Effects of training, exercise and diet on muscle glycolysis and liver gluconeogenesis

Huston, R. L.; Weiser, Philip C.; Dohm, G. Lynis; Askew, E. W.; Boyd, Joe B.

doi:10.1016/0024-3205(75)90486-5

Cited by 24 publications

(10 citation statements)

References 17 publications

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“…The effect of training on PEPCK and PC has been assessed in several studies (19,20,34,41). However, no change in the maximal activity of PEPCK (19,20,34,41) and PC (19,20) and in PEPCK mRNA content (19) was reported after training.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of increased gluconeogenesis from alanine in rat isolated hepatocytes after endurance training

Burelle

Fillipi

Péronnet

et al. 2000

American Journal of Physiology-Endocrinology and Metabolism

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This work aimed at further investigating the mechanisms by which liver gluconeogenic capacity from alanine is improved after training in rats, with an isolated hepatocyte model. Compared with controls in hepatocytes from trained rats incubated with gluconeogenic precursors (20 mM), the glucogenic flux (J(glucose)) was increased by 64% from alanine (vs. 21% for glycerol, 18% for lactate-pyruvate 10:1, and 10% for dihydroxyacetone). Maximal intracellular alanine accumulation capacity was also increased by 50%. Further experiments conducted on perifused hepatocytes showed that the putative adaptation at the level of the phosphoenolpyruvate-pyruvate cycle, which could be involved in the increased J(glucose) from lactate-pyruvate, was not involved in the increased J(glucose) from alanine after training. For alanine concentration higher than approximately 1 mM, an increased flux through alanine aminotransferase appeared responsible for the increased J(glucose). This could, in turn, depend on an increased supply of cytosolic 2-oxoglutarate because of the higher mitochondrial respiration observed in hepatocytes from trained rats and the activation of the malate-aspartate shuttle. At lower alanine concentration, the increase in J(glucose) appeared to be entirely due to the improved transport capacity.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of increased gluconeogenesis from alanine in rat isolated hepatocytes after endurance training

Burelle

Fillipi

Péronnet

et al. 2000

American Journal of Physiology-Endocrinology and Metabolism

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“…2A). Endurance training has also been shown to increase the conversion of lactate to glucose in hepatocytes isolated from rats after exercise [2], despite there being no effect of training on key gluconeogenic enzymes [15,18]. In rats, endurance training improves the removal of lactate via gluconeogenesis, rather than by oxidation [10,11].…”

Section: Discussionmentioning

confidence: 99%

Effects of endurance training on lactate removal by oxidation and gluconeogenesis during exercise

1995

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This report describes the effects of 9 weeks of endurance-training on the relative rates of lactate removal via oxidation and gluconeogenesis in humans. Before and after training, eight subjects performed incremental (60 W plus 40 W every 6 min) exercise tests, while 14C-lactate was infused into one forearm vein and arterialized venous blood was sampled from the other forearm. During the trial, the volume of expired 14CO2 and circulating 14C-lactate and 14C-glucose specific radioactivities were measured. Such measurements revealed that training increased the estimated oxidation of equivalent venous blood lactate concentrations [VLa] of greater than 1.6 mmol/l. These increases in lactate oxidation were more than would be predicted from the approximately 40% higher O2 uptake values at any [VLa] after training. At a [VLa] of 6 mmol/l, rates of lactate oxidation were increased by some 100% following training, from 105 +/- 12 to 208 +/- 33 micromol/min/kg (P < 0.01). Improvements in lactate oxidation after training reduced the estimated rates of lactate-to-glucose conversion from 40 +/- 3 to 9 +/- 2 micromol/min/kg at a [VLa] of 2.5 mmol/l (P < 0.01). Thus, unlike in rats, human endurance-training does not increase gluconeogenesis. In the final stages of progressive exercise after training, more than 80% of lactate was oxidised and accounted for approximately 45% of overall carbohydrate oxidation.

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“…Evidence that intrahepatic gluconeogenic mechanisms are stimulated during exercise is twofold. First, gluconeogenic enzyme activities [e.g., phosphoenolpyruvate carboxykinase (PEPCK), fructose-1,6-bisphosphatase, glucose 6-phosphatase] are elevated (73,74,130), whereas the activity of the glycolytic enzyme, phosphofructokinase, is diminished by exercise (73). Second, the intrahepatic gluconeogenic efficiency, as determined by the fraction of 14C-alanine consumed by the liver that is channeled into 14C-glucose, is increased (312).…”

Section: Exercise Responsementioning

confidence: 99%

“…The intrahepatic mechanism for this increase in gluconeogenic capacity is unclear. The activity of the key gluconeogenic enzyme phosphoenolpyruvate carboxykinase is not elevated in the basal state, but may increase more in response to exercise in the trained state (130). In addition, a reduction in hepatic phosphodiesterase activity has been reported to occur in response to endurance training (75).…”

Section: Physical Trainingmentioning

confidence: 99%

Regulation of Extramuscular Fuel Sources During Exercise

Wasserman

Cherrington

1996

Comprehensive Physiology

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The sections in this article are: Fuel Requirements of the Working Muscle Effect of Exercise Duration Effect of Exercise Intensity Exercise Responses of Hormones and Nerves Involved in Acute Metabolic Regulation Insulin Response Glucagon Response Catecholamine Responses Extramuscular Fuel Sources NEFA Mobilization from Adipose Tissue Basic Mechanisms that Influence NEFA Availability Regulatory Factors Hepatic Glucose Production Exercise Response Regulation by the Endocrine Pancreas Role of Epinephrine Role of Sympathetic Nerve Activity and Norepinephrine Role of Cortisol Regulation during High‐Intensity Exercise Hepatic Fat Metabolism: Oxidation and Triglyceride Synthesis Regulation of Ketogenesis Triglyceride Synthesis Splanchnic Bed Amino Acid Metabolism Protein Breakdown Amino Acids as a Carbon Source for Gluconeogenesis and Oxidation Uptake of Nitrogenous Compounds by the Splanchnic Bed Fate of Nitrogenous Compounds in the Liver Gastrointestinal Tract as a Source of Glucose: Effect of Carbohydrate Ingestion Importance Determinants of the Metabolic Availability of Ingested Carbohydrates Effect of Carbohydrate Ingestion on Endogenous Substrates Training‐Induced Adaptations in Extramuscular Fuel Mobilization Endocrine Adaptations to Physical Training Adaptations of Extramuscular Fuel Sources to Physical Training Summary

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Effects of training, exercise and diet on muscle glycolysis and liver gluconeogenesis

Cited by 24 publications

References 17 publications

Mechanisms of increased gluconeogenesis from alanine in rat isolated hepatocytes after endurance training

Mechanisms of increased gluconeogenesis from alanine in rat isolated hepatocytes after endurance training

Effects of endurance training on lactate removal by oxidation and gluconeogenesis during exercise

Regulation of Extramuscular Fuel Sources During Exercise

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