Effect of the classic 1-week glycogen-loading regimen on fat-loading in rats and humans

The purpose of this study was to elucidate the fat-loading effect of the classic 1-wk glycogen-loading regimen histologically in rats and physiologically in humans. In the rat and human studies, an exhaustive swimming exercise and cycle ergometer exercise were loaded on day 1 of a 6-d feeding period, respectively. Thereafter, both the rats and humans were divided into a glycogen-loading regimen consisting of a 3-d high-fat diet and a 3-d high-carbohydrate diet or a 6-d high-carbohydrate diet. After the feeding period in the human study, the human subjects performed a test exercise on day 7 using a cycle ergometer. In the rat study, the intramuscular triglyceride (IMTG) content was 69% greater (p<0.05) after the glycogen-loading regimen than after the high-carbohydrate diet feeding on day 7. In the human study, the respiratory exchange ratios (RER) after the glycogen-loading regimen were 4.9-6% lower than those after the high-carbohydrate diet during the test exercise on day 7 (p<0.05). Our findings suggest that the classical 1-wk glycogen-loading regimen maintained the storage and enhanced the utilization of energy sources during exercise in the skeletal muscle, and that it provides a fat-loading effect, in addition to the glycogen-loading effect, to the skeletal muscle.     

High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.     

Effect of diet on glucose tolerance 36 hours after glycogen-depleting exercise.

In order to estimate the effect of muscle glycogen content on the glycaemic response, glucose tolerance and glucose oxidation were measured in eight healthy male subjects. Each subject followed three different treatments, consisting of either a physical exercise session followed by 36 h of a low-carbohydrate high-fat diet (glycogen depletion treatment); or a physical exercise followed by 36 h of a high carbohydrate diet (glycogen repletion treatment); or a low-carbohydrate high-fat diet alone (diet treatment). After both the glycogen depletion and the diet treatments, the subjects showed a high glycaemic response (443 +/- 57 and 419 +/- 63 mmol.min/l resp.), a high insulinaemic response (7158 +/- 671 and 7643 +/- 913 mU.min/l), and a low rate of glucose oxidation (27.5 +/- 2.4 and 31.0 +/- 5.8 g/3 h respiration). In contrast, after the glycogen repletion treatment, the subjects had a lower glycaemic response (197 +/- 21 mmol.min/l), a lower insulinaemic response (4645 +/- 327 mU.min/l) and a higher glucose oxidation level (47.4 +/- 2.0 g/3h). Fasting free fatty acids (FFA) were positively correlated with glucose area (P less than 0.001) and negatively with glucose oxidation (P less than 0.01). These results show a strong inhibitory effect of the low-carbohydrate high-fat diet on glucose tolerance despite prior strenuous exercise. Because of this, the effect of the muscle glycogen content could not be tested. However, the results suggest that the FFA/glucose interrelationship may override exercise-induced changes in insulin-stimulated glucose uptake.     

Dietary whey protein increases liver and skeletal muscle glycogen levels in exercise-trained rats

We investigated the effect of different types of dietary protein on glycogen content in liver and skeletal muscle of exercise-trained rats. Twenty-four male Sprague-Dawley rats (approximately 100 g; n 6 per group) were divided into sedentary or exercise-trained groups with each group being fed either casein or whey protein as the source of dietary protein. Rats in the exercised groups were trained during 2 weeks using swimming exercise for 120 min/d, 6 d/week. Exercise training resulted in an increase in the skeletal muscle glycogen content. Furthermore, the whey protein group significantly increased the skeletal muscle glycogen content compared with the casein group. The increase in glycogen content in liver was significantly greater in rats fed the whey protein diet compared with those fed the casein diet. We also found that the whey protein diet increased the activity of liver glucokinase, whereas it decreased the activities of 6-phosphofructokinase and pyruvate kinase compared with the casein diet. However, hepatic total glycogen synthase activity and mRNA expression were similar with the two diets. In the skeletal muscle, whey protein decreased only 6-phosphofructokinase activity compared with casein. Total glycogen synthase activity in the skeletal muscle in the whey protein group was significantly higher than that in the casein group. The present study is the first to demonstrate that a diet based on whey protein may increase glycogen content in liver and skeletal muscle of exercise-trained rats. We also observed that whey protein regulated glycogen metabolism in these two tissues by different mechanisms.     

