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13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-seven subjects with moderate obesity (50 +/- 3 percent above ideal body weight) were given an oral glucose tolerance test with the simultaneous measurement of rates of glucose and lipid oxidation by continuous indirect calorimetry. When the subjects were stratified into nine 5-year classes of duration of obesity, the prevalence of impaired glucose tolerance (IGT) and overt diabetes both increased with increasing duration of obesity. Both basal and post-OGTT lipid oxidation rates were, however, similar in all classes. To assess the independent influence of IGT, diabetes, age, and duration of obesity on glucose metabolism, the data were subjected to analysis of variance using a factorial design with metric covariates. Age by itself was found to be associated (P less than 0.05) with a decline in total post-OGTT glucose oxidation. Both IGT and diabetes, on the other hand, were associated with increased plasma insulin and free fatty acid (FFA) levels, both in the fasting state and following glucose ingestion (P = 0.05-P less than 0.002). Only diabetes, however, was associated with a drastic reduction in nonoxidative glucose disposal, which marked the appearance of, and strongly correlated with (r = -0.81, P less than 0.001), fasting hyperglycemia. Duration of obesity had significant metabolic consequences in its own right: a fall in the insulin response to glucose (P = 0.05) and in the rate of total glucose oxidation (P = 0.03), and a rise in post-OGTT glucose levels (P = 0.04). We conclude that: (a) increased lipid oxidation is common in obesity, but is not sufficient to explain the deterioration of glucose tolerance in long-term obesity; (b) very-long-term obesity may be associated with partial exhaustion of the beta cell, and the resultant insulinopenia may cause depressed glucose oxidation and impaired glucose tolerance, and (c) a defect in nonoxidative glucose disposal is a characteristic feature of frank diabetes at any stage of obesity.
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PMID:The metabolic consequences of long-term human obesity. 306 64

Fasting before an exercise event has been demonstrated to decrease endurance. The purpose of this study was to investigate whether this decrement in performance after fasting could be reversed by ingestion of a carbohydrate solution before and during exercise. Nine fit male subjects ran to exhaustion at approximately 70% VO2max in two counterbalanced trials. The subjects were fasted for 21 h before both trials, and the trials were arranged so that the subjects ingested either a carbohydrate (CHO) or placebo (PL) solution. Although ratings of perceived exertion were significantly lower in the CHO trial, there were no differences in endurance time to exhaustion in the two trials (102 +/- 8 min in the PL trial and 106 +/- 8 min in the CHO trial). There were no differences between trials for the VO2, heart rate, and blood lactate concentrations. As expected, the blood glucose and insulin concentrations were higher in the CHO trial. The respiratory exchange ratio was significantly higher in the CHO trial at 40 min of exercise and tended to be higher at all other times, suggesting a greater reliance on carbohydrate and less on fat as an energy source. This seemed to be confirmed by the significantly lower plasma glycerol concentration, which suggested less fat mobilization in the CHO trial. Ingestion of a glucose polymer solution increased carbohydrate utilization in fasted subjects, but exercise performance was not improved.
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PMID:Effect of carbohydrate ingestion on exercise endurance and metabolism after a 1-day fast. 324 66

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

Metabolic effects of an overnight fast (postabsorptive state, PA) or a 3.5-day fast (fasted state, F) were compared in eight healthy young men at rest and during exercise to exhaustion at 45% maximum O2 uptake. Glucose rate of appearance (Ra) and disappearance (Rd) were calculated from plasma glucose enrichment during a primed, continuous infusion of [6,6-2H]glucose. Serum substrates and insulin levels were measured and glycogen content of the vastus lateralis was determined in biopsies taken before and after exercise. At rest, whole-body glucose flux (determined by the deuterated tracer) and carbohydrate oxidation (determined from respiratory exchange ratio) were lower in F than PA, but muscle glycogen levels were similar. During exercise, glucose flux, whole-body carbohydrate oxidation, and the rate of muscle glycogen utilization were significantly lower during the fast. In the PA state, glucose Ra and Rd increased together throughout exercise. However, in the F state Ra exceeded Rd during the 1st h of exercise, causing an increase in plasma glucose to levels similar to those of the PA state. The increase in glucose flux was markedly less throughout F exercise. Lower carbohydrate utilization in the F state was accompanied by higher circulating fatty acids and ketone bodies, lower plasma insulin levels, and the maintenance of physical performance reflected by similar time to exhaustion.
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PMID:Influence of fasting on carbohydrate and fat metabolism during rest and exercise in men. 329 4

