scholarly journals Editorial: Possible Mechanisms to Explain Abdominal Fat Loss Effect of Exercise Training Other Than Fatty Acid Oxidation

2021 ◽  
Vol 12 ◽  
Author(s):  
Chia-Hua Kuo ◽  
M. Brennan Harris ◽  
Jørgen Arendt Jensen ◽  
Ahmad Alkhatib ◽  
John L. Ivy
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Fatty Acid Oxidation ◽  
Abdominal Fat ◽  
Acid Oxidation ◽  
Fat Loss ◽  
Loss Effect

Higher mitochondrial fatty acid oxidation following intermittent versus continuous endurance exercise training

1998 ◽  
Vol 76 (9) ◽  
pp. 891-894 ◽  
Author(s):  
P D Chilibeck ◽  
G J Bell ◽  
R P Farrar ◽  
T P Martin
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Fatty Acid Oxidation ◽  
Endurance Exercise ◽  
High Intensity ◽  
Treadmill Running ◽  
Acid Oxidation ◽  
Interval Exercise ◽  
Endurance Exercise Training ◽  
Mitochondrial Fatty Acid

It has been well documented that skeletal muscle fatty acid oxidation can be elevated by continuous endurance exercise training. However, it remains questionable whether similar adaptations can be induced with intermittent interval exercise training. This study was undertaken to directly compare the rates of fatty acid oxidation in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria following these different exercise training regimes. Mitochondria were isolated from the gastrocnemius-plantaris muscles of male Sprague-Dawley rats following exercise training 6 days per week for 12 weeks. Exercise training consisted of either continuous, submaximal, endurance treadmill running (n = 10) or intermittent, high intensity, interval running (n = 10). Both modes of training enhanced the oxidation of palmityl-carnitine-malate in both mitochondrial populations (p < 0.05). However, the increase associated with the intermittent, high intensity exercise training was significantly greater than that achieved with the continuous exercise training (p < 0.05). Also, the increases associated with the IMF mitochondria were greater than the SS mitochondria (p < 0.05). These data suggest that high intensity, intermittent interval exercise training is more effective for stimulation of fatty acid oxidation than continuous submaximal exercise training and that this adaptation occurs preferentially within IMF mitochondria.Key words: muscle, subsarcolemmal mitochondria, intermyofibrillar mitochondria.

Subsarcolemmal and intermyofibrillar mitochondria play distinct roles in regulating skeletal muscle fatty acid metabolism

2005 ◽  
Vol 288 (5) ◽  
pp. C1074-C1082 ◽  
Author(s):  
Timothy R. Koves ◽  
Robert C. Noland ◽  
Andrew L. Bates ◽  
Sarah T. Henes ◽  
Deborah M. Muoio ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Exercise Training ◽  
Fatty Acid Oxidation ◽  
Treadmill Running ◽  
Hill Coefficient ◽  
Acid Oxidation ◽  
Oxidation Rates ◽  
Malonyl Coa ◽  
Mitochondrial Fatty Acid

Skeletal muscle contains two populations of mitochondria that appear to be differentially affected by disease and exercise training. It remains unclear how these mitochondrial subpopulations contribute to fiber type-related and/or training-induced changes in fatty acid oxidation and regulation of carnitine palmitoyltransferase-1β (CPT1β), the enzyme that controls mitochondrial fatty acid uptake in skeletal muscle. To this end, we found that fatty acid oxidation rates were 8.9-fold higher in subsarcolemmal mitochondria (SS) and 5.3-fold higher in intermyofibrillar mitochondria (IMF) that were isolated from red gastrocnemius (RG) compared with white gastrocnemius (WG) muscle, respectively. Malonyl-CoA (10 μM), a potent inhibitor of CPT1β, completely abolished fatty acid oxidation in SS and IMF mitochondria from WG, whereas oxidation rates in the corresponding fractions from RG were inhibited only 89% and 60%, respectively. Endurance training also elicited mitochondrial adaptations that resulted in enhanced fatty acid oxidation capacity. Ten weeks of treadmill running differentially increased palmitate oxidation rates 100% and 46% in SS and IMF mitochondria, respectively. In SS mitochondria, elevated fatty acid oxidation rates were accompanied by a 48% increase in citrate synthase activity but no change in CPT1 activity. Nonlinear regression analyses of mitochondrial fatty acid oxidation rates in the presence of 0–100 μM malonyl-CoA indicated that IC50 values were neither dependent on mitochondrial subpopulation nor affected by exercise training. However, in IMF mitochondria, training reduced the Hill coefficient ( P < 0.05), suggesting altered CPT1β kinetics. These results demonstrate that endurance exercise provokes subpopulation-specific changes in mitochondrial function that are characterized by enhanced fatty acid oxidation and modified CPT1β-malonyl-CoA dynamics.

scholarly journals Enhanced Fatty Acid Oxidation and FATP4 Protein Expression after Endurance Exercise Training in Human Skeletal Muscle