Transient hypophagia in rats switched from high-fat diets with different fatty-acid pattern to a high-carbohydrate diet

The present study investigates the mechanisms underlying the transient hypophagia occurring when rats adapted to high-fat, carbohydrate-free diets are switched to high-carbohydrate, low-fat diets. The hypophagia after the high-fat, carbohydrate-free to high-carbohydrate, low-fat diet shift seems to depend on the amount of carbohydrate in the diet, since an attenuation of hypophagia was observed when high-fat, carbohydrate-free-adapted rats were switched to a medium-carbohydrate, medium-fat diet. A role of glucose intolerance in the hypophagia is supported by the attenuation of carbohydrate anorexia in rats adapted to a high-fat diet containing n -3 polyunsaturated fatty acids from fish oil (60% of fat as fish oil), which has been shown to improve glucose tolerance in rats. Furthermore, the increased plasma glucose concentration in the high-fat, carbohydrate-free diet to high-carbohydrate, low-fat shifted rats despite the suppression in food intake also suggests an involvement of glucose intolerance in the hypophagia. The failure of the inhibitor of hepatic-fatty-acid oxidation mercaptoacetate (400 micromol/kg, i.p.) to counteract carbohydrate anorexia in the HF-adapted rats argues against an involvement of fatty-acids oxidation in the inhibition of eating after high-fat, carbohydrate-free to high-carbohydrate, low-fat diet shift. This is also supported by the failure to demonstrate a relationship between plasma beta-hydroxybutyrate and the severity of the hypophagia. A role of leptin in the hypophagia seems unlikely, since plasma leptin after diet shift was unchanged. Ingestion of the high-carbohydrate, low-fat diet also produced an aversion towards this diet in high-fat, carbohydrate-free-adapted rats. It is concluded that the transient hypophagia induced by switching rats from a high-fat to a high-carbohydrate diet is not related to fatty acid oxidation but to transiently impaired carbohydrate utilization.     

Carbohydrate loading--a review.

The purpose of carbohydrate loading is to supersaturate with glycogen the muscles to be used in competition. The competition should be longer than 30 to 60 min. to fully utilize the glycogen stores. An exhausting exercise is first performed to deplete the glycogen stores, and a high-fat, high-protein diet is followed for three days to keep the glycogen stores low. After depletion of the muscles, a high-carbohydrate diet is followed for two to three days to restore and supersaturate the muscles with glycogen. The most important point to impress on the athlete is the nutritional adequacy of the entire diet. Though the technique of carbohydrate loading is a dietary manipulation emphasizing the intake of carbohydrate, the diet can be adequate with sound dietary planning.     

Effect of palatable hyperlipidic diet on lipid metabolism of sedentary and exercised rats

OBJECTIVE: The present study was designed to examine 1) whether continuous feeding with a palatable hyperlipidic diet and cycling this diet with chow diet would affect lipid and carbohydrate metabolism in a similar way; and 2) whether the effect of chronic exercise on lipid and carbohydrate metabolism would be modified by these diet regimens. METHODS: Male 25-d-old Wistar rats were assigned to one of six groups: sedentary rats fed with chow diet; exercised (swimming 90 min/d, 5 d/wk) rats fed with chow diet; sedentary rats fed with a palatable hyperlipidic diet; exercised rats fed with the palatable hyperlipidic diet; sedentary rats fed with food cycles (four cycles alternating the chow and hyperlipidic diets weekly); and exercised rats fed with food cycles. After 8 wk of treatment, the animals were killed 24 h after the last exercise session. RESULTS: The hyperlipidic diet and food cycles schedules caused similar increases in body weight gain, carcass lipogenesis rate and adiposity, lipid content of the liver and gastrocnemius muscle, and serum total lipid, triacylglycerol, insulin, and leptin levels. The exercise attenuated body weight gain, adipose tissue mass, and serum triacylglycerol, insulin, and leptin levels similarly in the hyperlipidic and food cycles groups. Carcass lipogenesis rate was not affected by exercise in any of the three groups. CONCLUSIONS: The data showed that the continuous intake of a hyperlipidic palatable diet for 8 wk and the alternation of the high-fat intake with periods of chow intake cause obesity and affected lipid metabolism in a similar way. Chronic exercise attenuated body weight gain and adiposity and improved serum lipid concentrations in both high-fat feeding regimens.     

Leucine supplementation enhances skeletal muscle recovery in rats following exercise.

