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

To determine whether a single carbohydrate feeding could rapidly restore and maintain plasma glucose availability late in exercise, six trained cyclists were studied on two occasions during exercise to fatigue at 70 +/- 1% of VO2max. After 135 min of exercise, the men were fed either an artificially sweetened placebo or glucose polymers (3 g.kg-1 in a 50% solution). Prolonged exercise led to a decline in plasma glucose from 4.6 +/- 0.1 mM at rest to 3.9 +/- 0.2 mM after 135 min (P less than 0.05). Plasma glucose decreased further (P less than 0.05) to 3.2 +/- 2.0 mM at fatigue following placebo ingestion but increased (P less than 0.05) and was then maintained at 4.5-4.9 mM following carbohydrate ingestion. Respiratory exchange ratio (R) fell gradually during the placebo trial from 0.88 +/- 0.01 after 10 min of exercise to 0.81 +/- 0.01 at fatigue (P less than 0.01). R also reached a minimum of 0.81-0.82 in each subject after 135-180 min of exercise during the carbohydrate feeding trial but increased again to 0.84-0.86 as plasma glucose rose following the carbohydrate feeding. Exercise time to fatigue was 21% longer (205 +/- 17 vs 169 +/- 12 min; P less than 0.01) during the carbohydrate ingestion trial. Plasma insulin did not increase significantly, whereas plasma free fatty acids and blood glycerol plateaued following carbohydrate ingestion. These data indicate that a single carbohydrate feeding late in exercise can supply sufficient carbohydrate to restore euglycemia and increase carbohydrate oxidation, thereby delaying fatigue.
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PMID:Metabolism and performance following carbohydrate ingestion late in exercise. 292 2

Twelve trained males, in a fed state, were studied to examine the effect of pre-exercise fructose ingestion on endurance capacity during prolonged cycling exercise. Sixty minutes prior to exercise, subjects ingested either 60 or 85 g fructose or a sweet placebo. Mean exercise intensity initially required 62% of the maximal aerobic power and thereafter increased to elicit 72 and 81% of maximal aerobic power at 90 and 120 min of exercise, respectively. Exercise time (mean +/- SE) to exhaustion was significantly increased after fructose ingestion, as compared to placebo ingestion (145 +/- 4 vs 132 +/- 3 min, P less than 0.01). During the exercise, no differences were observed between both trials for oxygen uptake, heart rate, or perceived exertion. Serum glucose and insulin levels between both trials were not significantly different throughout the experiment. There were also no significant differences in serum-free fatty acids and glycerol levels as well as respiratory exchange ratio between fructose and placebo trials during the exercise. The results suggest that fructose ingestion is of benefit before prolonged exercise, because it provides a carbohydrate source to contracting muscles without transient hypoglycemia and a depression of fat utilization, and thereby delays the fatigue.
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PMID:Effect of pre-exercise fructose ingestion on endurance performance in fed men. 328 17

The effects of the addition and removal of glycerol on the metabolic activities of human platelets were studied. Platelet concentrates (PC) with 20 ml plasma were stored with 3-7% (v/w) glycerol in 150-ml polyvinylchloride plastic bags for 2 days at 22 degrees C with constant agitation. Incubation of glycerol with platelets produced a dose-dependent inhibition of oxygen consumption. The inhibitions of glucose utilization and lactate production had reached the plateau level at 3% glycerol. The rate of adenosine triphosphate (ATP) generation of control platelets was 9.8 nmol/min/10(9) platelets, in which over 90% ATP generation was derived from oxidative phosphorylation. There was a dose-dependent decrease (up to 20%) by glycerol in the rate of platelet ATP generation. Glycerol inhibited glycolysis more than oxidative phosphorylation. However, the inhibition potency diminished with increasing concentrations of glycerol. The energy metabolism of platelets after removal of 5% glycerol was examined. Deglycerolized platelets after 1 hr incubation facilitated energy metabolism more strongly than that of 24 hr incubation. The platelet aggregation response to collagen was not impaired by a cycle of the addition and removal of glycerol. The results indicate that glycerol lowered the rate of ATP generation of platelets stored at 22 degrees C. However, the removal of glycerol reversed the decreased energy metabolism.
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PMID:Reversible effects of glycerol on the metabolism of platelets kept at room temperature. 337 Oct 61

