| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada
2 Department of Medicine, McMaster University, Hamilton, Ontario, Canada
* To whom correspondence should be addressed. E-mail: vbezaire{at}uoguelph.ca.
CPTI is considered the rate-limiting enzyme in the transfer of long chain fatty acids into the mitochondria and is reversibly inhibited by malonyl-CoA (M-CoA) in vitro. In rat skeletal muscle, MCoA levels decrease during exercise releasing the inhibition of CPTI and increasing LCFA oxidation. However, in human skeletal muscle, M-CoA levels do not change during moderate intensity exercise despite large increases in fat oxidation, suggesting that M-CoA is not the sole regulator of increased CPTI activity during exercise. In the present study, we measured CPTI activity in intermyofibrillar (IMF) and subsarcolemmal (SS) mitochondria isolated from human vastus lateralis (VL), and rat soleus (Sol) and red gastrocnemius (RG) muscles. We tested whether exercise-related levels (~65% maximal O2 uptake) of calcium and adenylate charge metabolites (free AMP, ADP, and Pi) could override the M-CoA-induced inhibition of CPTI activity and explain the increased CPTI flux during exercise. Protein content was ~25-40% higher in IMF than SS mitochondria in all muscles. Maximal CPTI activity was similar in IMF and SS mitochondria in all muscles (VL: 282 ± 46 vs. 280 ± 51, Sol: 390 ± 81 vs. 368 ± 82, RG: 252 ± 71 vs. 278 ± 44 nmol.min-1.mg protein-1). Sensitivity to M-CoA did not differ between the IMF and SS mitochondria in all muscles (25-31% inhibition in VL and 52-70% in Sol and RG). Calcium and the adenylate charge metabolites did not override the M-CoA-induced inhibition of CPTI activity in mitochondria isolated from VL, Sol and RG muscles. Decreasing pH from 7.1 to 6.8 reduced CPTI activity by ~34-40% in both VL mitochondrial fractions. In summary, this study reports no differences in CPTI activity or sensitivity to M-CoA between IMF and SS mitochondria isolated from human and rat skeletal muscles. Exercise-induced increases in calcium and adenylate charge metabolites do not appear responsible for upregulating CPTI activity in human or rat skeletal muscle during moderate aerobic exercise.
This article has been cited by other articles:
|
|
 |
|
  G. P. Holloway, S. S. Jain, V. Bezaire, X. X. Han, J. F. C. Glatz, J. J. F. P. Luiken, M.-E. Harper, and A. Bonen FAT/CD36-null mice reveal that mitochondrial FAT/CD36 is required to upregulate mitochondrial fatty acid oxidation in contracting muscle Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2009; 297(4): R960 - R967. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. B. Wilkinson, S. M. Phillips, P. J. Atherton, R. Patel, K. E. Yarasheski, M. A. Tarnopolsky, and M. J. Rennie Differential effects of resistance and endurance exercise in the fed state on signalling molecule phosphorylation and protein synthesis in human muscle J. Physiol., August 1, 2008; 586(15): 3701 - 3717. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. R. Bruce, C. Brolin, N. Turner, M. E. Cleasby, F. R. van der Leij, G. J. Cooney, and E. W. Kraegen Overexpression of carnitine palmitoyltransferase I in skeletal muscle in vivo increases fatty acid oxidation and reduces triacylglycerol esterification Am J Physiol Endocrinol Metab, April 1, 2007; 292(4): E1231 - E1237. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Roepstorff, M. Thiele, T. Hillig, H. Pilegaard, E. A. Richter, J. F. P. Wojtaszewski, and B. Kiens Higher skeletal muscle {alpha}2AMPK activation and lower energy charge and fat oxidation in men than in women during submaximal exercise J. Physiol., July 1, 2006; 574(1): 125 - 138. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Bezaire, C. R. Bruce, G. J. F. Heigenhauser, N. N. Tandon, J. F. C. Glatz, J. J. J. F. Luiken, A. Bonen, and L. L. Spriet Identification of fatty acid translocase on human skeletal muscle mitochondrial membranes: essential role in fatty acid oxidation Am J Physiol Endocrinol Metab, March 1, 2006; 290(3): E509 - E515. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. P. Holloway, V. Bezaire, G. J. F. Heigenhauser, N. N. Tandon, J. F. C. Glatz, J. J. F. P. Luiken, A. Bonen, and L. L. Spriet Mitochondrial long chain fatty acid oxidation, fatty acid translocase/CD36 content and carnitine palmitoyltransferase I activity in human skeletal muscle during aerobic exercise J. Physiol., February 15, 2006; 571(1): 201 - 210. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Kiens Skeletal Muscle Lipid Metabolism in Exercise and Insulin Resistance Physiol Rev, January 1, 2006; 86(1): 205 - 243. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. R. Koves, R. C. Noland, A. L. Bates, S. T. Henes, D. M. Muoio, and R. N. Cortright Subsarcolemmal and intermyofibrillar mitochondria play distinct roles in regulating skeletal muscle fatty acid metabolism Am J Physiol Cell Physiol, May 1, 2005; 288(5): C1074 - C1082. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
