Formoterol

long-acting beta-2 adrenergic agonist (LABA)

Also sold as Perforomist, Foradil, Oxis, Fostair with a steroid.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Formoterol has no classical depletion machinery. It is cleared mainly by direct glucuronidation (UGT1A1, 1A8, 1A9, 2B7, 2B15) with a minor O-demethylation route (CYP2D6, 2C19, 2C9, 2A6), it did not inhibit CYP450 enzymes at therapeutic concentrations, and only 1.1 to 3.4% of an inhaled dose appears unchanged in urine (about 8% in the budesonide/formoterol label) [1][2][3]. No vitamin, mineral or antacid interaction is listed in the three labels read or on the Drugs.com food-interaction page, which lists only caffeine for additive blood pressure and heart rate effects [31]. What formoterol does have is its own beta-2 pharmacology: within hours of dosing it moves potassium into cells and raises glucose and lactate. These are acute changes in blood concentrations, not losses from the body, and none of them is a dietary deficiency.

long-acting beta-2 adrenergic agonist (LABA) · ATC R03AC13 (WHO ATC/DDD Index [4]); R03CC15 per Wikipedia [4] · also sold as Perforomist and Foradil and Oxis and Oxeze; in Symbicort and Fostair with a steroid · reviewed 2026-10-08. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Formoterol in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe: Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit.
Yellow — Low: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction.
Not graded — disclosed evidence gap: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: Not gradeable under the rules above because nothing has been measured. Published as a documented gap, never as reassurance that there is no effect.

What the research found

Potassium: transient serum fall by cellular redistribution, clinically sized at high cumulative or acute-care doses (not store depletion)

Orange — Moderate

See study details

Formoterol lowers serum potassium within hours of dosing by moving potassium into cells; the fall is dose-dependent, was clinically sized in cumulative-dose and emergency-room studies, and the labels say it is usually transient and needs no supplementation.

Full detail, limits and 1 references

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

Null findings: At recommended dosing the labels state clinically significant potassium changes were infrequent [1][2]; the Symbicort adverse-reaction tables (sec 6.1 and 6.2) do not list hypokalemia, which appears only under postmarketing reports (sec 6.3) [3]. Formoterol lowered potassium less than terbutaline at the compared doses in both head-to-head trials [5][7]. The effect attenuated after a week of formoterol dosing in healthy volunteers [13], and the Ankerst authors judged the significant potassium change at 45 mcg added formoterol clinically unimportant [11]. A class meta-analysis of beta-2 agonists (Salpeter 2004 [14]) found a single-dose potassium fall of 0.36 mmol/L (95% CI 0.18 to 0.54); its abstract does not name the agents, so formoterol inclusion is unconfirmed and it is CLASS EXTRAPOLATION context only, not used for the grade.
At-risk subgroups: People also taking non-potassium-sparing diuretics, xanthines or corticosteroids [1]; acute severe asthma with repeated high cumulative dosing [7][8]; children given cumulative doses [5]; overdose.

Direction

Redistribution (a disturbance of the blood level). Not depletion, not renal wasting, not a dietary shortfall.

Regulatory status

Named in all three labels. Perforomist sec 5.7: "Beta-agonist medications may produce significant hypokalemia in some patients"; the decrease is usually transient, "not requiring supplementation," and clinically significant changes in serum potassium were infrequent in long-term studies at the recommended dose [1]. Foradil sec 5.9 adds "possibly through intracellular shunting" [2]; Symbicort sec 5.18 [3]. Xanthines, steroids and non-potassium-sparing diuretics may potentiate the effect (Perforomist sec 7.2 and 7.3) [1]. Perforomist sec 12.2: a single 244 mcg dose lowered serum potassium by 0.68 +/- 0.4 mEq/L [1]. Foradil sec 12.2: 120 mcg (10 times the recommended dose) in 12 healthy volunteers lowered plasma potassium in all subjects, maximum reductions 0.55 to 1.52 mmol/L, median 1.01 [2].