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e29391 ◽  
Author(s):  
Jacob Jeppesen ◽  
Andreas B. Jordy ◽  
Kim A. Sjøberg ◽  
Joachim Füllekrug ◽  
Andreas Stahl ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Exercise Training ◽  
Protein Expression ◽  
Fatty Acid Oxidation ◽  
Endurance Exercise ◽  
Human Skeletal Muscle ◽  
Acid Oxidation ◽  
Endurance Exercise Training

scholarly journals Exercise Intensity Modulation of Hepatic Lipid Metabolism

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Fábio S. Lira ◽  
Luiz C. Carnevali ◽  
Nelo E. Zanchi ◽  
Ronaldo VT. Santos ◽  
Jean Marc Lavoie ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Exercise Training ◽  
Fatty Acid Oxidation ◽  
Ketone Bodies ◽  
Hepatic Metabolism ◽  
Acid Oxidation ◽  
Hepatic Lipid Metabolism ◽  
Very Low Density Lipoproteins ◽  
Obesity And Cancer

Lipid metabolism in the liver is complex and involves the synthesis and secretion of very low density lipoproteins (VLDL), ketone bodies, and high rates of fatty acid oxidation, synthesis, and esterification. Exercise training induces several changes in lipid metabolism in the liver and affects VLDL secretion and fatty acid oxidation. These alterations are even more conspicuous in disease, as in obesity, and cancer cachexia. Our understanding of the mechanisms leading to metabolic adaptations in the liver as induced by exercise training has advanced considerably in the recent years, but much remains to be addressed. More recently, the adoption of high intensity exercise training has been put forward as a means of modulating hepatic metabolism. The purpose of the present paper is to summarise and discuss the merit of such new knowledge.

Daily exercise increases hepatic fatty acid oxidation and prevents steatosis in Otsuka Long-Evans Tokushima Fatty rats

2008 ◽  
Vol 294 (3) ◽  
pp. G619-G626 ◽  
Author(s):  
R. Scott Rector ◽  
John P. Thyfault ◽  
R. Tyler Morris ◽  
Matthew J. Laye ◽  
Sarah J. Borengasser ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Hepatic Steatosis ◽  
Fatty Acid Oxidation ◽  
Wheel Running ◽  
Acid Oxidation ◽  
Oletf Rats ◽  
Hepatic Fatty Acid ◽  
Long Evans ◽  
Hepatic Fatty Acid Oxidation

Exercise training is commonly prescribed for treatment of nonalcoholic fatty liver disease (NAFLD). We sought to determine whether exercise training prevents the development of NAFLD in Otsuka Long-Evans Tokushima Fatty (OLETF) rats and to elucidate the molecular mechanisms underlying the effects of exercise on hepatic steatosis. Four-week-old OLETF rats were randomly assigned to either a sedentary control group (Sed) or a group given access to voluntary running wheels for 16 wk (Ex). Wheels were locked 2 days before euthanasia in the Ex animals, and both groups were euthanized at 20 wk old. Voluntary wheel running attenuated weight gain and reduced serum glucose, insulin, free fatty acids, and triglycerides in Ex animals compared with Sed ( P < 0.001). Ex animals exhibited significantly reduced hepatic triglyceride levels and displayed fewer lipid droplets (Oil Red O staining) and reduced lipid droplet size compared with Sed. Wheel running increased by threefold the percent of palmitate oxidized completely to CO2 in the Ex animals but did not alter AMP-activated protein kinase-α (AMPKα) or AMPK phosphorylation status. However, fatty acid synthase and acetyl-coenzyme A carboxylase (ACC) content were significantly reduced (∼70 and ∼35%, respectively), and ACC phosphorylation and cytochrome c content were significantly elevated (∼35 and ∼30%, respectively) in the Ex animals. These results unequivocally demonstrate that daily physical activity attenuates hepatic steatosis and NAFLD in an obese rodent model and suggest that this effect is likely mediated, in part, through enhancement of hepatic fatty acid oxidation and reductions in key protein intermediates of fatty acid synthesis.

Plasma metabolic signatures reveal the regulatory effect of exercise training in db/db mice

2015 ◽  
Vol 11 (9) ◽  
pp. 2588-2596 ◽  
Author(s):  
L. Xiang ◽  
W. S. Cheang ◽  
S. H. Lin ◽  
L. Wang ◽  
Y. L. Li ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Moderate Exercise ◽  
Regulatory Effect ◽  
Moderate Exercise Training ◽  
Metabolic Signatures

Regulatory effect of moderate exercise training on fatty acid oxidation.

Glucocorticoids promote mitochondrial fatty acid oxidation in the fetal heart

2019 ◽  
Author(s):  
Helena Urquijo ◽  
Emma N Panting ◽  
Roderick N Carter ◽  
Emma J Agnew ◽  
Caitlin S Wyrwoll ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fetal Heart ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Mitochondrial Fatty Acid
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