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Computational analyses of oxygen transport suggest that perfusion heterogeneity, not overall oxygen delivery, limits muscle performance in metabolic syndrome (674.7)
Author(s) -
Frisbee Jefferson,
Wu Fan
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.674.7
Subject(s) - perfusion , skeletal muscle , microcirculation , metabolic syndrome , oxygenation , capillary action , oxygen , blood flow , cardiology , oxygen transport , medicine , chemistry , anatomy , mechanics , physics , thermodynamics , obesity , organic chemistry
The ability of in situ skeletal muscle to perform is compromised with development of metabolic syndrome in obese Zucker rats (OZR); a model of vascular disease without atherosclerosis. At 17 weeks, skeletal muscle function appears to be normal, implicating the microcirculation as a major contributor to poor performance; yet actual contributors to this are unclear. We performed computational analyses on single capillary O2 transport in LZR and OZR, using the Krogh model to compute axial PO2 distribution given metabolic rate and capillary diameter. The target variable is ΔPO2 between the capillary center and outer wall of a tissue cylinder. Initial analyses suggest that, assuming uniform microvascular perfusion, the maximum axial ΔPO2 is 13 mmHg in LZR and 10 mmHg in OZR at fatiguing contractions, suggesting that oxygenation in both is sufficient to support metabolism and that O2 consumption is not limited by bulk perfusion in LZR or OZR. Combined with our previous findings on capillary‐level flow distributions [Wu et al., 2011], this implies that increased muscle fatigue in OZR is associated with heterogeneous flow distribution, causing local mismatch between O2 supply and metabolic demand. Grant Funding Source : Supported by National Institutes of Health and American Heart Association