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Biomedical subjects

W W Winder

Publications and source records attributed to W W Winder.

At least 73 records · Page 4Linked to original sources
PubMed1988

Liver fructose 2,6-bisphosphate in rats running at different treadmill speeds.

To determine the effect of work rate on liver fructose 2,6-bisphosphate (fructose 2,6-P2), rats were run for 5 min on a treadmill up a 15% grade at 16, 21, 26, 31, and 36 m/min. The liver content of fructose 2,6-P2 decreased 25, 42, 50, 62, and 71% from resting values after 5 min of running at these work rates. The time course of the decline in liver fructose 2,6-P2 was also studied in rats run at 16 m/min for times ranging from 5 to 100 min, at 23 m/min for times ranging from 5 to 60 min, and at 31 m/min for times of 5, 10, and 20 min. The hepatic content of fructose 2,6-P2 declined significantly after 5 min in all three groups of rats. The rate of decline was greatest in rats run at 31 m/min. After 100 min of running, fructose 2,6-P2 in livers of rats running at 16 m/min declined to levels seen in rats run at 31 m/min for 20 min. Changes in fructose 2,6-P2 occurred before a detectable decline in liver glycogen and in the absence of any significant change in blood glucose. Liver adenosine 3',5'-cyclic monophosphate (cAMP) was elevated after 5 min of exercise in rats running at 23 and 31 m/min but not in rats running at 16 m/min. By the end of exercise, hepatic cAMP was elevated in rats running at all speeds. The rapid decline in fructose 2,6-P2 probably plays a role in decreasing hepatic glycolysis, thereby ensuring that glucose 6-phosphate derived from glycogenolysis is diverted to blood glucose.

Animals↗
PubMed1988

Effects of glucose infusion in exercising rats.

To determine whether feedforward control of liver glycogenolysis during exercise is subject to negative feedback by elevated blood glucose, glucose was infused into exercising rats at a rate that elevated blood glucose greater than 10 mM. Liver glycogen content decreased 22.4 mg/g in saline-infused rats compared with 13.6 mg/g in glucose-infused rats during the first 40 min of treadmill running (21 m/min, 15% grade). Liver adenosine 3',5'-cyclic monophosphate (cAMP) concentration was significantly lower in the glucose-infused rats during the exercise bout. The concentration of hepatic fructose 2,6-bisphosphate remained elevated throughout the exercise bout in glucose-infused rats but decreased markedly in saline-infused rats. Plasma insulin concentration was higher and plasma glucagon concentration lower in glucose-infused rats than in saline-infused rats during exercise. Early in exercise, liver glycogenolysis proceeds in the glucose-infused rats despite the fact that glucose and insulin concentrations are markedly elevated and liver cAMP is unchanged from resting values. These observations suggest the existence of a cAMP-independent feedforward system for activation of liver glycogenolysis that can override classical negative feedback mechanisms during exercise.

Animals↗
PubMed1988

Effect of the exercise-induced increase in glucocorticoids on endurance in the rat.

To investigate the effect of the increase in glucocorticoids during exercise on endurance, rats were either sham operated (SO) or adrenalectomized. All adrenalectomized rats were given a subcutaneously implanted corticosterone pellet at the time of adrenalectomy. Adrenalectomized rats were injected with corticosterone (ADX Cort) or corn oil (ADX) 5 min before exercise. Rats were killed at rest or after running on a treadmill (21 m/min, 15% grade) until exhaustion. SO rats ran 138 +/- 6 min compared with 114 +/- 9 min for ADX Cort and 89 +/- 8 min for ADX. All differences in run times were significant (P less than 0.05). Corticosterone levels were similar in exhausted SO and ADX Cort groups. ADX exhausted rats had corticosterone levels similar to resting values in SO and ADX rats. Inhibition of the rise in glucocorticoids during exercise had no effect on liver glycogen, liver adenosine 3',5'-cyclic monophosphate, plasma insulin, blood glucose, lactate, glycerol, or 3-hydroxybutyrate, plasma norepinephrine, or red quadriceps and soleus glycogen. Plasma free fatty acids were significantly depressed at exhaustion in ADX rats compared with SO. These data show that glucocorticoids exert effects within the time frame of a prolonged exercise bout and play a role in increasing endurance.

