The influence of free fatty acids on glycogen recovery in rat heart after exercise

Summary Glycogen supercompensation is the term used to denote the abnormally high levels of glycogen found in the heart shortly after an exercise-induced reduction of the substrate. Using rats, we tested whether this condition was linked to the use of plasma free fatty acids (FFA), which normally rise with exercise. Before a 1-h swim, animals received an injection of either saline (S) or nicotinic acid (NA). The nicotinic acid treatment dramatically suppressed the rise in plasma FFA observed in the S-group. Exercise caused a significant but similar reduction (35–38%) of the myocardial glycogen content in both groups. After 1 h of recovery in the S-group, myocardial glycogen reached a value of 30.3±1.7 Μmol·g⁻¹ or 113% of that measured before the exercise began. In contrast, the value for hearts from the NA-group with reduced FFA levels was 24.0±1.9 Μmol·g⁻¹ or only 91% of that measured before exercise. After 2 h the values were 33.8±1.4 and 29.0±1.9 Μmol·g⁻¹ respectively. These data indicate that glycogen repletion in rat heart after exercise is related to the amount of FFA present in the plasma. We suggest that carbohydrate metabolism is diverted towards synthesis and storage as a result of the glycolytic inhibition exerted by the increased use of fat as an energy source as previously observed in hearts from fasted or diabetic animals. This work was supported by a grant from the Utah Heart Association and the Deseret Gym Corporation     

Metabolite accumulation increases adenine nucleotide degradation and decreases glycogenolysis in ischaemic rat skeletal muscle

Adenine nucleotides and glycogen are degraded in skeletal muscle during no-flow ischaemia. Past investigations have ascribed these metabolic changes to the severe energetic stress which arises with the removal of exogenous substrates (principally oxygen). We tested this hypothesis by measuring the high-energy phosphagen and glycogen contents of stimulated rat hindlimb muscles (1 twitch s^?1) prior to and following 40 min of no-flow ischaemia or hypoxic perfusion without glucose (P_ao₂ = 4.6 ± 0.1 torr, plasma glucose = 0.3 ± 0.1 mmol L^?1). Both experimental protocols eliminated exogenous substrate supply; however, the maintenance of flow during hypoxic perfusion ensured the removal of metabolic by-products. A period of forty minutes of skeletal muscle ischaemia was characterized by reductions in the total adenine nucleotide pool, phosphocreatine and glycogen in the slow oxidative soleus, fast oxidative-glycolytic plantaris and the fast glycolytic white gastrocnemius. Compared to ischaemia, the total adenine nucleotide pool was higher (by 7.2–13.3 μmol g^?1 dry wt) and the glycogen content lower (by 10.0–16.6 μmol g^?1 dry wt) in skeletal muscle exposed to hypoxic perfusion without glucose. The ability of hypoxic perfusion to attenuate TAN degradation and augment glycogenolysis can be attributed to metabolic by-product removal. By limiting muscle lactate and PCO ₂ accumulation, hypoxic perfusion without glucose attenuates cellular acidification; this could in turn limit AMP deaminase activation and glycogen phosphorylase inhibition. We conclude that the ischaemia-induced alterations in adenine nucleotide and glycogen metabolism arise in response to the elimination of exogenous substrates and to the accumulation of metabolic by-products.     

The effect of acute exercise on glycogen synthesis rate in obese subjects studied by 13C MRS

In obesity, insulin-stimulated glucose uptake in skeletal muscle is decreased. We investigated whether the stimulatory effect of acute exercise on glucose uptake and subsequent glycogen synthesis was normal. The study was performed on 18 healthy volunteers, 9 obese (BMI?=?32.6?±?1.2?kg/m², mean?±?SEM) and 9 lean (BMI?=?22.0?±?0.9?kg/m²), matched for age and gender. All participants underwent a euglycemic hyperinsulinemic clamp, showing reduced glucose uptake in the obese group (P?=?0.01), during which they performed a short intense local exercise (single-legged toe lifting). Dynamic glucose incorporation into glycogen in the gastrocnemius muscle before and after exercise was assessed by ¹³C magnetic resonance spectroscopy combined with infusion of [1-¹³C]glucose. Blood flow was measured to investigate its potential contribution to glucose uptake. Before exercise, glycogen synthesis rate tended to be lower in obese subjects compared with lean (78?±?14 vs. 132?±?24???mol/kg muscle/min; P?=?0.07). Exercise induced highly significant rises in glycogen synthesis rates in both groups, but the increase in obese subjects was reduced compared with lean (112?±?15 vs. 186?±?27???mol/kg muscle/min; P?=?0.03), although the relative increase was similar (184?±?35 vs. 202?±?51%; P?=?0.78). After exercise, blood flow increased equally in both groups, without a temporal relationship with the rate of glycogen synthesis. In conclusion, this study shows a stimulatory effect of a short bout of acute exercise on insulin-induced glycogen synthesis rate that is reduced in absolute values but similar in percentages in obese subjects. These results suggest a shared pathway between insulin- and exercise-induced glucose uptake and subsequent glycogen synthesis.     