Population evidence

All Tier A, formoterol in the cohort, potassium measured directly. Kaae 2004 [5]: 20 children with asthma aged 6 to 11, randomized crossover; cumulative formoterol 45 mcg over 2.5 hours; minimum plasma potassium 2.98 mmol/L versus 3.56 on a no-treatment day, difference -0.58 (95% CI -0.70 to -0.46); terbutaline 5000 mcg gave 2.71. ERJ 2001 [7]: 47 emergency-room patients with acute bronchial obstruction (formoterol n=23), cumulative delivered 90 mcg over 3 hours; mean serum potassium fell from 4.02 to a minimum of 3.43 mmol/L (terbutaline 10 mg: 4.22 to 3.16; difference in minimum 0.32, 95% CI 0.14 to 0.50). Boonsawat 2003 [8]: 88 emergency patients with acute severe asthma; formoterol 54 mcg caused a greater potassium decrease than salbutamol 2400 mcg by pMDI plus spacer (difference -0.2 mmol/L). Guhan 2000 [6] (full text opened on the repair pass): 16 healthy adults, formoterol 24, 48 and 96 mcg Turbuhaler versus salmeterol and placebo, double-blind crossover; baseline plasma potassium 4.0 to 4.1 mmol/L on all days; dose-related fall that was faster with formoterol, further falls after lunch, and drug effects still present at 8 hours with salmeterol but not formoterol; relative dose potency versus salmeterol 5.8 (95% CI 4.1 to 8.6) up to 4 hours and 3.0 (1.2 to 5.7) over 8 hours; five serum potassium values above 6.5 mmol/L were excluded from the analysis; absolute falls are shown only in a graph (Figure 3), not in text or tables, so no mmol/L fall could be retrieved. Singh 2008 [9]: 18 adults with asthma, formoterol 60 mcg (10 puffs of 6 mcg) on top of maintenance therapy lowered 12-hour serum potassium more than placebo or beclomethasone/formoterol (p<0.05); the magnitudes could not be read from the abstract summary. van den Berg 1998 [13] (PubMed abstract opened on the repair pass): healthy volunteers given single inhaled doses of formoterol 72 mcg and salbutamol 1200 mcg, repeated after 1 week of medication; both drugs lowered potassium significantly, with a longer duration after formoterol (p<0.05 by two analyses); after 1 week of formoterol the maximum fall and the area under the potassium-effect curve were smaller (p<0.05), which is tolerance; the abstract gives no sample size or absolute potassium values. Ankerst 2003 [11] (PubMed abstract opened on the repair pass): 14 adults with asthma on budesonide/formoterol maintenance, randomized double-blind double-dummy crossover; added formoterol 45 mcg (or high-dose budesonide/formoterol 1600/45 mcg) versus placebo; serum potassium monitored for 12 hours; changes in potassium were statistically significant versus placebo (P<0.05) but judged clinically unimportant by the authors, with no clinically relevant difference between the active treatments; the abstract does not state the direction of each change or give values. Potassium is also listed among measured outcomes in Rosenborg 2000 [10] (12 healthy, 11 asthmatic, cumulative 54 mcg) but the Springer page is paywalled beyond the abstract and no values were retrieved.

Mechanism

Named in the label: intracellular shunting of potassium after beta-agonist stimulation [2]. Not renal loss. The Guhan authors add that the early potassium fall and slower glucose rise are consistent with greater insulin release with formoterol [6] (their inference, not a measured insulin result).

QTc (clinical outcome, not a nutrient)

Not filed as a separate entry (Hard Rule 2). Perforomist 12-week trial: mean QTcB rise up to 4.8 ms versus up to 4.6 ms with placebo [1]. Foradil single 120 mcg dose: maximum QTcB +25 ms (QTcF +8 ms), and a 12-month COPD study showed no clinically meaningful ECG effect [2]. Kaae [5]: maximum QTc 453.3 versus 429 ms untreated, +25.7 ms (95% CI 16.1 to 35.4) after 45 mcg cumulative in children, less than terbutaline (+40.8). ERJ 2001 [7]: no significant QTc difference from terbutaline (12-hour mean difference 0.0 ms, 95% CI -11.9 to 12.0).

Near-red note

Seven Tier A formoterol cohorts agree on direction with a named mechanism, which is close to red. Held at orange because the clinically sized falls came from cumulative dosing several times a single labeled dose, the labels bound the clinical significance at recommended doses, and two trials compared against another potassium-lowering beta-agonist rather than placebo. Missing for red: a numeric potassium fall at 12 to 24 mcg labeled dosing with a clinical consequence. Repair pass: Guhan full text opened (thorax.bmj.com PDF; potassium shown only in Figure 3, no numeric falls), van den Berg 1998 and Ankerst 2003 abstracts opened via PubMed (no absolute potassium values, no sample size for van den Berg), Rosenborg full text not retrievable (Springer paywall), Singh and Boonsawat magnitudes unchanged. The second independent Tier A requirement is met in count and direction, but the magnitude test is not: the labels, the Ankerst authors and the tolerance finding bound clinical significance at labeled dosing, so orange stands.

Boundary string (customer-visible)

Formoterol can lower blood potassium for a few hours by moving it into cells; clinically sized falls were seen with cumulative or emergency-room dosing well above a single labeled dose, and the label says supplementation is usually not needed.

Counter-evidence held on record

Counter-evidence and confounding The direction is not contradicted by any Tier A source, but size depends on dose. Both head-to-head trials [7][8] used another potassium-lowering beta-agonist as comparator and had no placebo arm, so they show direction under high-dose conditions, not the size attributable to formoterol alone. Acute-asthma patients also receive other drugs that lower potassium. Kaae [5] used an untreated day rather than a blinded placebo, and its subjects were children given a cumulative dose over 2.5 hours. Framing caution This is a short-lived shift of potassium into cells after dosing, not a dietary potassium deficiency. The label says it is usually temporary and does not require supplementation. This entry is an excess-and-disturbance risk, never a prompt to supplement potassium.

Safety of formoterol Turbuhaler at cumulative dose of 90 mcg in patients with acute bronchial obstruction. Eur Respir J 2001;18(6):928-934. — Tier A. Randomized double-blind parallel-group trial; 47 analyzed (formoterol n=23, terbutaline n=24). Authors, PMID and DOI were not shown on the page read and are not given. Potassium and QTc values read through a summarizing fetch. Formoterol in cohort: yes; comparator was terbutaline, not placebo.

