Peptide Health Lab

Goal

Endurance

Also known as: Aerobic capacity, Stamina

A research reference for the compounds mapped to aerobic capacity and stamina. Every one of them is prohibited in tested sport at all times, and only one has a randomized human trial using an endurance endpoint.

Last reviewed August 3, 2026

What "endurance" actually means in the research

Endurance is the goal on this site where the reader is most likely to be a tested athlete, so this page states the anti-doping position before it states anything else: every compound mapped here is prohibited in tested sport at all times, in and out of competition. The section numbers are at the bottom of the page and the short version is in the first framework entry. If you compete under anti-doping rules, that is the whole answer and the rest of this page is background.[7]

With that said, the studies underneath these compounds measured four different things, and none of them is a training block. One measured running performance in mice at three ages, plus circulating and muscle MOTS-c in exercising humans.[8] One measured plasma growth hormone and IGF-1 concentrations in healthy adult volunteers who were not training for anything.[2] One measured the time course of a single growth-hormone release across five infusion rates.[1] One measured treadmill time to exhaustion in physically active young women.[7]

Only the last of those is an endurance endpoint in a human, and it belongs to the compound on this page that is a controlled prescription hormone rather than a research peptide. That inversion, the strongest endurance evidence sitting with the least peptide-shaped compound, is the most useful thing this page can tell an endurance reader.

What the evidence supports

MOTS-c improves physical performance in mice, at every age tested. MOTS-c significantly enhanced physical performance in young, middle-aged, and old mice; it regulated nuclear genes related to metabolism and proteostasis, altered skeletal muscle metabolism, and changed myoblast adaptation to metabolic stress. Intermittent treatment begun late in life increased physical capacity and healthspan.[8] The founding work established what the peptide is doing: skeletal muscle appears to be its primary target organ, it inhibits the folate cycle and de novo purine biosynthesis leading to AMPK activation, and in mice it prevented age-dependent and diet-induced insulin resistance and diet-induced obesity.[5] This is a coherent, well-executed body of animal work.

In humans, exercise raises MOTS-c, not the other way round. The same paper reports that in humans, exercise induces endogenous MOTS-c expression in skeletal muscle and in circulation.[8] That is a real human finding and it is frequently reported as though it were an efficacy result. It is the opposite shape: it makes MOTS-c a marker of the training stimulus, not a demonstrated substitute for it.

Growth hormone and IGF-1 do rise, measurably and for days. Two randomized, placebo-controlled ascending-dose trials of CJC-1295 in healthy adults produced dose-dependent increases in plasma growth hormone of two- to ten-fold lasting six days or more and in IGF-1 of 1.5- to three-fold lasting nine to eleven days, with IGF-1 still above baseline for up to 28 days after multiple doses.[2] Ipamorelin produced a single episode of growth hormone release at every infusion rate tested.[1] These are competent human pharmacology studies. They measured hormone concentrations.

One randomized human trial on this page used an endurance endpoint and hit it. 48 healthy, physically active women aged 18 to 35 were randomized to a daily testosterone cream or placebo for ten weeks. Running time to exhaustion increased by 21.17 seconds over placebo, a gain of 8.5%, and total lean mass rose by 923 g against 135 g. The anaerobic Wingate result did not reach significance, and counter-movement jump, squat jump, and knee extension did not change.[7]

Where the evidence is weak

The surrogate has been tested and it does not carry. If a higher growth hormone concentration were sufficient for endurance, growth hormone itself would deliver it. Pooled across 27 randomized study samples in fit young adults, lean body mass rose about 2.1 kg, strength did not appear to improve, exercise capacity may have worsened, lactate during exercise was significantly higher in two of three studies measuring it, and soft-tissue edema and fatigue were more common. The authors' conclusion is unambiguous: claims that growth hormone enhances physical performance are not supported by the literature.[3] Every argument on this page that runs from "it raises growth hormone" to "it raises endurance" has to get past that result first.

Nobody has given MOTS-c to a person in a published trial. Not for endurance, not for anything. The animal performance data is genuine and the human data is observational and points the other way, and the gap between them is the whole distance between this page and a recommendation.[8]

The one randomized human efficacy trial in this group failed. Ipamorelin was tested in bowel-resection patients for postoperative ileus in a randomized, controlled, proof-of-concept study. It was well tolerated and did not separate from placebo on its key or secondary efficacy endpoints.[4] A negative trial is information, and it is the most rigorous human efficacy information any peptide on this page has produced.

