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1 University of California San Diego, La Jolla, California 92093; 2 University of Kansas Medical Center, Kansas City, Kansas 66160; and 3 Medical College of Ohio, Toledo, Ohio 43614
To
attempt to explain the difference in intrinsic (untrained) endurance
running capacity in rats selectively bred over seven generations for
either low (LCR) or high running capacity (HCR), the relationship among
skeletal muscle capillarity, fiber composition, enzyme activity, and
O2 transport was studied. Ten females from each
group [body wt: 228 g (HCR), 247 g (LCR); P = 0.03] were studied at 25 wk of age. Peak normoxic maximum
O2 consumption and muscle O2 conductance were
previously reported to be 12 and 33% higher, respectively, in HCR,
despite similar ventilation, arterial O2 saturation, and a
cardiac output that was <10% greater in HCR compared with LCR. Total
capillary and fiber number in the medial gastrocnemius were similar in
HCR and LCR, but, because fiber area was 37% lower in HCR, the number
of capillaries per unit area (or mass) of muscle was higher in HCR by
32% (P < 0.001). A positive correlation
(r = 0.92) was seen between capillary density and
muscle O2 conductance. Skeletal muscle enzymes citrate
synthase and
-hydroxyacyl-CoA dehydrogenase were both ~40% higher
(P < 0.001) in HCR (12.4 ± 0.7 vs. 8.7 ± 0.4 and 3.4 ± 0.2 vs. 2.4 ± 0.2 mmol · kg
1 · min
1,
respectively), whereas phosphofructokinase was significantly (P = 0.02) lower in HCR (27.8 ± 1.2 vs. 35.2 ± 2.5 mmol · kg
1 · min
1)
and hexokinase was the same (0.65 ± 0.04 vs. 0.65 ± 0.03 mmol · kg
1 · min
1).
Resting muscle ATP, phosphocreatine, and glycogen contents were not
different between groups. Taken together, these data suggest that, in
rats selectively bred for high-endurance exercise capacity, most of the
adaptations for improved O2 utilization occur peripherally
in the skeletal muscles and not in differences at the level of the
heart or lung.
oxidative capacity; vascularization; genetic variation; mitochondria; aerobic exercise; genetic models
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