Blood glucose: small transient rise after dosing, larger at high doses (excess direction)

Orange — Moderate

See study details

Formoterol raises blood glucose by a small, temporary amount after a dose; the rise is dose-related and is a metabolic disturbance, not a nutrient shortfall.

Full detail and limits

Limits on what this shows

Null findings: The labels call clinically significant changes infrequent at recommended doses [1][2]. In a four-arm athlete crossover with formoterol, salbutamol, both and placebo (Bizjak 2023 [32]), insulin fell from before to after the time trial in the active arms; formoterol-only glucose values were not in the text read.
At-risk subgroups: People with diabetes (Mayo Clinic: the medicine "may affect blood sugar levels") [29]; high cumulative or overdose exposure.

Direction

Excess (transient hyperglycemia). Not a deficiency.

Regulatory status

Perforomist sec 5.7: beta-agonists "may produce transient hyperglycemia in some patients"; clinically significant changes in serum potassium and blood glucose were infrequent in long-term studies [1]. Perforomist sec 12.2: serum glucose 1 hour after 10, 20 and 244 mcg rose by 26 +/- 30, 29 +/- 28 and 38 +/- 44 mg/dL [1]. Foradil sec 12.2: in 10 healthy males urinary formoterol excretion correlated linearly with increases in plasma glucose [2]. Symbicort sec 5.18 and postmarketing hyperglycemia (sec 6.3); the adverse-reaction tables do not list it [3]. Overdose lists hyperglycemia [3].

Population evidence

Kaae 2004 [5]: 20 children, cumulative formoterol 45 mcg; maximum plasma glucose 6.10 versus 5.52 mmol/L untreated, difference +0.58 (95% CI 0.1 to 1.07); terbutaline 6.75. Singh 2008 [9]: 18 adults with asthma, formoterol 60 mcg cumulative; mean maximum glucose increase 0.4 mmol/L (p<0.01 versus placebo). Guhan 2000 [6] (full text opened): 16 healthy adults; baseline plasma glucose 5.2 to 5.4 mmol/L; an increase in glucose at the higher doses of formoterol and salmeterol, faster with salmeterol, gone by 4 hours for formoterol; relative dose potency versus salmeterol 1.6 (95% CI 0.7 to 2.7) up to 4 hours (the interval includes 1, so no potency difference), not calculated over 8 hours because the effect of lunch exceeded the drug effect; no absolute mmol/L rise is given in text or tables (graph only). Ankerst 2003 [11] (abstract opened): 14 adults with asthma, added formoterol 45 mcg or high-dose budesonide/formoterol versus placebo, blood glucose monitored for 3 hours; the change was statistically significant versus placebo (P<0.05) but judged clinically unimportant; direction and values not in the abstract. Glucose was also measured in Rosenborg 2000 [10] (values not retrieved; paywalled) and in Yamakido 1985 [12] (oral formoterol 40 to 80 mcg in healthy adults; direction not stated in the abstract).

Mechanism

The labels list the glucose rise among the expected systemic beta-agonist effects (sec 12.2) [1][2]; the tissue pathway is not described in the sources read.

Near-red note

Four formoterol cohorts plus label pharmacology agree in direction (Kaae, Singh, Guhan, Ankerst). Held at orange because the sizes are small (about 0.4 to 0.6 mmol/L in trials; label means 26 to 38 mg/dL at 1 hour) and the labels call clinically significant change infrequent. Missing for red: a placebo-controlled trial at labeled dosing in people with diabetes, and a numeric glucose rise from the Guhan, Ankerst or Rosenborg trials (Guhan gives only graphs and ratios; Ankerst and Rosenborg give no values in the text read). The Ankerst authors judged the change clinically unimportant. Glucose is a metabolic variable rather than a nutrient, so by Hard Rule 2 it can only be an excess-direction entry.

Boundary string (customer-visible)

Formoterol can raise blood sugar slightly and briefly after a dose, more at high doses; people with diabetes should be aware of this.

Counter-evidence held on record

Counter-evidence and confounding Glucose and potassium were measured in the same subjects in [5][9], so they share one sampling series (see the Overlap map). Acute-asthma patients often receive corticosteroids that also raise glucose. The trials sampled over hours, so persistence beyond the dosing session is not shown. Framing caution A brief rise in blood glucose is a disturbance, not a nutrient deficiency, and implies no dietary change.

Lactate: rise during high cumulative dosing in children, one numeric trial (excess direction)

Orange — Moderate

See study details

In one randomized pediatric trial, cumulative inhaled formoterol raised plasma lactate by about 1.2 mmol/L; other formoterol trials measured lactate but no values were retrieved.

Full detail and limits

Limits on what this shows

Null findings: No acidosis or lactate-related outcome with formoterol was found in the sources read. The Guhan trial [6] reports no lactate measurement. Riiser 2006 [16] measured post-exercise lactate after 18 mcg formoterol in 20 athletes, but the abstract reports no lactate result, so it neither supports nor contradicts the entry.
At-risk subgroups: Children given cumulative dosing [5]; acute severe asthma with repeated high-dose beta-agonist; overdose.

Direction

Excess (acute, dose-related). Not a deficiency.

