Changes In Muscle Glycogen Content Research Articles

The relation between dietary polysaccharide intake and urinary excretion of tetraglucoside.

The urinary metabolite tetraglucoside (Glc4) is a potential biomarker for hepatic glycogen storage diseases (GSDs). Glc4 is believed to reflect body glycogen content and/or turnover. However, dietary polysaccharide intake may influence Glc4 excretion, potentially limiting the utility of Glc4 as a monitoring biomarker in hepatic GSDs. We aimed to investigate the association of dietary polysaccharide intake with Glc4 excretion. Urinary Glc4 excretion (mmol/mmol creatinine and mmol/24 h) was analyzed using a validated LC-MS/MS method. Data was analyzed from 65 kidney transplant recipients and 58 healthy kidney donors in the TransplantLines cohort study. Spearman's correlation and multivariable linear regression analyses were performed. In the multivariable analysis, dry lean body mass (DLBM), dietary polysaccharide intake, transplantation status, age, sex, and glycated hemoglobin (HbA1c) served as independent variables. Daily variation was examined in 21 healthy individuals of urinary Glc4 excretion in 2-h collections over a 24-h period. Mixed generalized additive models were built to study the association of prior polysaccharide intake with Glc4 excretion. No (univariate) associations were found between polysaccharide intake and Glc4 excretion. However, a significant interaction between DLBM and polysaccharide on 24 h Glc4 excretion was observed in the multivariate analysis. Glc4 excretion throughout the day exhibited no relationship to prior polysaccharide intake. Our findings suggest an indirect effect of polysaccharide intake on Glc4 excretion, potentially due to changes in muscle glycogen content and/or turnover. We have found no evidence that dietary polysaccharides under normal intakes increase urinary Glc4 directly.

Augmented muscle glycogen utilization following a single session of sprint training in hypoxia.

This study determined the effect of a single session of sprint interval training in hypoxia on muscle glycogen content among athletes. Ten male college track and field sprinters (mean ± standard error of the mean: age, 21.1 ± 0.2years; height, 177 ± 2cm; body weight, 67 ± 2kg) performed two exercise trials under either hypoxia [HYPO; fraction of inspired oxygen (FiO2), 14.5%] or normoxia (NOR: FiO2, 20.9%). The exercise consisted of 3 × 30s maximal cycle sprints with 8-min rest periods between sets. Before and immediately after the exercise, the muscle glycogen content was measured using carbon magnetic resonance spectroscopy in vastus lateralis and vastus intermedius muscles. Moreover, power output, blood lactate concentrations, metabolic responses (respiratory oxygen uptake and carbon dioxide output), and muscle oxygenation were evaluated. Exercise significantly decreased muscle glycogen content in both trials (interaction, P = 0.03; main effect for time, P < 0.01). Relative changes in muscle glycogen content following exercise were significantly higher in the HYPO trial (- 43.5 ± 0.4%) than in the NOR trial (- 34.0 ± 0.3%; P < 0.01). The mean power output did not significantly differ between the two trials (P = 0.80). The blood lactate concentration after exercise was not significantly different between trials (P = 0.31). A single session of sprint interval training (3 × 30s sprints) in hypoxia caused a greater decrease in muscle glycogen content compared with the same exercise under normoxia without interfering with the power output.

Does Muscle Glycogen Content Account For The Contralateral Force Deficit During Unilateral Fatigue?