Effect of low glycogen on glycogen synthase in human muscle during and after exercise

Subjects cycled at a work load calculated to elicit 75% of maximal oxygen uptake on two occasions: the first to fatigue (34.5 ± 5.3 min; mean ± SE), and the second at the same workload and for the same duration as the first. Biopsies were obtained from the quadriceps femoris muscle before and immediately after exercise, and 5 min post-exercise. Before the first experiment, muscle glycogen was lowered by a combination of exercise and diet, and before the second, experiment muscle glycogen was elevated. In the low glycogen condition (LG), muscle glycogen decreased from 169 ± 15 mmol glucosyl units kg^-1dry wt at to rest to 13 ± 6 after exercise. In the high glycogen condition (HG) glycogen decreased from 706 ± 52 at rest to 405 ± 68 after exercise. Glycogen synthase fractional activity (GSF) was always higher during the LG treatment. During exercise in the HG condition, those subjects who cycled for < 35 min (n= 3) had GSF values in muscle which were lower than at rest, whereas those subjects who cycled for > 35 min (n= 4) had values which were similar to or higher than at rest. Thus the change in GSF in muscle during HG was positively related to the exercise duration (r= 0.94; y = 254–17x + 0.3x²; P < 0.001) and negatively related to the glycogen content at the end of exercise (r=–0.82; y= 516–2x + 0.001x²; P < 0.05). During LG exercise GSF remained constant. GSF increased markedly after 5 min post-exercise in both HG and LG conditions. cAMP dependent protein kinase activity increased similarly during both LG and HG exercise and reverted to the preexercise values 5 min post-exercise. It is concluded that muscle contraction decreases GSF, but low glycogen levels can attenuate or abolish the decrease in GSF. The rapid increase of GSF during recovery from exercise does not require glycogen depletion during the exercise.     

Effect of glycogen loading on skeletal muscle cross‐sectional area and T2 relaxation time

This study was performed to investigate if glycogen loading of skeletal muscles, by binding water, would effect the cross‐sectional area (CSA) and if an altered water content would alter the transverse relaxation time (T2) measured by magnetic resonance imaging (MRI). Five healthy volunteers participated in a programme with 4 days of extremely carbohydrate‐restricted meals followed by 4 days of extremely high carbohydrate intake. The CSA and T2 of thigh and calf muscles were related to the intramuscular glycogen content evaluated at days 4 and 8. An increase in glycogen content from 281 to 634 mmol kg^–1 dry wt increased the CSA of the vastus muscles by 3.5% from 78 ± 11 to 80 ± 12 cm² and the thigh circumference by 2.5% from 146 ± 20 to 150 ± 23 cm². Calf circumference increased non‐significantly by 4% from 78 ± 15 to 82 ± 19 cm². Mono‐exponential T2 decreased in m tibialis anterior from 27.8 ± 1.2 to 26.9 ± 1.7 ms, did not change in m. vastus lateralis 26.5 ± 1.9 ms/26.6 ± 1.3 ms or in m. gastrocnemius 29.5 ± 1.0 ms/29.8 ± 1.9 ms. Glycogen loading increased the signal intensity mainly at different echo times (TE) 15 and 30 ms. The study shows that increased glycogen filling in the muscles increases muscle CSA and that this can be detected by MRI. The signal intensity increased the most at shorter TEs suggesting a more tight intracellular binding of water in glycogen loaded muscles.     