Regulatory status

No lactate wording in the label text read. The Foradil label lists "metabolic acidosis" among adverse reactions common to long-acting beta-agonists (sec 6) and with overdose (sec 10) [2]; the Symbicort overdose section lists metabolic acidosis, hyperglycemia and hypokalemia [3]; the Perforomist text read names metabolic acidosis only in the same places [1].

Population evidence

Kaae 2004 [5]: 20 children with asthma, cumulative formoterol 45 mcg over 2.5 hours; maximum plasma lactate 2.77 mmol/L versus 1.57 untreated, difference +1.21 (95% CI 0.78 to 1.64); terbutaline 3.97. Ankerst 2003 [11] (abstract opened on the repair pass; independent cohort): 14 adults with asthma, randomized double-blind crossover, added formoterol 45 mcg or high-dose budesonide/formoterol versus placebo, plasma lactate monitored for 3 hours; the change was statistically significant versus placebo (P<0.05) but the authors judged it clinically unimportant; the abstract gives no lactate value and no direction. Lactate was also measured but numbers were not retrieved in Rosenborg 2000 [10] (paywalled), Singh 2008 [9] (lactate with beclomethasone/formoterol did not differ from formoterol alone) and Yamakido 1985 [12] (lactic acid measured after oral formoterol 40 to 80 mcg; direction not stated in the abstract).

Mechanism

Not named for lactate in the sources read. The lactate rise accompanies the potassium and glucose changes of the same beta-2 action in [5].

Near-red note

One numeric Tier A source with a bounded setting meets orange. A second independent cohort now exists (Ankerst 2003 [11]) with a significant lactate change versus placebo, but without values or direction, and its authors call the change clinically unimportant, so it supports consistency but not a clinically meaningful magnitude. Missing for red: a second independent formoterol cohort with lactate values and a clinically meaningful size. Tried: Rosenborg Springer page and PDF (paywalled, no values), Ankerst PubMed abstract (opened, no values), Singh abstract (no numbers), Guhan full text (lactate not measured), PubMed "formoterol lactate" (listing worked once and surfaced these studies).

Boundary string (customer-visible)

Formoterol raised blood lactate during high cumulative dosing in one study of 20 children (mean peak 2.77 mmol/L versus 1.57 without treatment).

Counter-evidence held on record

Counter-evidence and confounding One cohort of 20 children with an untreated comparison day. Lactate was sampled during a 2.5-hour cumulative-dose session, so duration of the rise and any link to acidosis are not shown. Muscle activity and tremor can also raise lactate. Framing caution This is an acute rise in a blood metabolite after high-dose exposure, not a nutrient deficiency, and implies no supplement.

Magnesium: plasma fall shown with intravenous salbutamol; no formoterol measurement found (CLASS EXTRAPOLATION)

Yellow — Low

See study details

A magnesium shift into cells is plausible for beta-2 agonists in general, but no study measured magnesium after formoterol.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

Null findings: A PubMed listing for salbutamol and plasma magnesium included inhaled salbutamol and salmeterol studies that the listing summary described as showing no magnesium change; their abstracts were not opened (the OpenAlex record for the inhaled salbutamol study had no abstract), so they are not used.

Direction

Redistribution (cellular uptake lowers the blood level). Not depletion and not renal wasting.

Cohort test

CLASS EXTRAPOLATION. Whyte 1987 [28]: placebo-controlled study of 8 normal subjects given adrenaline infusion and intravenous salbutamol. Formoterol was NOT in the cohort. Tier C for this drug; capped at yellow.

Class evidence

Plasma magnesium fell significantly during adrenaline infusion and also fell, more slowly, during salbutamol infusion, and had not recovered 1 hour after the infusions ended; potassium fell and recovered within 30 minutes; insulin did not change significantly. The authors concluded the shifts are intracellular and beta-adrenergic [28]. The abstract gives no magnesium effect size.

Formoterol-specific search

Kaae 2004 [5] measured potassium, glucose, lactate and QTc after formoterol but did not report magnesium. PubMed "formoterol magnesium" returned eight records, none measuring serum magnesium after formoterol (acute-asthma reviews on magnesium sulfate, magnesium stearate in inhaler formulations). No label read mentions magnesium [1][2][3].

Counter-evidence held on record

Counter-evidence and confounding Intravenous infusion in 8 volunteers is a different exposure from inhaled formoterol, and extension to this drug is untested. Framing caution A possible short-lived shift of magnesium into cells, not a dietary shortfall. No magnesium supplementation is suggested.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden: lower muscle mitochondrial respiratory capacity after 6 weeks of inhaled formoterol in endurance-trained adults (one trial; opposite to the preclinical biogenesis signal)

Orange — Moderate

See study details

In the one human trial that measured it, therapeutic-dose inhaled formoterol lowered maximal muscle mitochondrial respiration and mitochondrial protein content in endurance-trained adults, and lowered maximal oxygen uptake.

Full detail and limits

Limits on what this shows

Null findings: In vitro and animal work shows no mitochondrial harm from formoterol. In the human trial, intrinsic (content-normalized) respiration, HAD activity, capillarization, cardiac structure and blood volumes were unchanged [15].
At-risk subgroups: The only group studied was endurance-trained adults with high baseline mitochondrial content. Effects in people with asthma or COPD, untrained people, or at other doses are untested.