Even the positive human trial has boundaries. It ran ten weeks, in women, using a treadmill test to exhaustion, and its jump and knee-extension outcomes did not move.[7] In older men, testosterone did not significantly change six-minute walking distance in the trial designed to test physical function, and the investigators stated their sample was too small to draw conclusions about the risks of treatment.[6] Two human trials with different populations, different endpoints, and different answers is not a body of evidence for "endurance".

Four weak bases do not sum to a strong one. Mapping four compounds to one goal can suggest convergence. They converge on a mechanism story of mitochondrial efficiency, growth hormone, and anabolic signalling. They do not converge on a measured endurance outcome for any of the three peptides.[2]

How to decide between these

The framework above the citations is the short version, and on this goal it has an unusual property: the first entry ends the analysis outright for a large share of the people reading. For a tested athlete, there is no compound comparison to make.[7]

For everyone else, three filters do the work. First, decide what counts as evidence, because "published human trial with an endurance endpoint" leaves exactly one compound on this page and it is a controlled prescription hormone.[6] Second, interrogate the mechanism story directly rather than through the compound. If the argument is growth hormone, the pooled growth hormone data is the argument's own best test.[3] Third, name the endpoint before starting rather than after, because endurance is one of the few goals where a genuinely objective before-and-after measurement is cheap and available.[7]

The stack assessment on this site is built to structure that conversation rather than to answer it, and its output is a starting point for a provider visit.

Questions to bring to a provider

The productive version of this conversation is not "should I try MOTS-c." It is "here is the performance I want, here is what I have measured, and here is what has been shown to move it."

  • What is limiting the performance in question, and which of those candidates has actually been tested: aerobic capacity, substrate availability, recovery between sessions, sleep, or iron status?[3]
  • Given that no published trial has administered MOTS-c to a human, what would have to exist before it were worth considering?[8]
  • If the proposal rests on raising growth hormone, how does the pooled finding that exercise capacity may have worsened change the reasoning?[3]
  • If testosterone is under discussion, what was measured, in whom, and how does the evidence in older men differ from the evidence in young women?[6]
  • What objective test would be run before and after (a time to exhaustion, a threshold assessment, a repeated time trial), and who interprets it?[7]
  • If the plan is a growth-hormone secretagogue, is a single pulse of hormone release per administration the thing that was actually wanted?[1]
  • If competing in a tested sport, what does this year's prohibited list say, and who at the national anti-doping organization confirms it?

Anti-doping status

Every compound mapped on this page is prohibited in tested sport at all times, both in and out of competition, under the World Anti-Doping Agency Prohibited List in force for 2026:

  • MOTS-c: section S4.4.1, metabolic modulators. The List names activators of AMP-activated protein kinase and gives "mitochondrial open reading frame of the 12S rRNA-c (MOTS-c)" as an example alongside AICAR and BAM15.
  • CJC-1295: section S2.2.4, growth hormone releasing factors, under growth hormone-releasing hormone and its analogues, listed beside CJC-1293, sermorelin and tesamorelin.
  • Ipamorelin: section S2.2.4, under growth hormone secretagogues and their mimetics, listed beside anamorelin, ibutamoren and macimorelin.
  • Testosterone: section S1.1, anabolic androgenic steroids, listed by name.

The classification differs across those sections and the difference has practical consequences. Substances in S1 and S2 are non-Specified Substances; S4.4 is also non-Specified, while S4.1 and S4.2 are Specified. Specified and non-Specified status changes how a case is handled rather than whether a substance is prohibited, and it is a question for a national anti-doping organization rather than a web page.

The status above is read from the published Prohibited List itself rather than from any research paper, because a citation can be real, correctly quoted, and still carry a false statement of regulatory fact. A review is a source for what the literature shows and never for what a regulator has done. What the literature contributes here is the reason these compounds are listed at all: a randomized, placebo-controlled trial showed a causal effect of a moderate testosterone increase on aerobic running time in physically active women.[7] The List is reissued every year and sections renumber, so a competing athlete should confirm the current year's edition rather than this page.

What the evidence supports for this goal

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

MOTS-c and physical performance in animals
Animal studies only animal

MOTS-c significantly enhanced physical performance in young, middle-aged, and old mice, regulated nuclear genes related to metabolism and proteostasis, and altered skeletal muscle metabolism and myoblast adaptation to metabolic stress; intermittent treatment begun in late life increased physical capacity and healthspan. The founding paper had separately shown that the peptide acts principally on skeletal muscle and activates AMPK, and that treatment prevented diet-induced obesity and insulin resistance in mice.

