Influence of fasting and hormone deficiency on myocardial glycogen levels in rats.

This study was undertaken because of uncertainties regarding the influence of hormones on myocardial glycogen metabolism of fed and fasted rats. The results indicate that adrenal hormones exert a stabilizing effect on myocardial glycogen levels in fed animals but are not necessary for synthesis to occur. Hypophysectomy eliminates the glycogen increase that occurs from fasting in normal animals while insulin deficiency leads to elevated glycogen stores in both fed and fasted conditions. These findings suggest that changes in myocardial glycogen metabolism are the results of a synergetic relationship between a variety of hormonal and nutritional factors.     

Effect of glycogen depletion on the ventilatory response to exercise

Five male subjects performed two graded exercise studies, one during control conditions and the other after reduction of muscle glycogen content by repeated maximum exercise and a high fat-protein diet. Reduction in preexercise muscle glycogen from 59.1 to 17.1 mumol X g-1 (n = 3) was associated with a 14% reduction in maximum power output but no change in maximum O2 intake; at any given power output O2 intake, heart rate, and ventilation (VE) were significantly higher, CO2 output (VCO2) was similar, and the respiratory exchange ratio was lower during glycogen depletion compared with control. The higher VE during glycogen depletion was associated with a higher VE/VCO2 ratio, lower end-tidal and mixed venous CO2 partial pressures, and higher blood pH than in the control studies. Changes in exercise VE accompanying glycogen depletion were not explained by changes in CO2 flux to the lungs suggesting that other factors served to modulate VE in these experimental conditions.     

Muscle glycogen depletion during exercise at 9 degrees C and 21 degrees C

This study compared glycogen depletion in active skeletal muscle after light and moderate exercise in both cold and comfortable ambient conditions. Twelve male subjects (Ss) were divided into two groups equally matched for the submaximal exercise intensity corresponding to a blood lactate concentration of 4 mM (W4) during cycle exercise. On two separate days Ss rested for 30 min at ambient temperatures of either 9 degrees C or 21 degrees C, with the order of temperature exposure being counter-balanced among Ss. Following rest a tissue specimen was obtained from the m. vastus lateralis with the needle biopsy technique. Six Ss then exercised on a cycle ergometer for 30 min at 30% W4 (range = 50 - 65 W) while the remaining group exercised at 60% W4 (range = 85 - 120 W). Another biopsy was taken immediately after exercise and both samples were assayed for glycogen content. Identical procedures were repeated for the second environmental exposure. No significant glycogen depletion was observed in the Ss exercising at 30% W4 in 21 degrees C, but a 23% decrease (p = 0.04) was observed when the same exercise was performed at 9 degrees C. A 22% decrease (p = 0.002) in glycogen occurred in the 60% W4 group at 21 degrees C, which was not significantly different from that observed during the same exercise at 9 degrees C. The results suggest that muscle substrate utilization is increased during light exercise in a cold environment as compared to similar exercise at a comfortable temperature, probably due to shivering thermogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of depletion exercise and light training on muscle glycogen supercompensation in men

Supercompensated muscle glycogen can be achieved by using several carbohydrate (CHO)-loading protocols. This study compared the effectiveness of two "modified" CHO-loading protocols. Additionally, we determined the effect of light cycle training on muscle glycogen. Subjects completed a depletion (D, n = 15) or nondepletion (ND, n = 10) CHO-loading protocol. After a 2-day adaptation period in a metabolic ward, the D group performed a 120-min cycle exercise at 65% peak oxygen uptake (VO2 peak) followed by 1-min sprints at 120% VO2 peak to exhaustion. The ND group performed only 20-min cycle exercise at 65% VO2 peak. For the next 6 days, both groups ate the same high-CHO diets and performed 20-min daily cycle exercise at 65% VO2 peak followed by a CHO beverage (105 g of CHO). Muscle glycogen concentrations of the vastus lateralis were measured daily with 13C magnetic resonance spectroscopy. On the morning of day 5, muscle glycogen concentrations had increased 1.45 (D) and 1.24 (ND) times baseline (P < 0.001) but did not differ significantly between groups. However, on day 7, muscle glycogen of the D group was significantly greater (p < 0.01) than that of the ND group (130 +/- 7 vs. 104 +/- 5 mmol/l). Daily cycle exercise decreased muscle glycogen by 10 +/- 2 (D) and 14 +/- 5 mmol/l (ND), but muscle glycogen was equal to or greater than preexercise values 24 h later. In conclusion, a CHO-loading protocol that begins with a glycogen-depleting exercise results in significantly greater muscle glycogen that persists longer than a CHO-loading protocol using only an exercise taper. Daily exercise at 65% VO2 peak for 20 min can be performed throughout the CHO-loading protocol without negatively affecting muscle glycogen supercompensation.     

