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  • Title: Effects of chronic heart failure on microvascular oxygen exchange dynamics in muscles of contrasting fiber type.
    Author: Behnke BJ, Delp MD, McDonough P, Spier SA, Poole DC, Musch TI.
    Journal: Cardiovasc Res; 2004 Feb 01; 61(2):325-32. PubMed ID: 14736549.
    Abstract:
    UNLABELLED: 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. OBJECTIVE: 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]). METHODS: 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. RESULTS: 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). CONCLUSION: 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.
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