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

Lactic acid is thought to be a stimulant of muscle metaboreceptors. The goal of the present study was to determine if inhibition of lactic acid production by dichloroacetate (DCA) would attenuate muscle sympathetic nerve activity (MSNA) during static forearm exercise. DCA increases pyruvate dehydrogenase levels. Thus, for a given amount of pyruvate produced, less lactic acid is formed. Seven subjects performed static forearm exercise at 20% maximal voluntary contraction until fatigue followed by posthandgrip circulatory arrest (PHG-CA) (trial.1). Subjects then received DCA (35 mg/kg) and repeated the exercise protocol (trial 2). We observed an attenuated rise in forearm venous lactate and MSNA. The trial 2 MSNA value during PHG-CA was 51 +/- 11% less than the value during trial 1 (P less than 0.01). In seven control subjects, two bouts of static forearm exercise were performed with an intervening saline infusion. This intervention had no effect on lactate or MSNA responses to exercise. We conclude that DCA attenuates lactate responses to static exercise, and this is associated with a blunted MSNA response.
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PMID:Dichloroacetate reduces sympathetic nerve responses to static exercise. 195 52

Lactic acid is formed and accumulated in the muscle under conditions of high energy demand, rapid fluctuations of the energy requirement and insufficient supply of O2. During intense exercise sustained to fatigue muscle pH decreases to about 6.4-6.6. Force generation does not appear to be limited by the high H+ ion concentration per se but is more related to the PCr level. Phosphofructokinase may be inhibited by high H+ concentration but the inhibition is adequately overcome by increases in the activators AMP and ADP. A high concentration of H+ will decrease PCr by a direct effect on the creatine kinase equilibrium and indirectly by an increase in ADP. The effect of acidosis on glycolysis and on the PCr level will result in a decreased rate of ADP rephosphorylation, and it is suggested that ADP increases transiently above the steady-state level in the contracting muscle fibre. It is further suggested that the function of Na-K-ATPase is impaired by the increase of ADP resulting in an altered ionic balance over the muscle cell membrane. Muscle fatigue is thus considered to be due to an insufficient rate of ADP rephosphorylation resulting in a block in the activation process or in the excitation/contraction coupling.
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PMID:Muscle fatigue and lactic acid accumulation. 347 Oct 61

Lactic acid and H+ evoke muscle reflexes that raise sympathetic nerve activity. Whether these substances are direct afferent stimulants or markers for the acidification of other substances is unknown. Diprotonated phosphate (H2PO4-), a possible mediator of fatigue, increases as the cell acidifies and phosphate is produced. Its role in evoking muscle reflexes is unknown. We used 31P-nuclear magnetic resonance to measure forearm muscle H+ and H2PO4- and microneurography to measure muscle sympathetic nerve activity (MSNA, peroneal nerve) during a handgrip protocol designed to dissociate H+ from H2PO4-. Ischemic handgrip (50% maximal voluntary contraction x 2 min) was followed by a 1-min rest period during which the muscle was freely perfused. This was followed by a second bout of ischemic handgrip and a 5-min recovery. In seven of eight subjects, MSNA correlated with H2PO4-, whereas it correlated with pH in only one subject. To determine whether muscle reflex responses are evoked by H+, lactic acid, monoprotonated phosphate (HPO4(2-), or H2PO4-, we injected H+, lactate, H2PO4- [all 50 mM in 10 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) buffered to pH 6], and HPO4(2-) (50 mM, pH 7.5 in 10 mM HEPES) into the arterial supply of the triceps surae of the cat (n = 9) as we measured mean arterial blood pressure (MAP). H2PO4- increased MAP more than HPO4(2-), H+, or lactate (27.1 +/- 3.7 vs. 5.0 +/- 1.3, 4.6 +/- 3.1, and 7.7 +/- 3.2 rise in mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of diprotonated phosphate in evoking muscle reflex responses in cats and humans. 806 33