Adrenalectomy↗
PubMed1988

Role of cyclic AMP in regulation of hepatic glucose production during exercise.

Cyclic AMP increases in liver during exercise, the magnitude of the increase being dependent on duration and intensity of the exercise. Within limits, the increase in cAMP is closely correlated with the rate of glycogenolysis and with the exercise intensity. It is unlikely that epinephrine is involved in determining cAMP concentration in liver during exercise. Adrenodemedullated rats show no impairment in exercise-induced liver glycogenolysis or in the increase in cAMP. When epinephrine is infused at different rates into exercising rats, liver cAMP appears to be unrelated to plasma epinephrine. The rise in plasma glucagon is likely responsible for the increase in hepatic cAMP during exercise. The increase in cAMP is apparently necessary for maintaining low levels of fructose-2,6-bisphosphate (the activator of PFK-1 and inhibitor of fructose-1,6-bisphosphate) in liver. The low fructose-2,6-bisphosphate concentration would be expected to result in an increase rate of gluconeogenesis during exercise.

Animals↗
PubMed1987

Insulin does not influence muscle glycogenolysis in adrenodemedullated exercising rats.

Previous reports have indicated that adrenodemedullated (ADM) rats exhibit an impairment in muscle glycogenolysis and elevated plasma insulin during exercise. This study was designed to determine whether the impaired muscle glycogenolysis in ADM rats is due to absence of epinephrine or to the inappropriately elevated plasma insulin. Fasted ADM rats were infused with saline, with epinephrine (0.045 micrograms . 100 g-1 . min-1), or with epinephrine + insulin (1.6, 3.3, 6.6, and 8.3 ng . 100 g-1 . min-1) during a 30-min run on the treadmill (21 m/min, 10% grade). Soleus muscle glycogen decreased from 5.1 +/- 0.2 mg/g in resting ADM rats to 4.0 +/- 0.2, 0.8 +/- 0.1, and 0.8 +/- 0.1 mg/g in the exercising saline-, epinephrine-, and epinephrine + insulin (8.3 ng . 100 g-1 . min-1)-infused rats, respectively. Glycogen utilization in gastrocnemius and red and white quadriceps muscles during exercise was likewise unaffected by insulin infusion. Blood glucose concentrations were 3.75 +/- 0.08, 2.65 +/- 0.14, 3.93 +/- 0.20, and 2.03 +/- 0.09 mM in the same groups at the end of exercise. Blood lactate was 50% lower and the blood 3-hydroxybutyrate and plasma free fatty acid concentrations were significantly higher in the ADM + saline rats than the other exercising rats. We conclude that inappropriately elevated plasma insulin does not impair epinephrine-stimulated muscle glycogenolysis in fasted ADM rats during exercise.

Adrenal Medulla↗
PubMed1987

Epinephrine, glucose, and lactate infusion in exercising adrenodemedullated rats.

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.

Adrenal Medulla↗
PubMed1987

Blood collection and processing for measurement of catecholamines in exercising rats.

We have studied the time course of the decline in plasma catecholamines in the postexercise period in rats. Male Sprague-Dawley rats were run on the treadmill for 5 min at 31 m/min up a 15% grade. At the end of the exercise the rats were quickly anesthetized by intravenous injection of pentobarbital. Blood samples were collected as soon as possible (average of 43 s), at 2 and 7 min postexercise. Plasma epinephrine decreased from 0.79 +/- 0.09 ng/ml to 0.51 +/- 0.05 after 2 min and to 0.35 +/- 0.09 after 7 min. Plasma norepinephrine decreased from 0.89 +/- 0.16 ng/ml to 0.61 +/- 0.05 after 2 min and to 0.50 +/- 0.07 after 7 min. We also studied the effect of time of centrifugation with respect to time of blood collection on plasma catecholamines. If blood samples were kept on ice no significant change in plasma epinephrine occurred over a period of 1 h. A small (14%) but significant decrease in norepinephrine was observed after 15 and 60 min. These studies emphasize the importance of collecting rat blood samples as quickly as possible after the end of exercise. Catecholamines decline very quickly in the rat after intravenous pentobarbital anesthesia.