The effect of forced liquid (L) or solid (S) carbohydrate (CHO)-rich feedings on plasma glucose, insulin, and glycogenesis after glycogen depletion was investigated. The relationship between glycogen restoration and maximal physical working capacity (MPWC) was studied as well. Eight males performed two experiments, with 2 weeks interval, on a bicycle ergometer. In each experiment, MPWC was determined in a graded test, which was immediately followed by interval work until exhaustion. After exercise cessation (EC), the subjects started to consume a standardized amount of concentrated L or CHO-rich food. Insulin and glucose concentration in blood were determined. Muscle glycogen was determined before, immediately after, 5 h after, and 22 h after EC. MPWC was determined again 22 h after EC. Four subjects performed a third experiment, in which solid food consumption was left ad libitum (AL). A rapid glycogen repletion was found 5 h after EC, i.e., from 72 +/- 40 to 198 +/- 38 mmol/kg in the S, and from 69 +/- 39 to 192 +/- 40 mmol/kg in the L experiment. The higher plasma glucose and insulin levels (P less than 0.05) during the 5 h after EC in the S experiments did not elicit a difference in glycogen repletion. Glycogen synthesis rate in the AL experiment was lower (P less than 0.05) than in the L and S experiments. Glycogen restoration in the L and S experiments was complete 22 h after depletion. However, despite repletion of glycogen, MPWC was decreased (P less than 0.05) in both experiments.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of liquid and solid meals on muscle glycogen resynthesis, plasma fuel hormone response, and maximal physical working capacity. 329 88

The purpose of this study was to determine the metabolic function of the marked increase in plasma epinephrine which occurs in fasted rats during treadmill exercise. Fasted adrenodemedullated (ADM) and sham-operated (SHAM) rats were run on a rodent treadmill (21 m/min, 15% grade) for 30 min or until exhaustion. ADM rats were infused with saline, epinephrine, glucose, or lactate during the exercise bouts. ADM saline-infused rats showed markedly reduced endurance, hypoglycemia, elevated plasma insulin, reduced blood lactate, and reduced muscle glycogenolysis compared with exercising SHAM's. Epinephrine infusion corrected all deficiencies. Glucose infusion restored endurance run times and blood glucose to normal without correcting the deficiencies in blood lactate and muscle glycogenolysis. Infusion of lactate partially corrected the hypoglycemia at 30 min of exercise, but endurance was not restored to normal and rats were hypoglycemic at exhaustion. We conclude that in the fasted exercising rat, actions of epinephrine in addition to provision of gluconeogenic substrate are essential for preventing hypoglycemia and allowing the rat to run for long periods of time.
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PMID:Epinephrine, glucose, and lactate infusion in exercising adrenodemedullated rats. 329 92

Nine healthy subjects were studied to determine their performance and the metabolic and hormonal responses to prolonged exercise after ingestion of a carbohydrate or a lipid diet. Subjects exercised on a bicycle ergometer (60% VO2max) until exhaustion four times at weekly intervals. The exercise test was performed 1 h after ingestion of three different isocaloric meals (400 Kcal) containing either glucose, medium-chain triglycerides (MCTs) or long-chain triglycerides (LCTs). The fourth test was performed after a night fast. The metabolism of these nutriments was followed using [U-13C]glucose, [1-13C]octanoate, and [1-13C]palmitate added as tracers. The average work time was comparable whatever nutriment used (116 +/- 11 min). Oxidation of the ingested nutriment over this period was 80% for glucose, 45% for MCTs, and 9% for LCTs. Glucose ingestion produced an early insulin peak associated at the end of the exercise with a lower glycemia compared to the fat diets. After MCT ingestion, an increase in ketone bodies was observed. Catecholamine response to physical exercise was decreased by all the meals when compared to fasting. Thus, we conclude that a different lipid meal, MCTs, or LCTs, compared to glucose feeding, do not modify exhaustion time in spite of differences in hormonal and metabolic responses.
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PMID:Metabolic and hormonal responses to lipid and carbohydrate diets during exercise in man. 329 29

