Effects of chronic heart failure on microvascular oxygen exchange dynamics in muscles of contrasting fiber type

In rat spinotrapezius muscle, chronic heart failure (CHF) speeds microvascular O2 pressure (pO2; index of O2 delivery-to-O2 uptake) dynamics across the rest-contractions transition [Cardiovasc. Res. 56 (2002) 479]. Due to the mosaic nature of this muscle, the effect of CHF on microvascular pO2 dynamics in different fiber types remains unclear.

Based upon derangements of endothelial function and blood flow responses, we hypothesized that CHF would speed microvascular pO2 dynamics (reduced O2 delivery-to-O2 uptake ratio) in type I muscle (soleus, approximately 84% type I), but not in type II muscle (peroneal, approximately 86% type II [J. Appl. Physiol. 80 (1996) 261]).

Using phosphorescence quenching, microvascular pO2 was measured at rest and across the rest-contractions transition (1 Hz) in soleus and peroneal of non-infarcted control (control; n=7), and Sprague-Dawley rats with moderate (moderate; elevated left ventricular end-diastolic pressure (LVEDP) 10 +/- 2 mm Hg; n=10) and severe (severe; LVEDP 28 +/- 4 mm Hg; n=5) CHF.

The microvascular pO2 mean response time (time delay+time constant) was progressively speeded with increasing severity of CHF in soleus (control, 38.7 +/- 2.0; moderate, 29.1 +/- 1.5; severe, 22.5 +/- 3.9 s; P< or =0.05), but not in peroneal (control=moderate=severe).

As type I fibers are recruited predominately for moderate intensity exercise, the more rapid lowering of soleus microvascular pO2 in CHF would reduce the blood-muscle O2 driving gradient, exacerbate phosphocreatine and glycogen breakdown, and provide a mechanism for slowed O2 uptake kinetics and premature fatigue in CHF.