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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the possible contribution of bioenergetic failure in the particular brain regions to the pathomechanism of hepatic encephalopathy (HE), local cerebral metabolic rate for glucose (LCMRglue) was evaluated from [3H]-deoxyglucose uptake in frontal, visual and auditory cortex, striatum, cerebellum and medulla oblongata of rats with acute HE induced with a hepatotoxin--thioacetamide (TAA). HE caused a decrease of LCMRglue in all the regions studied. The strongest decrease (about 65%) was noted in hippocampus and cerebral cortex--the two regions rich in glutamatergic neurons. The results indicate a possible link between decreased energy metabolism and impaired excitatory, glutamatergic neurotransmission--the two factors whose contribution to HE has so far been implicated separately.
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PMID:Decreased glucose utilization in discrete brain regions of rat in thioacetamide-induced hepatic encephalopathy as measured with [3H]-deoxyglucose. 188 55

Muscle glycogen and blood glucose are important substrates for contracting skeletal muscle during exercise and fatigue often coincides with depletion of these carbohydrate reserves. Carbohydrate utilization during exercise is influenced by several factors including exercise intensity and duration, training status, diet, environment and gender. In view of the importance of carbohydrates for exercise performance, active individuals should ensure their diet contains sufficient carbohydrate. For athletes engaged in heavy training the daily carbohydrate requirement may be as high as 9-10 g carbohydrate per kg body mass in order to guarantee adequate carbohydrate availability prior to and during exercise and to allow full recovery of carbohydrate reserves following exercise.
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PMID:Carbohydrates and exercise. 189 61

Based upon the fact that fatigue during intense prolonged exercise is commonly due to depletion of muscle and liver glycogen which limits both training and competitive performance, this paper has proposed extraordinary dietary practices which generally advocate high carbohydrate intake at all times before, during and after exercise. The simple goal is to have as much carbohydrate in the body as possible during the latter stages of prolonged intense exercise when the ability for intense exercise usually becomes limiting to performance. This theory is put into practice by recommending that carbohydrate intake after exhaustive exercise should average 50 g per 2 h of mostly moderate and high glycaemic carbohydrate foods. The aim should be to ingest a total of about 600 g in 24 h. Carbohydrate intake should not be avoided during the 4 h period before exercise and in fact it is best to eat at least 200 g during this time. When possible, carbohydrate should be ingested during exercise, generally in the form of solutions containing glucose/sucrose/maltodextrins, at a rate of 30-60 g h-1. Emphasis has been placed upon eating the optimal amount and best type of carbohydrate at the proper times because these practices demand a large amount of food. When diet is not carefully planned according to these guidelines, endurance athletes tend to consume too little carbohydrate because they become satiated with high fat in their diet and they go through periods in the day when recovery of glycogen stores is suboptimal and thus precious time is wasted.
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PMID:Timing and method of increased carbohydrate intake to cope with heavy training, competition and recovery. 189 62

This is a report on an eight-year-old girl who presented with facial palsy, headache, fatigue, arthralgias and myalgias six weeks after two tick bites. Physical examination was unremarkable with the exception of a left-sided facial palsy. Laboratory investigation revealed normal complete blood count, ESR and CRP. The spinal tap showed a protein of 63 mg/dl, glucose 45 mg/dl and no cells. IFT titres to Borrelia burgdorferi in serum and CSF were significantly elevated. The diagnosis was supported by Western blot analysis. Treatment was started with ceftriaxone i.v. for a total of 14 days. Under this therapeutic regimen the patient improved substantially within five days. Investigation of CSF in patients with facial palsy may help to establish the diagnosis of Lyme disease by simultaneously measuring IFT to B. burgdorferi in serum and spinal fluid, even in cases where CSF shows little or no signs of inflammation.
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PMID:Facial palsy with elevated protein in otherwise normal CSF in a child with Lyme disease. 191 37

