Carbohydrate ingestion and muscle glycogen depletion during marathon and ultramarathon racing

1988 ◽  
Vol 57 (4) ◽  
pp. 482-489 ◽  
Author(s):  
Timothy D. Noakes ◽  
Estelle V. Lambert ◽  
Michael I. Lambert ◽  
Penelope S. McArthur ◽  
Kathryn H. Myburgh ◽  
...  
Author(s):  
Lee M. Margolis ◽  
Marques A. Wilson ◽  
Claire C. Whitney ◽  
Christopher T. Carrigan ◽  
Nancy E. Murphy ◽  
...  

Abstract Background The effects of low muscle glycogen on molecular markers of protein synthesis and myogenesis before and during aerobic exercise with carbohydrate ingestion is unclear. The purpose of this study was to determine the effects of initiating aerobic exercise with low muscle glycogen on mTORC1 signaling and markers of myogenesis. Methods Eleven men completed two cycle ergometry glycogen depletion trials separated by 7-d, followed by randomized isocaloric refeeding for 24-h to elicit low (LOW; 1.5 g/kg carbohydrate, 3.0 g/kg fat) or adequate (AD; 6.0 g/kg carbohydrate, 1.0 g/kg fat) glycogen. Participants then performed 80-min of cycle ergometry (64 ± 3% VO2peak) while ingesting 146 g carbohydrate. mTORC1 signaling (Western blotting) and gene transcription (RT-qPCR) were determined from vastus lateralis biopsies before glycogen depletion (baseline, BASE), and before (PRE) and after (POST) exercise. Results Regardless of treatment, p-mTORC1Ser2448, p-p70S6KSer424/421, and p-rpS6Ser235/236 were higher (P < 0.05) POST compared to PRE and BASE. PAX7 and MYOGENIN were lower (P < 0.05) in LOW compared to AD, regardless of time, while MYOD was lower (P < 0.05) in LOW compared to AD at PRE, but not different at POST. Conclusion Initiating aerobic exercise with low muscle glycogen does not affect mTORC1 signaling, yet reductions in gene expression of myogenic regulatory factors suggest that muscle recovery from exercise may be reduced.


2020 ◽  
Vol 30 (3) ◽  
pp. 203-209
Author(s):  
Campbell Menzies ◽  
Michael Wood ◽  
Joel Thomas ◽  
Aaron Hengist ◽  
Jean-Philippe Walhin ◽  
...  

The timing of carbohydrate ingestion and how this influences net muscle glycogen utilization and fatigue has only been investigated in prolonged cycling. Past findings may not translate to running because each exercise mode is distinct both in the metabolic response to carbohydrate ingestion and in the practicalities of carbohydrate ingestion. To this end, a randomized, cross-over design was employed to contrast ingestion of the same sucrose dose either at frequent intervals (15 × 5 g every 5 min) or at a late bolus (1 × 75 g after 75 min) during prolonged treadmill running to exhaustion in six well-trained runners ( 61 ± 4 ml·kg−1·min−1). The muscle glycogen utilization rate was lower in every participant over the first 75 min of running (Δ 0.51 mmol·kg dm−1·min−1; 95% confidence interval [−0.02, 1.04] mmol·kg dm−1·min−1) and, subsequently, all were able to run for longer when carbohydrate had been ingested frequently from the start of exercise compared with when carbohydrate was ingested as a single bolus toward the end of exercise (105.6 ± 3.0 vs. 96.4 ± 5.0 min, respectively; Δ 9.3 min, 95% confidence interval [2.8, 15.8] min). A moderate positive correlation was apparent between the magnitude of glycogen sparing over the first 75 min and the improvement in running capacity (r = .58), with no significant difference in muscle glycogen concentrations at the point of exhaustion. This study indicates that failure to ingest carbohydrates from the outset of prolonged running increases reliance on limited endogenous muscle glycogen stores—the ergolytic effects of which cannot be rectified by subsequent carbohydrate ingestion late in exercise.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 644-644
Author(s):  
Lee Margolis ◽  
Marques Wilson ◽  
Claire Whitney ◽  
Christopher Carrigan ◽  
Nancy Murphy ◽  
...  