Resistance of hepatic glycogen to depletion in obese Zucker rats

Glycogen stores (liver and carcass) have been studied in lean and obese Zucker rats. The animals were submitted to one of three feeding conditions: ad libitum, a 48-h fast, or a 48-h fast and food ad libitum for 24 h, and to two environmental conditions, either thermoneutrality or an acute cold exposure (2 days at 4-7 degrees C). After a 2-day fast at 25 degrees C, the liver glycogen store was reduced by 45 times in the lean rats, while it was decreased by only 3 times in the obese rats. Under these conditions, the liver glycogen store was 45 times higher in the obese than in the lean rats. After 2 days in the cold, liver glycogen store was 4.4 times higher in obese rats than in lean rats. After a 2-day fast in the cold, the liver glycogen store in the obese rats was 30 times higher than in the lean rats. In comparison to fasting at thermoneutrality, fasting in the cold did not lead to a further reduction in hepatic glycogen in obese Zucker rats. The differences observed in the mobilization of the hepatic glycogen store between obese and lean rats have not been found in the mobilization of the carcass glycogen store. Drastic conditions, such as a 2-day fast in the cold, did not exhaust the glycogen store in obese Zucker rats. The present observations point out that obese Zucker rats cannot mobilize the entire hepatic glycogen store, as seen in lean control rats. The role of this abnormality in the high hyperlipogenesis that maintains the obese state is still to be evaluated.     

Cardiac glycogen depletion in Amphiuma means during induced anoxia

Giant salamanders, Amphiuma means, measuring 240 to 280 mm from snout to vent, tolerate induced anoxia for six hours. Most of the cardiac glycogen (beta units) is depleted within the first hour of anoxia but a few scattered units remain after six hours. The suggestion that cardiac glycogen is a stand-by energy source which enhances the energy available to the heart during anoxic strain is reasonable. Beta units are stored in the heart as opposed to the larger alpha units in the liver. The smaller beta units are probably more easily metabolized than the larger alpha units due to their greater surface area per volume ratio and dispersal around the numerous cardiac mitochondria.     

The effect of portocaval shunt on hepatic glycogen stores during fasting

The effect of a prolonged fast was studied in surgically portocaval shunted (PCS) rats. This shunt excludes the liver from the direct effect of pancreatic and enteric hormones, thus facilitating the study of the biochemical and metabolic effects of these hormones. In portocaval shunted rats, liver glycogen was lower than that of control rats, and remained unaffected during fasting. No remarkable difference was observed in blood glucose, plasma and liver free fatty acids and blood ketone bodies. Among blood nitrogen compounds, total protein, alanine and urea did not show any significant variation, while, in PCS rats, the initial low levels of creatinine resulted in an increase after fast. Skeletal muscle protein decreased only slightly in control rats, while their loss was remarkable in PCS rats. The possibility of a differential activation of gluconeogenesis and glycogenolysis in control and PCS rats is discussed.     

Exercise-induced muscle glycogen depletion and repletion in diabetic rats.

