scholarly journals Effects of Oral Resveratrol Supplementation on Glycogen Replenishment and Mitochondria Biogenesis in Exercised Human Skeletal Muscle

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3721
Author(s):  
Chun-Ching Huang ◽  
Chia-Chen Liu ◽  
Jung-Piao Tsao ◽  
Chin-Lin Hsu ◽  
I-Shiung Cheng
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Young Male ◽  
Gene Expressions ◽  
Plasma Parameters ◽  
Post Exercise ◽  
Glycogen Resynthesis ◽  
Mitochondria Biogenesis

The present study aimed to investigate the effect of oral resveratrol supplementation on the key molecular gene expressions involved in mitochondria biogenesis and glycogen resynthesis in human skeletal muscle. Nine young male athletes participated in the single-blind and crossover designed study. All subjects completed a 4-day resveratrol and placebo supplement in a randomized order while performing a single bout of cycling exercise. Immediately after the exercise challenge, the subjects consumed a carbohydrate (CHO) meal (2 g CHO/Kg body mass) with either resveratrol or placebo capsules. Biopsied muscle samples, blood samples and expired gas samples were obtained at 0 h and 3 h after exercise. The muscle samples were measured for gene transcription factor expression by real-time PCR for glucose uptake and mitochondria biogenesis. Plasma glucose, insulin, glycerol, non-esterified fatty acid concentrations and respiratory exchange ratio were analyzed during post-exercise recovery periods. The results showed that the muscle glycogen concentrations were higher at 3 h than at 0 h; however, there were no difference between resveratrol trial and placebo trial. There were no significantly different concentrations in plasma parameters between the two trials. Similarly, no measured gene expressions were significant between the two trials. The evidence concluded that the 4-day oral resveratrol supplementation did not improve post-exercise muscle glycogen resynthesis and related glucose uptake and mitochondrial biosynthesis gene expression in men.

scholarly journals Effect of green tea extract supplementation on glycogen replenishment in exercised human skeletal muscle

2017 ◽  
Vol 117 (10) ◽  
pp. 1343-1350 ◽  
Author(s):  
Tsen-Wei Tsai ◽  
Chia-Chen Chang ◽  
Su-Fen Liao ◽  
Yi-Hung Liao ◽  
Chien-Wen Hou ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Green Tea ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Recovery Period ◽  
Glycogen Resynthesis ◽  
Postexercise Recovery ◽  
Exercise Induced ◽  
Tea Extract

AbstractThe purpose of this study was to investigate the effects of 8-week green tea extract (GTE) supplementation on promoting postexercise muscle glycogen resynthesis and systemic energy substrate utilisation in young college students. A total of eight healthy male participants (age: 22·0 (se 1·0) years, BMI: 24·2 (se 0·7) kg/m2, VO2max: 43·2 (se 2·4) ml/kg per min) participated in this study. GTE (500 mg/d for 8 weeks) was compared with placebo in participants in a double-blind/placebo-controlled and crossover study design with an 8-week washout period. Thereafter, all participants performed a 60-min cycling exercise (75 % VO2max) and consumed a carbohydrate-enriched meal immediately after exercise. Vastus lateralis muscle samples were collected immediately (0 h) and 3 h after exercise, and blood and gaseous samples were collected during the 3-h postexercise recovery period. An 8-week oral GTE supplementation had no effects on further promoting muscle glycogen resynthesis in exercised human skeletal muscle, but the exercise-induced muscle GLUT type 4 (GLUT4) protein content was greater in the GTE supplementation trial (P<0·05). We observed that, during the postexercise recovery period, GTE supplementation elicited an increase in energy reliance on fat oxidation compared with the placebo trial (P<0·05), although there were no differences in blood glucose and insulin responses between the two trials. In summary, 8-week oral GTE supplementation increases postexercise systemic fat oxidation and exercise-induced muscle GLUT4 protein content in response to an acute bout of endurance exercise. However, GTE supplementation has no further benefit on promoting muscle glycogen resynthesis during the postexercise period.

