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

This study examined the effect of (a) creatine supplementation on exercise metabolism and performance and (b) changes in intramuscular total creatine stores following a 5 day supplementation period and a 28 day wash-out period. Six men performed four exercise trials, each consisting of four 1 min cycling bouts, punctuated by 1 min of rest followed by a fifth bout to fatigue, all at a workload estimated to require 115 or 125% VO2,max. After three familiarization trials, one trial was conducted following a creatine monohydrate supplementation protocol (CREAT); the other after 28 d without creatine supplementation, in which the last 5 d involved placebo ingestion (CON). Intramuscular TCr was elevated (P < 0.05) in CREAT compared with the final familiarization trial (FAM 3) and CON. Concentrations of this metabolite in these latter trials were not different. In addition, a main effect (P < 0.05) for treatment was observed for PCr when the data from CREAT were compared with CON. In contrast, no differences were observed in the total adenine nucleotide pool (ATP+ADP+AMP), inosine 5'-monophosphate, ammonia, lactate or glycogen when comparing CREAT with CON. Despite the differences in TCr and PCr concentrations when comparing CREAT with other trials, no difference was observed in exercise duration in the fifth work bout. These data demonstrate that creatine supplementation results in an increase in TCr but this has no effect on performance during exercise of this nature, where the creatine kinase system is not the principal energy supplier. In addition 28 d without supplementation is a sufficient time to return intramuscular TCr stores to basal levels.
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PMID:Effect of creatine supplementation on intramuscular TCr, metabolism and performance during intermittent, supramaximal exercise in humans. 871 58

This study investigated the effect of the serotonin receptor antagonist pizotifen on endurance performance during treadmill exercise in humans. Eight healthy men exercised to exhaustion on a treadmill at an intensity corresponding to 70% of their maximal oxygen uptake (VO2max). Pizotifen was administered orally in a 1-mg dose 5 h before the start of exercise. The study was double blind, using a randomized, placebo-controlled crossover design. Oxygen uptake, heart rate, and ratings of perceived exertion were measured and blood samples taken for determination of concentrations of lactate, glucose, amino acids, ammonia, and haematocrit. Measurements were made at intervals of 30 min during the run and at exhaustion. There was no significant difference between the placebo and the pizotifen trials for any of the variables except for the plasma free-tryptophane: branched chain amino acid ratio which was somewhat lower after pizotifen at postexercise. Pizotifen did not increase exercise time to exhaustion, which was even shorter after pizotifen than after placebo in seven out of the eight subjects; the difference between pizotifen and placebo did not reach the level of statistical significance [109.4 (SD 6.7) min after pizotifen versus 119.8 (SD 12.5) min after placebo]. The results do not support the hypothesis that there is a central component to fatigue which is mediated by the serotoninergic neurones.
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PMID:The antiserotonin agent pizotifen does not increase endurance performance in humans. 878 90

The purpose of this investigation was to study the relationship between both blood ammonia thresholds (AmT) and lactate thresholds (LT) during dynamic exercise in cardiac transplant patients (CTPs). Eleven male patients who had undergone orthotopic cardiac transplantation (age: 54 +/- 11 years, mean +/- SD; height: 165.1 +/- 6.6 cm; body mass: 78.3 +/- 16.1 kg) participated in this study. Each of them performed a bicycle ergometer test (ramp protocol) until volitional fatigue. During each test, gas exchange parameters and ECG responses were determined continuously. In addition, blood lactate and ammonia concentrations were measured every 2 min for determination of both LT and AmT, respectively. Peak values of oxygen uptake (Vo2), respiratory exchange ratio, ventilation, and heart rate averaged 15.9 +/- 3.03 mL.Kg-1.min-1, 1.02 +/- 0.06, 46.69 +/- 5.69 L.min-1, and 124 +/- 16 beats per minute, respectively. However, blood concentrations of lactate and ammonia at peak exercise were 3.7 +/- 0.4 mmol.L-1 and 85.6 +/- 31.7 micrograms.dL-1, respectively. LT and AmT were detected in 8 (72.7% of total) and 9 (81.8% of total) of 11 subjects, respectively. No significant differences were found between mean values of LT and AmT, when both were expressed either as Vo2 (10.01 +/- 1.19 vs 10.5 +/- 2.38 mL.kg-1.min-1, respectively) or as percent Vo2 peak (64.62 +/- 11.362 vs 66.48 +/- 9.19%, respectively). In addition, LT and AmT were significantly correlated (p < 0.05) when both were expressed either as Vo2 (mL.kg-1.min-1) or as percent Vo2 peak (r = 0.70 and r = 0.68, respectively). Our findings suggest that in CTPs, both LT and AmT occur at similar workloads, probably as a result of skeletal muscle alterations associated with chronic deconditioning and immunosuppressive therapy.
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PMID:Relationship between lactate and ammonia thresholds in heart transplant patients. 879 13

