Lower-load (LL), higher-repetition resistance exercise training (RET) can increase muscle mass in a similar degree as higher-load (HL), lower-repetition RET. However, little is known about how LL and HL RET modulate other aspects of the RET phenotype such as satellite cells, myonuclei, and mitochondrial proteins. We aimed to investigate changes in muscle mass, muscle strength, satellite cell activity, myonuclear addition, and mitochondrial protein content after prolonged RET with LL and HL RET.
We recruited 21 young men and randomly assigned them to perform 10 wk RET (leg press, leg extension, and leg curl) three times per week with the following conditions: 80FAIL (80% one-repetition maximum [1RM] performed to volitional fatigue), 30WM (30%1RM with volume matched to 80FAIL), and 30FAIL (30%1RM to volitional fatigue). Skeletal muscle
biopsies were taken from the vastus lateralis pre- and post-RET intervention.
After 10 wk of RET, only 30FAIL and 80FAIL showed an increase in peak torque and type I fiber cross-sectional area (P
< 0.05). Moreover, only 30FAIL resulted in a significant decrease in the myonuclear domain of type II muscle fibers and an increase in mitochondrial proteins related to autophagy, fission, and fusion (all P
We discovered that LL RET was effective at increasing the content of several mitochondrial proteins. Similar to previous research, we found that changes in muscle mass and strength were independent of load when repetitions were performed to volitional fatigue.