scholarly journals Repeated bouts of high-intensity exercise and muscle glycogen sparing in the rat

2003 ◽  
Vol 206 (13) ◽  
pp. 2159-2166 ◽  
Author(s):  
G. Raja
2021 ◽  
Author(s):  
Jeppe F. Vigh-Larsen ◽  
Niels Ørtenblad ◽  
Lawrence L. Spriet ◽  
Kristian Overgaard ◽  
Magni Mohr

1999 ◽  
Vol 165 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Balsom ◽  
Gaitanos ◽  
Söderlund ◽  
Ekblom

2019 ◽  
Vol 120 (1) ◽  
pp. 127-135 ◽  
Author(s):  
Hamid Mohebbi ◽  
Iain T. Campbell ◽  
Marie A. Keegan ◽  
James J. Malone ◽  
Andrew T. Hulton ◽  
...  

Abstract Purpose The effect of hyperglycaemia with and without additional insulin was explored at a low and high intensity of exercise (40% vs 70% VO2peak) on glucose utilization (GUR), carbohydrate oxidation, non-oxidative glucose disposal (NOGD), and muscle glycogen. Methods Eight healthy trained males were exercised for 120 min in four trials, twice at 40% VO2peak and twice at 70% VO2peak, while glucose was infused intravenously (40%G; 70%G) at rates to “clamp” blood glucose at 10 mM. On one occasion at each exercise intensity, insulin was also infused at 40 mU/m2/per min (i.e. 40%GI and 70%GI). The glucose and insulin infusion began 30 min prior to exercise and throughout exercise. A muscle biopsy was taken at the end of exercise for glycogen analysis. Results Hyperglycaemia significantly elevated plasma insulin concentration (p < 0.001), although no difference was observed between the exercise intensities. Insulin infusion during both mild and severe exercise resulted in increased insulin concentrations (p < 0.01) and GUR (p < 0.01) compared with glucose (40%GI by 25.2%; 70%GI by 26.2%), but failed to significantly affect carbohydrate, fat and protein oxidation. NOGD was significantly higher for GI trials at both intensities (p < 0.05) with storage occurring during both lower intensities (62.7 ± 19.6 g 40%GI; 127 ± 20.7 g 40%GI) and 70%GI (29.0 ± 20.0 g). Muscle glycogen concentrations were significantly depleted from rest (p < 0.01) after all four trials. Conclusion Hyperinsulinaemia in the presence of hyperglycaemia during both low- and high-intensity exercise promotes GUR and NOGD, but does not significantly affect substrate oxidation.


2000 ◽  
Vol 88 (1) ◽  
pp. 219-225 ◽  
Author(s):  
Jeffrey F. Horowitz ◽  
Ricardo Mora-Rodriguez ◽  
Lauri O. Byerley ◽  
Edward F. Coyle

This investigation determined whether ingestion of a tolerable amount of medium-chain triglycerides (MCT; ∼25 g) reduces the rate of muscle glycogen use during high-intensity exercise. On two occasions, seven well-trained men cycled for 30 min at 84% maximal O2 uptake. Exactly 1 h before exercise, they ingested either 1) carbohydrate (CHO; 0.72 g sucrose/kg) or 2) MCT+CHO [0.36 g tricaprin (C10:0)/kg plus 0.72 g sucrose/kg]. The change in glycogen concentration was measured in biopsies taken from the vastus lateralis before and after exercise. Additionally, glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the rate of glucose disappearance from plasma (Rd glucose), as measured by stable isotope dilution techniques. The change in muscle glycogen concentration was not different during MCT+CHO and CHO (42.0 ± 4.6 vs. 38.8 ± 4.0 μmol glucosyl units/g wet wt). Furthermore, calculated glycogen oxidation was also similar (331 ± 18 vs. 329 ± 15 μmol ⋅ kg− 1 ⋅ min− 1). The coingestion of MCT+CHO did increase ( P < 0.05) Rd glucose at rest compared with CHO (26.9 ± 1.5 vs. 20.7 ± 0.7 μmol ⋅kg− 1 ⋅ min− 1), yet during exercise Rd glucose was not different during the two trials. Therefore, the addition of a small amount of MCT to a preexercise CHO meal did not reduce muscle glycogen oxidation during high-intensity exercise, but it did increase glucose uptake at rest.


2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Kenya Takahashi ◽  
Yu Kitaoka ◽  
Yutaka Matsunaga ◽  
Hideo Hatta

Objective High-intensity exercise, which increases blood lactate concentration, is known as an effective method to induce mitochondrial biogenesis compared to traditional endurance exercise. In addition, it has been reported that lactate acts as a signaling molecule inducing mitochondrial biogenesis. Therefore, we hypothesized that efficacy of high-intensity exercise is partly induced by lactate. The purpose of this study was to investigate the effects of lactate administration on signaling related to mitochondrial biogenesis. Methods 8-week-old male ICR mice were used in this study. Mice were intraperitoneally administrated phosphate buffered saline (PBS) or 1 g/kg of body weight of sodium lactate. Immediately after the administration, mice were kept sedentary or performed treadmill exercise (20 m/min) for 60 min. Hence, there are the following four groups in this study: the PBS-sedentary, the Lactate-sedentary, the PBS-exercised and the Lactate-exercised. The blood, and the soleus and the plantaris muscles were harvested immediately after the rest or exercise. Nucleus and mitochondria were isolated to assess the localization of p53. Two-way ANOVA (Lactate x Exercise) was performed for statistical analysis. Results We first measured blood substrates and muscle glycogen concentrations. Lactate administration significantly increased blood lactate and plasma free fatty acid concentrations. Exercise significantly decreased glycogen concentration both in the soleus and the plantaris muscles. Furthermore, lactate administration significantly decreased muscle glycogen concentration only in the soleus muscle. To clarify the effects of lactate administration on intramuscular signaling, we assessed kinases related to mitochondrial biogenesis. Main effect of exercise was observed in phosphorylation state of AMPK, ACC, p38 MAPK, and CaMKII in the soleus and the plantaris muscles. There was a trend of negative effect of lactate in CaMKII phosphorylation in the soleus muscle. However, there was no effect of lactate administration on the other kinases. We also investigated phosphorylation and localization of p53. As a result, lactate administration tended to increase p53 phosphorylation in the plantaris muscle. However, p53 was not translocated to nucleus or mitochondria. Conclusions Lactate administration affected plasma FFA concentration and muscle glycogen concentration. However, acute lactate administration did not dramatically change intracellular signaling assessed in this study. 


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