Frequent Carbohydrate Ingestion Reduces Muscle Glycogen Depletion and Postpones Fatigue Relative to a Single Bolus

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.

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.


1986 ◽  
Vol 60 (5) ◽  
pp. 1518-1523 ◽  
Author(s):  
S. H. Constable ◽  
R. J. Favier ◽  
J. O. Holloszy

Phosphorylase activation reverses during prolonged contractile activity. Our first experiment was designed to determine whether this loss of ability to activate phosphorylase by stimulation of muscle contraction persists following exercise. Phosphorylase activation by stimulation of muscle contraction was markedly inhibited in rats 25 min after exhausting exercise. To evaluate the role of glycogen depletion, we accelerated glycogen utilization by nicotinic acid administration. A large difference in muscle glycogen depletion during exercise of the same duration did not influence the blunting of phosphorylase activation. Phosphorylase activation by stimulation of contraction was more severely inhibited following prolonged exercise than after a shorter bout of exercise under conditions that resulted in the same degree of glycogen depletion. A large difference in muscle glycogen repletion during 90 min of recovery was not associated with a significant difference in the ability of muscle stimulation to activate phosphorylase, which was still significantly blunted. Phosphorylase activation by epinephrine was also markedly inhibited in muscle 25 min after strenuous exercise but had recovered completely in glycogen-repleted muscle 90 min after exercise. These results provide evidence that an effect of exercise other than glycogen depletion is involved in causing the inhibition of phosphorylase activation; however, they do not rule out the possibility that glycogen depletion also plays a role in this process.


1988 ◽  
Vol 57 (4) ◽  
pp. 482-489 ◽  
Author(s):  
Timothy D. Noakes ◽  
Estelle V. Lambert ◽  
Michael I. Lambert ◽  
Penelope S. McArthur ◽  
Kathryn H. Myburgh ◽  
...  

1977 ◽  
Vol 43 (4) ◽  
pp. 695-699 ◽  
Author(s):  
D. L. Costill ◽  
E. Coyle ◽  
G. Dalsky ◽  
W. Evans ◽  
W. Fink ◽  
...  

Seven men were studied during 30 min of treadmill exercise (approximately 70% VO2 max) to determine the effects of increased availability of plasma free fatty acids (FFA) and elevated plasma insulin on the utilization of muscle glycogen. This elevation of plasma FFA (1.01 mmol/1) with heparin (2,000 units) decreased the rate of muscle glycogen depletion by 40% as compared to the control experiment (FFA = 0.21 mmol/1). The ingestion of 75 g of glucose 45 min before exercise produced a 3.3-fold increase in plasma insulin and a 38% rise in plasma glucose at 0 min of exercise. Subsequent exercise increased muscle glycogen utilization and total carbohydrate (CHO) oxidation 17 and 13%, respectively, when compared to the control trial. This elevation of plasma insulin produced hypoglycemia (less than 3.5 mmol/1) in most subjects throughout the exercise. These data illustrate the regulatory influence of both plasma insulin and FFA on the rate of CHO usage during prolonged severe muscular activity.


2000 ◽  
Vol 278 (1) ◽  
pp. E65-E75 ◽  
Author(s):  
Anna Casey ◽  
Rob Mann ◽  
Katie Banister ◽  
John Fox ◽  
Peter G. Morris ◽  
...  

This study investigated the effect of carbohydrate (CHO) ingestion on postexercise glycogen resynthesis, measured simultaneously in liver and muscle ( n = 6) by 13C magnetic resonance spectroscopy, and subsequent exercise capacity ( n = 10). Subjects cycled at 70% maximal oxygen uptake for 83 ± 8 min on six separate occasions. At the end of exercise, subjects ingested 1 g/kg body mass (BM) glucose, sucrose, or placebo (control). Resynthesis of glycogen over a 4-h period after treatment ingestion was measured on the first three occasions, and subsequent exercise capacity was measured on occasions four through six. No glycogen was resynthesized during the control trial. Liver glycogen resynthesis was evident after glucose (13 ± 8 g) and sucrose (25 ± 5 g) ingestion, both of which were different from control ( P < 0.01). No significant differences in muscle glycogen resynthesis were found among trials. A relationship between the CHO load (g) and change in liver glycogen content (g) was evident after 30, 90, 150, and 210 min of recovery ( r = 0.59–0.79, P< 0.05). Furthermore, a modest relationship existed between change in liver glycogen content (g) and subsequent exercise capacity ( r= 0.53, P < 0.05). However, no significant difference in mean exercise time was found (control: 35 ± 5, glucose: 40 ± 5, and sucrose: 46 ± 6 min). Therefore, 1 g/kg BM glucose or sucrose is sufficient to initiate postexercise liver glycogen resynthesis, which contributes to subsequent exercise capacity, but not muscle glycogen resynthesis.


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.


2001 ◽  
Vol 91 (5) ◽  
pp. 2125-2134 ◽  
Author(s):  
Melissa J. Arkinstall ◽  
Clinton R. Bruce ◽  
Vasilis Nikolopoulos ◽  
Andrew P. Garnham ◽  
John A. Hawley

The effects of carbohydrate or water ingestion on metabolism were investigated in seven male subjects during two running and two cycling trials lasting 60 min at individual lactate threshold using indirect calorimetry, U-14C-labeled tracer-derived measures of the rates of oxidation of plasma glucose, and direct determination of mixed muscle glycogen content from the vastus lateralis before and after exercise. Subjects ingested 8 ml/kg body mass of either a 6.4% carbohydrate-electrolyte solution (CHO) or water 10 min before exercise and an additional 2 ml/kg body mass of the same fluid after 20 and 40 min of exercise. Plasma glucose oxidation was greater with CHO than with water during both running (65 ± 20 vs. 42 ± 16 g/h; P < 0.01) and cycling (57 ± 16 vs. 35 ± 12 g/h; P < 0.01). Accordingly, the contribution from plasma glucose oxidation to total carbohydrate oxidation was greater during both running (33 ± 4 vs. 23 ± 3%; P < 0.01) and cycling (36 ± 5 vs. 22 ± 3%; P < 0.01) with CHO ingestion. However, muscle glycogen utilization was not reduced by the ingestion of CHO compared with water during either running (112 ± 32 vs. 141 ± 34 mmol/kg dry mass) or cycling (227 ± 36 vs. 216 ± 39 mmol/kg dry mass). We conclude that, compared with water, 1) the ingestion of carbohydrate during running and cycling enhanced the contribution of plasma glucose oxidation to total carbohydrate oxidation but 2) did not attenuate mixed muscle glycogen utilization during 1 h of continuous submaximal exercise at individual lactate threshold.


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