This study was designed to determine the ability of leucine to enhance muscle recovery after exercise. Male rats (200 g) were divided into five groups: sedentary, food-deprived (SF); exercised, food-deprived (EF); exercised, fed a carbohydrate meal (EC); exercised, fed a leucine meal (EL); and exercised, fed a combination of carbohydrate and leucine (ECL). All meals were administered by oral gavage immediately following exercise. EC and ECL meals were isocaloric and provided 15% of daily energy intake. EL and ECL meals each provided 270 mg leucine. Rats ran on a motor-driven treadmill for 2 h at 36 m/min and were killed 1 h postexercise. Plasma glucose and insulin were measured, and the gastrocnemius and plantaris muscles were excised as a unit to determine glycogen levels and the fractional rate of skeletal muscle protein synthesis (Ks). Exercise did not alter plasma glucose or insulin. In contrast, prolonged exercise reduced muscle glycogen (-51%) and Ks (-18%). Refeeding a combination of carbohydrate and leucine increased plasma insulin relative to the EF and SF groups and produced complete recovery of muscle Ks and glycogen to values not different from those in SF rats. Feeding leucine alone restored Ks to that in the SF group without affecting plasma glucose or insulin concentrations. Feeding carbohydrate alone enhanced the rate of glycogen repletion compared to the EF group, concomitant with increases in plasma glucose and insulin. The degree of glycogen recovery correlated with plasma insulin concentrations (r = 0.58, P < 0.05). These data suggest that leucine stimulates muscle protein synthesis following exercise, independent of increased plasma insulin. This is the first demonstration that orally administered leucine stimulates recovery of skeletal muscle protein synthesis after exercise.     

Tracing metabolic routes of dietary carbohydrate and protein in rainbow trout (Oncorhynchus mykiss) using stable isotopes ([¹³C]starch and [¹⁵N]protein): effects of gelatinisation of starches and sustained swimming

Here we examined the use of stable isotopes, [13C]starch and [1?N]protein, as dietary tracers to study carbohydrate assimilation and distribution and protein utilisation, respectively, by rainbow trout (Oncorhynchus mykiss). The capacity of glucose uptake and use by tissues was studied, first, by varying the digestibility of carbohydrate-rich diets (30 % carbohydrate), using raw starch and gelatinised starch (GS) and, second, by observing the effects of two regimens of activity (voluntary swimming, control; sustained swimming at 1·3 body lengths/s, exercise) on the GS diet. Isotopic ratio enrichment (13C and 1?N) of the various tissue components (protein, lipid and glycogen) was measured in the liver, muscles, viscera and the rest of the fish at 11 and 24 h after a forced meal. A level of 30 % of digestible carbohydrates in the food exceeded the capacity of rainbow trout to use this nutrient, causing long-lasting hyperglycaemia that raises glucose uptake by tissues, and the synthesis of glycogen and lipid in liver. Total 13C recovered 24 h post-feeding in the GS group was lower than at 11 h, indicating a proportional increase in glucose oxidation, although the deposition of lipids in white muscle (WM) increased. Prolonged hyperglycaemia was prevented by exercise, since sustained swimming enhances the use of dietary carbohydrates, mainly through conversion to lipids in liver and oxidation in muscles, especially in red muscle (RM). Higher recoveries of total 15N for exercised fish at 24 h, mainly into the protein fraction of both RM and WM, provide evidence that sustained swimming improves protein deposition, resulting in an enhancement of the protein-sparing effect.     

Postprandial glycogen and lipid synthesis in prednisolone-treated rats maintained on high-protein diets with varied carbohydrate levels

OBJECTIVE: The present experiment was designed to study the effect of a high-protein, high-carbohydrate diet versus a high-protein, low-carbohydrate diet on in vivo postprandial glycogen and lipid synthesis of rats treated with prednisolone. METHODS: Thirty-two 6-wk-old male Sprague-Dawley rats were randomly assigned to one of four equal groups: high-protein, high-carbohydrate; high-protein, high-carbohydrate with prednisolone; high-protein, low-carbohydrate; and high-protein, low-carbohydrate with prednisolone. Rats were sham operated or subcutaneously implanted with prednisolone pellets while being maintained on their respective diets (39% of energy from protein) for 6 wk. Food intake and body weight were monitored throughout the experiment. At the end of the feeding period, overnight-fasted rats were fed a test meal and injected with 3H2O to measure in vivo rates of glycogen and lipid synthesis. Final plasma glucose, insulin, and triacylglycerol concentrations and hepatic glycogen content were also measured. RESULTS: Results showed that hepatic glycogen content (milligrams per gram of liver) was similar across all four experimental groups. Total hepatic glycogen synthesis and its percentage synthesis via pyruvate (indirect pathway) were higher in rats maintained on the high-protein, high-carbohydrate diet compared with those on the high-protein, low-carbohydrate diet and this was not substantially affected by prednisolone administration. Hepatic and epididymal fat pad lipid syntheses were not altered by diet or prednisolone treatments. CONCLUSION: Under long-term high-protein conditions, prednisolone administration does not seem to affect hepatic glycogen synthesis, which was increased with the increased carbohydrate content of the diet.     