We performed 93 sclerotherapy sessions on liver cirrhosis patients with recurrent variceal bleedings. In each session, hypertonic glucose, thrombin and 1% polidocanol were consecutively injected into the varices, and changes in the hemostatic system were examined in relation to the symptoms observed during the treatment. Patients underwent sclerotherapy with no complaints in 62 (67%) sessions, and complained of slight symptoms of general fatigue and headache in 19 (20%). In the other 12 (13%) sessions, the procedure was discontinued due to marked manifestations of these symptoms. All symptoms were temporary and disappeared completely after the procedure. These temporary symptoms were closely related to changes in coagulation tests similar to those of disseminated intravascular coagulation, which were observed just after the treatment. Possible activation of the renal kallikrein-kinin system following injection sclerotherapy was also demonstrated.
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PMID:Manifestations of temporary symptoms during endoscopic variceal sclerotherapy using thrombin as a sclerosant. 192 Sep 57

It is well recognized that energy from CHO oxidation is required to perform prolonged strenuous (greater than 60% VO2 max) exercise. During the past 25 years, the concept has developed that muscle glycogen is the predominant source of CHO energy for strenuous exercise; as a result, the potential energy contribution of blood glucose has been somewhat overlooked. Although during the first hour of exercise at 70-75% VO2max, most of the CHO energy is derived from muscle glycogen, it is clear that the contribution of muscle glycogen decreases over time as muscle glycogen stores become depleted, and that blood glucose uptake and oxidation increase progressively to maintain CHO oxidation (Fig. 1.7). We theorize that over the course of several hours of strenuous exercise (i.e., 3-4 h), blood glucose and muscle glycogen contribute equal amounts of CHO energy, making blood glucose at least as important as muscle glycogen as a CHO source. During the latter stages of exercise, blood glucose can potentially provide all of the CHO energy needed to support exercise at 70-75% VO2max if blood glucose availability is maintained. During prolonged exercise in the fasted state, however, blood glucose concentration often decreases owing to depletion of liver glycogen stores. This relative hypoglycemia, although only occasionally severe enough to result in fatigue from neuroglucopenia, causes fatigue by limiting blood glucose (and therefore total CHO) oxidation. The primary purpose of CHO ingestion during continuous strenuous exercise is to maintain blood glucose concentration and thus CHO oxidation and exercise tolerance during the latter stages of prolonged exercise. CHO feeding throughout continuous exercise does not alter muscle glycogen use. It appears that blood glucose must be supplemented at a rate of approximately 1 g/min late in exercise. Feeding sufficient amounts of CHO 30 minutes before fatigue is as effective as ingesting CHO throughout exercise in maintaining blood glucose availability and CHO oxidation late in exercise. Most persons should not wait, however, until they are fatigued before ingesting CHO, because it appears that glucose entry into the blood does not occur rapidly enough at this time. It also may be advantageous to ingest CHO throughout intermittent or low-intensity exercise rather than toward the end of exercise because of the potential for glycogen synthesis in resting muscle fibers. Finally, CHO ingestion during prolonged strenuous exercise delays by approximately 45 minutes but does not prevent fatigue, suggesting that factors other than CHO availability eventually cause fatigue.
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PMID:Carbohydrate ingestion during prolonged exercise: effects on metabolism and performance. 193 83

Using the mixed type musculus latissimus dorsi of the dog in the present work, we show the effect of carnitine on an in situ fatigue test. L-Carnitine appears to improve force of this muscle by 34% while stimulated in situ. This effect of carnitine is acute and (stereo)specific, since neither D-carnitine nor the structural analogue choline (also a tertiary amine) has a positive effect on contractile force. Because skeletal muscle is rich in carnitine and because carnitine transport is slow, its effect must be exerted outside the striated muscle cells. Insulin (with glucose) administration abolished the carnitine effect. It is speculated that facilitation of fatty acid oxidation in the blood vessel wall is the basis for this positive effect of carnitine.
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PMID:Acute effect of L-carnitine on skeletal muscle force tests in dogs. 199 22