Effect of exercise on glycogen metabolism in muscles of triiodothyronine-treated rats

The aim of the present study was to examine the rate of glycogen mobilization during exercise and the rate of the postexercise glycogen replenishment in different muscle types [white (WG), and red (RG) gastrocnemius, soleus (S) and diaphragm (D)] in rats treated with triiodothyronine (T₃, group T). Rats of the control group (C) were treated with saline. The animals were made to run on a treadmill set at 0° gradient and at a speed of 1200 m·h^–1. The time taken to reach exhaustion in group C was 188 (SD 23) min, whereas in group T, it was only 63 (SD 12) min. The content of glycogen in all muscles of the rats from group T at rest and during exercise was significantly lower than in group C at each corresponding time. At exhaustion, the glycogen content was in WG(C) 34.79 (SD 4.65), (T) 20.10 (SD 4.10); in RG(C) 22.82 (SD 4.66), (T) 16.50 (SD 2.00); in S(C) 14.85 (SD 2.48), (T) 11.90 (SD 2.93); in D(C) 18.18 (SD 3.49), (T) 7.54 (SD 3.36) (mol of glucosyl units·g^–1). The amount of glycogen mobilized during exhausting exercise in RG, S and D was similar in both groups whereas in WG it was much higher in rats of group T than in group C. The concentration of glycogen returned to pre-exercise values in each muscle 3 h after exercise. The net amount of glycogen resynthetized during 3 h of recovery depended on the muscle type. It was in WG(C) 3.30, (T) 18.03; in RG(C) 21.34, (T) 25.88, in S(C) 34.00, (T) 17.68, and in D(C) 17.25, (T) 12.22 mol of glucosyl units·g^–1 (each number represents the difference between the means). It concluded that treatment with T₃ markedly affects this exercise-induced metabolism of glycogen in each muscle type.From our study it is suggested that low muscle glycogen content may contribute to a reduction in exercise performance in hyperthyroidism.     

Glycogen depletion and resynthesis in the rat after downhill running

Summary to study the effect of downhill running on glycogen metabolism, 94 rats were exercised by running for 3 h on the level or down an 18° incline. Muscle and liver glycogen concentrations were measured before exercise and 0, 48 and 52 h postexercise. Rats were not fed during the first 48 h of recovery but ingested a glucose solution 48 h postexercise. Downhill running depleted glycogen in the soleus muscle and liver significantly more than level running (P<0.01). The amount of glycogen resynthesized in the soleus muscle and liver in fasting or nonfasting rats was not altered significantly by downhill running (P>0.05). On every day of recovery the rats were injected with dexamethasone, which induced similar increases in glycogen concentration in the soleus muscle and liver after the 52nd h of the postexercise period in the case of downhill and level running. The glycogen depletion and repletion results indicated that, under our experimental conditions, downhill running in the rat, a known model of eccentric exercise, affected muscle glycogen metabolism differently from eccentric cycling in humans.     

Fuel substrate turnover and oxidation and glycogen sparing with carbohydrate ingestion in non-carbohydrate-loaded cyclists

This study examined the effects of ingesting 500 ml/h of either a 10% carbohydrate (CHO) drink (CI) or placebo (PI) on splanchnic glucose appearance rate (endogenous + exogenous) (R _a), plasma glucose oxidation and muscle glycogen utilisation in 17, non-carbohydrate-loaded, male, endurance-trained cyclists who rode for 180 min at 70% of maximum oxygen uptake. Mean muscle glycogen content at the start of exercise was 130 ± 6 mmol/kg ww; (mean ± SEM). Total CHO oxidation was similar in CI and PI subjects and declined during the trial. R _a increased significantly during the trial (P < 0.05) in both groups. Plasma glucose oxidation also increased significantly during the trial, reaching a plateau in the PI subjects, but was significantly (P < 0.05) higher in CI than PI subjects at the end of exercise [(98 ± 14 vs. 72 ± 10 μmol/min/kg fat-free mass) (FFM) (1.34 ± 0.19 vs. 0.93 ± 0.13 g/min)]. However, mean endogenous R _a was significantly (P < 0.05) lower in the CI than PI subjects throughout exercise (35 ± 7 vs. 54 ± 6 μmol/min/kg FFM), as was the oxidation of endogenous plasma glucose, which remained almost constant in CI subjects, and reached values at the end of exercise of 42 ± 13 and 72 ± 10 μmol/min/kg FFM in the CI and PI groups respectively. Of the 150 g CHO ingested during the trial, 50% was oxidised. Muscle glycogen disappearance was identical during the first 2 h of exercise in both groups and continued at the same rate in PI subjects, however no net muscle glycogen disappearance occurred during the final hour in CI subjects. We conclude that ingestion of 500 ml/h of a 10% CHO solution during prolonged exercise in non carbohydrate loaded subjects has a marked liver glycogen-sparing effect or causes a reduction in gluconeogenesis, or both, maintains plasma glucose concentration and has a muscle glycogen-sparing effect. Received: 25 August 1995/Received after revision: 25 March 1996/Accepted: 29 April 1996     

