Load-matched acute and chronic exercise induce changes in mitochondrial biogenesis and metabolic markers.

We investigated the effects of acute and chronic exercise, prescribed in different intensity zones, but with total load-matched on mitochondrial markers (cytochrome C oxidase subunit IV (COX-IV), mitochondrial transcription factor A (Tfam), and citrate synthase (CS) activity in skeletal muscles, heart, and liver), glycogen stores, aerobic capacity, and anaerobic index in swimming rats. For this, 2 experimental designs were performed (acute and chronic efforts). Load-matched exercises were prescribed below, above, and on the anaerobic threshold (AnT), determined by the lactate minimum test. In chronic programs, 2 training prescription strategies were assessed (monotonous and linear periodized model). Results show changes in glycogen stores but no modification in the COX-IV and Tfam contents after acute exercises. In the chronic protocols, COX-IV and Tfam proteins and CS adaptations were intensity- and tissue-dependent. Monotonous training promoted better adaptations than the periodized model. Training at 80% of the AnT improved both performance variables, emphasizing the anaerobic index, concomitant to CS and COX-IV improvement (soleus muscle). The aerobic capacity and CS activity (gastrocnemius) were increased after 120% AnT training. In conclusion, acute exercise protocol did not promote responses in mitochondrial target proteins. An intensity and tissue dependence were reported in the chronic protocols, highlighting training at 80 and 120% of the AnT. Load-matched acute exercise did not enhance COX-IV and Tfam contents in skeletal muscles, heart, and liver. In chronic exercise, COX-IV, Tfam, and CS activity adaptations were intensity- and tissue-dependent. Monotonous training was more efficient than the periodized linear model in adaptations of target proteins and enzymatic activity.