scholarly journals The Acute Effects Of Pre-exercise Glucose Ingestion On Respiratory Quotient, Carbohydrate, And Lipid Oxidation Rates In Overweight/obese Adults

2021 ◽  
Vol 53 (8S) ◽  
pp. 237-237
Author(s):  
Miguel Alejandro Atencio-Osorio ◽  
Hugo Alejandro Carrillo-Arango ◽  
Carlos Alejandro López Alban ◽  
Diana Isabel Martínez-García ◽  
Jenny Reyes Castillo ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Respiratory Quotient ◽  
Acute Effects ◽  
Obese Adults ◽  
Oxidation Rates ◽  
Glucose Ingestion

Effect of physical training on utilization of a glucose load given orally during exercise

1984 ◽  
Vol 246 (5) ◽  
pp. E412-E417 ◽  
Author(s):  
G. Krzentowski ◽  
F. Pirnay ◽  
A. S. Luyckx ◽  
M. Lacroix ◽  
F. Mosora ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Physical Training ◽  
Glucose Oxidation ◽  
Exercise Bout ◽  
Moderate Intensity ◽  
Glucose Load ◽  
Total Carbohydrate ◽  
Oxidation Rates ◽  
Exogenous Glucose ◽  
Glucose Ingestion

The effect of a 6-wk training period on the oxidation of a 100-g glucose load given orally during exercise was investigated in six healthy male volunteers. The subjects were submitted before and 24 h after the training program to a 105-min exercise bout (performed at about 40% of the pretraining VO2max) followed by a 90-min resting period. Naturally labeled [13C]glucose was given 15 min after the beginning of exercise. Exogenous glucose oxidation was derived from 13CO2 measurements in expired air, and total glucose and lipid oxidation were evaluated by indirect calorimetry. Training (60-min bicycling 5 days a week at 30-40% VO2max) resulted in a 29% increase in VO2max. During the 15 min of exercise that preceded glucose ingestion, the rate of total carbohydrate oxidation was slightly decreased after training, whereas the rate of lipid oxidation was slightly increased. Training did not affect the response of blood glucose, plasma insulin, or plasma free fatty acids to the glucose ingested during exercise; in contrast, the circulating levels of epinephrine, glycerol, and lactate were significantly reduced after training. Substrate utilization measurements revealed similar oxidation rates of carbohydrates (106.9 +/- 2.7 before vs. 100.2 +/- 4.7 g/3 h after training) and of lipids. However, detailed analysis revealed a significant 17% increase in exogenous glucose oxidation, thus indicating a significant sparing of endogenous carbohydrates. In conclusion, physical training induces a modest but significant increase in the oxidation of an oral load of glucose given during subsequent exercise of moderate intensity, a phenomenon reinforcing the sparing of endogenous carbohydrate stores.

Effects of puberty and diabetes on metabolism of insulin-sensitive fuels

1994 ◽  
Vol 266 (6) ◽  
pp. E885-E891 ◽  
Author(s):  
S. Caprio ◽  
G. Cline ◽  
S. Boulware ◽  
C. Permanente ◽  
G. I. Shulman ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Lipid Oxidation ◽  
Insulin Infusion ◽  
Plasma Free Fatty Acid ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Healthy Controls ◽  
Oxidation Rates ◽  
Acid Protein ◽  
Insulin Dependent

Insulin's ability to stimulate glucose metabolism is reduced during normal puberty; these changes are exaggerated in adolescents with insulin-dependent diabetes mellitus (IDDM). Because the effects of puberty and IDDM on the other actions of insulin have not been established, we studied leucine kinetics (using [1-13C]leucine) and fat metabolism during euglycemic hyperinsulinemia (20 mU.m2.min-1) for 3 h in eight healthy and nine IDDM (HbA1 14 +/- 2%) adolescents and six healthy young adult controls. IDDM subjects received overnight low-dose insulin infusion to normalize fasting glucose. Basal and steady-state insulin values (approximately 240 pM) during the study were similar in all three groups. Insulin-stimulated glucose metabolism was reduced by 40% in healthy adolescents vs. adults (P < 0.05) and by an additional 40% in poorly controlled IDDM (P < 0.05 vs, normal adolescents). Although basal glucose and lipid oxidation rates (measured by indirect calorimetry) were similar in all three groups, when insulin was infused, glucose oxidation increased and lipid oxidation decreased only in the two nondiabetic groups. Similarly, insulin significantly reduced plasma free fatty acid levels only in the nondiabetics. Basal leucine flux (an index of protein degradation) was similar in healthy controls but was markedly increased in IDDM adolescents. Despite similar increments in plasma insulin during the clamp, leucine flux remained higher in IDDM adolescents than in healthy controls. Basal leucine oxidation rates were also increased in IDDM subjects compared with nondiabetic groups and declined to a lesser extent during insulin infusion. We conclude that insulin resistance of puberty is selective for glucose metabolism, sparing amino acid/protein metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Lipid Oxidation during Thermogenesis in High-Altitude Deer Mice (Peromyscus maniculatus)

2021 ◽  
Author(s):  
Sulayman Aslan Lyons ◽  
Kevin B Tate ◽  
Kenneth Collins Welch ◽  
Grant B. McClelland
Keyword(s):  
Lipid Oxidation ◽  
Palmitic Acid ◽  
High Altitude ◽  
Deer Mice ◽  
Acid Oxidation ◽  
Cold Environments ◽  
Oxidation Rates ◽  
Low Altitude ◽  
Land Mammal ◽  
Specific Lipid