Intramyocellular lipid and glycogen content are reduced following resistance exercise in untrained healthy males

Resistance exercise has recently been shown to improve whole-body insulin sensitivity in healthy males. Whether this is accompanied by an exercise-induced decline in skeletal muscle glycogen and/or lipid content remains to be established. In the present study, we determined fibre-type-specific changes in skeletal muscle substrate content following a single resistance exercise session. After an overnight fast, eight untrained healthy lean males participated in a ~45 min resistance exercise session. Muscle biopsies were collected before, following cessation of exercise, and after 30 and 120 min of post-exercise recovery. Subjects remained fasted throughout the test. Conventional light and (immuno)fluorescence microscopy were applied to assess fibre-type-specific changes in intramyocellular triacylglycerol (IMTG) and glycogen content. A significant 27±7% net decline in IMTG content was observed in the type I muscle fibres (P<0.05), with no net changes in the type IIa and IIx fibres. Muscle glycogen content decreased with 23±6, 40±7 and 44±7% in the type I, IIa and IIx muscle fibres, respectively (P<0.05). Fibre-type-specific changes in intramyocellular lipid and/or glycogen content correlated well with muscle fibre-type oxidative capacity. During post-exercise recovery, type I muscle fibre lipid content returned to pre-exercise levels within 120 min. No changes in muscle glycogen content were observed during recovery. We conclude that intramyocellular lipid and glycogen stores are readily used during resistance exercise and this is likely associated with the reported increase in whole-body insulin sensitivity following resistance exercise.     

Muscle glycogen repletion and pre-exercise glycogen content: effect of carbohydrate loading in rats previously fed a high fat diet

We have recently reported that rates of muscle glycogen repletion during the early period of recovery were increased by carbohydrate (CHO) loading in rats previously fed a high fat diet. However, the reason for this remained unanswered. The purpose of this study was to examine whether an increase of glycogen utilization due to an elevated pre-exercise glycogen store would enhance rates of glycogen repletion in muscle. Despite an equal degree of glycogen depletion, the rates of glycogen repletion of soleus, red and white gastrocnemius muscles by postexercise administration of glucose (3.0 g · kg^–1 body mass) and citrate (0.5 g · kg^–1 body mass) were faster in the CHO loaded (3 days) rats than in the nonloaded rats, as a result of elevated pre-exercise glycogen content and consequently the greater glycogen utilization. The higher rate of muscle glycogen repletion may in part be explained by increased postexercise glycogen synthase activity.     

Fuel metabolism during ultra-endurance exercise

 Cyclists either ingested 300 ml 100 g/l U-[¹⁴C] glucose solution every 30 min during 6 h rides at 55% of VO_2max (n=6) or they consumed unlabelled glucose and were infused with U-[¹⁴C] lactate (n=5). Maintenance of euglycaemia limited rises in circulating free fatty acids, noradrenaline and adrenaline concentrations to 0.9±0.1 mM, 27±4 nM and 2.0±0.5 nM, respectively, and sustained the oxidation of glucose and lactate. As muscle glycogen oxidation declined from 100±13 to 71±9 μmol/min/kg in the last 3 h of exercise, glucose and lactate oxidation and interconversion rates remained at approximately 60 and 50 and at about 4 and 5 μmol/min/kg, respectively. Continued high rates of carbohydrate oxidation led to a total oxidation of around 270 g glucose, 130 g plasma lactate and 530 g muscle glycogen. Oxidation of some 530 g of muscle glycogen far exceeded the predicted (about 250 g) initial glycogen content of the active muscles and suggested that there must have been a considerable diffusion of unlabelled lactate from glycogen breakdown in inactive muscle fibres to adjacent active muscle fibres via the interstitial fluid that did not equilibrate with ¹⁴C lactate in the circulation. Received: 19 September 1997 / Received after revision: 15 December 1997 / Accepted: 22 January 1998     

Post-exercise glycogen resynthesis in trained high-protein or high-fat-fed rats after glucose feeding