Effect of Capsinoids Supplementation on Fat Oxidation and Muscle Glycogen Restoration During Post-exercise Recovery in Humans

2020 ◽  
Vol 26 ◽  
Author(s):  
Su-Fen Liao ◽  
Mallikarjuna Korivi ◽  
Jung-Piao Taso ◽  
Chun-Ching Huang ◽  
Chia-Chen Chang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Young Adults ◽  
Muscle Glycogen ◽  
Vastus Lateralis ◽  
Recovery Period ◽  
Fat Oxidation ◽  
Exercise Recovery ◽  
Post Exercise ◽  
Glycogen Resynthesis ◽  
Post Exercise Recovery

Background: Capsinoids (CSN), the novel non-pungent capsaicin analogs have been reported to promote metabolic health and exercise tolerance. However, the effect of CSN on fat oxidation and changes in skeletal muscle glycogen levels during post-exercise recovery has not been investigated in humans. Purpose: We examined the effect of CSN supplementation on energy reliance, glycogen resynthesis and molecular proteins in the skeletal muscle of young adults during post-exercise recovery. Methods: In this crossover-designed study, nine healthy adult male volunteers (aged 21.4±0.2 years, BMI 21.9±1.3 kg/m2 ) completed a 60-min cycling exercise at 70% VO2max. Participants consumed either CSN (12 mg, single dosage) or placebo capsules with a high-carbohydrate meal (2 g carb/kg bodyweight) immediately after exercise. Biopsied muscle samples (vastus lateralis), blood and gaseous samples were obtained during 3h post-exercise recovery period. Results: We found that oral CSN supplementation right after exercise significantly altered the energy reliance on fat oxidation during recovery. This was evidenced by lower respiratory exchange ratio (RER) and higher fat oxidation rate in CSN trial. Despite, acute CSN dosage does not contribute to enhance the glycogen replenishment in skeletal muscle during 3h recovery. We identified no significant differences in postprandial glucose and insulin area under the curve in both trials. Western blot data showed increased muscle GLUT4 expression, but no significant response of p-Akt/Akt ratio with CSN during post-exercise recovery. Conclusion: Our findings conclude that acute CSN intake could change energy reliance on fat oxidation, but unable to enhance muscle glycogen resynthesis during post-exercise recovery. Thus, ergogenic properties of CSN in relevance to muscle glycogen restoration following exercise needs to be further investigated in young adults.

scholarly journals Oral Capsinoids Supplementation May not Enhance Glycogen Recovery against Exercise-Induced Loss in Exercised Human Skeletal Muscle

2018 ◽  
Author(s):  
Jung-Piao Taso ◽  
Su-Fen Liao ◽  
Duen-Kai Shiau ◽  
Mei-Fang Wu ◽  
Chia-Chen Chang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Postprandial Glucose ◽  
Exercise Recovery ◽  
Post Exercise ◽  
Glycogen Resynthesis ◽  
Glut4 Expression ◽  
Before And After ◽  
Post Exercise Recovery

We investigated whether post-exercise capsinoids (CSN) supplementation could enhance muscle glycogen resynthesis via GLUT4/Akt expressions in human skeletal muscle. Nine male college students (aged 21.4&plusmn;0.2 years, BMI 21.9&plusmn;1.3 kg/m2, VO2max 47.1&plusmn;1.8 ml/kg/min) participated in this crossover designed study, and completed a 60-min cycling exercise at 70% VO2max. Immediately after exercise, participants consumed high-carbohydrate diet (2 g carb/kg bodyweight) with CSN (12 mg, single dosage) or placebo. Biopsied muscle samples (vastus lateralis) were obtained immediately (0h) and 3h after exercise. Blood and expired gas samples were collected before and after exercise. We found oral CSN supplementation immediately after exercise was unable to enhance glycogen resynthesis in exercised human skeletal muscle. Despite, CSN could alter the energy reliance on fat oxidation during post-exercise recovery, based on gaseous exchange measurement (NEFA and glycerol). We further identified no significant differences in postprandial glucose/insulin area under curve in both trials. Western blot data showed no significant response of p-Akt/Akt ratio with CSN during post-exercise recovery. Inconsistent with glycogen levels, muscle GLUT4 expression was significantly elevated at 3h in CSN trial. Our findings emphasize the necessity of further evidences to confirm the ergogenic properties of CSN in connection with glycogen recovery in exercised human skeletal muscle.