[8] [5]

MOTS-c and endurance in humans
Anecdotal reports only animal

The human finding is that exercise induces endogenous MOTS-c expression in skeletal muscle and in circulation. In that data the peptide is a marker of the training stimulus, not an intervention tested against one. No published study has administered MOTS-c to a human being and measured an endurance, capacity, or performance outcome. There is no human efficacy evidence to grade here, which is the honest statement of the claim.

[8]

Raising growth hormone and IGF-1 in humans
Human RCT evidence human RCT · human observational

Two randomized, placebo-controlled ascending-dose trials of CJC-1295 in healthy adults produced dose-dependent increases in mean plasma growth hormone of two- to ten-fold for six days or more and in IGF-1 of 1.5- to three-fold for nine to eleven days, with IGF-1 remaining above baseline for up to 28 days after multiple doses. Ipamorelin produced a single episode of growth hormone release at every infusion rate tested in healthy male volunteers. Both programmes measured hormone concentrations and nothing about exercise.

[2] [1]

Growth hormone and athletic performance
Human RCT evidence review

A systematic review of randomized controlled trials in fit young adults pooled 27 study samples and 303 growth-hormone recipients. Lean body mass increased by 2.1 kg, strength did not appear to improve, exercise capacity may have worsened, lactate during exercise was statistically significantly higher in two of three studies measuring it, and soft-tissue edema and fatigue were more frequent. The authors concluded that claims growth hormone enhances physical performance are not supported by the literature.

[3]

Testosterone and aerobic endurance in humans
Human RCT evidence human RCT

In a double-blind, randomized, placebo-controlled trial, 48 healthy, physically active women aged 18 to 35 received a daily testosterone cream or placebo for ten weeks. Running time to exhaustion increased by 21.17 seconds, or 8.5%, over placebo, and total lean mass rose; the anaerobic Wingate result did not reach significance, and there were no significant changes in counter-movement jump, squat jump, or knee extension. In older men, by contrast, the six-minute walking distance endpoint was not met in the trial designed to test physical function.

[7] [6]

Endurance or performance outcomes for the peptides on this page
Anecdotal reports only human RCT

No published randomized controlled trial has tested MOTS-c, CJC-1295, or ipamorelin against an endurance, aerobic capacity, or performance endpoint in humans. The only randomized human efficacy trial any of the three has produced was of ipamorelin for postoperative ileus in bowel-resection patients, where it was well tolerated and showed no significant difference from placebo on the key or secondary efficacy endpoints. A negative trial in an unrelated indication is the most rigorous human efficacy information this group has generated.

[4] [2]

Compounds people map to this goal

Each card carries the compound's FDA status and its overall evidence grade, plus why it shows up on this goal in particular. Follow the card to the full library page for the claim-by-claim evidence review and what published research reported. Dosing and protocol ranges are never on this page.

FOR RESEARCH PURPOSES ONLY

MOTS-c

Also known as: Mitochondrial open reading frame of the 12S rRNA-c, Mitochondrial-derived peptide MOTS-c

Research only Animal studies only

A research reference for MOTS-c, a mitochondria-encoded peptide with a strong mouse metabolic literature, real human biomarker data, and no published trial in which anyone has been given it.

Why it's on this page

The compound this goal is built around, and the one whose headline result is genuinely about physical performance. That result is in mice, at three different ages. In humans the arrow runs the other way: exercise induces the body's own MOTS-c, and no published trial has administered it to a person. Prohibited at all times under WADA section S4.4.1 as an AMPK activator.

Last reviewed August 2, 2026

FOR RESEARCH PURPOSES ONLY

CJC-1295

Also known as: CJC-1295 with DAC, DAC:GRF, hGRF(1-29) albumin bioconjugate

Research only Anecdotal reports only

A research reference for CJC-1295, a long-acting GHRH analog with two small human pharmacology studies showing raised GH and IGF-1 and no trial of any clinical outcome.

Why it's on this page

A long-acting GHRH analogue, mapped here because "more growth hormone means more aerobic capacity" is the mechanism story endurance readers arrive with. The hormone rise is real, dose-dependent, and measured in humans over days; no endurance outcome was measured in any of it. Prohibited at all times under WADA section S2.2.4.

Last reviewed August 2, 2026

FOR RESEARCH PURPOSES ONLY

Ipamorelin

Research only Anecdotal reports only

A research reference for ipamorelin, a selective growth-hormone secretagogue with solid rodent pharmacology, one human dose-ranging study, and one phase 2 trial that missed its endpoint.

Why it's on this page

A selective growth-hormone secretagogue, almost always discussed beside CJC-1295 for the same mechanism. Its human pharmacology produces one episode of growth hormone release per administration, and its one randomized human efficacy trial did not separate from placebo. That trial was in postoperative ileus, not in sport. Prohibited at all times under WADA section S2.2.4.

