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Chronic heart failure (CHF) induces muscle fiber-type specific alterations in skeletal muscle O(2) delivery and utilization during metabolic transitions. As a result, the recovery of microvascular Po(2) (Pmv(O(2))) is prolonged in slow-twitch skeletal muscle but not fast-twitch skeletal muscle in rats with CHF. We tested the hypothesis that CHF slows Pmv(O(2)) recovery in rat skeletal muscle of a mixed fiber-type analogous to human locomotory muscles and that the degree of slowing correlates with central indexes of heart failure. Healthy control [n = 6, left ventricular end-diastolic pressure (LVEDP): 10 ± 1 mmHg], moderate CHF (n = 6, LVEDP: 18 ± 2 mmHg), and severe CHF (n = 4, LVEDP: 34 ± 2 mmHg) female Sprague-Dawley rats had their right spinotrapezius muscles (41% type I, 7% type IIa, and 52% type IIb and d/x) exposed, and Pmv(O(2)) was measured via phosphorescence quenching during 180 s of recovery from 180 s of electrically induced twitch contractions (1 Hz, 4-6 V). CHF progressively slowed the mean response time (MRT; the time to reach 63% of the overall dynamic response) of Pmv(O(2)) recovery (MRT(off); control: 60.2 ± 6.9, moderate CHF: 72.8 ± 6.6, and severe CHF: 109.8 ± 6.6 s, P &lt; 0.05 for all). MRT(off) correlated positively with central hemodynamic (LVEDP: r = 0.76, P &lt; 0.01) and morphological (right ventricle-to-body weight ratio: r = 0.74, P &lt; 0.01; and lung weight-to-body weight ratio: r = 0.79, P &lt; 0.01) indexes of heart failure. The present investigation suggests that slowed Pmv(O(2)) kinetics during recovery in CHF constitutes a mechanistic link between impaired circulatory and metabolic recovery after contractions in CHF.

Progressive chronic heart failure slows the recovery of microvascular O2pressures after contractions in the rat spinotrapezius muscle

Progressive chronic heart failure slows the recovery of microvascular O₂pressures after contractions in the rat spinotrapezius muscle