In rat spinotrapezius muscle, chronic heart failure (CHF) speeds microvascular O 2 pressure ( p O 2 ; index of O 2 delivery-to-O 2 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 p O 2 dynamics in different fiber types remains unclear. Objective: Based upon derangements of endothelial function and blood flow responses, we hypothesized that CHF would speed microvascular p O 2 dynamics (reduced O 2 delivery-to-O 2 uptake ratio) in type I muscle (soleus, <IMG SRC="/math/sim.gif" ALT="~" BORDER="0">84% type I), but not in type II muscle (peroneal, <IMG SRC="/math/sim.gif" ALT="~" BORDER="0">86% type II [J. Appl. Physiol. 80 (1996) 261]). Methods: Using phosphorescence quenching, microvascular p O 2 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. Results: The microvascular p O 2 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 <IMG SRC="/math/le.gif" ALT="≤" BORDER="0">0.05), but not in peroneal (control=moderate=severe). Conclusion: As type I fibers are recruited predominately for moderate intensity exercise, the more rapid lowering of soleus microvascular p O 2 in CHF would reduce the blood-muscle O 2 driving gradient, exacerbate phosphocreatine and glycogen breakdown, and provide a mechanism for slowed O 2 uptake kinetics and premature fatigue in CHF.
Copyright (C) 2004, European Society of Cardiology
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