Direction

Reduction of mitochondrial capacity in muscle (a functional finding, not a nutrient deficiency). Reverse of the preclinical direction, where formoterol raised mitochondrial markers.

Regulatory status

No mitochondrial statement in the Perforomist, Foradil or Symbicort text read [1][2][3].

Population evidence

Jessen 2023 [15]: randomized, double-blind, placebo-controlled, parallel-group trial of 51 endurance-trained adults (31 men, 20 women; formoterol n=26, placebo n=25), 6 weeks of inhaled formoterol (12 mcg twice daily in week 1, then 24 mcg twice daily per the PMC summary; the OpenAlex abstract gives 24 mcg twice daily). Muscle protein was analyzed in 41 and respirometry in 20. Versus placebo: maximal complex I-linked respiration -14% (p=0.044), complex I+II-linked respiration -16% (p=0.017), citrate synthase activity -15% (p=0.063, not significant), complex II and III protein lower (p=0.028 and p=0.007), oligomycin-induced leak respiration lower (p=0.009). Respiration normalized to citrate synthase did not change, and HAD activity (-7%, p=0.105) and the capillarization marker PECAM-1 did not change. Outcomes: maximal oxygen uptake -5% (p=0.013), incremental exercise performance -3% (p<0.001), lean mass +0.7 kg (95% CI 0.2 to 1.2). On the repair pass the PMC full text was re-read: the text reports percent changes and treatment-by-trial p values for the mitochondrial and VO2max endpoints (VO2max relative to lean mass -6%, p=0.002; relative to body weight -5%, p=0.009) but no confidence intervals; absolute differences appear only in figures. Group sizes: respirometry 5 men and 5 women per arm (n=20); protein and citrate synthase 21 formoterol and 20 placebo (n=41); VO2max formoterol 26 (16 men, 10 women), placebo 25 (15 men, 10 women).

Mechanism

Not established. The authors link the loss of aerobic capacity to reduced muscle mitochondrial capacity. My reading of the reported pattern (not stated by the authors in the text read): respiration per unit of mitochondrial content was unchanged, which points to less mitochondrial machinery rather than damaged mitochondria.

Reverse-direction context (Tier B)

Formoterol raised FCCP-uncoupled oxygen consumption and mtDNA copy number in primary renal proximal tubule cells and feline cardiomyocytes, and raised PGC-1alpha, mtDNA and electron-transport gene expression in mouse kidney and heart (Wills 2012 [19]); restored renal mitochondrial function and renal function after ischemia-reperfusion injury in mice (Jesinkey 2014 [20], daily intraperitoneal dosing; dose not on the page read); acutely raised PGC-1alpha and mitochondrial biogenesis gene expression, but not after consecutive days, in cultured human skeletal myotubes at 30 nM for 3 hours (Gordon 2023 [21], gene expression only). In cachectic rats formoterol did not change mitochondrial complex activities (Salazar-Degracia 2017 [22]). None of these used inhaled human dosing.

Near-red note

One Tier A trial with a bounded group meets orange. Missing for red: a second independent human trial of formoterol measuring muscle mitochondrial function, and confidence intervals for the mitochondrial endpoints (not reported in the text; figures only). Tried: ERJ Open Research full text (too many redirects), PMC full text re-read on the repair pass (percent changes and p values only), OpenAlex reconstructed abstract, PubMed "formoterol mitochondrial" (invalid-form error then HTTP 429), PubMed "formoterol muscle biopsy respiration" (two animal or cell records only). No second human formoterol mitochondrial trial exists in the records seen, so the red test is not met.

Boundary string (customer-visible)

In one 6-week trial in endurance-trained adults, inhaled formoterol lowered muscle mitochondrial respiration and maximal oxygen uptake; effects in other groups have not been tested.

Counter-evidence held on record

Counter-evidence and confounding A single trial; the muscle endpoints come from 20 to 41 participants, several have p values between 0.01 and 0.1, and adjustment for multiple comparisons was not stated in the text read. The performance decline (maximal oxygen uptake, exercise performance) is a clinical outcome and is not filed as a nutrient or category entry. The preclinical literature points the other way, and the human gene-expression finding was transient [21]. Framing caution This is a measured change in muscle respiratory capacity in trained adults, not a nutrient shortfall, and it does not support any supplement. It is not evidence of mitochondrial toxicity in people with asthma or COPD.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress: reverse direction (protective) in a rat disease model and a mouse liver-injury model; no human formoterol redox data

Yellow — Low

See study details

Formoterol attenuated oxidative and nitrosative protein damage in a rat cancer-cachexia model and hepatic lipid peroxidation in a mouse liver-injury model; no human study of formoterol and a redox marker was found that names the drug.

Full detail and limits

Direction

Reverse (protective). Not a depletion.

Regulatory status

No antioxidant or oxidative-stress statement in the labels read [1][2][3].

