REF-1180 · Burd et al., 2012 · Journal of Physiology · Paper · PubMed · Free full text

Do slow reps switch on mitochondria?

One bout of 30% 1RM at 6 s up/6 s down to failure raised mitochondrial protein synthesis 114% at 0-6 h; fast reps short of failure did not, but both did by 24-30 h. n=8, acute, not mitochondrial growth.

C+thin evidenceMeasured on recreational people

Burd, Phillips and colleagues had 8 resistance-trained men do unilateral knee extension at 30% of 1RM. One leg did three sets with 6-s concentric and 6-s eccentric actions with no pauses until failure (SLOW); the other leg did the same load and the same number of repetitions with 1-s actions, which did not reach failure (CTL).

Sets lasted 198, 119 and 90 s in SLOW against 25, 14 and 11 s in CTL (total 407 vs 50 s). They took 20 g whey after exercise and again at 24 h, and biopsies under a labelled phenylalanine infusion at rest, 6 h, 24 h and 30 h.

Mitochondrial protein synthesis rose 2.1-fold over rest at 0-6 h only in SLOW (the abstract's +114%); sarcoplasmic synthesis rose 1.8-fold (+77%) only in SLOW. Myofibrillar synthesis did not rise in the first 6 h in either leg, then rose 2.3-fold at 24-30 h in SLOW only. At 24-30 h mitochondrial synthesis was raised in both legs (2.8-fold SLOW, 2.3-fold CTL).

PGC-1α mRNA rose about 3-fold at 6 h with no difference between legs. The authors conclude that longer time under tension increased the acute amplitude of mitochondrial and sarcoplasmic synthesis and produced a delayed rise in myofibrillar synthesis.

How this bears on the Russian static-dynamic method (Seluyanov): indirect, acute only, though in form it is close. 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 with short rests, grow type I fibres and their mitochondria and so improve endurance.

SLOW used a light load, continuous movement with no pauses, failure and long sets (90-198 s), so it is one of the nearest acute analogues in the literature; the repetitions (12 s) were much slower and the rest (2 min) longer than the method usually prescribes. It shows a faster early rise in mitochondrial protein synthesis after one session.

It does not show more mitochondria, fibre-type-specific effects, or any training or endurance outcome, and by the next day the fast, non-failure bout had raised mitochondrial synthesis too. Because the control leg also differed in failure, the effect cannot be pinned on tempo or tension time alone.

Protocol

Participants: 8 men, 23.5 ± 1 years (SEM), 88.3 ± 5 kg, BMI 26.5; lower-body resistance training at least 2 times a week for at least 2 years. Unilateral 1RM 105 ± 6 and 101 ± 6 kg (right and left).
SLOW leg: 30% 1RM (31 ± 2 kg); 6 s concentric, 6 s eccentric, "no pauses", to volitional failure (unable to lift through full range, or other joints joining in); 3 sets, 2 min rest; repetitions 12 ± 1, 7 ± 1 and 6 ± 1.
CTL leg: same load (30 ± 2 kg) and same repetitions, 1 s concentric and 1 s eccentric, not to failure; 3 sets, 2 min rest.
Relaxation and range: continuous movement through the full range in SLOW; no isometric hold described.
Time under tension: SLOW 198 ± 10, 119 ± 9 and 90 ± 7 s per set (407 ± 23 s total); CTL 25 ± 2, 14 ± 1 and 11 ± 1 s (50 ± 3 s).
Nutrition and sampling: overnight fast; 20 g whey immediately after exercise and again at 24 h; L-[ring-13C6]phenylalanine infusion; vastus lateralis biopsies fasted at rest, then at 6 h, 24 h and 30 h in both legs; EMG during exercise.
Single session; no training period.

Key Results

Outcome (n = 8)SLOWCTLStatistics
Total time under tension407 ± 23 s50 ± 3 sP < 0.001
Mitochondrial protein synthesis, 0-6 h2.1-fold over rest (abstract +114%)not raisedSLOW P = 0.018 vs fasted
Mitochondrial protein synthesis, 24-30 h2.8-fold (abstract +175%)2.3-fold (abstract +126%)SLOW P < 0.001, CTL P = 0.002 vs fasted; no SLOW vs CTL difference reported
Sarcoplasmic protein synthesis, 0-6 h1.8-fold (abstract +77%)not raisedSLOW P < 0.001; SLOW > CTL P = 0.001
Myofibrillar protein synthesis, 0-6 hnot raisednot raisedboth P > 0.05
Myofibrillar protein synthesis, 24-30 h2.3-foldnot raisedP < 0.001; SLOW > CTL (abstract P < 0.001)
p70S6K phosphorylation, 24 h3.4-foldnot raisedP = 0.002; SLOW > CTL P = 0.004; r = 0.42 with 24-30 h myofibrillar synthesis (P = 0.02)
PGC-1α mRNA, 6 h~3-fold~3-foldtime effect P = 0.001 (abstract P < 0.001); no difference between conditions
Vastus lateralis EMGhigher than CTL late in sets 1-2 and throughout set 3P < 0.05

