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Muscle & PerformanceHuman studies cited: 6

Clenbuterol

Clenbuterol hydrochloride, selective beta-2 adrenergic agonist

Written by Reviewed Sep 2026

Also known as: Spiropent, Ventipulmin, Clen

The first randomised trial in humans, published in 2025, found clenbuterol added 0.91 kg of lean mass in two weeks, changed fat mass not at all, and cut maximal oxygen uptake by 7 percent. It is not approved for human use in the United States, and it has caused documented poisoning outbreaks from contaminated meat and from adulterated heroin.

Overview

Clenbuterol is a long-acting beta-2 adrenergic agonist. It is a licensed human bronchodilator in a handful of countries, a veterinary bronchodilator elsewhere, and in the United States it is neither: there is no FDA approval for human use, and the American product is a horse medicine.

For decades the muscle claim rested on rats. In 2025 a Copenhagen group ran the trial that had never been run. Eleven healthy men took oral clenbuterol at 80 micrograms a day or placebo for two weeks each, in a crossover with a three week washout. Lean mass rose by 0.91 kg against placebo, muscle protein content rose, and fat mass did not move at all, which is worth pausing on given that fat loss is the reason most people buy it. Maximal oxygen uptake fell by 7 percent and exercise capacity by 4 percent. Muscle fat oxidation enzymes were repressed. The beta-2 signalling that drove the anabolic effect faded over the two weeks.

The harm record is not theoretical. In 1992 an outbreak in Catalonia produced 113 cases of poisoning traced to veal liver from cattle illegally fed clenbuterol, with tachycardia, tremor, myalgia and headache lasting up to six days. Between 2005 and 2015, clenbuterol-adulterated heroin caused clusters of emergency presentations in the United States: 34 cases across five states in one outbreak, with tachycardia, hypotension, hypokalaemia, raised lactate and biochemical evidence of myocardial injury in six patients, and a second, separate 13-patient cluster in Richmond, Virginia.

Cardiac hypertrophy is documented in animals given clenbuterol. In the one human trial that measured it, two weeks of dosing did not change left ventricular mass. Two weeks is not a long enough exposure to settle the question, and nobody has run a longer one.

Mechanism of action

Selective beta-2 adrenergic receptor agonism. In skeletal muscle the receptor couples to cyclic AMP and protein kinase A, which in the 2025 human trial was markedly activated along with phosphorylation of ribosomal protein S6, the anabolic signal that drove the lean mass gain. The same receptor class in the heart and vasculature produces the tachycardia, tremor and hypokalaemia that define the poisoning syndrome. Repeated dosing desensitises the receptor: the signalling response in that trial declined across the two weeks, which is the pharmacological basis of the cycling practice users have arrived at empirically.

Human evidence

There is real human data, and it is better than most compounds on this site have: one randomised crossover trial in healthy men, one small open trial in heart failure patients, a human pharmacokinetic study, and three separate public health investigations of mass poisoning.

  • Randomised crossover, 11 healthy men, 80 micrograms a day for 2 weeks: +0.91 kg lean mass, no change in fat mass, maximal oxygen uptake down 7 percent, exercise capacity down 4 percent, sprint power unchanged.
  • Left ventricular assist device patients, 7 subjects at 720 micrograms a day for 3 months: lean mass and quadriceps strength rose, ejection fraction did not, exercise capacity did not.
  • Catalonia 1992: 113 poisonings from contaminated veal liver, symptoms lasting up to 6 days, no deaths.
  • United States 2005 to 2007: 34 emergency presentations from clenbuterol-adulterated heroin, with myocardial injury in 6 patients.
  • Richmond, Virginia 2015: a further 13 patients from the same adulteration practice.
  • Human pharmacokinetics: plasma half-life about 35 hours, so a daily dose accumulates for several days before steady state.

What this does not tell you: The only randomised trial ran for two weeks in eleven young men. It cannot tell you what months of use do, which is what the people who buy clenbuterol actually do. Left ventricular mass did not change in those two weeks, so the cardiac hypertrophy documented in animals is neither confirmed nor ruled out in humans. No trial has tested clenbuterol for fat loss in people who want fat loss, and the one trial that measured fat mass found no effect. The poisoning literature describes acute overdose in people who did not choose the dose, which is informative about the toxic syndrome and not about chronic self-administration.

Reading the research record

Clenbuterol is the rare case where the community claim and the trial result point in opposite directions on the headline benefit. It is sold overwhelmingly as a fat burner. The only randomised trial that measured body composition found no effect on fat mass and a clear effect on lean mass, alongside a fall in aerobic capacity that no endurance athlete would accept. The authors' own conclusion was that the adverse effects alongside the anabolic action justify its prohibition in sport.

The two contamination routes are worth separating. Meat contamination happens where clenbuterol is used illegally as a growth promoter in cattle and pigs, and it has produced outbreaks in Spain, China and elsewhere; it is also the standard defence offered by athletes who test positive. Heroin adulteration is a different phenomenon, documented in at least two US clusters, in which the drug appears in the illicit supply and users receive doses far above any therapeutic range.

The cardiac question remains genuinely open. Beta-2 agonism at high dose causes cardiac hypertrophy in animals, and the myocardial injury markers in the heroin outbreak are real. The one human study designed to look at cardiac structure ran for two weeks and found nothing. Absence of a signal at two weeks is not evidence of safety at two years.

The evidence, charted

Fig. 1 · evidence composition

6of 7 citations (86%) are in people

Counted from the citation list on this page. The Human count is the same number shown in the badge at the top. Both understate any literature larger than the sources we cite.