Tier B evidence

Salazar-Degracia 2017 [22]: rats inoculated with AH-130 hepatoma (cancer cachexia), formoterol 0.3 mg/kg/day subcutaneously for 7 days. Cachectic rats had more protein carbonylation and nitration in the gastrocnemius; formoterol attenuated the increases in oxidative stress and myosin loss in respiratory and limb muscles and reduced inflammatory infiltration. No numeric marker values appear in the reconstructed abstract. Mitochondrial complex activities were not different between groups. Teng 2025 [23] (PubMed abstract opened on the repair pass; Tier B, formoterol itself): a drug screen identified formoterol as a ferroptosis inhibitor in multiple human and rodent cell lines; the effect did not depend on GPX4, FSP1 or iron chelation and appears to be direct scavenging of lipid peroxyl radicals through its ortho-amino phenol group; in male C57BL mice with acetaminophen-induced acute liver injury, formoterol reduced hepatic lipid peroxidation and preserved tissue (doses, cell lines and numeric marker values not in the abstract). This is a second, independent reverse-direction (antioxidant) Tier B source. A human bronchial epithelial cell record exists for beclomethasone plus formoterol on cigarette-smoke oxidative and nitrosative stress (Montalbano 2013 [24], abstract not available, not opened; a PubMed retry was rate limited on the repair pass); it is not used to support the grade.

Excluded human source

Alzoghaibi 2007 [25]: 20 asthmatics on inhaled steroid plus a long-acting beta-2 agonist had higher serum lipid peroxides than controls (TBARS 4.2 versus 3.6 umol/mL) after 3 months. The record does not name which long-acting agonist was used, so the cohort test is not met for formoterol, and asthma itself is a confounder. Not used.

Mechanism

In the mouse and cell work the authors propose direct scavenging of lipid peroxyl radicals by the ortho-amino phenol group, independent of GPX4, FSP1 and iron chelation [23]. In the rat study the effect may be indirect (less inflammatory infiltration) [22]. Doses per kilogram are not comparable with inhaled human dosing.

Counter-evidence held on record

Counter-evidence and confounding Disease-model rats; oxidative stress there is driven by cachexia. The human mitochondrial trial [15] points toward lower muscle oxidative capacity, not a redox marker, and measured no redox marker. Framing caution If anything, the animal signal is protective. This entry is not a reason to add an antioxidant supplement.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Iron: lower serum iron in rats given other beta-agonists and methylxanthines at necrosis-inducing doses; formoterol not tested (CLASS EXTRAPOLATION, animal toxicology)

Yellow — Low

See study details

A single rat toxicology study reported lower serum iron after isoproterenol, fenoterol or terbutaline (alone or with aminophylline or caffeine) given at doses that caused heart muscle necrosis; formoterol was not in that study, and no human or formoterol iron measurement was found.

Full detail and limits

Direction

Lower serum iron in an acute toxicity setting. Not shown to be loss of iron from the body or an iron deficiency (Hard Rule 2: drug toxicity, tissue-injury response).

Cohort test

CLASS EXTRAPOLATION. Whitehurst 1994 [35]: male heavy Sprague-Dawley rats given single subcutaneous doses of isoproterenol 15 micrograms/kg, fenoterol 40 micrograms/kg or terbutaline hemisulfate 0.4 mg/kg, alone or with aminophylline 20 mg/kg or caffeine 40 mg/kg. Formoterol was NOT in the cohort and neither was salmeterol. Tier C for this drug (a Tier B animal study of other agonists); capped at yellow.

Regulatory status

No iron, anemia or mineral statement in the three labels read [1][2][3].

Class evidence

Per the abstract (reconstructed from the OpenAlex inverted index, paraphrased; the number of animals is not stated): beta-agonist-induced myocardial necrosis was seen, enhanced by aminophylline with sudden death in some animals, and "a decrease in serum iron levels was observed in rats of all beta-agonist and/or methylxanthine-treated groups." No serum iron values are given and the finding is not stratified by drug. Because the methylxanthine-only groups also showed it, the lower iron is not specific to beta-2 stimulation.

Formoterol-specific search

PubMed "formoterol iron" (4 records), "formoterol ferritin" (1 record) and "formoterol hemoglobin" (3 records) returned nothing measuring iron status after formoterol (details under the earlier search record: a 2025 mouse and cell ferroptosis paper, a 2026 sarcoidosis anemia case report, and two comparator-only records). Repair-pass PubMed "salbutamol serum iron" returned 20 records, none with a beta-agonist exposure. Teng 2025 [23] (formoterol itself, mice and cells) found that formoterol's anti-ferroptotic effect did not depend on iron chelation, so there is no formoterol iron-binding mechanism on record; the abstract measures no iron status. Hemoglobin mass was unchanged in the 6-week trial [15] and sits in the oxygen entry; it is not iron evidence.

Mechanism

Not named. The decrease coincided with myocardial necrosis, so an acute systemic response to tissue injury is a competing explanation that was not tested. No formoterol mechanism for iron handling was found.

Counter-evidence held on record

Counter-evidence and confounding Toxic-dose rat model, other drugs, no values, no stratification, and a methylxanthine-only effect of the same kind. No human serum iron, ferritin or transferrin study with formoterol or any beta-2 agonist was found. This entry is carried at yellow only because the dossier protocol grades any Tier B or C record at yellow at minimum; it is the weakest yellow in this dossier. Framing caution Not evidence that formoterol lowers iron in people. Do not present as an iron deficiency, as a reason to take iron, or as an explanation for anemia.