In a controlled, double-blind, crossover study, the effects of guanadrel sulfate and propranolol on blood pressure (BP) and selected cardiopulmonary and metabolic variables were compared in 15 physically active and moderately hypertensive subjects. Guanadrel sulfate reduced systolic and diastolic BP at rest by -16 and -15 mm Hg, and at maximal exercise by -33 and -13 mm Hg, respectively (p less than 0.005), without affecting submaximal oxygen consumption (VO2), maximal VO2, ventilatory threshold, forced vital capacity, forced expiratory volume in 1 second, or fatigue, as assessed by perceived exertion. In contrast, propranolol significantly decreased diastolic BP at rest (-16 mm Hg) and systolic BP at maximal exercise (-44 mm Hg); however, it significantly decreased submaximal VO2 (-3.9 ml.kg-1.min-1), maximal VO2 (-3.9 ml.kg-1.min-1), ventilatory threshold (-0.3 liters.min-1), minute ventilation at submaximal exercise (-7.3 liters.min-1), forced expiratory volume in 1 second (-0.27 liters), and concomitantly increased the rating of perceived exertion at maximal exercise (1.9 U). Guanadrel sulfate was also associated with significant decreases in mean fasting plasma glucose and total serum cholesterol, whereas propranolol resulted in an increase in serum triglycerides (p less than 0.05). In contrast to propranolol, guanadrel sulfate appears to decrease BP without evoking negative metabolic consequences or impairing exercise tolerance.
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PMID:Comparison of the effects of guanadrel sulfate and propranolol on blood pressure, functional capacity, serum lipoproteins and glucose in systemic hypertension. 200 Jul 92

The effect of bicycle exercise (75% of maximal oxygen uptake) on glucose uptake by the inferior limb (LGU) and glycolysis in human skeletal muscle has been investigated. Biopsies were obtained from the quadriceps femoris muscle before exercise, after 5 and 40 min of exercise, and at fatigue [74.9 +/- 4.7 (SE) min]. LGU was 0.05 +/- 0.02 mmol/min at rest, increased approximately sevenfold after 5 min of exercise, and continued to increase linearly during the first 40 min of exercise. Thereafter LGU stabilized at approximately 1.4 mmol/min until fatigue. Intracellular glucose was low at rest but increased sixfold after 5 min of exercise (P less than 0.01 vs. rest); thereafter, intracellular glucose decreased and was not significantly different from the value at rest after 40 min or at fatigue (P greater than 0.05). D-Glucose 6-phosphate (G-6-P) and alpha-D-glucose 1,6-bisphosphate (G-1,6-P2) (inhibitors of hexokinase) increased significantly after 5 min of exercise (approximately 300% G-6-P; approximately 25% G-1,6-P2) and then decreased continuously. The muscle glycolytic rate (glycogenolysis + glucose uptake) averaged 7.7 mmol.kg dry wt-1.min-1 during the first 40 min of exercise and 3.7 mmol.kg dry wt-1.min-1 during the last 35 min of exercise. The contribution of extracellular glucose to muscle glycolysis was estimated to be only 5 and 19% during the initial and latter phases of exercise, respectively. It is concluded that, during the initial phase of exercise, glucose utilization is limited by phosphorylation, probably due to G-6-P-dependent inhibition of hexokinase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of glucose utilization in human skeletal muscle during moderate dynamic exercise. 200 94

In order to examine whether there are sex-differences in the response of energy balance to physical training slightly obese men and women participated in the same 3 months physical training program with the same individual relative intensity. The men became somewhat lighter (-2 kg) and leaner (-2.9 kg body fat) and showed decreases in sum of insulin and sum of C-peptide values during an oral glucose tolerance test as well as cholesterol values. The women showed decrease of 2.6 kg body fat, and also increased lean body mass (1.9 kg) and similar metabolic changes. The women had, however, a larger body fat mass at the outset. When women with similar body fat mass as that of men were analysed separately, no change in body weight or body fat had occurred, and the metabolic adaptations were less pronounced. No compensatory increase of energy intake could be discovered in any of the groups, the most obese women actually showed a decrease. Taken together with previous information these results suggest that men, like male rats, become leaner during physical training due to a lack of energy intake compensation. Women with similar body fat mass, however, like female rats, may react with such a compensation, causing a protection of their body fat. Women usually have more body fat than men, however. Obese women in this study showed a decrease of body fat.
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PMID:The effects of exercise, training on body composition and metabolism in men and women. 201 Feb 62


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