Summary This study examined the effect on glycogen resynthesis during recovery from exercise of feeding glucose orally to physically trained rats which had been fed for 5 weeks on high-protein low fat (HP), high-protein/long-chain triglyceride (LCT) or high carbohydrate (CHO) diets. Muscle glycogen remained low and hepatic gluconeogenesis was stimulated by long-term fat or high-protein diets. The trained rats received, via a stomach tube, 3 ml of a 34% glucose solution immediately after exercise (2 h at 20 m · min^–1), followed by 1ml portions at hourly intervals until the end of the experiments. When fed glucose soleus muscle glycogen overcompensation occurred rapidly in the rats fed all three diets following prolonged exercise. In LCT- and CHO-fed rats, glucose feeding appeared more effective for soleus muscle repletion than in HP-fed rats. The liver demonstrated no appreciable glycogen overcompensation. A complete restoration of liver glycogen occurred within a 2- to 4-h recovery period in the rats fed HP-diet, while the liver glycogen store had been restored by only 67% in CHO-fed rats and 84% in LCT-fed rats within a 6-h recovery period. This coincides with low gluconeogenesis efficiency in these animals.     

Effect of exercise on metabolism of glycogen and triglycerides in the respiratory muscles

It was shown that during muscular exertion the diaphragm muscle and the intercostal muscles utilize endogenous glycogen whereas only the diaphragm muscle utilizes endogenous triglycerides. The post-excercise glycogen repletion in the diaphragm muscle was much faster than in the intercostal muscles. In the diaphragm muscle, marked overshoot of the glycogen level occurred early after the exercise.The work was supported by Polish Academy of Sciences within the project 10.4.2.01.3.2.     

Effect of a 20-day ski trek on fuel selection during prolonged exercise at low workload with ingestion of <Superscript>13</Superscript>C-glucose

Fuel selection was measured in five subjects (36.0 ± 10.5 years old; 87.3 ± 12.5 kg; mean ± SD) during a 120-min tethered walking with ski poles (1.12 l O₂ min⁻¹) with ingestion of ¹³C-glucose (1.5 g kg⁻¹), before and after a 20-day 415-km ski trek [physical activity level (PAL) ~3], using respiratory calorimetry, urea excretion, and ¹³C/¹²C in expired CO₂ and in plasma glucose. Before the ski trek, protein oxidation contributed 9.7 ± 1.6% to the energy yield (%En) while fat and carbohydrate (CHO) oxidation provided 73.5 ± 5.5 and 16.7 ± 6.5%En. Plasma glucose was the main source of CHO (52.9 ± 9.5%En) with similar contributions from exogenous glucose (27.2 ± 3.1%En), glucose from the liver (25.6 ± 8.3%En) and muscle glycogen (20.9 ± 4.0%En). Endogenous CHO contributed 46.6 ± 3.9%En. Following the ski trek %En from protein, fat, CHO, exogenous glucose and endogenous CHO were not significantly modified (10.1 ± 1.3, 15.8 ± 6.7, 74.1 ± 6.5, 28.7 ± 3.0 and 45.5 ± 7.5%En, respectively) but the %En from plasma glucose and glucose from the liver (41.1 ± 3.6 and 12.4 ± 4.0%En) were reduced, while that from muscle glycogen increased (33.0 ± 4.5%En). These results show that in subjects in the fed state with glucose ingestion during exercise, CHO is the main substrate oxidized, with major contributions from both exogenous and endogenous CHO. Following a ~3-week period of prolonged low intensity exercise, the %En from protein, fat, CHO, exogenous glucose and endogenous CHO were not modified. However, the %En from glucose released from the liver was reduced (possibly due to an increased insulin sensitivity of the liver) while that from muscle glycogen was increased. Ethical standards: the experiments reported in this study comply with the current laws of Canada.     