The purpose of this experiment was to examine glycogen depletion in muscles of chronic diabetic rats during treadmill running of moderate intensity and glycogen repletion following the exercise bouts. Diabetes was induced with a single intravenous injection of streptozotocin (70 mg × kg^?1). Glycogen concentrations in muscles from diabetic and normal animals were determined at rest, after running either 10 or 30 min at 23 m × min^?1 (5% incline), or 2, 4, or 8 hr following 30 min of running at the same speed and incline. With the exception of soleus muscle after 30 min of running, there were no differences in muscle glycogen contents between normal and diabetic rats before exercise, immediately after exercise, or during the recovery period. All muscles showed a significant loss of glycogen during exercise, and most muscles had completely restored their glycogen by 2 hr following exercise. Blood lactate concentrations were also similar for normal and diabetic rats at rest and after exercise. It is concluded that the diabetic condition studied in this experiment did not significantly alter muscle glycogen metabolism during exercise of moderate intensity or during recovery from the activity.     

Effect of exercise on glycogen level in muscles and liver in rats

The effect of exercise of glycogen level in skeletal muscles and liver was studied in Wistar rats. The previously untrained animals were subjected to one-time exercise in form of swimming in water at 32 degrees C for 10, 20 and 30 min. The glycogen level in the muscles (in g per 100 g of tissue) fell down during the first 10 minutes of the exercise by a mean value of 0.45 g. During the following 10 minutes the decrease was smaller amounting on the average to 0.1 g. After 30 min the glycogen level in the muscles was about 0.1 g/100 g of tissue. Respective falls of glycogen level in the liver were on the average 0.99 g and 0.40 g/100 g of tissue. After 30 min of exercise the glycogen level in the liver was 1.2 g/100 g of tissue. The fall of glycogen level in the muscles was similar at all times during exercise in all animals, but in the liver fairly significant differences were observed in the first 10 min between individual groups of rats. Later on during exercise the differences in the liver glycogen falls decreased.     

Effect of streptozotocin-induced diabetes on glycogen resynthesis in fasted rats post-high-intensity exercise

It has recently been shown that food intake is not essential for the resynthesis of the stores of muscle glycogen in fasted animals recovering from high-intensity exercise. Because the effect of diabetes on this process has never been examined before, we undertook to explore this issue. To this end, groups of rats were treated with streptozotocin (60 mg/kg body mass ip) to induce mild diabetes. After 11 days, each animal was fasted for 24 h before swimming with a lead weight equivalent to 9% body mass attached to the tail. After exercise, the rate and the extent of glycogen repletion in muscles were not affected by diabetes, irrespective of muscle fiber composition. Consistent with these findings, the effect of exercise on the phosphorylation state of glycogen synthase in muscles was only minimally affected by diabetes. In contrast to its effects on nondiabetic animals, exercise in fasted diabetic rats was accompanied by a marked fall in hepatic glycogen levels, which, surprisingly, increased to preexercise levels during recovery despite the absence of food intake.     

Effects of fasting and training on pyruvate dehydrogenase activation during exercise

1. The effect of exercise (2 hr treadmill running at 28 m/min) on PDHa (the activity of the active form of pyruvate dehydrogenase) in untrained rats, trained rats (2 hr/d at 25 m/min for 4 wk), and in 24 hr fasted rats was determined. 2. Exercise increased PDHa activity approximately 2 fold in fed-untrained rats. 3. Fasting decreased PDHa activity in sedentary rats to approximately half the activity in fed rats. 4. The increase in PDHa activity during exercise was less in fasted than fed rats. 5. Training did not change the total activity of PDH (phosphorylated plus nonphosphorylated forms) but the percent of PDH in the active form was increased in muscle of trained-rested rats. 6. PDHa activity was unchanged by acute exercise (2.5 hr at 40 m/min) in the trained rats.     

