Regulation of fuel metabolism by preexercise muscle glycogen content and exercise intensity

2004 ◽  
Vol 97 (6) ◽  
pp. 2275-2283 ◽  
Author(s):  
Melissa J. Arkinstall ◽  
Clinton R. Bruce ◽  
Sally A. Clark ◽  
Caroline A. Rickards ◽  
Louise M. Burke ◽  
...  

To date, the results of studies that have examined the effects of altering preexercise muscle glycogen content and exercise intensity on endogenous carbohydrate oxidation are equivocal. Differences in the training status of subjects between investigations may, in part, explain these inconsistent findings. Accordingly, we determined the relative effects of exercise intensity and carbohydrate availability on patterns of fuel utilization in the same subjects who performed a random order of four 60-min rides, two at 45% and two at 70% of peak O2 uptake (V̇o2 peak), after exercise-diet intervention to manipulate muscle glycogen content. Preexercise muscle glycogen content was 596 ± 43 and 202 ± 21 mmol/kg dry mass ( P < 0.001) for high-glycogen (HG) and low-glycogen (LG) conditions, respectively. Respiratory exchange ratio was higher for HG than LG during exercise at both 45% (0.85 ± 0.01 vs. 0.74 ± 0.01; P < 0.001) and 70% (0.90 ± 0.01 vs. 0.79 ± 0.01; P < 0.001) of V̇o2 peak. The contribution of whole body muscle glycogen oxidation to energy expenditure differed between LG and HG for exercise at both 45% (5 ± 2 vs. 45 ± 5%; P < 0.001) and 70% (25 ± 3 vs. 60 ± 3%; P < 0.001) of V̇o2 peak. Yet, despite marked differences in preexercise muscle glycogen content and its subsequent utilization, rates of plasma glucose disappearance were similar under all conditions. We conclude that, in moderately trained individuals, muscle glycogen availability (low vs. high) does not influence rates of plasma glucose disposal during either low- or moderate-intensity exercise.

2002 ◽  
Vol 282 (3) ◽  
pp. E688-E694 ◽  
Author(s):  
T. J. Stephens ◽  
Z.-P. Chen ◽  
B. J. Canny ◽  
B. J. Michell ◽  
B. E. Kemp ◽  
...  

The effect of prolonged moderate-intensity exercise on human skeletal muscle AMP-activated protein kinase (AMPK)α1 and -α2 activity and acetyl-CoA carboxylase (ACCβ) and neuronal nitric oxide synthase (nNOSμ) phosphorylation was investigated. Seven active healthy individuals cycled for 30 min at a workload requiring 62.8 ± 1.3% of peak O2consumption (V˙o 2 peak) with muscle biopsies obtained from the vastus lateralis at rest and at 5 and 30 min of exercise. AMPKα1 activity was not altered by exercise; however, AMPKα2 activity was significantly ( P < 0.05) elevated after 5 min (∼2-fold), and further elevated ( P < 0.05) after 30 min (∼3-fold) of exercise. ACCβ phosphorylation was increased ( P < 0.05) after 5 min (∼18-fold compared with rest) and increased ( P< 0.05) further after 30 min of exercise (∼36-fold compared with rest). Increases in AMPKα2 activity were significantly correlated with both increases in ACCβ phosphorylation and reductions in muscle glycogen content. Fat oxidation tended ( P = 0.058) to increase progressively during exercise. Muscle creatine phosphate was lower ( P < 0.05), and muscle creatine, calculated free AMP, and free AMP-to-ATP ratio were higher ( P < 0.05) at both 5 and 30 min of exercise compared with those at rest. At 30 min of exercise, the values of these metabolites were not significantly different from those at 5 min of exercise. Phosphorylation of nNOSμ was variable, and despite the mean doubling with exercise, statistically significance was not achieved ( P = 0.304). Western blots indicated that AMPKα2 was associated with both nNOSμ and ACCβ consistent with them both being substrates of AMPKα2 in vivo. In conclusion, AMPKα2 activity and ACCβ phosphorylation increase progressively during moderate exercise at ∼60% of V˙o 2 peak in humans, with these responses more closely coupled to muscle glycogen content than muscle AMP/ATP ratio.


Author(s):  
Ed A. Maunder ◽  
Helen E. Bradley ◽  
Colleen S. Deane ◽  
Adrian B. Hodgson ◽  
Michael Jones ◽  
...  

