FIGURE 1.

Bcl2-mediated autophagy is not required for mitochondrial respiratory adaptations to exercise training. Mitochondrial respiration of isolated mitochondria from quadriceps muscle of wild-type and Bcl2^AAA mice that performed 8 wk of exercise training (EX) or remained sedentary (SED). A, Complex I (CI) and complex II (CII) substrate-linked oxygen consumption (JO₂) during oxidative phosphorylation (P) with nonlimiting ADP. Rates of JO₂ are expressed as absolute units (pmol O₂/mL/sec; left) and relative to protein content (pmol O₂/μg protein/sec; right). B, CI and CII substrate-linked oxygen consumption (JO₂) during leak (L) respiration after the addition of oligomycin, a complex V inhibitor. Rates of JO₂ are expressed as relative units (pmol O₂/μg protein/sec). C, CI and CII substrate-linked oxygen consumption (JO₂) during uncoupled electron transfer system (E) respiration after the addition of the chemical uncoupler, FCCP (left) and after the addition of rotenone, a CI inhibitor (right). Rates of JO₂ are expressed as relative units (pmol O₂/μg protein/sec). Data are means ± SD; n = 12–17. Two-way ANOVAs were used to test for effects of exercise and genotype. P values are main effects