Why the study?
Does selective breeding for high endurance running capacity increase arteriolar microvasculature branching in the myocardium and gastrocnemius muscle of rats?
Does selective breeding for high endurance running capacity increase arteriolar microvasculature branching in the myocardium and gastrocnemius muscle of rats?
High endurance running capacity in selectively bred rats is achieved without alterations in the architecture of the microvasculature, suggesting increased endothelial tolerance for shear stress or metabolic efficiency.
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Challenges hypothesis that arteriolar branching drives endurance in this rat model; leaves open endothelial tolerance or metabolic efficiency as alternative mechanisms.
We tested the hypothesis that changes in the arteriolar branching architecture contributed to increased running capacity of rats subjected to two-way artificial selection for intrinsic aerobic endurance treadmill running capacity resulting in strains of low-capacity and high-capacity endurance rats. Hearts and gastrocnemius muscles were harvested from each strain, and the microvasculature's branching geometry measured from micro-CT images. The vascular branching geometry of the hearts and skeletal muscle from the high capacity was indistinguishable from low-capacity rats. Our hypothesis was not supported. Neither remodeling nor an increase in arteriolar microvasculature branching appears to play a role in the enhanced performance of the high capacity rats. We are led to speculate that endothelial tolerance for shear stress and/or increased coupling of myocardial muscle fiber metabolic-to-contractile function is increased in the high-capacity runner strain to the effect of allowing either higher flow rate per unit volume of muscle or more efficient use of oxygen and nutrients in the high-capacity endurance rats.
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Beighley et al. (2012) studied this question.
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