Near-infrared Raman spectroscopy can be a new technique for physical evaluations, allowing the measurement of lactic acid concentrations, in blood or muscles, during the physical activity in a transcutaneous non-invasive way. Lactic acid accumulation in the human body is one of the factors that leads to fatigue and therefore it should be continually monitored during physical training. Our proposal is to use Raman spectroscopy to monitor the lactic acid present in an athlete without interrupting his exercise for sample collection. The experimental set-up for Raman spectroscopy comprised a near infrared laser at 830 nm, a Kaiser f/1.8 spectrometer and a liquid nitrogen cooled CCD detector. The radiation from the exciting laser is blocked in the collecting system by Kaiser holographic filters. A personal computer controls the entire system, saving and processing the Raman spectra. Experiments were undertaken to verify the presence of lactic acid in the Raman spectra of solutions of lactic acid in human serum and in blood from a Wistar rat. After these two experiments, another was developed in vivo in a Wistar rat, injecting intraperitoneally 1 ml of a 0.12 mol/l lactic acid aqueous solution. An optical fibre catheter touching the skin of the rat groin, over the ileac vein collected the Raman signal. The presence of lactic acid was detected inside a live organism, in a transcutaneous non-invasive way. The minimum lactic acid concentration that the equipment can detect was also studied. An experiment was undertaken for that purpose, in which the laser illuminated directly a quartz cuvette containing solutions with decreasing lactic acid concentrations up to values near to the physiological level in the human body. The results indicated that the technique can be suitable for the physical evaluation of athletes.
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PMID:Analysis of near-infrared Raman spectroscopy as a new technique for a transcutaneous non-invasive diagnosis of blood components. 1148 34

Lactic acid accumulation is generally believed to be involved in muscle fatigue. However, one study reported that in rat soleus muscle (in vitro), with force depressed by high external K(+) concentrations a subsequent incubation with lactic acid restores force and thereby protects against fatigue. However, incubation with 20 mm lactic acid reduces the pH gradient across the sarcolemma, whereas the gradient is increased during muscle activity. Furthermore, unlike active muscle the Na(+)-K(+) pump is not activated. We therefore hypothesized that lactic acid does not protect against fatigue in active muscle. Three incubation solutions were used: 20 mM Na-lactate (which acidifies internal pH), 12 mM Na-lactate +8 mm lactic acid (which mimics the pH changes during muscle activity), and 20 mM lactic acid (which acidifies external pH more than internal pH). All three solutions improved force in K(+)-depressed rat soleus muscle. The pH regulation associated with lactate incubation accelerated the Na(+)-K(+) pump. To study whether the protective effect of lactate/lactic acid is a general mechanism, we stimulated muscles to fatigue with and without pre-incubation. None of the incubation solutions improved force development in repetitively stimulated muscle (Na-lactate had a negative effect). It is concluded that although lactate/lactic acid incubation regains force in K(+)-depressed resting muscle, a similar incubation has no or a negative effect on force development in active muscle. It is suggested that the difference between the two situations is that lactate/lactic acid removes the negative consequences of an unusual large depolarization in the K(+)-treated passive muscle, whereas the depolarization is less pronounced in active muscle.
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PMID:Lactate and force production in skeletal muscle. 1555 Apr 57

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

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

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

Lactic acid has played an important role in the traditional theory of muscle fatigue and limitation of endurance exercise performance. It has been called a waste product of anaerobic metabolism and has been believed to be responsible for the uncomfortable "burn" of intense exercise and directly responsible for the metabolic acidosis of exercise, leading to decreased muscle contractility and ultimately cessation of exercise. Although this premise has been commonly taught, it is not supported by the scientific literature and has led to a great deal of confusion among the sports medicine and exercise science communities. This review will provide the sports medicine clinician with an understanding of contemporary lactate theories, including lactate's role in energy production, its contributions to metabolic acidosis, and its function as an energy substrate for a variety of tissues. Lactate threshold concepts will also be discussed, including a practical approach to understanding prediction of performance and monitoring of training progress based on these parameters.
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PMID:Lactate: Friend or Foe. 2764 Jul 37


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