Abstract Objectives Maintaining low muscle glycogen content during recovery from aerobic exercise with low carbohydrate, high fat feeding has been shown to reduce insulin-mediated anabolic signaling compared to high carbohydrate feeding. The effects of low muscle glycogen content on intracellular regulators of muscle mass before and after aerobic exercise with carbohydrate ingestion is unclear. This study examined the effect of initiating aerobic exercise with low muscle glycogen content on postprandial insulin-dependent muscle anabolic signaling and myogenesis. Methods Twelve men (mean ± SD, age: 21 ± 4 y; body mass: 83 ± 11 kg; VO2peak: 44 ± 3 mL/kg/min) completed 2 cycle ergometry glycogen depletion trials separated by 7 d, followed by a 24-h period of isocaloric high fat (1.5 g/kg carbohydrate, 3.0 g/kg fat) or high carbohydrate (6.0 g/kg carbohydrate, 1.0 g/kg fat) refeeding to elicit low (LOW; 217 ± 103 mmol/kg dry wt) or adequate (AD; 396 ± 70 mmol/kg dry wt) glycogen content in randomized order. Participants then performed 80 min of cycle ergometry (64 ± 3% VO2peak) while ingesting 146 g of carbohydrate. Protein signaling (Western blotting) and gene transcription (RT-qPCR) were determined from vastus lateralis biopsies obtained before glycogen depletion (baseline, BASE), and before (PRE) and after (POST) exercise. Data presented as fold change relative to BASE for LOW and AD. Results Independent of time, carbohydrate sensing p-AMPKThr172 was higher (P &lt; 0.05) in LOW compared to AD, while p-p38MAPKThr180/Tyr182 was higher (P &lt; 0.05) in LOW at POST, but not different PRE. Insulin sensitive p-AKTThr473 was higher (P &lt; 0.05) in AD compared to LOW, regardless of time. Anabolic regulators, p-mTORC1Ser2448, p-p70S6KSer424/421, and p-rpS6Ser235/236 were higher (P &lt; 0.05) POST compared to PRE and BASE, independent of group. Regulators of myogenesis, MYOD and MYOGENIN were lower (P &lt; 0.05) in LOW compared to AD, regardless of time, while PAX7 was lower (P &lt; 0.05) in LOW compared to AD at PRE, but not different POST. Conclusions Initiating aerobic exercise with low muscle glycogen content does not appear to affect downstream insulin-dependent anabolic signaling, yet reductions in myogenic regulator factors suggest muscle repair and remodeling in recovery from exercise may be impaired. Funding Sources Work supported by DHP JPC-5/MOMRP; authors’ views not official U.S. Army or DoD policy.


Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2555 ◽  
Author(s):  
Takahashi ◽  
Matsunaga ◽  
Banjo ◽  
Takahashi ◽  
Sato ◽  
...  

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.


1988 ◽  
Vol 65 (4) ◽  
pp. 1553-1555 ◽  
Author(s):  
M. Hargreaves ◽  
C. A. Briggs

Five male cyclists were studied during 2 h of cycle ergometer exercise (70% VO2 max) on two occasions to examine the effect of carbohydrate ingestion on muscle glycogen utilization. In the experimental trial (CHO) subjects ingested 250 ml of a glucose polymer solution containing 30 g of carbohydrate at 0, 30, 60, and 90 min of exercise; in the control trial (CON) they received an equal volume of a sweet placebo. No differences between trials were seen in O2 uptake or heart rate during exercise. Venous blood glucose was similar before exercise in both trials, but, on average, was higher during exercise in CHO [5.2 +/- 0.2 (SE) mmol/l] compared with CON (4.8 +/- 0.1, P less than 0.05). Plasma insulin levels were similar in both trials. Muscle glycogen levels were also similar in CHO and CON both before and after exercise; accordingly, there was no difference between trials in the amount of glycogen used during the 2 h of exercise (CHO = 62.8 +/- 10.1 mmol/kg wet wt, CON = 56.9 +/- 10.1). The results of this study indicate that carbohydrate ingestion does not influence the utilization of muscle glycogen during prolonged strenuous exercise.