Nine male marathon runners were exercised to exhaustion to determine the effects of a 27-h fast on endurance performance. Each subject completed two exercise tests at the same treadmill speed (set at 70% maximal O2 uptake), one following a 27-h fast and one 3 h after a preexercise meal, in random order. Fasting caused a 44.7 +/- 5.8% (SE) decrease in endurance performance (P less than 0.01). Blood, muscle, psychological, and ventilatory data were examined to determine the cause of the decreased performance. Fasting caused significant increases in O2 uptake (9.3 +/- 2.0%), heart rate (8.4 +/- 2.4%), and rating of perceived exertion, ventilation, and psychological fatigue, evident within the first 60 min of exercise. There were no differences in plasma glucose or epinephrine levels. Muscle glycogen degraded at the same rate (0.482 +/- 0.146 vs. 0.470 +/- 0.281 mumol.g-1.min-1 in the nonfasted and fasted tests, respectively) despite lower respiratory exchange ratio and elevated free fatty acid levels, which may partially explain the elevated O2 uptake. Lactate, insulin, and norepinephrine were all increased in the fasted test (P less than 0.05). The increase in norepinephrine (r = 0.79, P less than 0.01), the diameter of type I muscle fibers (r = 0.70, P less than 0.05), and ending insulin levels (r = -0.88, P less than 0.01) were correlated with endurance time in the fasted state. Fatigue in endurance running for 27-h fasted humans appears to be related to a combination of physiological, psychological, metabolic, and hormonal changes.
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PMID:Running endurance in 27-h-fasted humans. 332 90

Plasma glucose and insulin levels were measured in genetically diabetic (subline L) hamsters from 2 1/2 weeks to over 1 year of age. This nonobese subline is known for subnormal pancreatic insulin release. Hyperglycemia was seen from 4 weeks onward. A short period of hyperinsulinemia was seen at 6 weeks of age, after which plasma insulin levels were not different from normal. During the hyperinsulinemia phase (age 6 weeks), pancreatic insulin content was subnormal, islet volume (as percent of pancreas cross-sectional area) and islet size (as islet cross-sectional area in micron2) were not different from normal, islet morphology appeared normal in electron micrographs, but granule volume was slightly but significantly below normal. Because the islets appeared morphologically normal, except for the slight degranulation during the hyperinsulinemic phase, these data suggest (a) that the islets "hypersecrete" to reduce hyperglycemia; but (b) synthesis does not increase enough to maintain a normal pancreatic insulin content; (c) that the first sign of pancreatic failure may be degranulation and decreased insulin synthesis or content; (d) that early peripheral resistance to insulin, rather than early islet failure, may cause the early hyperglycemia, and (e) that early hyperglycemia or insulin resistance contributes to the later islet exhaustion, which is seen in these diabetic animals when adult.
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PMID:Islet morphology in young, genetically diabetic Chinese hamsters during the hyperinsulinemic phase. 332 82

In 7 male cyclists glycogen synthesis during exercise and rest was studied. Each subject did two exercise trials (A and B), in random order. In both trials, after determining the maximal workload (Wmax), intermittent exercise was given to exhaustion. After the exhaustive exercise and taking a muscle biopsy the subjects either exercised at 40% Wmax for 3 h (trial A) or rested for 3 h (trial B), during which they consumed approximately 2 l of a 25% malto-dextrine drink in both trials. After 3 h rest (trial A) or 3 h of mild exercise (trial B) a second muscle biopsy was taken for total glycogen and histochemistry (ATPase and PAS). Blood glucose and insulin levels were elevated during the first 2 h of exercise (p less than 0.05). Glycogen depletion was most pronounced in type I and to a less extent in type IIA fibers. In trial A muscle glycogen increased from 136 +/- 66 to 199 +/- 71 mmol/kg DW, and in trial B from 145 +/- 56 to 257 +/- 79 mmol/kg DW. During exercise glycogen repletion was restricted to type IIA and IIB fibers, whereas during rest glycogen synthesis occurred both in type I and type II fibers. The present study demonstrates that oral carbohydrate administered during exercise may not only provide substrate for energy metabolism, but can also be utilized for glycogen synthesis in the non-active muscle fibers.
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PMID:Carbohydrate feeding and glycogen synthesis during exercise in man. 344 1


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