It has been hypothesized that fatigue and prolactin (PRL) changes during endurance exercise are influenced by serotonin synthesis, and in turn, release. Such a change is thought to occur through an increase in blood free tryptophan (TRP) and a concomitant decrease in those large neutral amino acids (LNAA) which compete with free TRP for entry into the brain. For further investigation, 10 healthy athletes were randomly subjected to three test units (TU), each consisting of a treadmill run for 90 min. The speed was adjusted to a blood lactate level of 2 mmol/l. During the first 30 min of exercise infusions of 500 ml saline (TU I), 500 ml saline with amino acids (TU II) or 500 ml saline with 30 U heparin/kg following an oral soy oil solution given 1 h before (TU III) were administered. Rate of perceived exertion (RPE), heart rate and running speed were recorded during exercise. Venous blood samples were taken after a 10 h fast, at rest, after 10, 50 and 90 min of exercise as well as 10 and 30 min post-exercise. PRL, insulin, glucose, ammonia, lactate, triglycerides (TG), free fatty acids (FFA) and amino acids were determined in each sample. No significant differences were found in RPE. PRL increased (p < 0.01) in all TU. TG and heparin administration resulted in an increase (p <0.01) in FFA, which correlated (p < 0.01) with free TRP and the ratio of free TRP/TRP. Artificial increase in free TRP in TU III did not affect plasma PRL level. The amino acid infusion in TU II induced an increase in LNAA but had no significant effect on PRL. PRL and ammonia peaked at the end of exercise. We conclude that neither exercise-induced PRL secretion nor RPE are affected by changes in circulating free TRP and LNAA under the present conditions.
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PMID:Alterations in plasma free tryptophan and large neutral amino acids do not affect perceived exertion and prolactin during 90 min of treadmill exercise. 883 6

The present experiment was designed to investigate whether a diet-induced metabolic acidosis was a major factor in the earlier onset of fatigue during high-intensity exercise. Six healthy males cycled to exhaustion at a workload equivalent to 95 percent of maximum oxygen uptake on four separate occasions. Exercise tests were performed after an overnight fast and each test was preceded by one of four experimental conditions. Two experimental diets were designed, either to replicate each subject's own normal diet [N diet, mean (SD) daily energy intake (E) = 13 (0.7) MJ, 14.5 (0.8) percent protein (Pro), 37.5 (2.2) percent fat (Fat) and 47.5 (2.1) percent carbohydrate (CHO)], or a low-carbohydrate diet [E = 12.6 (0.8) MJ, 33.6 (1.3) percent Pro, 64.4 (1.5) percent Fat and 2.2 (0.4) percent CHO]. These diets were prepared and consumed within the department over a 3-day period. Over a 3-period prior to the exercise trial subjects ingested either NaHCO(3) or CaCO(3) (3.6 and 3.0 mmol*kg body mass), thus giving four experimental conditions: N diet and treatment, N diet and placebo, low-CHO diet and treatment and low-CHO diet and placebo. Treatments were assigned using a randomised protocol. Arterialised venous blood samples were taken for the determination of acid-base status and metabolite concentrations at rest prior to exercise and at intervals for 30 min following exhaustion. Consumption of the low-CHO diet induced a mild metabolic acidosis which was reversed by the ingestion of NaHCO(3). Blood pH, bicarbonate (HCO-(3)) and base excess (BE) were higher following NaHCO(3) ingestion after the normal diet than all of the other experimental conditions (P <0.01). Exercise time following the low-CHO diet was less than on the normal diet conditions (P <0.05): bicarbonate ingestion had no effect on exercise time on either of the diet conditions. Post-exercise blood pH, HCO-(3); and BE were higher following the ingestion of NaHCO(3) irrespective of the pre-exercise diet (P <0.05). Blood lactate concentration was higher 2 min after exercise following the N diet with NaHCO(3) when compared to the low-CHO diets with either NaHCO(3) or placebo (P <0.05). Plasma ammonia accumulation was not significantly different between experimental conditions. These data confirm previous data showing that the ingestion of a low-CHO diet reduces the capacity to perform high-intensity exercise, but it appears that the metabolic acidosis induced by the low-CHO diet is not the cause of the reduced exercise capacity observed during high-intensity exercise under these conditions.
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PMID:The acute reversal of a diet-induced metabolic acidosis does not restore endurance capacity during high-intensity exercise in man. 886 77

