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1 Departments of Kinesiology, Anatomy & Physiology, Kansas State University, Manhattan, KS, USA
2 Department of Medicine, University of California, San Diego, La Jolla, CA, USA
* To whom correspondence should be addressed. E-mail: poole{at}vet.ksu.edu.
Chronic heart failure (CHF) reduces muscle blood flow at rest and during exercise and these alterations are associated with impaired muscle function and exercise intolerance. We utilized intravital microscopy techniques to study spinotrapezius muscle capillary hemodynamics in control (C) and CHF rats at rest and in response to electrically-induced muscle contractions. We tested the hypothesis that both the speed and amplitude of the capillary red blood cell (RBC) velocity (VRBC) and flux (FRBC) response to contractions would be reduced in CHF compared with C muscle. The proportion of capillaries supporting continuous RBC flow was less (p<0.05) in CHF (0.66 ± 0.04) compared with C (0.84 ± 0.01) muscle at rest and was not significantly altered (p>0.05) with contractions. At rest, VRBC (C, 270 ± 62; CHF, 179 ± 14 µm/s) and FRBC (C, 22.4 ± 5.5 vs. CHF, 15.2 ± 1.2 RBC's/s) were reduced (both p<0.05) in CHF compared with C muscle. Contractions significantly (both p<0.05) elevated VRBC (C, 428 ± 47 vs. CHF, 222 ± 15 µm/s) and FRBC (C, 44.3 ± 5.5 vs. CHF, 24.0 ± 1.2 RBC's/s) in both C and CHF muscle, however both VRBC and FRBC remained significantly (p<0.05) less in CHF vs. C. The speed of the increase at contractions onset, assessed via time to 50% of the overall amplitude, was slowed (both p<0.05) in CHF compared with C for both VRBC (C, 8 ± 4; CHF, 56 ± 11 s) and FRBC (C, 11 ± 3; CHF, 65 ± 11 s). Contractions elicited a significant rise (both p<0.05) in capillary hematocrit in C and CHF muscle, however values were not different (p>0.05) between the two groups either at rest, during or following contractions. These data demonstrate that CHF impairs both diffusive and conductive O2 delivery across the rest-to-contractions transition in rat skeletal muscle thus providing a mechanistic basis for the increased metabolic perturbations and slowed O2 uptake on-kinetics manifested in CHF at the onset of a given exercise workload.
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