Last reviewed August 2, 2026

Testosterone

Also known as: Testosterone replacement therapy, TRT

FDA approved Human RCT evidence

A research reference for testosterone therapy, the one compound in this library with a large randomized trial literature, and a prescription hormone that requires a diagnosis, a prescriber, and ongoing lab monitoring.

Why it's on this page

The only compound on this page with a randomized, placebo-controlled human trial that used an aerobic endurance endpoint and hit it. That trial was run in women by investigators advising anti-doping bodies, and its result is the reason the entry below it exists. Prohibited at all times under WADA section S1.1.

Last reviewed August 2, 2026

How to decide between them

These are the questions that actually change the answer. Work through them with a licensed provider. None of them can be answered by a page that does not know your labs, your history, or your medications.

  1. Do you compete in a tested sport, at any level?

    On this goal that question comes first, not last, because every compound mapped on this page is prohibited at all times, in and out of competition, under the WADA Prohibited List in force for 2026: MOTS-c under S4.4.1, CJC-1295 and ipamorelin under S2.2.4, testosterone under S1.1. If the answer is yes, the analysis ends here and no evidence question follows it. The status is read from the published list rather than from the research literature, and the reason the strongest compound here is prohibited is exactly the reason it appears on an endurance page: a randomized trial showed testosterone causally increased aerobic running time in women.

    [7]

  2. Are you asking for evidence in humans, or evidence in mice?

    Applying that filter removes the compound this page is named around. MOTS-c significantly enhanced physical performance in young, middle-aged, and old mice, and late-life intermittent administration increased physical capacity. All of that is in animals. The human data in the same paper runs in the opposite causal direction: exercise induces endogenous MOTS-c expression in skeletal muscle and in circulation. Nobody has published a trial in which a person was given MOTS-c and measured on anything.

    Animal studies only [8] [5]

  3. Would a higher growth hormone level actually settle it?

    This is the surrogate the GH-axis compounds trade on, and it has been tested directly. Pooling 27 randomized study samples of growth hormone given to fit young adults, lean body mass rose by about two kilograms, strength did not appear to improve, exercise capacity may have worsened, lactate during exercise was significantly higher in two of three studies that measured it, and soft-tissue edema and fatigue were more frequent. For an endurance reader, "exercise capacity may have worsened" is the finding that matters, and it sits upstream of every compound here that argues from a hormone concentration.

    Human RCT evidence [3] [2]

  4. Which endurance endpoint do you actually care about?

    Naming it changes which evidence is even relevant, and the two human trials on this page used two different ones with two different outcomes. Running time to exhaustion increased by 8.5% over placebo in physically active young women after ten weeks of a testosterone cream. Six-minute walking distance in men aged 65 and over did not differ significantly between testosterone and placebo in the trial designed to test physical function. A treadmill test to exhaustion and a walking distance in older men are not the same construct, and neither is a training block.

    Human RCT evidence [7] [6]

  5. Is one hormone pulse the same thing as a training adaptation?

    Ipamorelin's human pharmacology is a single episode of growth hormone release with a peak inside the first hour and an exponential decline to negligible concentrations, across every infusion rate tested. That is a pharmacodynamic description, not an adaptation. When ipamorelin was finally taken into a randomized human efficacy trial, in bowel-resection patients rather than athletes, it was well tolerated and did not separate from placebo on its key endpoint. A compound with a clean pharmacology profile and one failed efficacy trial is not a compound with an endurance result.

    Human RCT evidence [1] [4]

  6. How would you know afterwards whether anything worked?

    Endurance is measurable in a way most goals are not, which makes the absence of measurement harder to excuse. The testosterone trial that produced a positive result was double-blind and placebo-controlled with a pre-specified primary endpoint, and even it found no significant change in squat jump, counter-movement jump, or knee extension. Deciding in advance on one objective test, whether a time to exhaustion, a threshold power, or a repeated time trial, is what separates an outcome from a training block that happened to go well.

    Human RCT evidence [7]

Questions for your provider

Bring this goal page to a licensed provider. A provider can order labs, review your medications and history, and tell you whether anything here applies to your situation. This goal page cannot. Peptide Health Lab does not prescribe and does not sell peptides.

A goal is not a diagnosis. The most useful version of this conversation usually starts with what is actually driving the symptom, not with which compound to try.

Citations

8 sources · every identifier checked against PubMed

Before you act on any of this

This page is educational only and is not medical advice. It does not diagnose, treat, or prescribe. Review it with a licensed provider before making any health decision. Peptide Health Lab does not sell peptides.

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