Mechanisms

Measured: the slow failure bout raised mitochondrial and sarcoplasmic protein synthesis early (0-6 h) and myofibrillar synthesis late (24-30 h); EMG showed greater activation as sets approached failure.
Authors' interpretation: long time under tension, with fatigue leading to full motor-unit recruitment, increases the acute amplitude of mitochondrial and sarcoplasmic synthesis and gives a delayed, feeding-potentiated myofibrillar response; maximal fibre activation is not the sole driver, and volume also matters.
Measured, and against a tension-time-specific mitochondrial effect: at 24-30 h mitochondrial synthesis was raised after the fast non-failure bout as well (2.3-fold vs 2.8-fold), and PGC-1α mRNA rose equally in both legs. Authors' interpretation: the mitochondrial protein pool is sensitive to contraction regardless of the exercise stimulus during longer recovery.
Inference: a higher synthesis rate after one bout is not the same as more mitochondria after training; in REF-1179 six weeks of light lifting to failure raised respiration without raising mitochondrial protein content.
Inference: SLOW differed from CTL in time under tension, in reaching failure and in EMG, so the design cannot separate slow tempo from effort.

Practical Application

Do slow reps switch on mitochondria? One bout of 30% 1RM at 6 s up/6 s down to failure raised mitochondrial protein synthesis 114% at 0-6 h; fast reps short of failure did not, but both did by 24-30 h. n=8, acute, not mitochondrial growth.
Do not read this as "slow reps build mitochondria". It is an acute synthesis signal in 8 men; the training studies with biopsies (REF-1178, tempo not reported in its abstract; REF-1179, 1.75 s down and 1.75 s up) were not slow-tempo protocols and found mitochondrial remodelling or function changes, not a proven gain in mitochondrial content.
Static-dynamic method: an indirect, acute test of a protocol close in form (light load, continuous slow movement, long sets to failure). It supports the idea that such sets stimulate mitochondrial protein turnover more quickly; it does not test fibre-type growth, mitochondrial content, or endurance, and the tempo here (12 s per repetition) is slower than the range in which tempo was neutral for hypertrophy (REF-1176).
For endurance athletes, endurance training remains the base's main lever for mitochondria (REF-465); this paper is a mechanism, not a prescription.

Limitations

Eight men, one session; synthesis rates and signalling only, with no training, mitochondrial content, function or performance outcome.
The control leg differed in three ways at once (tempo, time under tension, failure), so the tempo effect is confounded with effort.
Biopsies at 6, 24 and 30 h only; the early signalling window (0.5-1.5 h) was missed, as the authors note.
Mitochondrial synthesis was measured in an enriched fraction; the protocol is, in the authors' words, far from resembling other resistance protocols studied (about 2 min 16 s per set).
Resistance-trained men fed whey; results may differ in untrained or endurance-trained people.
Funding: Natural Sciences and Engineering Research Council of Canada grant to S. M. Phillips; whey protein donated by Inbalance Nutrition. No competing-interest statement in the text read. The PubMed record also lists a Medical Research Council (UK) grant, MR/K00414X/1, which the paper itself does not mention.
How this entry was checked and changed
Why this level

mechanistic laboratory study, n=8, single session, protein synthesis rates and signalling only, no training or performance outcome; read from the full text

Full text (checked 2026-10-16)
Eight recreationally resistance-trained men (23.5 ± 1 years (sem); 88.3 ± 5 kg), lower body resistance exercise at least 2 times per week for ≥2 years (full text).
SLOW: 6 s concentric phase and a 6 s eccentric phase with no pauses until volitional fatigue; CTL: identical number of repetitions at an equivalent load, but not to failure, 1 s concentric and 1 s eccentric; three sets with 2 min rest (full text).
Load 31 ± 2 kg (SLOW) and 30 ± 2 kg (CTL); repetitions 12 ± 1, 7 ± 1 and 6 ± 1 for sets 1, 2 and 3 (full text).
Time under tension SLOW 198 ± 10 s, 119 ± 9 s, 90 ± 7 s; CTL 25 ± 2 s, 14 ± 1 s, 11 ± 1 s; total 407 ± 23 s vs 50 ± 3 s (full text).
Mitochondrial and sarcoplasmic protein synthesis elevated by 114% and 77% above rest at 0–6 h only in the SLOW condition (full text).
Mitochondrial protein synthesis stimulated 2.1-fold above fasted rest (the paper writes "above fast") (P = 0.018) at 0–6 h only in SLOW; at 24–30 h SLOW (P < 0.001) and CTL (P = 0.002) by 2.8- and 2.3-fold (full text).
Myofibrillar protein synthesis: no detectable increase during 6 h in either condition; 2.3-fold increase at 24–30 h in SLOW (P < 0.001) (full text).
p70S6K phosphorylation 3.4-fold at 24 h only in SLOW (P = 0.002); r = 0.42, P = 0.02 with myofibrillar synthesis (full text).
PGC-1α mRNA increased by ∼3-fold at 6 h, no difference between conditions (P = 0.001) (full text).
Research grant from Natural Sciences and Engineering Research Council of Canada to S.M.P.; whey protein isolate a gift of Inbalance Nutrition (full text).