1984 ◽  
Vol 247 (5) ◽  
pp. R880-R883 ◽  
Author(s):  
S. H. Constable ◽  
J. C. Young ◽  
M. Higuchi ◽  
J. O. Holloszy

This study was undertaken to determine whether glycogen resynthesis can occur in glycogen-depleted muscles in response to glucose feeding during prolonged exercise. Rats were exercised for 40 min with a treadmill running program designed to deplete muscle glycogen. One group was studied immediately after the glycogen-depletion exercise. A second group was given 1 g glucose by stomach tube and exercised for an additional 90 min at a running speed of 22 m/min on a treadmill set at an 8 degree incline; they were given additional 1-g glucose feedings after 30 and 60 min of running. The initial 40-min run resulted in liver glycogen depletion, large decreases in plasma glucose and insulin concentrations, and a marked lowering of muscle glycogen. The glucose feedings resulted in greater than twofold increases in the concentrations of glucose and insulin in plasma, and of glycogen in leg muscles, during the 90 min of running. No repletion of liver glycogen occurred. These results provide evidence that glycogen resynthesis can occur in glycogen-depleted muscle despite continued moderate intensity exercise if sufficient glucose is made available.


1996 ◽  
Vol 81 (4) ◽  
pp. 1495-1500 ◽  
Author(s):  
Adrianus J. Van Den Bergh ◽  
Sibrand Houtman ◽  
Arend Heerschap ◽  
Nancy J. Rehrer ◽  
Hendrikus J. Van Den Boogert ◽  
...  

Van Den Bergh, Adrianus J., Sibrand Houtman, Arend Heerschap, Nancy J. Rehrer, Hendrikus J. Van Den Boogert, Berend Oeseburg, and Maria T. E. Hopman. Muscle glycogen recovery after exercise during glucose and fructose intake monitored by13C-NMR. J. Appl. Physiol. 81(4): 1495–1500, 1996.—The purpose of this study was to examine muscle glycogen recovery with glucose feeding (GF) compared with fructose feeding (FF) during the first 8 h after partial glycogen depletion by using13C-nuclear magnetic resonance (NMR) on a clinical 1.5-T NMR system. After measurement of the glycogen concentration of the vastus lateralis (VL) muscle in seven male subjects, glycogen stores of the VL were depleted by bicycle exercise. During 8 h after completion of exercise, subjects were orally given either GF or FF while the glycogen content of the VL was monitored by13C-NMR spectroscopy every second hour. The muscular glycogen concentration was expressed as a percentage of the glycogen concentration measured before exercise. The glycogen recovery rate during GF (4.2 ± 0.2%/h) was significantly higher ( P < 0.05) compared with values during FF (2.2 ± 0.3%/h). This study shows that 1) muscle glycogen levels are perceptible by 13C-NMR spectroscopy at 1.5 T and 2) the glycogen restoration rate is higher after GF compared with after FF.


1983 ◽  
Vol 54 (2) ◽  
pp. 470-474 ◽  
Author(s):  
G. J. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones

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


1983 ◽  
Vol 72 (5) ◽  
pp. 1605-1610 ◽  
Author(s):  
C Bogardus ◽  
P Thuillez ◽  
E Ravussin ◽  
B Vasquez ◽  
M Narimiga ◽  
...  

2019 ◽  
Vol 51 (Supplement) ◽  
pp. 374-375
Author(s):  
Keisuke Shiose ◽  
Yosuke Yamada ◽  
Keiko Motonaga ◽  
Hideyuki Takahashi

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