When at their maximum thermogenic capacity (cold-induced V̇O2max), small endotherms reach levels of aerobic metabolism as high, or even higher, than running V̇O2max. How these high rates of thermogenesis are supported by substrate oxidation is currently unclear. The appropriate utilization of metabolic fuels that could sustain thermogenesis over extended periods may be important for survival in cold environments, like high altitude. Previous studies show that high capacities for lipid use in high-altitude deer mice may have evolved in concert with greater thermogenic capacities. The purpose of this study was to determine how lipid utilization at both moderate and maximal thermogenic intensities may differ in high- and low- altitude deer mice, and strictly low-altitude white-footed mice. We also examined the phenotypic plasticity of lipid use after acclimation to cold hypoxia (CH), conditions simulating high altitude. We found that lipids were the primary fuel supporting both moderate and maximal rates of thermogenesis in both species of mice. Lipid oxidation increased 3-fold in mice from 30oC to 0oC, consistent with increases in oxidation of [13C]-palmitic acid. CH acclimation led to an increase in [13C]-palmitic acid oxidation at 30oC but did not affect total lipid oxidation. Lipid oxidation rates at cold-induced V̇O2max were two- to four-fold those at 0oC and increased further after CH acclimation, especially in high-altitude deer mice. These are the highest mass-specific lipid oxidation rates observed in any land mammal. Uncovering the mechanisms that allow for these high rates of oxidation will aid our understanding of the regulation of lipid metabolism.

scholarly journals Exercise training improves cardiovascular autonomic modulation in response to glucose ingestion in obese adults with and without type 2 diabetes mellitus

Metabolism ◽  
2010 ◽  
Vol 59 (6) ◽  
pp. 901-910 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Tracy Baynard ◽  
Ruth M. Franklin ◽  
Bo Fernhall ◽  
Robert Carhart ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Exercise Training ◽  
Autonomic Modulation ◽  
Obese Adults ◽  
Glucose Ingestion

Acute effects of quinidine on K exchange and distribution in the dog ventricle

1960 ◽  
Vol 199 (1) ◽  
pp. 151-156 ◽  
Author(s):  
Hadley L. Conn ◽  
John C. Wood
Keyword(s):  
Oxygen Consumption ◽  
Gas Exchange ◽  
Action Potential ◽  
Respiratory Quotient ◽  
Resting Potential ◽  
Acute Effects ◽  
Dog Heart ◽  
Potassium Influx ◽  
Potassium Exchange ◽  
Potassium Metabolism

Some of the effects of quinidine on potassium metabolism and gas exchange were studied in the isolated perfused dog heart. The major changes found were an increase in cell K and transcellular K exchange, and a decrease in oxygen consumption and respiratory quotient. The increase in K exchange was apparently due to an increased resting potential potassium exchange with little or no alteration in exchange during the action potential. The accumulation of cell K seemed to be dependent mainly on an initial resting phase increase in potassium influx.

scholarly journals LMNA Mutations, Skeletal Muscle Lipid Metabolism, and Insulin Resistance

2010 ◽  
Vol 95 (4) ◽  
pp. 1634-1643 ◽  
Author(s):  
Michael Boschmann ◽  
Stefan Engeli ◽  
Cedric Moro ◽  
Angelika Luedtke ◽  
Frauke Adams ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Lipid Oxidation ◽  
Exercise Intolerance ◽  
Intrinsic Defect ◽  
Lamin A ◽  
Glucose Ingestion

Abstract Context: Type 2 familial partial lipodystrophy (FPLD) is an autosomal-dominant lamin A/C-related disease associated with exercise intolerance, muscular pain, and insulin resistance. The symptoms may all be explained by defective metabolism; however, metabolism at the tissue level has not been investigated. Objective: We hypothesized that in FPLD, insulin resistance and impaired aerobic exercise capacity are explained by a common underlying mechanism, presumably a muscular metabolic defect. Patients and Methods: Carbohydrate and lipid metabolism was studied on 10 FPLD patients, one patient with limb-girdle muscular dystrophy (LGMD1B, a different lamin A/C disease), and 10 healthy control subjects before and during an oral glucose tolerance test by indirect calorimetry and im microdialysis. Muscle biopsies were taken for in vitro studies. Results: We observed marked increased skeletal muscle fatty acid β-oxidation rate in vitro and in vivo, even after glucose ingestion in FPLD patients. However, fatty acid oxidation was largely incomplete and accompanied by increased ketogenesis. The lipid oxidation abnormality was associated with impaired glucose disposition through reduction in glucose oxidation, rather than decreased cellular glucose uptake. A microarray showed down-regulation of complex I respiratory chain, glycolysis, and nuclear transport genes. Although not overtly insulin resistant, the LGMD1B patient showed similar metabolic derangements as the FPLD patients. Conclusions: Our study suggests imbalance between lipid oxidation and oxidative glucose metabolism in FPLD and LGMD1B patients. The observation suggests an intrinsic defect in skeletal muscle metabolism due to lamin A/C dysfunction. The metabolic FPLD phenotype likely results from this intrinsic defect combined with lipodystrophic “lipid pressure” due to decreased adipose tissue lipid storage capacity.

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