Altering dietary carbohydrate (CHO) intake modulates fuel utilization during exercise. However, there has been no systematic evaluation of metabolic responses to graded changes in short-term (< 1 week) dietary CHO intake. Thirteen active men performed interval running exercise combined with isocaloric diets over 3 days before evaluation of metabolic responses to 60-min running at 65% V̇O2max on three occasions. Diets contained lower (LOW, 2.40 ± 0.66 g CHO.kg-1.d-1, 21.3 ± 0.5% of energy intake [EI]), moderate (MOD, 4.98 ± 1.31 g CHO.kg-1.d-1, 46.3 ± 0.7% EI), or higher (HIGH, 6.48 ± 1.56 g CHO.kg-1.d-1, 60.5 ± 1.6% EI) CHO. Pre-exercise muscle glycogen content was lower in LOW (54.3 ± 26.4 mmol.kg-1 wet weight [ww]) compared to MOD (82.6 ± 18.8 mmol.kg-1 ww) and HIGH (80.4 ± 26.0 mmol.kg-1 ww, P<0.001; MOD vs. HIGH, P=0.85). Whole-body substrate oxidation, systemic responses, and muscle substrate utilization during exercise indicated increased fat and decreased CHO metabolism in LOW (RER: 0.81 ± 0.01) compared to MOD (RER 0.86 ± 0.01, P = 0.0005) and HIGH (RER: 0.88 ± 0.01, P < 0.0001; MOD vs. HIGH, P=0.14). Higher basal muscle expression of genes encoding proteins implicated in fat utilization was observed in LOW. In conclusion, muscle glycogen availability and subsequent metabolic responses to exercise were resistant to increases in dietary CHO intake from ~5.0 to ~6.5 g CHO.kg-1.d-1 (46% to 61% EI), while muscle glycogen, gene expression and metabolic responses were sensitive to more marked reductions in CHO intake (~2.4 g CHO.kg-1.d-1, ~21% EI).


2004 ◽  
Vol 287 (6) ◽  
pp. E1195-E1201 ◽  
Author(s):  
Theodore W. Zderic ◽  
Simon Schenk ◽  
Christopher J. Davidson ◽  
Lauri O. Byerley ◽  
Edward F. Coyle

We have recently reported that, during moderate intensity exercise, low muscle glycogen concentration and utilization caused by a high-fat diet is associated with a marked increase in fat oxidation with no effect on plasma glucose uptake (Rd glucose). It is our hypothesis that this increase in fat oxidation compensates for low muscle glycogen, thus preventing an increase in Rd glucose. Therefore, the purpose of this study was to determine whether low muscle glycogen availability increases Rd glucose under conditions of impaired fat oxidation. Six cyclists exercised at 50% peak O2 consumption (V̇o2 peak) for 1 h after 2 days on either a high-fat (HF, 60% fat, 24% carbohydrate) or control (CON, 22% fat, 65% carbohydrate) diet to manipulate muscle glycogen to low and normal levels, respectively. Two hours before the start of exercise, subjects ingested 80 mg of propanolol (βB), a nonselective β-adrenergic receptor blocker, to impair fat oxidation during exercise. HF significantly decreased calculated muscle glycogen oxidation ( P < 0.05), and this decrease was partly compensated for by an increase in fat oxidation ( P < 0.05), accompanied by an increase in whole body lipolysis ( P < 0.05), despite the presence of βB. Although HF increased fat oxidation, plasma glucose appearance rate, Rd glucose, and glucose clearance rate were also significantly increased by 13, 15, and 26%, respectively (all P < 0.05). In conclusion, when lipolysis and fat oxidation are impaired, in this case by βB, fat oxidation cannot completely compensate for a reduction in muscle glycogen utilization, and consequently plasma glucose turnover increases. These findings suggest that there is a hierarchy of substrate compensation for reduced muscle glycogen availability after a high-fat, low-carbohydrate diet, with fat being the primary and plasma glucose the secondary compensatory substrate. This apparent hierarchy likely serves to protect against hypoglycemia when endogenous glucose availability is low.


1995 ◽  
Vol 5 (1) ◽  
pp. 25-36 ◽  
Author(s):  
Laurie H.G. Rauch ◽  
Ian Rodger ◽  
Gary R. Wilson ◽  
Judy D. Belonje ◽  
Steven C. Dennis ◽  
...  

This study compared the effects of supplementing the normal diets of 8 endurance-trained cyclists with additional carbohydrate (CHO), in the form of potato starch, for 3 days on muscle glycogen utilization and performance during a 3-hr cycle ride. On two occasions prior to the trial, the subjects ingested in random order either their normal CHO intake of 6.15 ± 0.23 g/kg body mass/day or a high-CHO diet of 10.52 ± 0.57 g/kg body mass/day. The trial consisted of 2 hr of cycling at ~75% ofwith five 60-s sprints at 100%at 20-min intervals, followed by a 60-min performance ride. Increasing CHO intake by 72 ± 9% for 3 days prior to the trial elevated preexercise muscle glycogen contents, improved power output, and extended the distance covered in 1 hr. Muscle glycogen contents were similar at the end of the 3-hr trial, indicating a greater utilization of glycogen when subjects were CHO loaded, which may have been responsible for their improved cycling performance.