Effect Of Post-exercise Carbohydrate Supplementation On Glucose Uptake-associated Gene Expression In Human Skeletal Muscle

2007 ◽  
Vol 39 (Supplement) ◽  
pp. S7 ◽  
Author(s):  
Yu-Ching Chen ◽  
I-Shiung Cheng ◽  
Ning-Yuean Lee ◽  
Su-Fen Liao ◽  
Chiung-Hsueh Huang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Human Skeletal Muscle ◽  
Post Exercise ◽  
Carbohydrate Supplementation

scholarly journals Carbohydrate restriction following strenuous glycogen-depleting exercise does not potentiate the acute molecular response associated with mitochondrial biogenesis in human skeletal muscle

2021 ◽  
Vol 121 (4) ◽  
pp. 1219-1232
Author(s):  
Catarina Ramos ◽  
Arthur J. Cheng ◽  
Sigitas Kamandulis ◽  
Andrejus Subocius ◽  
Marius Brazaitis ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Mitochondrial Biogenesis ◽  
Muscle Glycogen ◽  
Oxidative Metabolism ◽  
Human Skeletal Muscle ◽  
Recovery Period ◽  
Mrna Levels ◽  
Cycling Exercise ◽  
Post Exercise

Abstract Purpose Carbohydrate (CHO) restriction could be a potent metabolic regulator of endurance exercise-induced muscle adaptations. Here, we determined whether post-exercise CHO restriction following strenuous exercise combining continuous cycling exercise (CCE) and sprint interval exercise could affect the gene expression related to mitochondrial biogenesis and oxidative metabolism in human skeletal muscle. Methods In a randomized cross-over design, 8 recreationally active males performed two cycling exercise sessions separated by 4 weeks. Each session consisted of 60-min CCE and six 30-s all-out sprints, which was followed by ingestion of either a CHO or placebo beverage in the post-exercise recovery period. Muscle glycogen concentration and the mRNA levels of several genes related to mitochondrial biogenesis and oxidative metabolism were determined before, immediately after, and at 3 h after exercise. Results Compared to pre-exercise, strenuous cycling led to a severe muscle glycogen depletion (> 90%) and induced a large increase in PGC1A and PDK4 mRNA levels (~ 20-fold and ~ 10-fold, respectively) during the acute recovery period in both trials. The abundance of the other transcripts was not changed or was only moderately increased during this period. CHO restriction during the 3-h post-exercise period blunted muscle glycogen resynthesis but did not increase the mRNA levels of genes associated with muscle adaptation to endurance exercise, as compared with abundant post-exercise CHO consumption. Conclusion CHO restriction after a glycogen-depleting and metabolically-demanding cycling session is not effective for increasing the acute mRNA levels of genes involved in mitochondrial biogenesis and oxidative metabolism in human skeletal muscle.

scholarly journals Effects of Nutrient Intake Timing on Post-Exercise Glycogen Accumulation and its Related Signaling Pathways in Mouse Skeletal Muscle

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2555 ◽  
Author(s):  
Takahashi ◽  
Matsunaga ◽  
Banjo ◽  
Takahashi ◽  
Sato ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Nutrient Intake ◽  
Matched Control ◽  
Control Group ◽  
Glycogen Depletion ◽  
Post Exercise ◽  
Glycogen Accumulation ◽  
Matched Control Group ◽  
Significant Difference

We investigated the effects of nutrient intake timing on glycogen accumulation and its related signals in skeletal muscle after an exercise that did not induce large glycogen depletion. Male ICR mice ran on a treadmill at 25 m/min for 60 min under a fed condition. Mice were orally administered a solution containing 1.2 mg/g carbohydrate and 0.4 mg/g protein or water either immediately (early nutrient, EN) or 180 min (late nutrient, LN) after the exercise. Tissues were harvested at 30 min after the oral administration. No significant difference in blood glucose or plasma insulin concentrations was found between the EN and LN groups. The plantaris muscle glycogen concentration was significantly (p < 0.05) higher in the EN group—but not in the LN group—compared to the respective time-matched control group. Akt Ser473 phosphorylation was significantly higher in the EN group than in the time-matched control group (p < 0.01), while LN had no effect. Positive main effects of time were found for the phosphorylations in Akt substrate of 160 kDa (AS160) Thr642 (p < 0.05), 5'-AMP-activated protein kinase (AMPK) Thr172 (p < 0.01), and acetyl-CoA carboxylase Ser79 (p < 0.01); however, no effect of nutrient intake was found for these. We showed that delayed nutrient intake could not increase muscle glycogen after endurance exercise which did not induce large glycogen depletion. The results also suggest that post-exercise muscle glycogen accumulation after nutrient intake might be partly influenced by Akt activation. Meanwhile, increased AS160 and AMPK activation by post-exercise fasting might not lead to glycogen accumulation.

