acid on the maintenance of contractility in rat fast-twitch [extensor digitorum longus (EDL)] and slow-twitch (soleus) muscles. Intact muscles were mounted on force transducers and stimulated electrically to evoke short isometric tetani. Elevated [K+]o (11 and 13 mM) was used to reduce force to approximately 20% of control force at 4 mM K+. In EDL, the beta2-agonist salbutamol (10(-5) M) restored tetanic force to 83 +/- 2% of control force, whereas in soleus salbutamol restored tetanic force to 93 +/- 1%. In both muscles, salbutamol induced hyperpolarization (5-8 mV), reduced intracellular Na+ content and increased Na+-K+ pump activity, leading to an increased K+ tolerance. Lactic acid (24 mM) restored force from 22 +/- 4% to 58 +/- 2% of control force in EDL, an effect that was significantly lower than in soleus muscle. These results amplify and generalize the concept that the exercise-induced acidification and increase in plasma catecholamines counterbalance fatigue arising from rundown of Na+ and K+ gradients.
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PMID:Effects of lactic acid and catecholamines on contractility in fast-twitch muscles exposed to hyperkalemia. 1574 86

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

The power needs of muscle are supplied by rapid anaerobic glycogenolytic ATP generation. Lactate is built up by the mismatch between steady state energy needs and short-term power demands and the increased concentration drives the lactate shuttle. In this model, contributions to fatigue should be looked for in the flux of glucose through glycogen rather than in the concentrations of fuel.
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PMID:Glycogen turnover forms lactate during exercise. 1623 31

Lactic acid is considered the end product of glycolysis and is a major cause of muscle fatigue. However, the lactate dehydrogenase (LDH) reaction is bidirectional: Lactate can be oxidized to pyruvate and used as a substrate for the Krebs cycle. Therefore, our hypothesis was that lactate sustains the contractile function of rat extraocular muscles during periods of increased activity. The study used extraocular and extensor digitorum longus (EDL) muscles from adult Sprague-Dawley rats to determine LDH isoform expression, total LDH activity, and contractile function in vitro. To evaluate the role of lactate on fatigue, we tested the effect of cinnamate, a blocker of lactate transport, and exogenous lactate on fatigue resistance. Cinnamate accelerated fatigue in the extraocular muscles: Endurance and residual force decreased significantly. Conversely, cinnamate did not affect the endurance or residual force of EDL muscles. Replacing glucose with exogenous lactate increased EDL fatigability but had no effect on the extraocular muscles. However, the extraocular muscles fatigued faster when exposed to exogenous lactate combined with cinnamate. The LDH-A and LDH-C isoforms were expressed at lower levels in extraocular muscle; LDH-B was equally abundant in the EDL and extraocular muscles. Total LDH activity in the extraocular muscles was only approximately 32% of the level in EDL. These results support the hypothesis that lactate sustains the contractile performance of the extraocular muscles.
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PMID:Lactate is a metabolic substrate that sustains extraocular muscle function. 1632 56

Aged garlic extract (AGE) has recently received attention as a potent anti-fatigue agent. The principal aim of this study was to elucidate the mechanism responsible for the ameliorating effect of AGE on physical fatigue in rats caused by repeated endurance exercise on a mechanical treadmill apparatus. Rats were subjected to endurance exercise 5 times per week for 4 weeks. AGE at a dosage of 2.86 g/kg was administrated to rats 30 min before every exercise. Succinate dehydrogenase (SDH) activity in the gastrocnemius and soleus muscles and superoxide dismutase (SOD) activity, nitric oxide (NO) metabolites, and lactic acid concentration in plasma were evaluated as biomarkers of physical fatigue. SDH activity was increased 2-4-fold by repeated endurance exercise in comparison with unexercised (intact) rats, and AGE further up-regulated this activity by 40%. SOD activity was increased 5-fold, whereas AGE maintained it at a level equivalent to that in intact rats. Levels of NO metabolites were slightly decreased, whereas AGE enhanced them 2-fold. Lactic acid concentration was not changed in any of the groups. These results indicate that AGE may facilitate the turnover of aerobic glucose metabolism, attenuate oxidative stress, and promote oxygen supply based on vasodilation, suggesting that AGE ameliorates the various impairments associated with physical fatigue.
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PMID:Aged garlic extract ameliorates physical fatigue. 1665 27

Lactate production under anaerobic conditions is indicative of human performance levels, fatigue, and hydration. Elevated lactate levels result from several medical conditions including congestive heart failure, hypoxia, and diabetic ketoacidosis. Real-time detection of lactate can therefore be useful for monitoring these medical conditions, posttrauma situations, and in evaluating the physical condition of a person engaged in strenuous activity. This paper represents a proof-of-concept demonstration of a lactate sensor based on surface-enhanced Raman spectroscopy (SERS). Furthermore, it points the direction toward a multianalyte sensing platform. A mixed decanethiol/mercaptohexanol partition layer is used herein to demonstrate SERS lactate sensing. The reversibility of the sensor surface is characterized by exposing it alternately to aqueous lactate solutions and buffer without lactate. The partitioning and departitioning time constants were both found to be approximately 30 s. In addition, physiological lactate levels (i.e., 6-240 mg/dL) were quantified in phosphate-buffered saline medium using multivariate analysis with a root-mean-square error of prediction of 39.6 mg/dL. Finally, reversibility was tested for sequential glucose and lactate exposures. Complete partitioning and departitioning of both analytes was demonstrated.
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PMID:Lactate and sequential lactate-glucose sensing using surface-enhanced Raman spectroscopy. 1768 22

