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Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle
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| Zeitschriftentitel: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| In: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 287, 2004, 6, S. R1419-R1426 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
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| Schlagwörter: |
| author_facet |
Putman, Charles T. Dixon, Walter T. Pearcey, Jean A. MacLean, Ian M. Jendral, Michelle J. Kiricsi, Mónika Murdoch, Gordon K. Pette, Dirk Putman, Charles T. Dixon, Walter T. Pearcey, Jean A. MacLean, Ian M. Jendral, Michelle J. Kiricsi, Mónika Murdoch, Gordon K. Pette, Dirk |
|---|---|
| author |
Putman, Charles T. Dixon, Walter T. Pearcey, Jean A. MacLean, Ian M. Jendral, Michelle J. Kiricsi, Mónika Murdoch, Gordon K. Pette, Dirk |
| spellingShingle |
Putman, Charles T. Dixon, Walter T. Pearcey, Jean A. MacLean, Ian M. Jendral, Michelle J. Kiricsi, Mónika Murdoch, Gordon K. Pette, Dirk American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle Physiology (medical) Physiology |
| author_sort |
putman, charles t. |
| spelling |
Putman, Charles T. Dixon, Walter T. Pearcey, Jean A. MacLean, Ian M. Jendral, Michelle J. Kiricsi, Mónika Murdoch, Gordon K. Pette, Dirk 0363-6119 1522-1490 American Physiological Society Physiology (medical) Physiology http://dx.doi.org/10.1152/ajpregu.00421.2004 <jats:p>The purpose of this investigation was to examine the temporal changes in uncoupling protein (UCP)-3 expression, as well as related adaptive changes in mitochondrial density and fast-to-slow fiber type transitions during chronically enhanced contractile activity. We examined the effects of 1–42 days of chronic low-frequency electrical stimulation (CLFS), applied to rat tibialis anterior (TA) for 10 h/day, on the expression of UCP-3 and concomitant changes in myosin heavy chain (MHC) protein expression and increases in oxidative capacity. UCP-3 protein content increased from 1 to 12 days, reaching 1.5-fold over control ( P < 0.0005); it remained elevated for up to 42 days. In contrast, UCP-3 mRNA decreased in response to CLFS, reaching a level that was threefold lower than control ( P < 0.0007). The activities of the mitochondrial reference enzymes citrate synthase (EC 4.1.3.7) and 3-hydroxyacyl-CoA-dehydrogenase (EC 1.1.1.35), which are known to increase in proportion to mitochondrial density, progressively increased up to an average of 2.3-fold ( P < 0.00001). These changes were accompanied by fast-to-slow fiber type transitions, characterized by a shift in the pattern of MHC expression ( P <0.0002): MHCI and MHCIIa expression increased by 1.7- and 4-fold, whereas MHCIIb displayed a 2.4-fold reduction. We conclude that absolute increases in UCP-3 protein content in the early adaptive phase were associated with the genesis of mitochondria containing a normal complement of UCP-3. However, during exposure to long-term CLFS, mitochondria were generated with a lower complement of UCP-3 and coincided with the emergence of a growing population of oxidative type IIA fibers.</jats:p> Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle American Journal of Physiology-Regulatory, Integrative and Comparative Physiology |
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| title |
Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_unstemmed |
Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_full |
Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_fullStr |
Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_full_unstemmed |
Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_short |
Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_sort |
chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| topic |
Physiology (medical) Physiology |
| url |
http://dx.doi.org/10.1152/ajpregu.00421.2004 |
| publishDate |
2004 |
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R1419-R1426 |
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<jats:p>The purpose of this investigation was to examine the temporal changes in uncoupling protein (UCP)-3 expression, as well as related adaptive changes in mitochondrial density and fast-to-slow fiber type transitions during chronically enhanced contractile activity. We examined the effects of 1–42 days of chronic low-frequency electrical stimulation (CLFS), applied to rat tibialis anterior (TA) for 10 h/day, on the expression of UCP-3 and concomitant changes in myosin heavy chain (MHC) protein expression and increases in oxidative capacity. UCP-3 protein content increased from 1 to 12 days, reaching 1.5-fold over control ( P < 0.0005); it remained elevated for up to 42 days. In contrast, UCP-3 mRNA decreased in response to CLFS, reaching a level that was threefold lower than control ( P < 0.0007). The activities of the mitochondrial reference enzymes citrate synthase (EC 4.1.3.7) and 3-hydroxyacyl-CoA-dehydrogenase (EC 1.1.1.35), which are known to increase in proportion to mitochondrial density, progressively increased up to an average of 2.3-fold ( P < 0.00001). These changes were accompanied by fast-to-slow fiber type transitions, characterized by a shift in the pattern of MHC expression ( P <0.0002): MHCI and MHCIIa expression increased by 1.7- and 4-fold, whereas MHCIIb displayed a 2.4-fold reduction. We conclude that absolute increases in UCP-3 protein content in the early adaptive phase were associated with the genesis of mitochondria containing a normal complement of UCP-3. However, during exposure to long-term CLFS, mitochondria were generated with a lower complement of UCP-3 and coincided with the emergence of a growing population of oxidative type IIA fibers.</jats:p> |
