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

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 (Qo(2)) and utilize (Vo(2)) oxygen in skeletal muscle. Whether aging potentiates the CHF-induced alterations in the Qo(2)-to-Vo(2) relationship [which determines microvascular Po(2) (Pmv(O(2)))] 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(O(2)) than observed in young rats with CHF. Phosphorescence quenching was utilized to measure spinotrapezius Pmv(O(2)) 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(O(2)) (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(O(2)) fall at the onset of contractions. Moreover, across the on-transient and in the subsequent steady state, Pmv(O(2)) 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 O(2) diffusion (Pmv(O(2))) 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(O(2)) to facilitate blood-muscle O(2) exchange and support mitochondrial ATP production.