Effect of muscle glycogen availability on maximal exercise performance

This investigation determined the influence of pre-exercise muscle glycogen availability on performance during high intensity exercise. Nine trained male cyclists were studied during 75 s of all-out exercise on an air-braked cycle ergometer following muscle glycogen-lowering exercise and consumption of diets (energy content approximately 14 MJ) that were either high (HCHO – 80% CHO) or low (LCHO – 25% CHO) in carbohydrate content. The exercise-diet regimen was successful in producing differences in pre-exercise muscle glycogen contents [HCHO: 578(SEM?55) mmol?·?kg^?1 dry mass; LCHO: 364 (SEM 58) P??1 dry mass]. Despite this difference in muscle glycogen availability, there were no between trial differences for peak power [HCHO 1185 (SEM 50)W, LCHO 1179 (SEM?48)W], mean power [HCHO 547 (SEM?5)W, LCHO 554 (SEM ?8)W] and maximal accumulated oxygen deficit [HCHO 54.4 (SEM?2.3)?ml?·?kg^?1, LCHO 54.6 (SEM?2.0) ml?·?kg^?1]. Postexercise muscle lactate contents (HCHO 95.9 (SEM?4.6)?mmol?·?kg^?1 dry mass, LCHO 82.7 (SEM?12.3) mmol?·?kg^?1 dry mass, n?=?8] were no different between the two trials, nor were venous blood lactate concentrations immediately after and during recovery from exercise. These results would indicate that increased muscle glycogen availability has no direct effect on performance during all-out high intensity exercise.     

Non-invasive techniques for assessing carbohydrate flux:

Glycogen forms the smallest yet most labile energy substrate store. Therefore studying carbohydrate flux may be crucial to understanding the regulation of energy balance. Indirect calorimetry has been used to measure carbohydrate oxidation overnight and during exercise in nine fasted subjects. Overnight carbohydrate oxidation (averaging 2.85 ± 0.8 g h^-1) was assumed to be derived primarily from hepatic glycogen since subjects were inactive or asleep, and since glucose oxidized after gluconeogenesis from protein is measured as protein oxidation. Lower-limb muscle glycogen stores were depleted by repeated 30-min periods of cycle ergometry at 45%Vo_2max until exhaustion (8 ± 1 periods). The carbohydrate oxidation rate decreased as exercise progressed. Quadratic curves yielded a close fit to each individual's exercise carbohydrate depletion data (mean multiple correlation r= 0.9996) and provided excellent inter-subject discrimination. Total (muscle plus liver) glycogen stores prior to exercise were estimated by extrapolation of the depletion curves to zero oxidation rate. This produced an estimate (174 ± 61 g) which compared well with predictions (208 ± 43 g) based on reference values for muscle mass and initial glycogen content. The results demonstrate that non-invasive estimates of glycogen status can be obtained from accurate respiratory exchange data.     

In humans IL-6 is released from the brain during and after exercise and paralleled by enhanced IL-6 mRNA expression in the hippocampus of mice

Aim: Plasma interleukin‐6 (IL‐6) increases during exercise by release from active muscles and during prolonged exercise also from the brain. The IL‐6 release from muscles continues into recovery and we tested whether the brain also releases IL‐6 in recovery from prolonged exercise in humans. Additionally, it was evaluated in mice whether brain release of IL‐6 reflected enhanced IL‐6 mRNA expression in the brain as modulated by brain glycogen levels. Methods: Nine healthy male subjects completed 4 h of ergometer rowing while the arterio‐jugular venous difference (a‐v diff) for IL‐6 was determined. The IL‐6 mRNA and the glycogen content were determined in mouse hippocampus, cerebellum and cortex before and after 2 h treadmill running (N = 8). Results: At rest, the IL‐6 a‐v diff was negligible but decreased to ?2.2 ± 1.9 pg ml^?1 at the end of exercise and remained low (?2.1 ± 2.1 pg ml^?1) 1 h into the recovery (P < 0.05 vs. rest). IL‐6 mRNA was expressed in the three parts of the brain with the lowest content in the hippocampus (P < 0.05) coupled to the highest glycogen content (3.2 ± 0.8 mmol kg^?1). Treadmill running increased the hippocampal IL‐6 mRNA content 2–3‐fold (P < 0.05), while the hippocampal glycogen content decreased to 2.6 ± 0.6 mmol kg^?1 (P < 0.05) with no significant changes in the two other parts of the brain. Conclusion: Human brain releases IL‐6 both during and in recovery from prolonged exercise and mouse data suggest that concurrent changes in IL‐6 mRNA and glycogen levels make the hippocampus a likely source of the IL‐6 release from the brain.     