Copper

Not graded — disclosed evidence gap

See study details

No study was found that measured copper status, absorption or loss in people or animals exposed to formoterol.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

Why no grade: Dual condition met: no Tier B or C evidence supports a yellow grade (the only copper hits are analytical materials) and no circulating copper claim was found to rebut. This is a disclosed gap, not a finding of safety. Copper stays a separate entry from Iron (Hard Rule 7).

What was searched

PubMed "formoterol copper" (2 records: an inhaler plume paper that uses a copper disc to measure force, and an electrochemical sensor built from copper oxide to detect formoterol residues in swine feed; neither studies copper status). PubMed "formoterol trace elements" (1 record, the same sensor paper). The three labels read contain no copper content [1][2][3]. Mayo Clinic, Medical News Today, the Drugs.com food-interaction page and Wikipedia mention no copper or mineral interaction [4][29][30][31].

Channel outcomes

Two PubMed listing phrasings returned results; two further phrasings for the class ("beta2-agonist serum copper ceruloplasmin" and "beta2 agonist copper status") returned HTTP 404 and were not read. Repair pass: Crossref "formoterol serum copper" (10 records: regulatory and pharmacopoeia entries and two copper papers with no beta-agonist exposure, none relevant) [37] and PubMed "beta-adrenergic agonist ceruloplasmin copper" (13 records, read at listing level only, abstracts not opened [36]). The closest class records were catecholamine items: an in vivo rat study in which adrenaline injection produced no significant short-term change in plasma copper or ceruloplasmin (PMID 694204, 1978), in vitro rat hepatocyte studies in which adrenaline changed copper uptake into ceruloplasmin (PMIDs 6882374 and 6889313, 1983), and an isoproterenol challenge in diet-induced copper-deficient mice (PMID 12876300, 2003) in which copper was the manipulated variable, not the outcome. Adrenaline is a mixed adrenergic agonist, not a beta-2 agonist, and none of these is formoterol, so they do not meet the cohort or mechanism test for a class-extrapolated yellow. The shared web-search budget ran out before any copper-specific web query was run and stayed exhausted, and Europe PMC, Semantic Scholar and eutils are blocked by policy. This is mostly a genuine gap with a tooling limit on web search and abstract access; a ceruloplasmin phrasing for formoterol and salbutamol should be re-run when search access returns.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk

Not graded — disclosed evidence gap

See study details

No study was found that measured gut or fecal microbiome composition in people or animals exposed to formoterol as the studied variable.

Full detail, limits and 1 references

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

Why no grade: Dual condition met: no gut-specific Tier B or C evidence exists to support a yellow grade (the airway data are a different compartment), and no circulating consumer claim about formoterol and the microbiome was found to rebut. The label notes that most inhaled formoterol is swallowed [3], which is a reason the gut question is reasonable, not evidence. A disclosed gap, not a finding of safety.

What was searched

Three web-search phrasings before the budget ran out (formoterol with gut microbiome, fecal microbiota or dysbiosis, with stool 16S, and budesonide/formoterol with intestinal microbiota); PubMed "formoterol microbiome" (5 records). Gut records: an asthma probiotics trial in which budesonide/formoterol was background therapy in both arms and formoterol was not the studied exposure, and a hawthorn mouse study that detected formoterol only as a fecal metabolite (both listing level, not opened [33]). A COPD gut-microbiota study of budesonide plus probiotics was opened and contains no formoterol (Liu 2024 [34]). The only formoterol-containing microbiome trials sampled the airway: DISARM (Leitao Filho 2021 [26]; 63 randomized COPD patients: budesonide/formoterol 20, fluticasone/salmeterol 22, formoterol alone 21; 4-week formoterol run-in; alpha-diversity changes differed across groups, driven by fluticasone/salmeterol, with less pronounced shifts in the formoterol-only and budesonide/formoterol arms) and MUSIC (Richardson 2025 [27]; budesonide/formoterol arm; no significant change in alpha-diversity). Airway is a different compartment and is not used for grading. The Perforomist adverse-reaction table lists diarrhea 4.9% versus 3.5% and nausea 4.9% versus 2.6% (n=123 versus 114) [1]; symptoms, not microbiome measures, and no inference is drawn.

Channel outcomes

PubMed listing worked for this phrasing; a second phrasing ("formoterol intestinal bacteria") was rate limited and not read. Europe PMC and Semantic Scholar are blocked by policy. Repair pass: PubMed "formoterol AND (feces OR fecal OR gut OR intestinal) AND (microbiota OR dysbiosis OR 16S)" returned the same two non-qualifying records (an asthma probiotic trial with budesonide/formoterol as background in both arms, and the hawthorn mouse study that detected formoterol only as a fecal metabolite [33]); PubMed "beta2-agonist gut microbiota" returned one record (PMID 29928672, a 2018 rat colonic-inflammation study in which a formoterol product, Foradil, was one treatment; the abstract describes stress hormones and histone acetylation at the IL1B promoter and measures no microbiota, so it does not qualify [36]); an earlier boolean phrasing with several agonist names was mis-parsed and returned unrelated records; a Crossref "formoterol intestinal microbiota" query and an OpenAlex search were rejected or rate limited. A genuine gap for the gut, with a partial tooling limit (web search exhausted, Europe PMC and Semantic Scholar blocked, Crossref and OpenAlex search not readable).