Does impaired mitochondrial function affect insulin signaling and action in cultured human skeletal muscle cells?

2008 ◽  
Vol 294 (1) ◽  
pp. E97-E102 ◽  
Author(s):  
Audrey E. Brown ◽  
Matthias Elstner ◽  
Stephen J. Yeaman ◽  
Douglass M. Turnbull ◽  
Mark Walker
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Mitochondrial Respiration ◽  
Respiratory Function ◽  
Insulin Action ◽  
Human Skeletal Muscle ◽  
Human Skeletal Muscle Cells ◽  
Basal Glucose Uptake

Insulin-resistant type 2 diabetic patients have been reported to have impaired skeletal muscle mitochondrial respiratory function. A key question is whether decreased mitochondrial respiration contributes directly to the decreased insulin action. To address this, a model of impaired cellular respiratory function was established by incubating human skeletal muscle cell cultures with the mitochondrial inhibitor sodium azide and examining the effects on insulin action. Incubation of human skeletal muscle cells with 50 and 75 μM azide resulted in 48 ± 3% and 56 ± 1% decreases, respectively, in respiration compared with untreated cells mimicking the level of impairment seen in type 2 diabetes. Under conditions of decreased respiratory chain function, insulin-independent (basal) glucose uptake was significantly increased. Basal glucose uptake was 325 ± 39 pmol/min/mg (mean ± SE) in untreated cells. This increased to 669 ± 69 and 823 ± 83 pmol/min/mg in cells treated with 50 and 75 μM azide, respectively (vs. untreated, both P < 0.0001). Azide treatment was also accompanied by an increase in basal glycogen synthesis and phosphorylation of AMP-activated protein kinase. However, there was no decrease in glucose uptake following insulin exposure, and insulin-stimulated phosphorylation of Akt was normal under these conditions. GLUT1 mRNA expression remained unchanged, whereas GLUT4 mRNA expression increased following azide treatment. In conclusion, under conditions of impaired mitochondrial respiration there was no evidence of impaired insulin signaling or glucose uptake following insulin exposure in this model system.

scholarly journals Endurance training reduces the contraction-induced interleukin-6 mRNA expression in human skeletal muscle

2004 ◽  
Vol 287 (6) ◽  
pp. E1189-E1194 ◽  
Author(s):  
Christian P. Fischer ◽  
Peter Plomgaard ◽  
Anne K. Hansen ◽  
Henriette Pilegaard ◽  
Bengt Saltin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Acute Exercise ◽  
Glycogen Content ◽  
Knee Extensor ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Resting Muscle

Contracting skeletal muscle expresses large amounts of IL-6. Because 1) IL-6 mRNA expression in contracting skeletal muscle is enhanced by low muscle glycogen content, and 2) IL-6 increases lipolysis and oxidation of fatty acids, we hypothesized that regular exercise training, associated with increased levels of resting muscle glycogen and enhanced capacity to oxidize fatty acids, would lead to a less-pronounced increase of skeletal muscle IL-6 mRNA in response to acute exercise. Thus, before and after 10 wk of knee extensor endurance training, skeletal muscle IL-6 mRNA expression was determined in young healthy men ( n = 7) in response to 3 h of dynamic knee extensor exercise, using the same relative workload. Maximal power output, time to exhaustion during submaximal exercise, resting muscle glycogen content, and citrate synthase and 3-hydroxyacyl-CoA dehydrogenase enzyme activity were all significantly enhanced by training. IL-6 mRNA expression in resting skeletal muscle did not change in response to training. However, although absolute workload during acute exercise was 44% higher ( P < 0.05) after the training period, skeletal muscle IL-6 mRNA content increased 76-fold ( P < 0.05) in response to exercise before the training period, but only 8-fold ( P < 0.05, relative to rest and pretraining) in response to exercise after training. Furthermore, the exercise-induced increase of plasma IL-6 ( P < 0.05, pre- and posttraining) was not higher after training despite higher absolute work intensity. In conclusion, the magnitude of the exercise-induced IL-6 mRNA expression in contracting human skeletal muscle was markedly reduced by 10 wk of training.

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