Rutin attenuates metabolic changes, nonalcoholic steatohepatitis, and cardiovascular remodeling in high-carbohydrate, high-fat diet-fed rats

Metabolic syndrome (obesity, diabetes, and hypertension) increases hepatic and cardiovascular damage. This study investigated preventive or reversal responses to rutin in high-carbohydrate, high-fat diet-fed rats as a model of metabolic syndrome. Rats were divided into 6 groups: 2 groups were fed a corn starch-rich diet for 8 or 16 wk, 2 groups were fed a high-carbohydrate, high-fat diet for 8 or 16 wk, and 2 groups received rutin (1.6 g/kg diet) in either diet for the last 8 wk only of the 16-wk protocol. Metabolic changes and hepatic and cardiovascular structure and function were then evaluated in these rats. The corn starch-rich diet contained 68% carbohydrate (mainly cornstarch) and 0.7% fat, whereas the high-carbohydrate, high-fat diet contained 50% carbohydrate (mainly fructose) and 24% fat (mainly beef tallow) along with 25% fructose in drinking water (total 68% carbohydrate using mean food and water intakes). The high-carbohydrate, high-fat diet produced obesity, dyslipidemia, hypertension, impaired glucose tolerance, hepatic steatosis, infiltration of inflammatory cells in the liver and the heart, higher cardiac stiffness, endothelial dysfunction, and higher plasma markers of oxidative stress with lower expression of markers for oxidative stress and apoptosis in the liver. Rutin reversed or prevented metabolic changes such as abdominal fat pads and glucose tolerance, reversed or prevented changes in hepatic and cardiovascular structure and function, reversed oxidative stress and inflammation in the liver and heart, and normalized expression of liver markers. These results suggest a non-nutritive role for rutin to attenuate chronic changes in metabolic syndrome.     

Coffee extract attenuates changes in cardiovascular and hepatic structure and function without decreasing obesity in high-carbohydrate, high-fat diet-fed male rats

Coffee, a rich source of natural products, including caffeine, chlorogenic acid, and diterpenoid alcohols, has been part of the human diet since the 15th century. In this study, we characterized the effects of Colombian coffee extract (CE), which contains high concentrations of caffeine and diterpenoids, on a rat model of human metabolic syndrome. The 8-9 wk old male Wistar rats were divided into four groups. Two groups of rats were fed a corn starch-rich diet whereas the other two groups were given a high-carbohydrate, high-fat diet with 25% fructose in drinking water for 16 wk. One group fed each diet was supplemented with 5% aqueous CE for the final 8 wk of this protocol. The corn starch diet contained ~68% carbohydrates mainly as polysaccharides, whereas the high-carbohydrate, high-fat diet contained ~68% carbohydrates mainly as fructose and sucrose together with 24% fat, mainly as saturated and monounsaturated fat from beef tallow. The high-carbohydrate, high-fat diet-fed rats showed the symptoms of metabolic syndrome leading to cardiovascular remodeling and nonalcoholic fatty liver disease. CE supplementation attenuated impairment in glucose tolerance, hypertension, cardiovascular remodeling, and nonalcoholic fatty liver disease without changing abdominal obesity and dyslipidemia. This study suggests that CE can attenuate diet-induced changes in the structure and function of the heart and the liver without changing the abdominal fat deposition.     

