Figure 7. Limb muscle mitochondrial response to non-ischemic injury.

Non-ischemic muscle regeneration was induced by cardiotoxin (CTX) injection. Paw tissue oxygen saturation (%SO₂), measured via white light reflectance spectroscopy, was analyzed to determine distal limb O₂ (A). B. Mitochondrial respiration (oxygen consumption rate-JO₂, as a measure of electron transport system flux) was measured in isolated mitochondria using high-resolution respirometry. The respiratory states assessed were: 1.) glutamate/malate supported state 2 respiration (GM) 2.) glutamate/malate supported state 3 (ADP) 3.) GM and succinate supported state 3 (SUCC) 4.) succinate supported state 3 (ROT) 5.) ascorbate/TMPD supported state 3 (ASC/TMPD) and 6.) FCCP supported state 3 uncoupled respiration (FCCP). Data are representative of the ratio of the injured limb (L) to the untreated control limb (R). * P<0.05 vs. C57BL/6. C. Ca²⁺ reuptake was measured in injured (L) and control (R) limb mitochondria isolated from the plantar flexors (gastrocnemius, plantaris, and soleus) as a function of mitochondrial integrity and resistance to permeability transition. Data are representative of the ratio of the ischemic (L) to the non-ischemic (R) limb, mean ± SEM and representative of N≥6/strain/time point. * P<0.05 vs. day matched C57BL/6.