Fig. 2 · evidence over time

Evidence spans 7 distinct years, 1985 to 2025, counted from the citation list on this page.

Fig. 3 · legal status at a glance

Not approved in any of the four jurisdictions shown. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.

Fig. 4 · dose response

No human dose response curve exists

We draw this figure where the data supports it. For this compound in humans it does not, so the panel stays empty rather than borrowing an animal curve and implying it transfers.

Awaiting a dose ranging studyProducing one takes a trial that gives different amounts to different groups and measures the difference. Nobody has funded that for this compound.

Key studies & citations

  • Human2025

    Clenbuterol induces lean mass and muscle protein accretion, but attenuates cardiorespiratory fitness and desensitizes muscle β2-adrenergic signalling

    The first randomised controlled trial. 11 healthy men aged 18 to 40, two 2-week cycles of oral clenbuterol at 80 micrograms a day versus placebo with a 3-week washout. Lean mass +0.91 kg (95% CI 0.02 to 1.81, p < 0.05), no effect on fat mass, maximal oxygen uptake -7% (p < 0.001), exercise capacity -4% (p < 0.001), no change in left ventricular mass, blood volume or haemoglobin mass. Muscle protein content rose while 3-hydroxyacyl CoA dehydrogenase activity and OXPHOS complex V fell. The beta-2 signalling response declined across the 2 weeks.

    The Journal of Physiology
  • Human1995

    Epidemiologic study of an outbreak of clenbuterol poisoning in Catalonia, Spain

    113 cases of poisoning in 1992 traced to veal liver from cattle given clenbuterol. More than half had nervousness, tachycardia, muscle tremors, myalgia and headache. Onset 15 minutes to 6 hours, symptoms lasting 90 minutes to 6 days. Urine clenbuterol 11 to 486 parts per billion in 47 samples. No deaths.

    Public Health Reports
  • Human2008

    A descriptive study of an outbreak of clenbuterol-containing heroin

    34 probable or confirmed emergency department presentations across 5 US states over 6 months. Blood clenbuterol 2.4 to 26 ng/mL. Significant tachycardia, hypotension, hyperglycaemia, hypokalaemia and raised lactate; 6 of the patients had biochemical evidence of myocardial injury.

    Annals of Emergency Medicine
  • Human2017

    Collaborative Public Health Investigation of Clenbuterol-Adulterated Heroin Outbreak-Richmond, Virginia, March-April 2015

    A second, later outbreak. 13 patients met clinical and epidemiological criteria, clenbuterol confirmed in clinical specimens, all linked to one supplier in one part of Richmond. The cluster stopped when the supplier was arrested.

    Journal of Public Health Management and Practice
  • Human2006

    Effect of clenbuterol on cardiac and skeletal muscle function during left ventricular assist device support

    7 heart failure patients on a left ventricular assist device given oral clenbuterol up-titrated to 720 micrograms a day for 3 months. No serious adverse events or arrhythmias, creatine phosphokinase rose in 4 patients. Ejection fraction did not improve and end-diastolic dimension increased; body weight and lean mass rose and quadriceps maximal voluntary contraction improved from 37.0 to 45.8 kg. Cardiac function did not improve.

    The Journal of Heart and Lung Transplantation
  • Human1985

    Pharmacokinetics of plasma and urine clenbuterol in man, rat, and rabbit

    Oral doses of 20, 40 and 80 micrograms in healthy volunteers. Peak plasma levels within 2.5 hours, plasma half-life about 35 hours, plasma protein binding 89 to 98 percent, and about 20 percent of the dose recovered unchanged in urine by 72 hours. Twice-daily dosing reached plateau within 4 days.

    Journal of Pharmacobio-Dynamics
  • Animal1991

    Effects of clenbuterol on skeletal muscle mass, body composition, and recovery from surgical stress in senescent rats

    Rats. One of the old animal studies the muscle claim rested on for three decades before a human randomised trial existed.

    Metabolism

Frequently asked questions

Does clenbuterol burn fat?

Not in the only randomised trial that measured it. Two weeks at 80 micrograms a day changed fat mass not at all in healthy men, while adding about 0.9 kg of lean mass. The thermogenic effect people feel is real, the tremor and raised heart rate are real, and the fat mass number did not move.

Is clenbuterol legal in the United States?

Not for human use. There is no FDA approval for people at any dose. The only US approval is veterinary, for horses. Anything sold for human consumption is unapproved, and WADA prohibits it in sport as an anabolic agent.

What does clenbuterol do to the heart?

Acutely it causes tachycardia, and in poisoning cases it has produced hypotension, hypokalaemia and biochemical evidence of myocardial injury. Cardiac hypertrophy is documented in animals. In humans, two weeks of dosing did not change left ventricular mass, which is the only structural measurement anyone has published, and it is far too short to answer the question.

Why do athletes test positive from eating meat?

Because clenbuterol is used illegally as a growth promoter in livestock in some countries, and it concentrates in liver. The Catalonia outbreak of 113 poisonings came from veal liver. Contaminated meat is a documented route of exposure, which is also why it is an unfalsifiable excuse in doping cases.

Why do people cycle it two weeks on, two weeks off?

There is a pharmacological basis, even if the schedule was arrived at by trial and error. In the human trial, beta-2 signalling and the downstream anabolic phosphorylation both declined over the two-week cycle, which is receptor desensitisation. What no data supports is that cycling makes chronic use safe.

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