Daily amylin replacement reverses hepatic glycogen depletion in insulin-treated streptozotocin diabetic rats

In streptozotocin-diabetic rats treated with insulin replacement, liver glycogen is some 35% depleted. Five consecutive daily subcutaneous injections with amylin dose-dependently restored liver glycogen to normal levels. Significant increases over insulin-only therapy occurred with amylin doses of 10, 30 and 100 micrograms/day, representing amylin: insulin ratios of 0.22, 0.75 and 2.79.     

Regulation of glycogen metabolism in rat respiratory muscles during exercise

The effect of prolonged exercise on the glycogen level in the respiratory muscles (diaphragm--D, external intercostal--IE and internal--II) has been studied in four groups of rats: 1-control, 2-fasted for 24 h, 3-treated with nicotinic acid and 4-treated with propranolol. There was a sharp reduction in glycogen level in each muscle after 30 min exercise in the control and fasted groups. Exercise till exhaustion further lowered the glycogen level in D in the control group and in IE and II in the fasted group. In the fasted group, the level of glycogen in each muscle, at rest, and after 30 min exercise, and in IE and II muscles after exercise till exhaustion was lower than in the control group. Nicotinic acid did not affect the glycogen level either at rest or during exercise as compared with the control group. Propranolol increased the glycogen level in the muscles at rest and during 30 min exercise. It partially prevented glycogen mobilization in D and IE and fully in II during exercise till exhaustion. In the control group, 24 and 48 h after exercise till exhaustion, the level of glycogen in each muscle exceeded the resting control value. It is concluded that exercise-induced glycogen metabolism in the respiratory muscles differs in some respects from that in the limb or heart muscles.     

Pregnancy and pentobarbital anaesthesia modify hepatic synthesis of acylglycerol glycerol and glycogen from gluconeogenic precursors during fasting in rats.

1. Incorporation of gluconeogenic precursors into blood glucose and hepatic glycogen and acylglycerol glycerol was examined in 24 h-fasted virgin rats by using a flooding procedure for substrate administration. At 10 min after their intravenous injection, the conversion of alanine or glycerol into liver glycogen or acylglycerol glycerol was proportional to glucose synthesis. 2. In 24 h-fasted 21-day-pregnant rats, the incorporation of alanine and glycerol into hepatic acylglycerol glycerol was markedly enhanced compared with the control group. In addition, during fasting at late pregnancy, the proportion of substrates directed to acylglycerol glycerol as compared with the fraction incorporated into glucose was augmented. 3. In pentobarbital-treated fasted rats, the incorporation of both alanine and pyruvate into circulating glucose and into hepatic glycogen and acylglycerol glycerol was increased. Pentobarbital treatment increased the proportion of substrates incorporated into liver glycogen, compared with the fraction appearing in circulating glucose. These changes were concomitant with a marked accumulation of glycogen. 4. The data indicate that, during fasting, gluconeogenesis provides glucose as well as hepatic glycogen and acylglycerol glycerol, independently of whether the substrates enter gluconeogenesis at the level of pyruvate or dihydroxyacetone phosphate.     

Muscle glycogen repletion after exercise in trained normal and diabetic rats

We hypothesize that training results in a faster and greater repletion of glycogen in skeletal muscles of normal and diabetic rats. Normal male Sprague-Dawley rats (100-140 g) were divided into two groups--one to train by treadmill running for 10 wk and the other to remain sedentary. Forty-eight hours after the last training session the rats of both groups were exercised to exhaustion. One subgroup of each was fed oral glucose (3 g/kg) at exhaustion and killed 60 min later. The other was killed at exhaustion. The glycogen concentration of soleus, plantaris, and red and white gastrocnemius was determined in all rats. The trained group had higher glycogen levels after glucose feeding in all muscles (P less than 0.002) and repleted their muscle glycogen more rapidly (P less than 0.05). However, in diabetic rats (45 mg streptozotocin/kg body wt) the trained and sedentary rats have similar glycogen levels and glycogen repletion rates in all muscles. Compared with the normal trained rats, the diabetic trained rats had slower glycogen repletion rates (P less than 0.05).