Carbohydrate-loading during the follicular phase of the menstrual cycle: effects on muscle glycogen and exercise performance

The effects of employing a high-carbohydrate diet (carbohydrate-loading) to increase glycogen storage in skeletal muscle are not well established in female athletes. On 4 occasions--2 familiarization trials and 2 experimental trials--6 well-trained female subjects completed 6 x 15-min continuous intervals of cycling (12 min at 72% VO2max, 1 min at maximal effort, and 2 min at 50% VO2max), followed by a time trial 15 min later. The women consumed their habitual diets (HD; 6-7 g carbohydrate/kg lean body mass) for 3 days after the second familiarization trial and before the first experimental trial. During the 3 days following the first experimental trial, the subjects consumed a high-carbohydrate diet (CD; 9-10 g carbohydrate/kg lean body mass) prior to the second experimental trial. Mean (+/-SEM) pre-exercise muscle glycogen concentrations were greater after CD versus HD (171.9+/-8.7 vs. 131.4+/-10.3 mmol/kg wet weight, P < 0.003). Although 4 of the 6 subjects improved their time-trial performance after CD, mean performance for the time trial was not significantly different between diets (HD: 763.9+/-35.6 s; CD: 752.9+/-30.1 s). Thus, female cyclists can increase their muscle glycogen stores after a carbohydrate-loading diet during the follicular phase of the menstrual cycle, but we found no compelling evidence of a dietary effect on performance of a cycling time trial performed after 90 min of moderate-intensity exercise.     

Effects of Thiamin Restriction on Exercise-Associated Glycogen Metabolism and AMPK Activation Level in Skeletal Muscle

This study aimed to investigate the direct influence of a decrease in the cellular thiamin level, before the onset of anorexia (one of the symptoms of thiamin deficiency) on glycogen metabolism and the AMP-activated protein kinase (AMPK) activation levels in skeletal muscle at rest and in response to exercise. Male Wistar rats were classified as the control diet (CON) group or the thiamin-deficient diet (TD) group and consumed the assigned diets for 1 week. Skeletal muscles were taken from the rats at rest, those that underwent low-intensity swimming (LIS), or high-intensity intermittent swimming (HIS) conducted immediately before dissection. There were no significant differences in food intake, locomotive activity, or body weight between groups, but thiamin pyrophosphate in the skeletal muscles of the TD group was significantly lower than that of the CON group. Muscle glycogen and lactate levels in the blood and muscle were equivalent between groups at rest and in response to exercise. The mitochondrial content was equal between groups, and AMPK in the skeletal muscles of TD rats was normally activated by LIS and HIS. In conclusion, with a lowered cellular thiamin level, the exercise-associated glycogen metabolism and AMPK activation level in skeletal muscle were normally regulated.     

Effects of high doses of leucine and ketoleucine on glycogen and protein metabolism in acute uremia

Binephrectomized rats treated with high doses of ketoleucine (0.5 g/rat per 20 hr) expired after about 45 hr. In contrast, survival time was 100% 60 hr after ureteral ligation. In comparison to animals receiving low-protein diets, addition of leucine to the diet almost doubled muscle and liver protein content whereas ketoleucine increased liver protein during the first 40 hr after operation about 1.5-fold. Skeletal muscle protein content was enhanced in the ureter-ligated rats with administration of ketoleucine. There was also about a 10-fold elevation in liver glycogen and total carbohydrate content between the 20th and 60th hr in binephrectomized rats fed leucine at 5-hr intervals. In skeletal muscle glycogen, there were no significant differences among the acutely uremic rats fed at 10-hr intervals low-protein diets alone or supplemented with leucine or ketoleucine. Leucine inhibits glycogenolysis by lowering phosphorylase alpha activity in muscle and liver, whereas ketoleucine enhances glycogenolysis in acute uremia. In rats supplemented with letoleucine, there is a progressive inactivation of glycogen synthetase I which occurs in parallel with increasing phosphorylase alpha activity. In binephrectomized rats receiving leucine supplements at 5-hr feeding intervals, the activity of liver glycogen synthetase I increases up to a maximum of 90% of total enzyme activity.     

Suppression of glycogen consumption during acute exercise by dietary branched-chain amino acids in rats

The effects of a diet supplemented with branched-chain amino acids (BCAA; 4.8% or 6.2%) on BCAA catabolism and glycogen metabolism in rats were examined. Rats were fed a BCAA diet or control diet for 4 wk and part of the rats were subjected to exercise training during the experimental period. Feeding the BCAA diet increased serum BCAA concentrations and activity of the hepatic branched-chain alpha-keto acid dehydrogenase complex, the rate-limiting enzyme in the catabolism of BCAA, suggesting that dietary BCAA promotes BCAA catabolism. Although the serum glucose concentration and glycogen contents in the liver and gastrocnemius muscle of rested rats were not significantly affected by feeding of the BCAA diet, those in rats exhausted by acute exercise were 2-4-fold higher in rats fed the BCAA diet than in rats fed the control diet. The activity of pyruvate dehydrogenase complex in the liver and gastrocnemius muscle after acute exercise showed reverse trends; the complex activities (especially in liver) tended to be less in the BCAA diet group than in the control diet group. These results suggest that dietary BCAA spares glycogen stores in liver and skeletal muscle during exercise and that the decrease in pyruvate dehydrogenase complex activity in these tissues by dietary BCAA is involved in the mechanisms.     

