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Aging potentiates the effect of congestive heart failure on muscle microvascular oxygenation

¹Division of Exercise Physiology, and the Center for Interdisciplinary Research in Cardiovascular Sciences, West Virginia University School of Medicine, Morgantown, West Virginia; and ²Departments of Anatomy, Physiology and Kinesiology, Kansas State University College of Veterinary Medicine, Manhattan, Kansas

Submitted 4 May 2007 ; accepted in final form 27 August 2007

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 (O₂) and utilize (O₂) oxygen in skeletal muscle. Whether aging potentiates the CHF-induced alterations in the O₂-to-O₂ relationship [which determines microvascular PO₂ (Pmv_O2)] 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 Pmv_O2 than observed in young rats with CHF. Phosphorescence quenching was utilized to measure spinotrapezius Pmv_O2 at 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 Y_CHF and O_CHF). In CHF muscle, aging significantly reduced resting Pmv_O2 (32.3 ± 3.4 Torr for Y_CHF and 21.3 ± 3.3 Torr for O_CHF; P < 0.05) and in both Y_CHF and O_CHF compared with their aged-matched counterparts, CHF reduced the rate of the Pmv_O2 fall at the onset of contractions. Moreover, across the on-transient and in the subsequent steady state, Pmv_O2 values in O_CHF vs. Y_CHF were substantially lower (for steady-state, 20.4 ± 1.7 Torr for Y_CHF and 16.4 ± 2.0 Torr for O_CHF; P < 0.05). At rest and during contractions in CHF, the pressure driving blood-muscle O₂ diffusion (Pmv_O2) is substantially decreased in old animals. This finding suggests that muscle dysfunction and exercise intolerance in aged CHF patients might be due, in part, to the failure to maintain a sufficiently high Pmv_O2 to facilitate blood-muscle O₂ exchange and support mitochondrial ATP production.

heart failure; skeletal muscle; oxygen exchange

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