The causes of fatigue during muscular exercise include factors that reside in the brain (central mechanisms) as well as the muscles themselves (peripheral mechanisms). Central fatigue is largely unexplored, but there is increasing evidence that increased brain serotonin (5-HT) can lead to central (mental) fatigue, thereby causing a deterioration in sport and exercise performance. Although there are also strong theoretical grounds for a beneficial role of nutrition in delaying central fatigue, the data are much more tenuous. Dietary supplementation with branched-chain amino acids (BCAA) in low doses produces small and probably inconsequential effects on peripheral markers of brain 5-HT synthesis (plasma free tryptophan/BCAA), whereas larger doses are likely to be unpalatable, reduce the absorption of water in the gut, and may increase potentially toxic ammonia concentrations in the plasma. Alternatively, carbohydrate supplementation results in large reductions in plasma free tryptophan/BCAA and exercise time to fatigue is significantly longer, but it is difficult to distinguish between the effects of carbohydrate feedings on central fatigue mechanisms and the well-established beneficial effects of carbohydrate supplements on the contracting muscle. These data support the exciting possibility that relationships exist among nutrition, brain neurochemistry and sport performance. However, while the evidence is intriguing and makes good intuitive sense, our knowledge in this area is rudimentary at best.
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PMID:Central and peripheral factors in fatigue. 889 20

Fatigue of voluntary muscular effort is a complex phenomenon. To date, relatively little attention has been placed on the role of the central nervous system (CNS) in fatigue during exercise despite the fact that the unwillingness to generate and maintain adequate CNS drive to the working muscle is the most likely explanation of fatigue for most people during normal activities. Several biological mechanisms have been proposed to explain CNS fatigue. Hypotheses have been developed for several neurotransmitters including serotonin (5-HT; 5-hydroxytryptamine), dopamine, and acetylcholine. The most prominent one involves an increase in 5-HT activity in various brain regions. Good evidence suggests that increases and decreases in brain 5-HT activity during prolonged exercise hasten and delay fatigue, respectively, and nutritional manipulations designed to attenuate brain 5-HT synthesis during prolonged exercise improve endurance performance. Other neuromodulators that may influence fatigue during exercise include cytokines and ammonia. Increases in several cytokines have been associated with reduced exercise tolerance associated with acute viral or bacterial infection. Accumulation of ammonia in the blood and brain during exercise could also negatively effect the CNS function and fatigue. Clearly fatigue during prolonged exercise is influenced by multiple CNS and peripheral factors. Further elucidation of how CNS influences affect fatigue is relevant for achieving optimal muscular performance in athletics as well as everyday life.
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PMID:Possible mechanisms of central nervous system fatigue during exercise. 900 Jan 55