Animals↗
PubMed1986

Effect of infusing epinephrine on liver and muscle glycogenolysis during exercise in rats.

To determine the possibility of a threshold concentration of plasma epinephrine that stimulates liver glycogenolysis during exercise, adrenodemedullated (ADM) and sham-operated (SHAM) rats were infused with saline or epinephrine at rates that produced plasma concentrations ranging between 0.01 ng/ml (0.06 nM) and 4.3 ng/ml (23.7 nM). During the infusion rats were run on a rodent treadmill for 0, 30, or 60 min at 21 m/min up a 15% grade. Liver glycogen decreased at similar rates in all exercising rats regardless of plasma epinephrine concentration. Epinephrine infusion stimulated significant muscle glycogen depletion in the soleus and red and white vastus lateralis muscles. ADM saline-infused animals exhibited the least muscle glycogen depletion. Blood glucose and lactate in exercising ADM rats increased as the epinephrine infusion concentration increased. During exercise, there was no epinephrine concentration that stimulated liver glycogenolysis more effectively than physiological saline.

Adrenal Medulla↗
PubMed1986

Effect of adrenodemedullation on metabolic responses to high-intensity exercise.

To determine the role of epinephrine in glycogenolysis during high-intensity exercise, rats were adrenodemedullated (ADM) or sham operated (SHAM) and run for either 30 min at 38 m/min or for 5 min at 27, 38, or 48 m/min up a 15% grade. At the end of exercise the rats were anesthetized by intravenous injection of pentobarbital sodium. Liver, blood, and muscle samples were obtained. Plasma epinephrine values were 5.9 and 0.3 nM for SHAM and ADM animals, respectively, after 30 min of exercise. Liver glycogen decreased by 16 and 21 mg/g in the SHAM and ADM groups, respectively, and liver cAMP increased significantly in both groups. Glycogen in the soleus muscle decreased 80% in the SHAM but only 43% in the ADM animals after 30 min of exercise. The exercise-induced hyperglycemia observed in the SHAM animals was not present in the ADM animals. The responses of cyclic AMP, soleus glycogen, and blood glucose were similar in both the 5- and 30-min exercise groups. During intense exercise, epinephrine is unessential for stimulating liver glycogenolysis but does play an important role in stimulating glycogenolysis in the soleus muscle and in establishing exercise-induced hyperglycemia.

Adrenal Medulla↗
PubMed1986

Liver glycogenolysis during exercise in adrenodemedullated male and female rats.

Previous studies have shown that adrenodemedullation has no effect on the rate of liver glycogenolysis during exercise in male rats. Mature female rats have been reported to have a higher hepatic beta-adrenergic receptor activity than do male rats of the same age. The present study was undertaken to determine the role of plasma epinephrine in stimulating liver glycogenolysis during exercise in female rats. Both male and female rats were adrenodemedullated or sham operated. Three weeks later rats were run for 60 min at 21 m/min up a 15% grade. The rate of liver glycogenolysis during exercise was not affected by adrenodemedullation in either female rats or male rats. Hepatic adenosine 3',5'-cyclic monophosphate increased to approximately the same extent in sham operated as in adrenodemedullated female rats during exercise. Adrenodemedullation caused a significant reduction in the amount of glycogen utilized by the soleus muscle and in the degree of hyperglycemia during exercise. We conclude that epinephrine is unessential for stimulation of liver glycogenolysis during exercise in either male or female rats.

Adrenal Medulla↗
PubMed1986

Effect of maternal exercise on fetal liver glycogen late in gestation in the rat.