Performing unilateral contractions to exhaustion has been shown to lead to force deficits of both the exercised and unexercised limbs. It has been proposed that the contralateral force deficits are of neural origin, and not due to peripheral mechanisms of fatigue (e.g. glycogen depletion). While this proposed model appears likely, it remains speculative as the absence of peripheral factors to contralateral force deficits have not been verified. PURPOSE: Therefore, the purpose of the study was to quantify the changes in muscle glycogen content and maximal force of both limbs in response to unilateral fatigue. METHODS: Nineteen healthy subjects performed two maximal voluntary isometric (MVC) knee extensions of each leg before (PRE) and after (POST) a fatiguing protocol of the right leg. The fatiguing protocol consisted of repeated 56 second long ramp contractions of the right leg at 30% MVC until failure. During the plateau phase of each contraction, ultrasound images were taken at the midpoint of the rectus femoris (RF). The echo intensity, which has been shown to be sensitive to acute changes in muscle glycogen content, was analyzed from each image of the RF muscle. RESULTS: A two way repeated measures ANOVA showed a significant time × limb interaction (p < 0.001) for MVCs. Follow-up paired sample t-tests indicated that both limbs showed significant force loss. However, the right leg (-33%, from 773.36±191.79 to 517.13±136.72, p < 0.001) demonstrated a much larger force deficit than the left leg (-9.7%, from 803.07±215.32 to 725.04±198.44, p = 0.002). For echo intensity, the right leg demonstrated a significant change (8.8%, from 48.64±7.70 to 52.58±8.68, p = 0.009) from PRE to POST. However, the left leg did not change (1.34%, from 53.93±7.65 to 54.65±7.72, p = 0.621). It is worth noting the increase in echo intensity, such as seen with the right leg, represents a decrease in tissue density (e.g. decreased muscle glycogen content). CONCLUSION: Our findings suggest peripheral fatigue mechanisms, such as muscle glycogen content, were not responsible for the decreased force in the contralateral limb. This absence of peripheral, intracellular changes supports the original proposal that the contralateral force deficit is of a central, neural origin.

Muscle Glycogen Content during Endurance Training under Low Energy Availability

The present study investigated the effects of three consecutive days of endurance training under conditions of low energy availability (LEA) on the muscle glycogen content, muscle damage markers, endocrine regulation, and endurance capacity in male runners. Seven male long-distance runners (19.9 ± 1.1 yr, 175.6 ± 4.7 cm, 61.4 ± 5.3 kg, maximal oxygen uptake [V˙O2max]: 67.5 ± 4.3 mL·kg·min) completed two trials consisting of three consecutive days of endurance training under LEA (18.9 ± 1.9 kcal·kg FFM·d) or normal energy availability (NEA) (52.9 ± 5.0 kcal·kg FFM·d). The order of the two trials was randomized, with a 2-wk interval between trials. The endurance training consisted of 75 min of treadmill running at 70% of V˙O2max. Muscle glycogen content, respiratory gas variables, and blood and urine variables were measured in the morning for three consecutive days of training (days 1-3) and on the following morning after training (day 4). As an indication of endurance capacity, time to exhaustion at 19.0 ± 0.8 km·h to elicit 90% of V˙O2max was evaluated on day 4. During the training period, body weight, fat-free mass, and skeletal muscle volume were significantly reduced in LEA (P = 0.02 for body weight and skeletal muscle volume, P = 0.01 for fat-free mass). Additionally, muscle glycogen content was significantly reduced in LEA (~30%, P < 0.001), with significantly lower values than those in NEA (P < 0.001). Time to exhaustion was not significantly different between the two trials (~20 min, P = 0.39). Three consecutive days of endurance training under LEA decreased muscle glycogen content with lowered body weight. However, endurance capacity was not significantly impaired.

Proglycogen and macroglycogen: artifacts of glycogen extraction?

Most recent studies on the physiology of proglycogen and macroglycogen in skeletal muscles have adopted a homogenization-free acid extraction protocol to separate these 2 pools of glycogen. The purposes of this study were to determine ( a) whether this protocol is suitable; ( b) if the acid-insoluble glycogen fraction corresponds to proglycogen; and ( c) if this fraction accounts for most of the changes in muscle glycogen content, irrespective of muscle fiber types. Using the rat as our experimental model, this study shows that when the conditions of acid extraction are optimized, 52% to 64% of glycogen in rat muscles is found as acid-soluble glycogen as opposed to approximately 16% when glycogen is extracted using a homogenization-free extraction protocol. Moreover, there is no evidence that the acid-insoluble glycogen corresponds to proglycogen because gel chromatography of the acid-insoluble and acid-soluble glycogen fractions shows similar elution profiles of high–molecular weight glycogen. Finally, irrespective of muscle fiber types, the acid-soluble glycogen accounts for most of the changes in total muscle glycogen levels during the fasting-to-fed transition, whereas the levels of the acid-insoluble glycogen remain stable or increase marginally. In conclusion, this study shows that the homogenization-free acid extraction of muscle glycogen underestimates the proportion of acid-soluble glycogen and that the findings of the studies that have adopted such an extraction protocol to examine the physiology of acid-insoluble and acid-soluble glycogens require reexamination.

