| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 University of Waterloo
2 University of Manitoba
3 Queens University
4 Queen's University
* To whom correspondence should be addressed. E-mail: green{at}healthy.uwaterloo.ca.
The objective of this study was to investigate the hypothesis that alterations in sarcoplasmic reticulum (SR) Ca2+-cycling properties would occur in skeletal muscle in patients with moderate to severe chronic obstructive pulmonary disease (COPD). To investigate this hypothesis, tissue samples were obtained from the vastus lateralis of 8 patients with COPD (age 67.4±2.4 yrs; FEV1/FVC=44±2%; mean±SE) and 10 healthy age-matched controls (CON, age 67.5±0.96 yrs; FEV1/FVC=77±2%) and homogenates analyzed for a wide range of SR properties. As compared to CON, COPD displayed (in umol.g protein.min-1) a 16% lower maximal Ca2+-ATPase activity (Vmax, 158±10 vs 133±7, P<0.05) and a 17% lower Ca2+-uptake (4.65±0.039 vs 3.85±0.26, P<0.05) which occurred in the absence of differences in Ca2+-release. The lower Vmax in COPD was also accompanied by an 11% lower (P<0.05) Ca2+-sensitivity, as measured by the Hill coefficient (defined as the relationship between Ca2+-ATPase activity and [Ca2+]f for 10-90% Vmax). For the SERCA isoforms, SERCA1a was 16% higher (P<0.05) and SERCA2a was 14% lower (P<0.05) in COPD. It is concluded that moderate to severe COPD results in abnormalities in SR Ca2+-ATPase properties, which cannot be explained by changes in the SERCA isoform phenotypes. The reduced catalytic properties of SERCA in COPD suggest a disturbance in Ca2+-cycling, possibly resulting in impairment in Ca2+-mediated mechanical function and/or second messenger regulated processes.
This article has been cited by other articles:
|
|
 |
|
  A. Ogawa, A. L. Firth, W. Yao, M. M. Madani, K. M. Kerr, W. R. Auger, S. W. Jamieson, P. A. Thistlethwaite, and J. X.-J. Yuan Inhibition of mTOR attenuates store-operated Ca2+ entry in cells from endarterectomized tissues of patients with chronic thromboembolic pulmonary hypertension Am J Physiol Lung Cell Mol Physiol, October 1, 2009; 297(4): L666 - L676. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M.-A. Caron, R. Debigare, P. N. R. Dekhuijzen, and F. Maltais Comparative assessment of the quadriceps and the diaphragm in patients with COPD J Appl Physiol, September 1, 2009; 107(3): 952 - 961. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. J. Green, M. E. Burnett, C. L. D'Arsigny, D. E. O'Donnell, J. Ouyang, and K. A. Webb Altered metabolic and transporter characteristics of vastus lateralis in chronic obstructive pulmonary disease J Appl Physiol, September 1, 2008; 105(3): 879 - 886. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. O'Donnell and K. Webb Last Word on Point:Counterpoint: The major limitation to exercise performance in COPD is 1) inadequate energy supply to the respiratory and locomotor muscles, 2) lower limb muscle dysfunction, 3) dynamic hyperinflation J Appl Physiol, August 1, 2008; 105(2): 765 - 765. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