To determine the effect of maternal exercise on fetal liver glycogen content, fed and fasted rats that were pregnant for 20.5 or 21.5 days were run on a rodent treadmill for 60 min at 12 m/min with a 0% grade or 16 m/min up a 10% grade. The rats were anesthetized by intravenous injection of pentobarbital sodium, and fetal and maternal liver and plasma samples were collected and frozen. Fetal liver glycogenolysis did not occur as a result of maternal exercise. Fetal blood levels of lactate increased 22-60%, but glucose, plasma glucagon, and insulin were unchanged during maternal exercise. Maternal liver glycogen decreased as a result of exercise in all groups of rats except the fasted 20.5-day-pregnant group. Plasma free fatty acids increased in all groups and blood lactate increased in fed (20.5 days) and fasted (21.5 days) pregnant rats. Maternal glucose, glucagon, and insulin values remained constant during exercise. The fetus appears to be well-protected from metabolic stress during moderate-intensity maternal exercise.

Animals↗
PubMed1986

Effects of 24-hour fast on cycling endurance time at two different intensities.

Ten competitive cyclists were exercised to exhaustion to test the potential of a 24-h fast for increasing endurance. One group (n = 4) was tested at an initial intensity of 86% maximum O2 uptake (VO2max) (HI) and a second group (n = 6) at 79% VO2max (MI). Both groups repeated test rides in fasted and normal-diet conditions. Time to fatigue was designated at two points: fatigue 1 occurred when pedal frequency could not be maintained at the initial percent VO2max; fatigue 2 occurred when pedal frequency could not be maintained at a workload of approximately 65% VO2max. In both HI and MI the 24-h fast had no effect on resting muscle glycogen stores but significantly increased plasma free fatty acid (FFA) levels. Despite the increased FFA availability, time to fatigue was reduced in the fasted groups. Fatigue 1 and 2 times (mean +/- SE) for HI-fasted were 42.0 +/- 6.2 and 170.0 +/- 20.4 min, respectively, compared with those of the HI-normal diet of 115.3 +/- 25.6 and 201.0 +/- 14.8 min. Fatigue 1 and 2 times for MI-fasted were 142.0 +/- 19.6 and 167.5 +/- 10.5 min compared with those of the MI-normal diet of 191.3 +/- 25.0 and 214.3 +/- 18.9 min. The cause of fatigue at fatigue 1 was not readily apparent. Fatigue 2 in all groups seemed to be related to hypoglycemia as well as muscle glycogen depletion.

3-Hydroxybutyric Acid↗
PubMed1986

Effect of intravenous caffeine on liver glycogenolysis during prolonged exercise.

Ingestion of caffeine has been reported to enhance performance during prolonged endurance exercise. This effect on performance has been attributed to a caffeine-induced enhancement of lipid oxidation, thereby sparing muscle glycogen. The purpose of this experiment was to determine the effect of caffeine on the rate of liver glycogenolysis during exercise. Adult male rats were given an intravenous injection of caffeine (5 mg X kg-1) or of 0.9% NaCl. One h later they were run on a motor driven treadmill at 28 m X min-1 up a 15% grade for 45 or 90 min. Liver and muscles were frozen, and blood was collected for analysis. No significant differences were found between caffeine- and saline-injected rats in liver or muscle glycogen, plasma free fatty acid, insulin, glucagon, blood glucose, or blood glycerol. Liver adenosine 3',5'-cyclic monophosphate was essentially the same in caffeine- and saline-injected rats after 90 min of exercise. In a separate study, injection of 5 or 25 mg caffeine per kg body weight immediately prior to a 60-min bout of exercise had no effect on the rate of liver muscle glycogenolysis or on any of the hormones and metabolites studied. We conclude that in the rat, blood levels of caffeine in the range of 3.7 to 29 micrograms X ml-1 have no effect on liver adenosine 3',5'-cyclic monophosphate or the rate of liver glycogenolysis during prolonged treadmill running.

Animals↗
PubMed1985

Attenuation of postexercise ketosis in fasted endurance-trained rats.