The effect of exercise training on glycogen,glycogen synthase and phosphorylase in muscle and liver

Summary It is thought that exercise training in both man and the rat results in a protective effect against the depletion of carbohydrate stores during exercise (glycogen-sparing). However there has been no comprehensive study of the effects of training on glycogen anabolic and catabolic enzymes with liver or muscle. The aim of this study was to examine whether changes in these enzymes occur and whether these changes may provide an explanation for the glycogen-sparing which results from exercise training.Male rats were trained by a treadmill running program at three different workloads. In addition, there were three control groups: free eating (SF), food restricted (SR), and one SF with a single bout of exercise prior to sacrifice.Exercise training was associated with a 60–150% increase in glycogen synthase and phosphorylase and a 50–70% increase in glycogen content in soleus, an intermediate muscle, but not in extensor digitorum longus (EDL), a white muscle nor in liver. The increase in glycogen synthase and phosphorylase in intermediate muscle was proportional to the degree of training and there was a significant correlation between glycogen content, glycogen synthase, and phosphorylase activity in intermediate muscle. Cytochrome c oxidase activity, an indicator of respiratory capacity, increased 50% in gastrocnemius of trained rats and was significantly correlated with glycogen synthase and phosphorylase in soleus.These results indicate a significant effect of exercise training on glycogen anabolic and catabolic enzymes in intermediate muscle, with no significant effects in white muscle or liver. The changes do not provide an explanation for glycogen-sparing, but are consistent with improved capacity of intermediate muscle for rapid glycogen mobilisation and repletion.     

13C MRS reveals a small diurnal variation in the glycogen content of human thigh muscle

There is marked diurnal variation in the glycogen content of skeletal muscles of animals, but few studies have addressed such variations in human muscles. ¹³C MRS can be used to noninvasively measure the glycogen content of human skeletal muscle, but no study has explored the diurnal variations in this parameter. This study aimed to investigate whether a diurnal variation in glycogen content occurs in human muscles and, if so, to what extent it can be identified using ¹³C MRS. Six male volunteers were instructed to maintain their normal diet and not to perform strenuous exercise for at least 3 days before and during the experiment. Muscle glycogen and blood glucose concentrations were measured six times in 24 h under normal conditions in these subjects. The glycogen content in the thigh muscle was determined noninvasively by natural abundance ¹³C MRS using a clinical MR system at 3 T. Nutritional analysis revealed that the subjects' mean carbohydrate intake was 463 ± 137 g, being approximately 6.8 ± 2.4 g/kg body weight. The average sleeping time was 5.9 ± 1.0 h. The glycogen content in the thigh muscle at the starting point was 64.8 ± 20.6 mM. Although absolute and relative individual variations in muscle glycogen content were 7.0 ± 2.1 mM and 11.3 ± 4.6%, respectively, no significant difference in glycogen content was observed among the different time points. This study demonstrates that normal food intake (not fat and/or carbohydrate rich), sleep and other daily activities have a negligible influence on thigh muscle glycogen content, and that the diurnal variation of the glycogen content in human muscles is markedly smaller than that in animal muscles. Moreover, the present results also support the reproducibility and availability of ¹³C MRS for the evaluation of the glycogen content in human muscles. Copyright © 2015 John Wiley & Sons, Ltd.     

The G-protein on cholesterol-rich membrane microdomains mediates mucosal sensing of short- chain fatty acid and secretory response in rat colon

Aim: The purpose of this study was to determine the anabolic response of a single bout of high intensity resistance exercise (RE) following 5 weeks of RE training. Methods: To complete these studies, Sprague–Dawley rats were assigned by body mass to RE, exercise control (EC), or sedentary cage control (CC) groups and studied over 36 h after 5 weeks of RE (squat‐like) training. Cumulative (final 36 h) fractional rates of muscle protein synthesis (FSR) were determined by ²H₂O, and acute (16 h post‐RE) rates of muscle protein synthesis (RPS) were determined by flooding with l ‐[2,3,4,5,6‐³H]phenylalanine. Regulators of peptide‐chain initiation, 4E‐BP1, eIF4E and the association of the two were determined by Western blotting and immunoprecipitation respectively. Results: No differences were observed with acute measures of RPS obtained 16 h following the final exercise bout in the plantaris or soleus muscles (P > 0.05). Consistent with this observation, 4E‐BP1 was similarly phosphorylated and bound to eIF4E among all groups. However, upon determination of the cumulative response, FSR was significantly increased in the plantaris of RE vs. EC and CC (0.929 ± 0.094, 0.384 ± 0.039, 0.300 ± 0.022% h^?1 respectively; P < 0.001), but not the soleus. Conclusion: With the advantage of determining cumulative FSR, the present study demonstrates that anabolic responses to RE are still evident after chronic RE training, primarily in muscle composed of fast‐twitch fibres.