Human metabolic response to exercise

The energy necessary to support prolonged submaximal exercise is provided by the aerobic metabolism of carbohydrate and fatty acids. Carbohydrate is stored as glycogen, a polymer of glucose, in the liver and in the skeletal muscles, whereas the fatty acids used by working muscles are mainly derived from triglycerides stored in white adipose tissue cells. The relative contributions of carbohydrate and fatty acids to muscle metabolism depend on the relative exercise intensity. The relative exercise intensity is defined as the oxygen cost of the exercise (V0₂) expressed as a percentage of the individual's maximum oxygen uptake (% V0₂ max). At exercise intensities which represent a large % V0₂ max for an individual, muscle glycogen is the main contributor to muscle metabolism. Fatigue is associated with the depletion of the limited intramuscular glycogen stores. When a carbohydrate-rich diet is consumed during recovery after exercise, the muscle glycogen stores are increased above theirpre-exercise concentrations. Thus an exercise and diet regime has been developed to exploit the glycogen supercompensa-tion phenomenon and so increase endurance capacity.     

Refeeding of rats fasted 36 hours with five different carbohydrates and with malt extract: differential effects on glycogen deposition in liver and muscle, on plasma insulin and on plasma triglyceride levels

Rats fasted for 36 h were refed for 1, 2, 4 or 6 h with a diet containing 12 g/100 g casein, 2 g/100 g NaCl and 86 g/100 g glucose, fructose, maltose, sucrose, starch or malt extract. Blood glucose reached constant levels after 1 to 2 h of refeeding. The increase in plasma insulin paralleled food intake rather than the increase in blood glucose. Plasma triglycerides decreased upon refeeding starch, maltose and malt extract and increased with sucrose and fructose. Recovery of absorbed carbohydrates was highest in rats refed malt extract. Glycogen deposition in muscle was highest in rats fed malt extract and lowest in those fed fructose; sucrose yielded intermediate values. Glucose, maltose and starch resulted in muscle glycogen depositions slightly lower than those obtained with malt extract. In liver, sucrose and fructose were better precursors for glycogen than glucose and starch. With carbohydrates containing only glucose units, much more glycogen was found to be deposited in total muscle than in liver. This asymmetry was less notable or even was reversed with sucrose and fructose. Glycogen deposition in muscle and in liver is influenced by the carbohydrate used for refeeding, and muscle, rather than liver, is the main glycogen storing tissue.     

Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats.

To investigate the efficacy of the ingestion of vinegar in aiding recovery from fatigue, we examined the effect of dietary acetic acid, the main component of vinegar, on glycogen repletion in rats. Rats were allowed access to a commercial diet twice daily for 6 d. After 15 h of food deprivation, they were either killed immediately or given 2 g of a diet containing 0 (control), 0.1, 0.2 or 0.4 g acetic acid/100 g diet for 2 h. The 0.2 g acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentration than the control group (P < 0.05). The concentrations of citrate in this group in both the liver and skeletal muscles were >1.3-fold greater than in the control group (P > 0.1). In liver, the concentration of xylulose-5-phosphate in the control group was significantly higher than in the 0.2 and 0.4 g acetic acid groups (P < 0.01). In gastrocnemius muscle, the concentration of glucose-6-phosphate in the control group was significantly lower and the ratio of fructose-1,6-bisphosphate/fructose-6-phosphate was significantly higher than in the 0.2 g acetic acid group (P < 0.05). This ratio in the soleus muscle of the acetic acid fed groups was <0.8-fold that of the control group (P > 0.1). In liver, acetic acid may activate gluconeogenesis and inactivate glycolysis through inactivation of fructose-2,6-bisphosphate synthesis due to suppression of xylulose-5-phosphate accumulation. In skeletal muscle, acetic acid may inhibit glycolysis by suppression of phosphofructokinase-1 activity. We conclude that a diet containing acetic acid may enhance glycogen repletion in liver and skeletal muscle.