Endurance-trained animals and human subjects have been reported to exhibit a lesser degree of postexercise ketosis than nontrained controls. We have studied the mechanism of this adaptation. Trained (2 h/day, 6 wk) and nontrained rats were fasted overnight and then run at 16 m/min up a 15% grade for 90 min. Trained rats had lower blood 3-hydroxybutyrate during exercise and during a 90-min postexercise period than nontrained rats. Liver malonyl coenzyme A (CoA), carnitine, and glycogen were not significantly different in the two groups at any time during and after exercise. Therefore these factors cannot be responsible for the difference in ketonemia. Plasma free-fatty acids and hepatic adenosine 3',5'-cyclic monophosphate were elevated in nontrained rats with respect to trained rats. These two differences could conceivably be responsible for a different ketogenic rate. In addition, 3-ketoacid CoA transferase activity of gastrocnemius muscle was increased by training. The increase in ketone oxidizing enzymes of muscle may also be partially responsible for the training-induced attenuation of postexercise ketonemia in these fasted rats.

3-Hydroxybutyric Acid↗
PubMed1985

Role of plasma epinephrine in fasted exercising rats.

We have investigated the physiological role of the marked increase in plasma epinephrine that occurs in fasted exercising rats. Fasted adrenodemedullated (ADM) rats show a marked reduction in endurance run times compared with sham-operated (SO) controls. After running for 30 min at 21 m/min up a 10% grade, ADM rats' blood glucose was 2.9 +/- 0.1 mM vs. 4.3 +/- 0.2 mM in SO rats. At the same time, blood lactate was 3.0 +/- 0.2 mM in SO rats compared with 1.0 +/- 0.1 mM in ADM rats. Glycogenolysis was impaired in ADM rats in the fast-twitch white region of the quadriceps, lateral gastrocnemius, and soleus muscles but not in the fast-twitch red region of the quadriceps muscle. Hepatic adenosine 3',-5'-cyclic monophosphate was increased to the same extent in ADM and SO rats during exercise. Infusion of epinephrine into ADM rats during exercise corrected the hypoglycemia, restored lactate to normal, and stimulated glycogenolysis in soleus, white quadriceps, and lateral gastrocnemius muscles. Epinephrine-dependent glycogenolysis in contracting type I and noncontracting type II muscle fibers apparently provides essential quantities of lactate for hepatic gluconeogenesis in fasted exercising rats.

Adrenal Medulla↗
PubMed1985

Epinephrine is unessential for stimulation of liver glycogenolysis during exercise.

To determine the role of adrenal medullary hormones in controlling the rate of liver glycogenolysis during exercise, adrenodemedullated (ADM) and sham-operated (SO) rats were run on a rodent treadmill at 21 m/min up a 15% grade for 0, 30, or 60 min. Rats were anesthetized by intravenous injection of pentobarbital sodium, and liver, muscle, and blood were collected and frozen. Liver glycogen decreased at similar rates in ADM and SO rats. Hepatic adenosine 3',5'-cyclic monophosphate (cAMP), plasma glucagon, and plasma free fatty acids increased to the same extent in both ADM and SO rats. The adrenodemedullation caused a reduction in glycogenolysis in the fast-twitch white region of the quadriceps, soleus, and lateral gastrocnemius during exercise. The normal exercise-induced increase in blood glucose and lactate and the decline in plasma insulin were not observed in the demedullated rats. During submaximal exercise the principal targets for epinephrine released from the adrenal medulla appear to be pancreatic beta-cells and skeletal muscle and not the liver.

Adrenal Medulla↗
PubMed1985

Control of hepatic glucose production during exercise.

Major advancements have occurred recently in study of the mechanisms of regulation of glycogenolysis and gluconeogenesis in perfused livers and isolated hepatocytes. Many questions remain unanswered, however, with respect to the control of these processes in the live exercising animal. Additional studies will be necessary to determine the relative roles of alpha- and beta-adrenergic receptor-mediated effects of circulating catecholamines, of glucagon, glucocorticoids, angiotensin II, vasopressin, insulin, and of the direct sympathetic innervation in regulation of hepatic glycogenolysis and gluconeogenesis during exercise.

Animals↗