High inborn running capacity (HCR) is a strong predictor for all-cause morbidity and
is considered to affect outcome in cardiac surgery. Mitochondria play a key role in
mediating exercise effects. We demonstrated that genetic predisposition influences
the mitochondrial response to exercise training as rats with HCR responded to exercise
training, while rats with low inborn running capacity did not. Since there are two
types of mitochondria (subsarcolemmal, SSM and interfibrillar, IFM), we assessed the
effect of exercise training on the properties of these two mitochondrial subpopulations
in skeletal muscle of HCR. It is the common notion that IFM generate ATP for contractile
function and SSM for cell and membrane maintenance.
IFM and SSM were isolated by differential centrifugation from M. gastrocnemius of
exercise trained or sedentary HCR. Citrate synthase activity and protein content were
determined photometrically, and respiratory capacity was measured using a Clark-type
electrode.
Exercise training resulted in increased body weight, cardiac hypertrophy, and increased
muscle weight. Exercise increased citrate synthase activity. Respiratory capacity
of SSM was higher than of IFM in sedentary animals with substrates for complex I (173 ± 29
vs. 86 ± 18 all nAtomO/min/mgprot), complex II (260 ± 37 vs. 202 ± 19), complex III
(431 ± 94 vs. 222 ± 34), and complex IV (574 ± 63 vs. 489 ± 42). ADP/O ratios were
not different between SSM and IFM. Exercise training led to an increase in respiratory
capacity in IFM (CI 86 ± 18 vs. 112 ± 17; CII 202 ± 19 vs. 278 ± 42; CIII 222 ± 34
vs. 422 ± 52; CIV 489 ± 42 vs. 620 ±85 nAtoms O/min/mgprot) but not in SSM reducing
the difference between both populations ADP/O ratio was not affected by exercise.
Exercise training in rats improves respiratory capacity only in interfibrillar mitochondria
of skeletal muscle. These data are consistent with the notion that IFM produce ATP
mainly for contractile function.