Exogenous carbohydrate oxidation was assessed in 6 male Category 1 and 2 cyclists who consumed CytoMax (C) or a leading sports drink (G) before and during continuous exercise (CE). C contained lactate-polymer, fructose, glucose and glucose polymer, while G contained fructose and glucose. Peak power output and VO2 on a cycle ergometer were 408+/-13 W and 67.4+/-3.2 mlO2 x kg(-1) x min(-1). Subjects performed 3 bouts of CE with C, and 2 with G at 62% VO2peak for 90 min, followed by high intensity (HI) exercise (86% VO(2)peak) to volitional fatigue. Subjects consumed 250 ml fluid immediately before (-2 min) and every 15 min of cycling. Drinks at -2 and 45 min contained 100 mg of [U-(13)C]-lactate, -glucose or -fructose. Blood, pulmonary gas samples and 13CO2 excretion were taken prior to fluid ingestion and at 5,10,15,30,45,60,75, and 90 min of CE, at the end of HI, and 15 min of recovery. HI after CE was 25% longer with C than G (6.5+/-0.8 vs. 5.2+/-1.0 min, P<0.05). 13CO2 from the -2 min lactate tracer was significantly elevated above rest at 5 min of exercise, and peaked at 15 min. 13CO2 from the -2 min glucose tracer peaked at 45 min for C and G. 13CO2 increased rapidly from the 45 min lactate dose, and by 60 min of exercise was 33% greater than glucose in C or G, and 36% greater than fructose in G. 13CO2 production following tracer fructose ingestion was greater than glucose in the first 45 minutes in C and G. Cumulative recoveries of tracer during exercise were: 92%+/-5.3% for lactate in C and 25+/-4.0% for glucose in C or G. Recoveries for fructose in C and G were 75+/-5.9% and 26+/-6.6%, respectively. Lactate was used more rapidly and to a greater extent than fructose or glucose. CytoMax significantly enhanced HI.
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PMID:Lactate, fructose and glucose oxidation profiles in sports drinks and the effect on exercise performance. 1789 68

We hypothesized that the changes in muscle temperature and interstitial pressure during thermoneutral immersion may affect the reflex adaptation of the motor drive during static contraction, assessed by the decrease in median frequency (MF) of electromyogram (EMG) power spectrum. Ten subjects were totally immersed for 6 h at 35 degrees C and repeated maximal voluntary contraction (MVC) and submaximal (60% MVC) leg extensions sustained until exhaustion. In vastus lateralis (VL) and soleus (SOL) muscles, the compound muscle potential evoked by muscle stimulation with single shocks (M-wave) was recorded at rest, and MF of surface EMG was calculated during 60% MVCs. We measured lactic acid and potassium venous blood concentrations and calculated plasma volume changes. Data were compared to those obtained in the same individuals exercising at 35 degrees C under dry conditions where the MF decrease during 60% MVCs was modest (-4 to-5%). During immersion, the rectal temperature remained stable, but the thigh and calf surface temperatures significantly increased. Lactic acid and potassium concentrations did not vary, but plasma volume decreased from the 180th min of immersion. The M-wave did not vary in VL but was prolonged in SOL from the 30th min of immersion. From the 220th min of immersion, the maximal MF decrease was majored in both muscles (-18 to -22%). Thus, compared to the dry condition, total body thermoneutral immersion enhances fatigue-induced EMG changes in leg muscles, perhaps through the activation of warm-sensitive muscle endings and/or the changes in interstitial pressure because of vasodilatation.
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PMID:Consequences of prolonged total thermoneutral immersion on muscle performance and EMG activity. 1790 53

For more than a century, the metabolic role of lactate has intrigued physiologists and biochemists. Yet, for the first half of the last century lactate had been designated as a waste product, and assigned no additional significance besides its controversial role in muscle fatigue. The decline of the lactate hypothesis for the onset of muscle fatigue and the defining of some modulatory properties attributed to lactate have increased the interest on this molecule. The present critical review aimed at evaluating some recent publications concerned with unveiling the regulatory actions of lactate in cellular function. Lactate has been described to modulate enzymes catalytic properties to affect hormonal release and responsiveness, and to control body homeostasis. Moreover, these properties are directly related to the genesis and the sustainability of pathological conditions, such as diabetes and cancer. In the end, we concluded that lactate should not be regarded as simply an anaerobic metabolite, but should be considered as a regulatory molecule that modulates the integration of metabolism.
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PMID:Metabolic regulation by lactate. 1850 40

The aetiology of muscle fatigue has yet not been clearly established. Administration of two nucleotides, cytosine monophosphate (CMP) and uridine monophosphate (UMP), has been prescribed for the treatment of neuromuscular affections in humans. Patients treated with CMP/UMP recover from altered neurological functions and experience pain relief, thus the interest to investigate the possible effect of the drug on exhausting exercise. With such aim, we have determined, in exercised rats treated with CMP/UMP, exercise endurance, levels of lactate, glucose and glycogen, and the activity of several metabolic enzymes such as, creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST). Our results show that rats treated with CMP/UMP are able to endure longer periods of exercise (treadmill-run). Before exercise, muscle glucose level is significantly higher in treated rats, suggesting that the administration of CMP/UMP favours the entry of glucose in the muscle. Liver glycogen levels remains unaltered during exercise, suggesting that CMP/UMP may be implicated in maintaining the level of hepatic glycogen constant during exercise. Lactate dehydrogenase and aspartate aminotransferase activity is significantly lower in the liver of treated rats. These results suggest that administration of CMP/UMP enable rats to endure exercise by altering some metabolic parameters.
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PMID:Effect of the nucleotides CMP and UMP on exhaustion in exercise rats. 1866 91


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