Five men were studied during exercise to exhaustion on an electrically braked cycle ergometer at 70% of VO2max. The four experimental treatments were as follows: fasted for 36 h (A); fasted (36 h) and refed with glucose (B) or glycerol (C); postabsorptive (overnight fast, D). In B and C the subjects were given a drink containing glucose or glycerol (1g per kg body weight) 45 min before starting exercise. A placebo drink was given 45 min before exercise on treatments A and D. Despite an increased availability of circulating free fatty acids, beta-hydroxybutyrate and glycerol exercise time to exhaustion was significantly lower after fasting (treatment A 77.7 +/- 6.8 min) compared with treatment D (119.5 +/- 5.8 min). Refeeding with glucose or glycerol did not significantly improve performance (92.4 +/- 11.8 min and 80.8 +/- 3.6 min respectively) compared with treatment A and lowered circulating levels of FFA and beta-HB during exercise compared with A. Despite the probability of low liver glycogen levels after fasting, none of the subjects became hypoglycaemic (blood glucose less than 4 mmol.l-1) during exercise and their blood lactate concentrations were not high at exhaustion. Plasma levels of branched chain amino acids (BCAA) decreased progressively during exercise on treatments A, B and C and were considerably lower at exhaustion compared with treatment D. Falling plasma concentrations of BCAA during prolonged exercise may be implicated in the generation of central fatigue.
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PMID:Influence of a 36 h fast followed by refeeding with glucose, glycerol or placebo on metabolism and performance during prolonged exercise in man. 339 74

Action potential fatigue has been studied in single short toe muscle fibres of Xenopus under three different conditions: in rested fibres which produced maximum tension, in fibres during post-contractile depression (PCD), a state of depressed tension generation but seemingly normal membrane properties, and in fibres de-tubulated by glycerol treatment. The fibres were stimulated continuously at 70 Hz (22.5 degrees C) and membrane potential was measured throughout the stimulation period with an intracellular microelectrode. Rested and PCD fibres exhibited similarities in the development of action potential fatigue during a 30 s stimulation period; the amplitude was reduced by 86 and 70 mV, respectively, and the duration, measured at a level of one-third of the peak amplitude, was increased from 1.1 to 4.2 and 1.3 to 3.7 ms, respectively. De-tubulated fibres were more resistant to action potential fatigue; the amplitude decreased by only 20 and 35 mV during 30 and 60 s of stimulation, respectively, and the duration was increased from 1.1 to 2.7 ms. It is concluded that action potential fatigue in skeletal muscle fibres is primarily caused by failing regenerative activity in the t-tubules, which is reflected in an altered shape of conventionally recorded action potentials.
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PMID:Action potential fatigue in single skeletal muscle fibres of Xenopus. 357 17

When the energy intake of (NZB X NZW)F1 female mice was reduced to 60% of the intake of simultaneously ad libitum-fed mice, the early death associated with autoimmune-based renal disease in this strain was greatly delayed. The length of prolongation of disease-free life depended not only on the decreased energy intake but also on the energy source. In the group of mice with 60% intake of a carbohydrate-free (i.e., high fat) diet, mean longevity was doubled as compared to that of ad libitum-fed mice. However, when the nonprotein energy was supplied by carbohydrate (sucrose and glycerol) the mean longevity was three times that of the ad libitum-fed groups, although survival times varied widely. With ad libitum feeding the nonprotein energy source did not significantly affect longevity. Clearly, although energy intake restriction provides significant influence on longevity, very high fat diets do not give the same protection as do high carbohydrate diets. The basis for this difference is not entirely clear and several explanations are possible.
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PMID:Crucial dietary factors in maximizing life span and longevity in autoimmune-prone mice. 359 24

