Adipose triglyceride lipase in human skeletal muscle is upregulated by exercise training

2009 ◽  
Vol 296 (3) ◽  
pp. E445-E453 ◽  
Author(s):  
Thomas J. Alsted ◽  
Lars Nybo ◽  
Martina Schweiger ◽  
Christian Fledelius ◽  
Poul Jacobsen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Human Skeletal Muscle ◽  
Hormone Sensitive Lipase ◽  
Adipose Triglyceride Lipase ◽  
Skeletal Muscle Biopsy ◽  
Triglyceride Lipase ◽  
Endurance Exercise Training ◽  
Molecule Inhibitor

Mobilization of fatty acids from stored triacylglycerol (TG) in adipose tissue and skeletal muscle [intramyocellular triacylglycerol (IMTG)] requires activity of lipases. Although exercise training increases the lipolytic capacity of skeletal muscle, the expression of hormone-sensitive lipase (HSL) is not changed. Recently, adipose triglyceride lipase (ATGL) was identified as a TG-specific lipase in various rodent tissues. To investigate whether human skeletal muscle ATGL protein is regulated by endurance exercise training, 10 healthy young men completed 8 wk of supervised endurance exercise training. Western blotting analysis on lysates of skeletal muscle biopsy samples revealed that exercise training induced a twofold increase in skeletal muscle ATGL protein content. In contrast to ATGL, expression of comparative gene identification 58 (CGI-58), the activating protein of ATGL, and HSL protein was not significantly changed after the training period. The IMTG concentration was significantly decreased by 28% at termination of the training program compared with before. HSL-phoshorylation at Ser660 was increased, HSL-Ser659 phosporylation was unchanged, and HSL-phoshorylation at Ser565 was decreased altogether, indicating an enhanced basal activity of this lipase. No change was found in the expression of diacylglycerol acyl transferase 1 (DGAT1) after training. Inhibition of HSL with a monospecific, small molecule inhibitor (76-0079) and stimulation of ATGL with CGI-58 revealed that significant ATGL activity is present in human skeletal muscle. These results suggest that ATGL in addition to HSL may be important for human skeletal muscle lipolysis.

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

Effects of Endurance Exercise Training on Insulin Signaling in Human Skeletal Muscle

Diabetes ◽  
2007 ◽  
Vol 56 (8) ◽  
pp. 2093-2102 ◽  
Author(s):  
Christian Frøsig ◽  
Adam J. Rose ◽  
Jonas T. Treebak ◽  
Bente Kiens ◽  
Erik A. Richter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Insulin Signaling ◽  
Human Skeletal Muscle ◽  
Endurance Exercise Training

Skeletal muscle biochemical adaptations to exercise training in miniature swine

1997 ◽  
Vol 82 (6) ◽  
pp. 1862-1868 ◽  
Author(s):  
Richard M. McAllister ◽  
Brian L. Reiter ◽  
John F. Amann ◽  
M. Harold Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Lactate Dehydrogenase ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Oxidative Capacity ◽  
Treadmill Running ◽  
Miniature Swine ◽  
Endurance Exercise Training ◽  
Hydroxyacyl Coa Dehydrogenase

McAllister, Richard M., Brian L. Reiter, John F. Amann, and M. Harold Laughlin. Skeletal muscle biochemical adaptations to exercise training in miniature swine. J. Appl. Physiol. 82(6): 1862–1868, 1997.—The primary purpose of this study was to test the hypothesis that endurance exercise training induces increased oxidative capacity in porcine skeletal muscle. To test this hypothesis, female miniature swine were either trained by treadmill running 5 days/wk over 16–20 wk (Trn; n = 35) or pen confined (Sed; n = 33). Myocardial hypertrophy, lower heart rates during submaximal stages of a maximal treadmill running test, and increased running time to exhaustion during that test were indicative of training efficacy. A variety of skeletal muscles were sampled and subsequently assayed for the enzymes citrate synthase (CS), 3-hydroxyacyl-CoA dehydrogenase, and lactate dehydrogenase and for antioxidant enzymes. Fiber type composition of a representative muscle was also determined histochemically. The largest increase in CS activity (62%) was found in the gluteus maximus muscle (Sed, 14.7 ± 1.1 μmol ⋅ min−1 ⋅ g−1; Trn, 23.9 ± 1.0; P < 0.0005). Muscles exhibiting increased CS activity, however, were located primarily in the forelimb; ankle and knee extensor and respiratory muscles were unchanged with training. Only two muscles exhibited higher 3-hydroxyacyl-CoA dehydrogenase activity in Trn compared with Sed. Lactate dehydrogenase activity was unchanged with training, as were activities of antioxidant enzymes. Histochemical analysis of the triceps brachii muscle (long head) revealed lower type IIB fiber numbers in Trn (Sed, 42 ± 6%; Trn, 10 ± 4; P < 0.01) and greater type IID/X fiber numbers (Sed, 11 ± 2; Trn, 22 ± 3; P < 0.025). These findings indicate that porcine skeletal muscle adapts to endurance exercise training in a manner similar to muscle of humans and other animal models, with increased oxidative capacity. Specific muscles exhibiting these adaptations, however, differ between the miniature swine and other species.

scholarly journals Exercise: Teaching myocytes new tricks

2017 ◽  
Vol 123 (2) ◽  
pp. 460-472 ◽  
Author(s):  
Scott K. Powers
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Cardiac Myocytes ◽  
Endurance Exercise ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
Cardiac Phenotype ◽  
Endurance Exercise Training ◽  
Skeletal Muscle Fibers ◽  
Exercise Induced

Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as “exercise preconditioning.” As few as 3–5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.

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