Do light loads to failure build slow fibres and mitochondria?

Lim, Phillips, Kim and colleagues randomised 21 young men to 10 weeks of leg press, leg extension and leg curl three times a week in one of three conditions: 80% of one-repetition maximum (1RM) to volitional fatigue (80FAIL), 30% 1RM to volitional fatigue (30FAIL), or 30% 1RM with volume matched to 80FAIL and therefore stopping short of fatigue (30WM).

They took vastus lateralis biopsies before and after. Only 30FAIL and 80FAIL increased peak torque and type I fibre cross-sectional area (P < 0.05). Only 30FAIL lowered the myonuclear domain of type II fibres and increased mitochondrial proteins related to autophagy, fission and fusion (all P < 0.05).

The authors conclude that low-load training increased the content of several mitochondrial proteins and that gains in muscle mass and strength were independent of load when repetitions went to volitional fatigue.

How this bears on the Russian static-dynamic method (Seluyanov): indirect, and not a slow-tempo protocol as far as the abstract states. The method's claims (practice descriptions, not this paper) are that slow, continuous-tension sets of roughly 30-60 s at a light load, taken to a burning sensation, grow type I fibres and their mitochondria and so improve endurance.

Here a light load to failure did grow type I fibres and raise some mitochondrial proteins, which is in the direction of those claims, but (1) the repetitions were not slow or no-relaxation as far as the abstract states, (2) heavy training to failure grew type I fibres too, so type I growth was not specific to light loads, (3) the proteins that rose govern mitochondrial turnover and remodelling, which the abstract does not equate with more mitochondria, and (4) no endurance outcome was measured.

The light load short of failure, at the same volume as heavy training, showed no significant change; 30FAIL differed from it in both effort (failure) and total volume, so the abstract cannot say which of the two carried the effect.