The purpose of the present study was to establish whether the performance of an all-out sprint could be replicated and the metabolic responses moderated in two further trials involving pre-set constant average pedalling rates. A total of 24 subjects (12 males and 12 females) completed a 30-s high-speed maximal all-out effort on a cycle ergometer against an applied resistance equal to 7.5% of their body mass. On two further occasions the applied resistance was increased so that the external work of the all-out effort could be replicated by adopting a pre-determined constant average pedal rate. When the required pedal rate was within the range of 60-90 rev.min-1 the subjects were able to maintain the rate for the full 30-s and so could replicate the external work of the all-out effort. They were unable to sustain a faster constant rate within the range of 97-150 rev.min-1 for the full 30 s, resulting in approximately 7% less external work being achieved (P < 0.05). A lower level of fatigue, reflected by less of a reduction in peak power output in a subsequent 6-s sprint (P < 0.05), arose as a result of similar work produced under constant paced conditions compared with the all-out effort. Also, post-exercise blood lactate, pH and ammonia were less disturbed (P < 0.05) following the paced trial compared with similar work produced in the all-out effort. A possible explanation for these findings is that there may be a partial sparing of some type II fibres as a consequence of an initial submaximal intensity of exercise during the paced trial.
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PMID:Constant external work cycle exercise--the performance and metabolic effects of all-out and even-paced strategies. 900 53

The aim of this investigation was to re-evaluate the relationship between electromyography and work intensity during incremental work in light of highly discrepant literature. Trained male subjects participated in the study (n = 14). Each subject completed a VO2max test on a cycle ergometer. Tests started at a power output of 60 Watts with a 30 Watt.4 min-1 work increment. Each test was terminated at exhaustion. Blood was collected at the end of each work intensity for lactate and ammonia analysis. EMG were recorded from the vastus lateralis, rectus femoris and vastus medialis using pre-amplified surface electrodes. EMG were collected at each intensity over a period of 60 cycle revolutions. EMG signals were analyzed using integration and EMG spectral analysis. Gas exchange variables were recorded on-line for each test (15 second interval). Ammonia and lactate threshold points were surpassed at the same absolute work intensity (200 Watts) which was equivalent to 64-69% VO2max. When a linear model was applied to the iEMG data, coefficients of determination achieved were greater than those obtained when an exponential model was used for the vastus lateralis and medialis. Gradients of regression lines fitted to iEMG data at pre- and post-lactate/ammonia threshold work intensities were not different. Alternatively, the iEMG-work intensity relationship for the rectus femoris muscle tended to be curvilinear. Significant increases in iEMG were observed at post-lactate/ammonia threshold work intensities for the rectus femoris reflecting increases in fatigue and type II motor unit recruitment at these intensities. In general, median frequency of the EMG power spectrum function were unchanged during incremental work, although highly individualistic results were observed between some subjects and muscles. Grouped median frequency values were insensitive to changes in recruitment, metabolite accumulation and fatigue associated with the increases in work intensity. Consequently, the usefulness of EMG spectral analysis during incremental work was questioned.
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PMID:The relationship between electromyography and work intensity revisited: a brief review with references to lacticacidosis and hyperammonia. 940 27

This review considers four experimental models for studying the dynamics of ammonia and amino acid metabolism in skeletal muscle: the rat hindlimb, the isolated dog gastrocnemius, the leg extensor for humans, and the traditional approach of humans performing two-legged exercise. The rat hindlimb is well suited for studying intense exercise with fast-twitch white fibers, but it is poorly suited for studying prolonged exercise because of rapid fatigue of major portions of the muscle and the restrictions of taking multiple blood samples. The traditional human model is limited because of the inability to quantify accurately the active muscle mass and to determine the true blood flow to the entire active tissue. Despite species differences and the various limitations of the paradigms, there are numerous consistencies in the literature. For example, human muscle and the canine gastrocnemius demonstrate similar magnitudes of efflux of ammonia, glutamine, and alanine (when indexed for the active mass) during prolonged exercise. Muscle has a large ammonia producing capacity during either intense or prolonged exercise. In prolonged exercise this is accompanied by similar productions of alanine and glutamine as well as a large uptake of glutamate. Despite the latter, the intramuscular glutamate concentration rapidly declines by more than 50% and remains constant throughout the exercise period. The leg extensor model and the canine gastrocnemius offer the greatest opportunities to quantify these responses during prolonged exercise.
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PMID:Ammonia and amino acid metabolism in skeletal muscle: human, rodent and canine models. 947 42


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