Muscle glycogen oxidation during prolonged exercise measured with oral [13C]glucose: comparison with changes in muscle glycogen content

Plasma glucose and muscle glycogen oxidation during prolonged exercise [75-min at 48 and 76% maximal O(2) uptake (Vo(2 max))] were measured in eight well-trained male subjects [Vo(2 max) = 4.50 l/min (SD 0.63)] using a simplified tracer technique in which a small amount of glucose highly enriched in (13)C was ingested: plasma glucose oxidation was computed from (13)C/(12)C in plasma glucose (which was stable beginning at minute 30 and minute 15 during exercise at 48 and 76% Vo(2 max), respectively) and (13)CO(2) production, and muscle glycogen oxidation was estimated by subtracting plasma glucose oxidation from total carbohydrate oxidation. Consistent data from the literature suggest that this small dose of exogenous glucose does not modify muscle glycogen oxidation and has little effect, if any, on plasma glucose oxidation. The percent contributions of plasma glucose and muscle glycogen oxidation to the energy yield at 48% Vo(2 max) [15.1% (SD 3.8) and 45.9% (SD 5.8)] and at 76% Vo(2 max) [15.4% (SD 3.6) and 59.8% (SD 9.2)] were well in line with data previously reported for similar work loads and exercise durations using conventional tracer techniques. The significant reduction in glycogen concentration measured from pre- and postexercise vastus lateralis muscle biopsies paralleled muscle glycogen oxidation calculated using the tracer technique and was larger at 76% than at 48% Vo(2 max). However, the correlation coefficients between these two estimates of muscle glycogen utilization were not different from zero at each of the two work loads. The simplified tracer technique used in the present experiment appears to be a valid alternative approach to the traditional tracer techniques for computing plasma glucose and muscle glycogen oxidation during prolonged exercise.

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 approximately 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.

Relationship Between Carbohydrate Supplementation and Perceived Exertion During Prolonged Running

0844 PURPOSE: The purpose of this study was to investigate the relationship between carbohydrate energy substrate and hormonal regulation on the perception of exertion during prolonged running. METHODS: Sixteen experienced marathoners ran on treadmills for 3 h at ∼70% VO2max on two occasions while receiving 1 l/h carbohydrate (C) or placebo (P) beverages. Blood and vastus lateralis muscle biopsy samples were collected before and after exercise. RESULTS: The pattern of change in RPE over time was significantly different between C and P ingestion (P<0.01) with attenuated RPE responses found in the latter part of the 3 h run. The pattern of change in the respiratory exchange ratio and carbohydrate oxidation rates were significantly greater (P<0.01) in the C than P condition. Change in muscle glycogen content did not differ between C and P (P = 0.246). C relative to P ingestion was associated with higher plasma levels of glucose, insulin, and lactate and lower levels plasma cortisol. CONCLUSIONS: These data indicate that a lower RPE was associated with a higher carbohydrate oxidation, plasma glucose, and insulin levels, and lower plasma cortisol during prolonged running following C supplementation as compared to P feeding despite no differences in muscle glycogen content. These findings support a physiological link between RPE and carbohydrate substrate availability as well as selected hormonal regulation during prolonged running.