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| author | Putman, Charles T., Dixon, Walter T., Pearcey, Jean A., MacLean, Ian M., Jendral, Michelle J., Kiricsi, Mónika, Murdoch, Gordon K., Pette, Dirk |
| author_facet | Putman, Charles T., Dixon, Walter T., Pearcey, Jean A., MacLean, Ian M., Jendral, Michelle J., Kiricsi, Mónika, Murdoch, Gordon K., Pette, Dirk, Putman, Charles T., Dixon, Walter T., Pearcey, Jean A., MacLean, Ian M., Jendral, Michelle J., Kiricsi, Mónika, Murdoch, Gordon K., Pette, Dirk |
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| description | <jats:p>The purpose of this investigation was to examine the temporal changes in uncoupling protein (UCP)-3 expression, as well as related adaptive changes in mitochondrial density and fast-to-slow fiber type transitions during chronically enhanced contractile activity. We examined the effects of 1–42 days of chronic low-frequency electrical stimulation (CLFS), applied to rat tibialis anterior (TA) for 10 h/day, on the expression of UCP-3 and concomitant changes in myosin heavy chain (MHC) protein expression and increases in oxidative capacity. UCP-3 protein content increased from 1 to 12 days, reaching 1.5-fold over control ( P < 0.0005); it remained elevated for up to 42 days. In contrast, UCP-3 mRNA decreased in response to CLFS, reaching a level that was threefold lower than control ( P < 0.0007). The activities of the mitochondrial reference enzymes citrate synthase (EC 4.1.3.7) and 3-hydroxyacyl-CoA-dehydrogenase (EC 1.1.1.35), which are known to increase in proportion to mitochondrial density, progressively increased up to an average of 2.3-fold ( P < 0.00001). These changes were accompanied by fast-to-slow fiber type transitions, characterized by a shift in the pattern of MHC expression ( P <0.0002): MHCI and MHCIIa expression increased by 1.7- and 4-fold, whereas MHCIIb displayed a 2.4-fold reduction. We conclude that absolute increases in UCP-3 protein content in the early adaptive phase were associated with the genesis of mitochondria containing a normal complement of UCP-3. However, during exposure to long-term CLFS, mitochondria were generated with a lower complement of UCP-3 and coincided with the emergence of a growing population of oxidative type IIA fibers.</jats:p> |
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| institution | DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Rs1, DE-Pl11, DE-105, DE-14, DE-Ch1, DE-L229 |
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| spelling | Putman, Charles T. Dixon, Walter T. Pearcey, Jean A. MacLean, Ian M. Jendral, Michelle J. Kiricsi, Mónika Murdoch, Gordon K. Pette, Dirk 0363-6119 1522-1490 American Physiological Society Physiology (medical) Physiology http://dx.doi.org/10.1152/ajpregu.00421.2004 <jats:p>The purpose of this investigation was to examine the temporal changes in uncoupling protein (UCP)-3 expression, as well as related adaptive changes in mitochondrial density and fast-to-slow fiber type transitions during chronically enhanced contractile activity. We examined the effects of 1–42 days of chronic low-frequency electrical stimulation (CLFS), applied to rat tibialis anterior (TA) for 10 h/day, on the expression of UCP-3 and concomitant changes in myosin heavy chain (MHC) protein expression and increases in oxidative capacity. UCP-3 protein content increased from 1 to 12 days, reaching 1.5-fold over control ( P < 0.0005); it remained elevated for up to 42 days. In contrast, UCP-3 mRNA decreased in response to CLFS, reaching a level that was threefold lower than control ( P < 0.0007). The activities of the mitochondrial reference enzymes citrate synthase (EC 4.1.3.7) and 3-hydroxyacyl-CoA-dehydrogenase (EC 1.1.1.35), which are known to increase in proportion to mitochondrial density, progressively increased up to an average of 2.3-fold ( P < 0.00001). These changes were accompanied by fast-to-slow fiber type transitions, characterized by a shift in the pattern of MHC expression ( P <0.0002): MHCI and MHCIIa expression increased by 1.7- and 4-fold, whereas MHCIIb displayed a 2.4-fold reduction. We conclude that absolute increases in UCP-3 protein content in the early adaptive phase were associated with the genesis of mitochondria containing a normal complement of UCP-3. However, during exposure to long-term CLFS, mitochondria were generated with a lower complement of UCP-3 and coincided with the emergence of a growing population of oxidative type IIA fibers.</jats:p> Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle American Journal of Physiology-Regulatory, Integrative and Comparative Physiology |
| spellingShingle | Putman, Charles T., Dixon, Walter T., Pearcey, Jean A., MacLean, Ian M., Jendral, Michelle J., Kiricsi, Mónika, Murdoch, Gordon K., Pette, Dirk, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle, Physiology (medical), Physiology |
| title | Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_full | Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_fullStr | Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_full_unstemmed | Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_short | Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_sort | chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| title_unstemmed | Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle |
| topic | Physiology (medical), Physiology |
| url | http://dx.doi.org/10.1152/ajpregu.00421.2004 |