1996 ◽  
Vol 270 (2) ◽  
pp. E336-E343 ◽  
Author(s):  
J. A. Tuominen ◽  
P. Ebeling ◽  
R. Bourey ◽  
L. Koranyi ◽  
A. Lamminen ◽  
...  

Acute physical exercise enhances insulin sensitivity in healthy subjects. We examined the effect of a 42-km marathon run on insulin sensitivity and lipid oxidation in 19 male runners. In the morning after the marathon run, basal serum free fatty acid concentration was 2.2-fold higher, muscle glycogen content 37% lower (P < 0.01), glycogen synthase fractional activity 56% greater (P < 0.01), and glucose oxidation reduced by 43% (P < 0.01), whereas lipid oxidation was increased by 55% (P < 0.02) compared with the control study. During euglycemic-hyperinsulinemic clamp, whole body glucose disposal was decreased by 12% (P < 0.01) because of a 36% lower glucose oxidation rate (P < 0.05), whereas the rate of lipid oxidation was 10-fold greater (P < 0.02) than in the control study. After the marathon, muscle glycogen content correlated positively with lipid oxidation (r = 0.60, P < 0.05) and maximal aerobic power (Vo2peak; r = 0.61, P < 0.05). Vo2peak correlated positively with basal lipid oxidation (r = 0.57, P < 0.05). In conclusion, 1) after the marathon run, probably because of increased lipid oxidation, the insulin-stimulated glucose disposal is decreased despite muscle glycogen depletion and the activation of glycogen synthase; 2) the contribution of lipid oxidation in energy expenditure is increased in proportion to physical fitness; 3) these adaptations of fuel homeostasis may contribute to the maintenance of physical performance after prolonged exercise.


2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S147
Author(s):  
M J. Arkinstall ◽  
P J. Saunders ◽  
C R. Bruce ◽  
C A. Rickards ◽  
S A. Clark ◽  
...  

2009 ◽  
Vol 106 (1) ◽  
pp. 91-100 ◽  
Author(s):  
Amanda P. Waller ◽  
George J. F. Heigenhauser ◽  
Raymond J. Geor ◽  
Lawrence L. Spriet ◽  
Michael I. Lindinger

We hypothesized that postexercise rehydration using a hypotonic electrolyte solution will increase the rate of recovery of whole body hydration, and that this is associated with increased muscle glycogen and electrolyte recovery in horses. Gluteus medius biopsies and jugular venous blood were sampled from six exercise-conditioned Standardbreds on two separate occasions, at rest and for 24 h following a competitive exercise test (CET) designed to simulate the speed and endurance test of a 3-day event. After the CETs, horses were given water ad libitum, and either a hypotonic commercial electrolyte solution (electrolyte) via nasogastric tube, followed by a typical hay/grain meal, or a hay/grain meal alone (control). The CET resulted in decreased total body water and muscle glycogen concentration of 8.4 ± 0.3 liters and 22.6%, respectively, in the control treatment, and 8.2 ± 0.4 liters and 21.9% in the electrolyte treatment. Electrolyte resulted in an enhanced rate of muscle glycogen resynthesis and faster restoration of hydration (as evidenced by faster recovery of plasma protein concentration, maintenance of plasma osmolality, and greater muscle intracellular fluid volume) during the recovery period compared with control. There were no differences in muscle Na, K, Cl, or Mg contents between the two treatments. It is concluded that oral administration of a hypotonic electrolyte solution after prolonged moderate-intensity exercise enhanced the rate of muscle glycogen resynthesis during the recovery period compared with control. It is speculated that postexercise dehydration may be one key contributor to the slow muscle glycogen replenishment in horses.


Aging Cell ◽  
2021 ◽  
Vol 20 (2) ◽  
Author(s):  
Carolyn Chee ◽  
Chris E. Shannon ◽  
Aisling Burns ◽  
Anna L. Selby ◽  
Daniel Wilkinson ◽  
...  

1996 ◽  
Vol 7 (1) ◽  
pp. 52-54 ◽  
Author(s):  
P. Mariani ◽  
K. Lundström ◽  
U. Gustafsson ◽  
A. -C. Enfält ◽  
R. K. Juneja ◽  
...  

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