CARBOHYDRATE INGESTION INFLUENCES SKELETAL MUSCLE CYTOKINE mRNA AND PLASMA CYTOKINE LEVELS AFTER A 3-H RUN

PURPOSE To determine the influence of carbohydrate ingestion on skeletal muscle cytokine mRNA content and plasma cytokine levels after a 3-h run. METHODS Sixteen experienced marathoners ran on treadmills for 3 h at ∼70% VO2max on two occasions while receiving 1 l/h carbohydrate (CHO) or placebo (PLA) beverages. Blood and vastus lateralis muscle biopsy samples were collected before and after exercise. Plasma was analyzed for IL-6, IL-10, IL-1ra, IL-8, cortisol, glucose, and insulin. Muscle was analyzed for glycogen content and relative gene expression of 13 cytokines (IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p35, IL-12p40, IL-15, IFN-γ, TNF-α) using real-time quantitative RT-PCR and the ΔΔCt method that monitors the degradation of a dual-labeled fluorescent probe (TaqMan) in real time concomitant with PCR amplification. The data were analyzed using a 2 × 2 repeated measures ANOVA. RESULTS Plasma glucose and insulin were higher and cortisol, IL-6, IL-10, and IL-1ra, but not IL-8, were significantly lower post-exercise in CHO vs PLA. Change in muscle glycogen content did not differ between CHO and PLA (P=0.246). Muscle cytokine mRNA was detected for IL-1β, IL-2, IL-6, IL-8, IL-10, IL-12p35, IL-15, IFN-γ, and TNF-α, but only IL-1β, IL-6, and IL-8 were significantly increased with exercise (P < 0.05). The increase in mRNA (fold difference from pre-exercise) was attenuated in CHO (15.9-fold) compared to PLA (35.2-fold) for IL-6 (P = 0.071) and IL-8 (CHO, 7.8-fold; PLA, 23.3-fold; P = 0.063). CONCLUSION CHO compared to PLA beverage ingestion attenuates the increase in plasma IL-6, IL-10, and IL-1ra, and gene expression for IL-6 and IL-8 in athletes running 3 h at 70% VO2max despite no differences in muscle glycogen content. Supported by a grant from the Gatorade Sports Science Institute.

Role of nonworking muscle on blood metabolites and ions with intense intermittent exercise

The exchange of ions between blood and inactive muscle was studied in healthy males (n = 11) who performed four 30-s bouts of maximum isokinetic leg exercise, with 4 min of rest between bouts; recovery was followed for 90 min. Blood was sampled from the brachial artery and antecubital vein from inactive arm, and biopsies were taken from the nonworking deltoid muscles. During exercise, whole blood and plasma arteriovenous (a-v) differences across the arm showed increased net uptake of lactate (Lac-), K+, Na+, Cl-, glycerol, and O2. Arm glucose uptake also increased during exercise and the last 30 min of recovery, but there was no change in muscle glycogen content. Deltoid intracellular Lac- concentration [( Lac-]) increased 2.5-fold to 8.2 +/- 1.4 meq/l during exercise and 25 min of recovery. Despite evidence of uptake from blood and plasma a-v differences, deltoid intracellular K+, Na+, and Cl- concentrations did not change. During recovery, arm a-v differences showed no Lac- release, but Cl- and Na+ were released to venous blood for at least 90 min of recovery. During repeated exercise, the elevated Lac- uptake (a-v [Lac-] is 5-8 meq/l) and a HCO3- release (a-v HCO3- concentration is -8-11 meq/l) by the arm was suggestive of a possible anion exchange (Lac-/HCO3-). It is concluded that during heavy exercise non-working muscles take up and oxidize significant amounts of Lac-. Other inactive tissues also play a role in the regulation of ion and metabolite concentrations of blood.

Glucose balance and muscle glycogen during TPN in the early post-operative phase

In order to study how muscle glycogen is influenced by different nutritional regimens in the early post-operative period we took muscle biopsies from 20 patients preoperatively and on the fourth post-operative day after abdominal aortic surgery. Ten patients received 93% of non-protein energy as glucose, 7% as fat (Intralipid ®) and insulin was given to keep the blood glucose below 10 mmol/l. The remaining patients had 80% of non-protein energy as fat (Intralipid ®). Amino acids constituting 12 g of nitrogen daily were given to both groups. Daily measurements of gas exchange (oxygen uptake, CO 2-production) were performed and from these data glucose balance was calculated as the difference between glucose intake and glucose expenditure. Muscle biopsies were analysed for glycogen, adenosine triphosphate, glucose-6-phosphate, lactate and citrate. We found that it was possible to maintain muscle glycogen stores at pre-operative levels with a glucose-insulin regimen. With the fat regimen there was a 31% decrease in muscle glycogen and two patients had a negative glucose balance despite the fact that 150 g of glucose were given. Average glucose balance throughout the study correlated positively with glucose intake. A significant correlation between glucose on the third day and change in muscle glycogen content was found. Muscle content of adenosine triphosphate, glucose-6-phosphate, lactate and citrate were similar in both groups.

