EFFECT OF HEART-FAILURE ON MUSCLE CAPILLARY GEOMETRY - IMPLICATIONS FOR O-2 EXCHANGE

There is strong evidence that chronic heart failure (CHF) impairs skel etal muscle function independent of blood flow and bulk O-2 delivery. Purpose: This investigation sought to determine whether alterations in muscle capillary geometry and surface area that are thought to be pri mary determinants of the efficacy for blood-tissue O-2 exchange might be altered in CHF and contribute to these changes. Methods: Plantaris (fast twitch) and soleus (slow twitch) muscles from control (C) and 6- to 7-wk post myocardial infarcted (CHF) rats were perfusion-fixed in situ. These muscles were analyzed using morphometric techniques that f acilitated determination of muscle sarcomere length, fiber cross-secti onal area, capillary tortuosity and branching coefficient (c(K,0), cap illary length; volume, and surface area. Results: Normalized to a sarc omere length of 2.1 mu m, plantaris fiber cross-sectional area decreas ed by 21% (P < 0.05), and capillary-to-fiber ratio decreased from 2.05 +/- 0.07 in C to 1.79 +/- 0.04 (P < 0.05) in CHF, but these variables were unchanged in soleus. There was no change in c(K,0) or capillary diameter in either muscle, and thus capillary length and surface area per fiber volume remained unchanged. From the measured fiber atrophy a nd capillary involution in plantaris reductions of total muscle capill ary length, volume, and surface area of 11%, 9% and 17%, respectively, are estimated. Conclusion: These changes, coupled with reduced blood flow may impair the effective matching of muscle fiber O-2 delivery to O-2 requirement during repeated muscle contractions (i.e., exercise). This scenario is expected to reduce intramyocyte O-2 partial pressure and thereby contribute to the greater fatigability characteristic of the CHF condition.