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Articles in PresS, published online ahead of print November 16, 2001
J Appl Physiol, 10.1152/jap.00116.2001
Submitted on February 5, 2001
Accepted on November 13, 2001
1 Medicine, Surgery, and Research Services, VA Medical Center, Philadelphia, PA, USA; Medicine, Surgery, and Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
2 Exercise Science, University of Georgia, Athens, GA, USA
3 Medicine, Surgery, and Research Services, VA Medical Center, Philadelphia, PA, USA
4 Medicine, Surgery, and Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA; Medicine, Surgery, and Research Services, VA Medical Center, Philadelphia, PA, USA
5 Medicine, Surgery, and Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: sdlevine{at}mail.med.upenn.edu.
To assess the effect of severe COPD on the ability of human diaphragmatic myofibers to aerobically generate adenosine triphosphate (ATP) relative to ATP utilization, we obtained biopsy specimens of the costal diaphragm from seven patients with severe COPD (mean±SEM, age 56±1 years; forced expiratory volume in one second 23±2% predicted; residual volume 267±30% predicted) and seven age-matched control subjects. We categorized all fibers in these biopsies using standard techniques and we carried out the following quantitative histochemical measurements by microdensitometry: (a) succinate dehydrogenase (SDH) activity as an indicator of mitochondrial oxidative capacity; and (b) calcium-activated myosin ATPase (mATPase) activity--the ATPase that represents over 70% of the ATP consumption by contracting muscle. We noted the following: (a) COPD diaphragms had a larger proportion of type I fibers, a lesser proportion of type IIax fibers and the same proportion of type IIa fibers as controls. (b) SDH activities of each of the fiber types was higher in COPD than control diaphragms (P<0.0001); the mean increases (expressed as percent of control values) in types I, IIa, and IIax were 84, 114, and 130%, respectively. (c) COPD elicited no change in mATPase activity of type I and IIa fibers, but qATPase decreased in type IIax fibers (P=0.02). (d) mitochondrial oxidative capacity relative to ATP demand (i.e., SDH/mATPase) was higher (P=0.03) in each of the fiber types in COPD diaphragms than in controls. These results demonstrate that severe COPD elicits an increase in aerobic ATP generating capacity relative to ATP utilization in all diaphragmatic fiber types as well as the previously described fast-to-slow fiber type transformation (Levine et al., N Engl J Med, 337:1799-1806,1997).
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