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 ( Pmvo(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 Pmvo(2) than observed in young rats with CHF. Phosphorescence quenching was utilized to measure spinotrapezius Pmvo(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 Pmvo(2) ( 32.3 +/- 3.4 Torr for Y-CHF and 21.3 +/- 3.3 Torr for O-CHF; P < 0.05) and in both YCHF and OCHF 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, PmvO2 values in OCHF vs. YCHF were substantially lower ( for steady- state, 20.4 +/- 1.7 Torr for YCHF and 16.4 +/- 2.0 Torr for OCHF; P < 0.05). At rest and during contractions in CHF, the pressure driving blood- muscle O-2 diffusion ( PmvO2) 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 O-2 exchange and support mitochondrial ATP production.