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1 Division of Exercise Physiology, West Virginia University Sch Med, Morgantown, West Virginia, United States
2 Division of Exercise Physiology, West Virginia Univ Sch Med, Morgantown, West Virginia, United States
3 Department of Kinesiology & Anatomy & Physiology, Kansas State University, Manhattan, Kansas, United States
4 Department of Anatomy and Physiology, Kansas State University - College of Vet. Med., Manhattan, United States
* To whom correspondence should be addressed. E-mail: musch{at}vet.k-state.edu.
Congestive heart failure (CHF) is most prevalent in aged individuals and elicits a spectrum of cardiovascular and muscular perturbations that impairs the ability to deliver (QO2) and utilize (VO2) oxygen in skeletal muscle. Whether aging potentiates the CHF- induced alterations in the QO2-to-VO2 relationship (which determines microvascular O2 pressure, PO2m) in resting and contracting skeletal muscle is unclear. We tested the hypothesis that old rats with CHF would demonstrate a greater impairment of skeletal muscle PO2m than observed in young rats with CHF. Phosphorescence quenching was utilized to measure spinotrapezius PO2mat rest and across the rest-to-contractions (1-Hz, 4-6 V) transition in young (Y) and old (O) male Fischer 344 Brown-Norway rats with CHF induced by myocardial infarction (mean left ventricular end-diastolic pressure >20 mmHg for YCHF and OCHF). In CHF muscle, aging significantly reduced resting PO2m(YCHF, 32.3 ± 3.4, OCHF, 21.3 ± 3.3 mmHg, P<0.05) and in both YCHF and OCHF compared with their aged-matched counterparts, CHF reduced the rate of PO2mfall at the onset of contractions. Moreover, across the on-transient and in the subsequent steady-state PO2mvalues in OCHF versus YCHF were substantially lower (steady-state, YCHF 20.4 ± 1.7, OCHF 16.4 ± 2.0 mmHg, P<0.05). At rest and during contractions in CHF the pressure driving blood-muscle O2 diffusion (PO2m) is decreased in old individuals. This suggests that muscle dysfunction and exercise intolerance in aged CHF patients might be due, in part, to the failure to maintain a sufficiently high PO2m to facilitate blood-muscle O2 exchange and support mitochondrial ATP production.
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