Comparative Efficacy of Mitochondrial Peptides vs. Anabolic Steroids

What this page compares

Most comparisons of mitochondrial peptides and anabolic steroids argue from mechanism. This page sticks to outcomes: what has actually been measured for each compound, and in whom. (For the mechanism side, see our mechanism comparison of mitochondrial peptides and anabolics.)

The evidence is lopsided. Testosterone's effects on muscle size and strength have been measured in randomized, placebo-controlled trials of healthy young men. SS-31 (elamipretide) has been tested in people, but only in rare mitochondrial diseases, and most of those trials missed their main goals. MOTS-c has never been given to people in a published study.

That gap matters more than any mechanism. When a vendor page says SS-31 "improves muscle strength," the claim traces back to about a dozen patients with Barth syndrome, not to trained lifters.

Testosterone: measured in healthy men

The best-known trial is Bhasin and colleagues' 1996 study in the New England Journal of Medicine. Researchers randomly assigned 43 healthy men to placebo or testosterone, each with or without supervised weight training three times a week. The testosterone groups received 600 mg of testosterone enanthate by injection every week for 10 weeks. Muscle size was measured by MRI and strength by bench press and squat.

The results were clear for a 10-week trial:

• Men who trained and took testosterone gained about 6.1 kg of fat-free mass. Their bench press rose by about 22 kg and their squat by about 38 kg.
• Testosterone without any training still beat placebo. Bench press rose about 9 kg on testosterone versus a 1 kg drop on placebo, and squat rose 16 kg versus 3 kg.
• The researchers found no change in mood or behavior in any group.

A 2001 follow-up from the same group tested whether the effect depends on dose. In 61 men aged 18-35, the researchers first suppressed the men's own testosterone with a GnRH agonist. They then gave weekly testosterone enanthate injections of 25, 50, 125, 300 or 600 mg for 20 weeks. Fat-free mass rose with the dose: about 3.4 kg at 125 mg, 5.2 kg at 300 mg and 7.9 kg at 600 mg. Leg-press strength and leg power also tracked testosterone levels. Fat mass fell as levels rose, while hemoglobin went up and HDL cholesterol went down.

These trials were short and used a single compound in screened, monitored men. Real-world steroid use often stacks several compounds over years of cycles, and trials can't ethically copy that, so long-term risk data come mostly from observational studies. A 2014 Endocrine Society scientific statement, drawing on that literature, links performance-enhancing drug use to a higher risk of death and to cardiovascular, psychiatric, endocrine and liver disorders, plus a withdrawal syndrome after stopping. The short trials and the observational data don't really conflict. They measured different exposures over very different time spans.

SS-31 (elamipretide): measured in rare disease

As of October 2026, elamipretide is a prescription medicine in the US. On September 19, 2025, the FDA granted it accelerated approval as Forzinity to improve muscle strength in people with Barth syndrome who weigh at least 30 kg. The labeled dose is 40 mg by subcutaneous injection once daily. Accelerated approval means the FDA accepted a measure it considers reasonably likely to predict benefit, in this case knee-extensor strength. The agency required a confirmatory randomized trial, which is ongoing.

The label is candid about how thin the evidence is. In a placebo-controlled crossover trial, 12 males with Barth syndrome received 40 mg a day for 12 weeks and placebo for 12 weeks. Elamipretide was not better than placebo on either primary endpoint, six-minute walk distance or a fatigue score. Knee strength didn't improve during the randomized phase either. It rose only in the open-label extension, where everyone got the drug: the median gain ranged from 34 to 68 newtons across visits, from a starting median of 124 newtons, in the 8-10 patients who stayed in. Without a control group, that rise is hard to separate from practice effects, which is why the confirmatory trial matters.

The largest efficacy trial also missed. MMPOWER-3 was a Phase 3 trial in 218 adults with primary mitochondrial myopathy, randomized to 40 mg a day or placebo for 24 weeks. Six-minute walk distance differed from placebo by -3.2 meters, which was not statistically significant, and fatigue scores didn't separate either. The authors did report that the drug was well tolerated, with mostly mild-to-moderate adverse events.

Tolerated isn't the same as side-effect free. In the Barth crossover trial, injection-site redness occurred in all 12 patients on elamipretide versus 3 of 12 on placebo. Injection-site pain affected 75% versus 42%, and hardening and itching each affected 67% versus 17%. The label also warns that serious allergic reactions have been reported, and eosinophil counts often rose with use lasting 30 days or more.

No published study has measured elamipretide's effect on performance in healthy people. Dose is another gap. Forum users commonly describe roughly 0.5-4 mg a day, according to the community reports summarized in our SS-31 entry, which is far below the 40 mg used in trials. So even the rare-disease results don't describe what most users take. The site rates SS-31's evidence as moderate: real human trials, but a narrow approval and several missed primary endpoints. As of October 2026, WADA doesn't name SS-31, and its status since approval is unverified.

MOTS-c: measured in mice

MOTS-c's performance reputation comes from mouse work. A 2015 Cell Metabolism paper reported that MOTS-c prevented diet-induced obesity and insulin resistance in mice. A 2021 Nature Communications study reported better physical performance in mice of all ages given MOTS-c, including old mice that started treatment three times a week late in life.

The human part of that 2021 study is observational. Exercise raised people's own MOTS-c levels in muscle and blood; nobody was given the peptide. Two of the authors disclosed that they were consultants and shareholders of CohBar, the company then developing a MOTS-c analog.

As of October 2026, we found no peer-reviewed study that gave native MOTS-c to people. The only related human trial used that analog, CB4211, which is a different molecule. CohBar's Phase 1b gave 25 mg by subcutaneous injection daily for 4 weeks to about 20 adults with obesity and fatty liver. The company reported lower liver enzymes (ALT and AST) than placebo, but liver fat fell substantially in both groups. CB4211 is no longer in development. A Phase 2 registry entry for native MOTS-c exists, but its sponsor's records are disputed, and it has reported nothing.

The site rates MOTS-c's evidence as emerging, based on consistent animal data. Users commonly report better endurance on MOTS-c, while others notice nothing, and itchy injection-site welts are a frequent complaint. None of these reports can rule out placebo effects or check what was in the vial. As of October 2026, WADA's 2026 Prohibited List names MOTS-c under metabolic modulators (S4.4.1), so it is banned at all times for tested athletes.

Side by side: what has been measured

One caution about reading this table. "No human data" means the question hasn't been tested, not that the answer is zero. For how these differences play out on strength versus endurance measures, see our performance-outcome comparison.

What we still don't know

• Whether elamipretide's confirmatory trial shows that the knee-strength change in Barth syndrome reflects real benefit.
• Whether SS-31 or MOTS-c changes any performance measure in healthy, trained people. As of October 2026, no such trial has been published.
• Whether the low doses users describe do anything measurable, since trials of SS-31 used 40 mg a day and native MOTS-c has no human dose-finding data.
• What long-term use of either peptide does in healthy people, which our page on long-term health implications covers in more detail.

For how SS-31 and MOTS-c compare with each other, see our comparison of mitochondrial peptides.