Effects of chronic heart failure in rats on the recovery of microvascular PO2 after contractions in muscles of opposing fibre type

Chronic heart failure (CHF) impairs muscle O-2 delivery (QO(2)) and, at a given O-2 uptake (V-O2), lowers microvascular O-2 pressures (P-mvO2: determined by the QO(2) -to- V-O2 ratio), which may impair recovery of high-energy phosphates following exercise. Because CHF preferentially decreases Q(O2) to slow-twitch muscles, we hypothesized that recovery P-mvO2 kinetics would be slowed to a greater extent in soleus (SOL: similar to 84% type I fibres) than in peroneal (PER: similar to 14% type I) muscles of CHF rats. P-mvO2 dynamics were determined in SOL and PER muscles of control (CON: n = 6; left ventricular end-diastolic pressure, LVEDP: similar to3 mmHg), moderate CHF (MOD: n = 7; LVEDP: similar to11 mmHg) and severe CHF (SEV. n = 4; LVEDP: similar to25 mmHg) following cessation of electrical stimulation (180 s; 1 Hz). In PER, neither the recovery P-mvO2 values nor the mean response time (MRT; a weighted average of the time to 63% of the overall response) were altered by CHF (CON: 66.8 +/- 8.0, MOD: 72.4 +/- 11.8, SEV: 69.1 +/- 9.5 s). In marked contrast, SOL P-mvO2, at recovery onset, was reduced significantly in the SEV group (similar to6 Torr) and P-mvO2 MRT was slowed with increased severity of CHF (CON: 45.1 +/- 5.3, MOD: 63.2 +/- 9.4, SEV: 82.6 +/- 12.3 s; P < 0.05 CON vs. MOD and SEV). These data indicate that CHF Slows P-mvO2 recovery following contractions and lowers capillary O-2 driving pressure in slow-twitch SOL, but not in fast-twitch PER muscle. These results may explain, in part, the slowed recovery kinetics (phosphocreatine and VO2) and pronounced fatigue following muscular work in CHF patients.