Correlation between muscle glycogen synthase activity and in vivo insulin action in man.

We have studied the relationship between in vivo insulin-mediated glucose disposal rates, muscle glycogen content, and muscle glycogen synthase activity in 25 southwest American Indians with normal glucose tolerance and with varying degrees of glucose intolerance. Insulin-mediated glucose disposal (M) was measured by using the hyperinsulinemic euglycemic clamp technique at plasma insulin concentrations of 134 +/- 7 and 1709 +/- 72 microU/ml, with simultaneous indirect calorimetry to assess glucose oxidation and storage rates. Muscle glycogen content and glycogen synthase activity were measured in percutaneous muscle biopsy samples obtained from the vastus lateralis muscle before and after the euglycemic clamp procedure. The results showed that muscle glycogen synthase activity at the end of the euglycemic clamp was well correlated with insulin-mediated glucose storage rates at both low (r = 0.50, P less than 0.02) and high (r = 0.78, P less than 0.0001) insulin concentrations; and also correlated with M (r = 0.66, P less than 0.001 and r = 0.76, P less than 0.0001). Similar correlations were observed between the change in muscle glycogen synthase activity and glucose storage rates and M. The change in muscle glycogen synthase activity correlated with the change in muscle glycogen content (r = 0.46, P less than 0.03) measured before and after the insulin infusions. The change in muscle glycogen content did not correlate with glucose storage rates or M. The data suggest the possible importance of glycogen synthesis in muscle in determining in vivo insulin-mediated glucose disposal rates in man.

Muscle glycogen synthesis after a glucose infusion during post-exercise recovery in diabetic and non-diabetic subjects.

Post-exercise muscle glycogen repletion after a glucose infusion was studied in diabetic (D) and non-diabetic (ND) subjects in two series of experiments; one in which muscle biopsies were examined and another in which arterial-femoral vein (a-fv) glucose differences were investigated. The results were compared with a control experiment where the subjects rested before the infusion. All experiments were performed after 12-14 h fast. The diabetics had not taken their morning insulin. The subjects bicycled till exhaustion. 15 min after cessation of exercise 0.5 g glucose per kg body weight was infused. Blood samples were drawn before exercise, in the last minute of exercise and repetetively during recovery. Biopsies were obtained before exercise, immediately after exercise and 65 min after the infusion. During exercise muscle glycogen content decreased from 68.7 ± 5.0 (D) and 81.4 ± 8.6 (ND) to 33.9 ± 5.1 (D) and 21.6 ± 3.3 (ND) mmol glucosyl units/kg w.w. After the glucose infusion muscle glycogen increased to 44.2 ± 3.8 (D) (P < 0.005) and 35.8 ± 5.7 (ND) (P < 0.005) mmol glucosyl units/kg w.w. Glycogen synthesis rates during recovery were 9.6 ± 1.5 (D) and 13.6 ± 2.6 (ND) mmol glucosyl units/kg w.w. per hr. No significant differences were observed in glycogen content or glycogen synthesis rate between the two groups. In the control experiments, no increase in muscle glycogen content was observed. The post-infusion a-fv-glucose differences were similar in diabetic and non-diabetic subjects during recovery, and in both groups larger than in the control experiments. It is concluded that during recovery after exercise a major portion of glucose infused as a single injection 15 min after exercise in diabetic and non-diabetic subjects, is utilized by muscle; mainly for glycogen synthesis. The rate of glycogen synthesis is similar in both groups. When glucose is infused without previous exercise, no changes in muscle glycogen content is observed.