Effects of chronic heart failure in rats on the recovery of microvascularPO2after contractions in muscles of opposing fibre type

Chronic heart failure (CHF) impairs muscle O2 delivery (QO2) and, at a given O2 uptake (VO2), lowers microvascular O2 pressures (PmvO2: determined by the QO2-to-VO2 ratio), which may impair recovery of high-energy phosphates following exercise. Because CHF preferentially decreases QO2 to slow-twitch muscles, we hypothesized that recovery PmvO2 kinetics would be slowed to a greater extent in soleus (SOL: ∼84% type I fibres) than in peroneal (PER: ∼14% type I) muscles of CHF rats. PmvO2 dynamics were determined in SOL and PER muscles of control (CON: n= 6; left ventricular end-diastolic pressure, LVEDP: ∼3 mmHg), moderate CHF (MOD: n= 7; LVEDP: ∼11 mmHg) and severe CHF (SEV: n= 4; LVEDP: ∼25 mmHg) following cessation of electrical stimulation (180 s; 1 Hz). In PER, neither the recovery PmvO2 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 PmvO2, at recovery onset, was reduced significantly in the SEV group (∼6 Torr) and PmvO2 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 PmvO2 recovery following contractions and lowers capillary O2 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.