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Continued divergence in O_{2 max} of rats artificially selected for running endurance is mediated by greater convective blood O₂ delivery

¹University of Kansas Medical Center, Kansas City, Kansas; ²University of California San Diego, La Jolla, California; and ³University of Michigan, Ann Arbor, Michigan

Submitted 6 December 2005 ; accepted in final form 9 June 2006

We previously showed that after seven generations of artificial selection of rats for running capacity, maximal O₂ uptake (O_{2 max}) was 12% greater in high-capacity (HCR) than in low-capacity runners (LCR). This difference was due exclusively to a greater O₂ uptake and utilization by skeletal muscle of HCR, without differences between lines in convective O₂ delivery to muscle by the cardiopulmonary system (O_{2 max}). The present study in generation 15 (G15) female rats tested the hypothesis that continuing improvement in skeletal muscle O₂ transfer must be accompanied by augmentation in O_{2 max} to support O_{2 max} of HCR. Systemic O₂ transport was studied during maximal normoxic and hypoxic exercise (inspired PO₂ 70 Torr). O_{2 max} divergence between lines increased because of both improvement in HCR and deterioration in LCR: normoxic O_{2 max} was 50% higher in HCR than LCR. The greater O_{2 max} in HCR was accompanied by a 41% increase in O_{2 max}: 96.1 ± 4.0 in HCR vs. 68.1 ± 2.5 ml STPD O₂·min^–1·kg^–1 in LCR (P < 0.01) during normoxia. The greater G15 O_{2 max} of HCR was due to a 48% greater stroke volume than LCR. Although tissue O₂ diffusive conductance continued to increase in HCR, tissue O₂ extraction was not significantly different from LCR at G15, because of the offsetting effect of greater HCR blood flow on tissue O₂ extraction. These results indicate that continuing divergence in O_{2 max} between lines occurs largely as a consequence of changes in the capacity to deliver O₂ to the exercising muscle.

intrinsic exercise capacity; genetic determinants; tissue O₂ diffusive conductance; maximal cardiac output

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