Literature DB >> 10904050

Exercise induces lipoprotein lipase and GLUT-4 protein in muscle independent of adrenergic-receptor signaling.

J S Greiwe1, J O Holloszy, C F Semenkovich.   

Abstract

Exercise increases the expression of lipoprotein lipase (LPL) and GLUT-4 in skeletal muscle. Intense exercise increases catecholamines, and catecholamines without exercise can affect the expression of both LPL and GLUT-4. To test the hypothesis that adrenergic-receptor signaling is central to the induction of LPL and GLUT-4 by exercise, six untrained individuals [age 28 +/- 4 (SD) yr, peak oxygen uptake 3.6 +/- 0.3 l/min] performed two exercise bouts within 12 days. Exercise consisted of cycling at approximately 65% peak oxygen uptake for 60 min with (block trial) and without (control trial) adrenergic-receptor blockade. Exercise intensity was the same during the block and control trials. Plasma catecholamine concentrations were significantly higher and heart rates were significantly lower during the block trial compared with the control trial, consistent with known effects of adrenergic-receptor blockade. However, blockade did not prevent the induction of either LPL or GLUT-4 proteins assayed in biopsies of skeletal muscle. LPL was significantly increased by 170-240% and GLUT-4 was significantly increased by 32-51% at 22 h after exercise compared with before exercise during both the control and block trials. These findings provide evidence that exercise increases muscle LPL and GLUT-4 protein content via signals generated by alterations in cellular homeostasis and not by adrenergic-receptor stimulation.

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Year:  2000        PMID: 10904050     DOI: 10.1152/jappl.2000.89.1.176

Source DB:  PubMed          Journal:  J Appl Physiol (1985)        ISSN: 0161-7567


  13 in total

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9.  Dietary exercise as a novel strategy for the prevention and treatment of metabolic syndrome: effects on skeletal muscle function.

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Journal:  J Nutr Metab       Date:  2011-06-06

10.  Does Branched-Chain Amino Acids Supplementation Modulate Skeletal Muscle Remodeling through Inflammation Modulation? Possible Mechanisms of Action.

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