scholarly journals Effects of short-term graded dietary carbohydrate intake on intramuscular and whole-body metabolism during moderate-intensity exercise

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 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.


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 ◽  
...  

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.


2000 ◽  
Vol 88 (5) ◽  
pp. 1777-1790 ◽  
Author(s):  
Raymond J. Geor ◽  
Kenneth W. Hinchcliff ◽  
Laura Jill McCutcheon ◽  
Richard A. Sams

This study examined the effects of preexercise glucose administration, with and without epinephrine infusion, on carbohydrate metabolism in horses during exercise. Six horses completed 60 min of treadmill exercise at 55 ± 1% maximum O2 uptake 1) 1 h after oral administration of glucose (2 g/kg; G trial); 2) 1 h after oral glucose and with an intravenous infusion of epinephrine (0.2 μmol ⋅ kg− 1 ⋅ min− 1; GE trial) during exercise, and 3) 1 h after water only (F trial). Glucose administration (G and GE) caused hyperinsulinemia and hyperglycemia (∼8 mM). In GE, plasma epinephrine concentrations were three- to fourfold higher than in the other trials. Compared with F, the glucose rate of appearance was ∼50% and ∼33% higher in G and GE, respectively, during exercise. The glucose rate of disappearance was ∼100% higher in G than in F, but epinephrine infusion completely inhibited the increase in glucose uptake associated with glucose administration. Muscle glycogen utilization was higher in GE [349 ± 44 mmol/kg dry muscle (dm)] than in F (218 ± 28 mmol/kg dm) and G (201 ± 35 mmol/kg dm). We conclude that 1) preexercise glucose augments utilization of plasma glucose in horses during moderate-intensity exercise but does not alter muscle glycogen usage and 2) increased circulating epinephrine inhibits the increase in glucose rate of disappearance associated with preexercise glucose administration and increases reliance on muscle glycogen for energy transduction.


2013 ◽  
Vol 38 (11) ◽  
pp. 1162-1165 ◽  
Author(s):  
Kym J. Guelfi ◽  
Rhiannon E. Halse

The effect of exercise on appetite and appetite-related hormones during pregnancy is not known. This study found that 30 min of moderate-intensity stationary cycling transiently attenuated hunger and increased fullness in late gestational women (n = 12). Exercise did not affect perceived appetite or appetite-related hormones in response to subsequent caloric consumption. These observations suggest that appetite responses do not intrinsically compensate for the additional energy expenditure induced by exercise, at least in the short term.


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.


2004 ◽  
Vol 36 (Supplement) ◽  
pp. S18
Author(s):  
Michael J. Carper ◽  
Samantha A. Whitman ◽  
Scott R. Richmond ◽  
Luke S. Acree ◽  
Brett D. Olson ◽  
...  

2017 ◽  
Vol 38 (10) ◽  
pp. 1828-1838 ◽  
Author(s):  
Sanna M Honkala ◽  
Jarkko Johansson ◽  
Kumail K Motiani ◽  
Jari-Joonas Eskelinen ◽  
Kirsi A Virtanen ◽  
...  

Brain insulin-stimulated glucose uptake (GU) is increased in obese and insulin resistant subjects but normalizes after weight loss along with improved whole-body insulin sensitivity. Our aim was to study whether short-term exercise training (moderate intensity continuous training (MICT) or sprint interval training (SIT)) alters substrates for brain energy metabolism in insulin resistance. Sedentary subjects ( n = 21, BMI 23.7–34.3 kg/m2, age 43–55 y) with insulin resistance were randomized into MICT ( n = 11, intensity≥60% of VO2peak) or SIT ( n = 10, all-out) groups for a two-week training intervention. Brain GU during insulin stimulation and fasting brain free fatty acid uptake (FAU) was measured using PET. At baseline, brain GU was positively associated with the fasting insulin level and negatively with the whole-body insulin sensitivity. The whole-body insulin sensitivity improved with both training modes (20%, p = 0.007), while only SIT led to an increase in aerobic capacity (5%, p = 0.03). SIT also reduced insulin-stimulated brain GU both in global cortical grey matter uptake (12%, p = 0.03) and in specific regions ( p < 0.05, all areas except the occipital cortex), whereas no changes were observed after MICT. Brain FAU remained unchanged after the training in both groups. These findings show that short-term SIT effectively decreases insulin-stimulated brain GU in sedentary subjects with insulin resistance.


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