Impaired skeletal muscle fatigue resistance in metabolic syndrome is associated with alterations in microvascular hematocrit levels and variability (675.3)

Vascular dysfunction in metabolic syndrome is associated with poor performance of in situ skeletal muscle. Prior to impaired function in skeletal muscle itself, this reflects a failure to effectively perfuse working muscle. While altered vascular reactivity, arteriolar wall stiffness and microvessel rarefaction have been implicated, the accumulated impact on mass transport/exchange is unknown. Using tracer washout and existing models for microvascular hematocrit (HMV) and permeability‐surface area product (PS), we determined these parameters for in situ skeletal muscle of lean (LZR) and obese Zucker (OZR) rats. HMV in OZR was less than for LZR; treatment with adrenergic blockers or anti‐oxidants improved HMV slightly, but imposition of all agents restored HMV fully. PS, reduced in OZR vs. LZR, was not impacted by intervention. Using in situ cremaster muscle, HMV was determined in individual microvessels. Similar to above, HMV was reduced in OZR vs. LZR, although variability was higher; with post‐intervention changes mirroring that from washout experiments. These data suggest a low, spatially variable, HMV and global loss in surface area are contributors to poor muscle performance in OZR. Grant Funding Source : Supported by National Institutes of Health and American Heart Association