The metabolic and ventilatory responses to steady state submaximal exercise on the cycle ergometer were compared at four intensities in 8 healthy subjects. The trials were performed so that, after a 10 min adaptation period, power output was adjusted to maintain steady state VO2 for 30 min at values equivalent to: (1) the aerobic threshold (AeT); (2) between the aerobic and the anaerobic threshold (AeTAnT); (3) the anaerobic threshold (AnT); and (4) between the anaerobic threshold and VO2max (AnTmax). Blood lactate concentration and ventilatory equivalents for O2 and CO2 demonstrated steady state values during the last 20 min of exercise at the AeT, AeAnT and AnT intensities, but increased progressively until fatigue in the AnTmax trial (mean time = 16 min). Serum glycerol levels were significantly higher at 40 min of exercise on the AeAnT and the AnT when compared to AeT, while the respiratory exchange ratios were not significantly different from each other. Thus, metabolic and ventilatory steady state can be maintained during prolonged exercise at intensities up to and including the AnT, and fat continues to be a major fuel source when exercise intensities are increased from the AeT to the AnT in steady state conditions. The blood lactate response to exercise suggests that, for the organism as a whole, anaerobic glycolysis plays a minor role in the energy release system at exercise intensities upt to and including the AnT during steady state conditions.
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PMID:Metabolic and ventilatory responses to steady state exercise relative to lactate thresholds. 369 10

The functional significance of gluconeogenesis in prolonging endurance during submaximal activity was assessed in untrained and endurance-trained rats. Gluconeogenesis was inhibited at the phosphoenolpyruvate carboxykinase reaction by 3-mercaptopicolinic acid (3-MPA). Endurance was significantly reduced by 3-MPA in untrained (-32%; P less than 0.005) and in trained rats (-26%; P less than 0.001). Metabolic correlates of fatigue were examined in trained rats. At exhaustion, 3-MPA-treated rats had only 3% of resting hepatic glycogen, 46% of resting white quadriceps glycogen, and 37% of resting blood glucose. All of these substrates were at higher levels in sham-injected controls after the same duration of running (130 min). Glycogen levels in red quadriceps, blood lactate levels, and blood glycerol levels were not different between groups. Plasma free fatty acid levels were elevated to the same extent in both groups after 90 min of activity, remained high at 130 min in controls, but had returned to resting levels in the severely hypoglycemic 3-MPA-treated rats at exhaustion. The results indicate that gluconeogenesis is important for maintaining blood glucose levels and for prolonging endurance time during submaximal activity.
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PMID:Reduced running endurance in gluconeogenesis-inhibited rats. 372 4

In vitro experiments were carried out under the premise that fatigue/stress could be defined bodily in terms of energy demand under conditions of limited supply. The experiments demonstrated some new biochemical correlates of stress and some of their hormonal control factors. It was seen that both physical and psychological stress--e.g., sleep deprivation, combat flying--caused an elevation of phospholipid G (phosphatidyl glycerol). This reaction was consistent, despite the type of stress. Other phospholipids varied with the stress conditions. The triggering factor for this raised phospholipid level may be explained by the fact that injection of various PGs (prostaglandins) causes major elevation in G and lesser changes in other phospholipids. The different types of PGs cause varying reactions in the different phospholipids. The work with PGs indicates a means of channelling biological energy in ways that will enhance bodily tolerance to stress.
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PMID:Some in vitro and in vivo effects of a new prostaglandin derivative. 467 92

The effects of oleate starvation on an oleate auxotroph of Escherichia coli K-12 were investigated. Following removal of oleate from the mutant growing in a minimal glycerol-peptone medium, the cells stopped making deoxyribonucleic acid, ribonucleic acid, protein, and phospholipids; they began to die exponentially and finally lysed. During oleate starvation in minimal medium minus peptone, inhibition of macromolecular syntheses and death occurred; however, lysis did not follow. When growth ceased, no further dying was observed. It is shown that none of the early effects (inhibition of macromolecular syntheses and death) can be due to leakiness of the cells, induction of a prophage or a colicin, or lack of energy sources. The cause of inhibition of macromolecular syntheses remained unknown. Since the rate of death was the same as the generation time under different conditions, it appears that death is due to the defective synthesis of some cellular structure (quite possibly, cytoplasmic membrane) during phospholipid deficiency. Lysis was found to require protein synthesis; electron microscopy revealed a peculiar type of "lysis from within"; i.e., the shape of the cells did not change but fragmentation of the inner layer of the cell envelope occurred. The murein was found to be unaltered. Most likely, lysis was a consequence of the cell's attempt to synthesize cytoplasmic membrane with altered phospholipid composition or during phospholipid deficiency. Several membrane functions (respiration, adenosine triphosphate formation, permeability) existing before oleate removal were not lost during starvation. Therefore, general damage to the membrane did not occur, and it could be that most, if not all, described effects were due to defective de novo membrane synthesis.
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PMID:Effects of oleate starvation in a fatty acid auxotroph of Escherichia coli K-12. 489 Dec 68


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