Exercise induces lipoprotein lipase and GLUT-4 protein in muscle independent of adrenergic-receptor signaling.
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.
Greiwe
J S
JS
Departments of Medicine and of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Holloszy
J O
JO
Semenkovich
C F
CF
D000317:Adrenergic alpha-Antagonists / Q000008:administration & dosage; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage; D000328:Adult; D004837:Epinephrine / Q000097:blood; D005080:Exercise Test; D005947:Glucose / Q000378:metabolism; D051275:Glucose Transporter Type 4; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D050356:Lipid Metabolism; D008071:Lipoprotein Lipase / Q000378:metabolism*; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D009124:Muscle Proteins; D018482:Muscle, Skeletal / Q000378:metabolism*; D009638:Norepinephrine / Q000097:blood; D010101:Oxygen Consumption / Q000502:physiology; D010643:Phenoxybenzamine / Q000008:administration & dosage; D005082:Physical Exertion / Q000187:drug effects / Q000502:physiology*; D011433:Propranolol / Q000008:administration & dosage; D011941:Receptors, Adrenergic / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D051275:Glucose Transporter Type 4; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; D011941:Receptors, Adrenergic; C495692:SLC2A4 protein, human; D010643:Phenoxybenzamine; D011433:Propranolol; D008071:Lipoprotein Lipase; D005947:Glucose; D009638:Norepinephrine; D004837:Epinephrine