Repair-pass search records read at listing level only (abstracts not opened): PubMed "beta-adrenergic agonist ceruloplasmin copper" (13 records; PMIDs 694204, 6882374, 6889313, 12876300 discussed in the copper card); PubMed "beta2-agonist gut microbiota" (1 record, PMID 29928672, no microbiota measured); PubMed "salbutamol serum iron" (20 records, none with a beta-agonist exposure); PubMed "formoterol AND (feces OR fecal OR gut OR intestinal) AND (microbiota OR dysbiosis OR 16S)" (2 records, same as [33]). — Listing level only. Used solely to document search results in the ungraded and iron cards; no claim rests on them.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization: hemoglobin mass and oxygen saturation unchanged; lower maximal oxygen uptake in trained adults is a drug effect shared with the mitochondrial entry

Yellow — Low

See study details

In two randomized formoterol trials, oxygen-carrying capacity (blood volume, hemoglobin mass) and arterial saturation did not change; the lower maximal oxygen uptake seen in trained adults is a utilization and performance outcome, not a delivery deficiency.

Full detail and limits

Direction

Neutral for carrying capacity. Reduced maximal aerobic capacity is an outcome, not a deficiency (Hard Rule 2); formoterol's intended bronchodilation is likewise not an oxygen-delivery deficiency.

Regulatory status

No hemoglobin, anemia, methemoglobin or oxygen-delivery statement in the label text read [1][2][3].

Evidence

Jessen 2023 [15], subgroup of 20 (formoterol 9 men and 1 woman, placebo 10 men; full text re-read on the repair pass): total hemoglobin mass 897 +/- 128 g to 904 +/- 135 g with formoterol and 897 +/- 76 g to 897 +/- 76 g with placebo, mean change 7 g (95% CI -24 to 39 g, treatment-by-trial p=0.631); blood volume 6.2 +/- 0.6 L to 6.3 +/- 0.8 L with formoterol and 6.3 +/- 0.6 L to 6.3 +/- 0.4 L with placebo, mean change 0.1 L (95% CI -0.4 to 0.4 L, p=0.796); maximal oxygen uptake -5% (p=0.013). Riiser 2006 [16]: 20 nonasthmatic male athletes, randomized double-blind crossover, 18 mcg formoterol versus placebo, run to exhaustion at simulated 2000 m; no change in arterial oxygen saturation, heart rate or time to exhaustion (P>0.05), while FEV1 improved. PubMed "formoterol hemoglobin" returned three records, none studying formoterol and hemoglobin, hematocrit or anemia.

Why yellow

There is a measured Tier A null for carrying capacity and an outcome (maximal oxygen uptake) that overlaps the mitochondrial entry, but no deficit in delivery. Graded yellow as a context flag, not as a deficiency claim. A ventilation-perfusion effect on arterial oxygen tension, known for beta-agonists as a class, was not retrieved and is not used.

Counter-evidence held on record

Counter-evidence and confounding Both trials were in healthy trained or nonasthmatic adults, not in people with COPD or asthma. The hemoglobin-mass subgroup was 20 people (almost all men), so the interval is wide. Numeric saturation values from Riiser were not retrieved. Framing caution No oxygen-carrying deficiency is shown. Do not use this entry to suggest iron or other blood-building supplements.

ATP production: not measured in people or animals with formoterol; surrogates point in opposite directions (human muscle respiration down, cell and mouse markers up)

Yellow — Low

See study details

No study measured ATP content or synthesis after formoterol; respiration surrogates and energy expenditure data exist but do not show lowered ATP synthesis.

Full detail and limits

Direction

Unknown for ATP itself. Surrogates: human muscle maximal respiration lower (reduction), cell oxygen consumption higher (reverse), whole-body energy expenditure higher (increased utilization, mechanism class I).

Regulatory status

No ATP or energy-production statement in the labels read [1][2][3].

Evidence

Human muscle respiration after 6 weeks (Jessen 2023 [15], shared with the mitochondrial entry): complex I-linked -14%, complex I+II-linked -16%; ATP not measured. Wills 2012 [19]: formoterol raised FCCP-uncoupled oxygen consumption in renal proximal tubule cells; the page read does not report ATP. Gordon 2023 [21]: ATP not measured; Jesinkey 2014 [20]: the page read does not mention ATP. Energy expenditure: Onslev 2017 [17], 19 overweight men (14 completed), inhaled racemic formoterol 2 x 27 mcg versus placebo; resting energy expenditure +12% (P<=0.001) and fat oxidation +38% (P=0.006), no difference in energy expenditure during submaximal exercise, carbohydrate oxidation +15% during exercise. Lee 2013 [18]: 8 men for one week at 160 mcg per day (route not stated in the abstract summary); resting energy expenditure, fat oxidation and plasma free fatty acids rose, heart rate did not change significantly.

Why yellow

Tier B in vitro respiration data and Tier A surrogates exist, so ungraded does not apply; none measures ATP. The higher energy expenditure is a drug effect, not lowered ATP synthesis.

Counter-evidence held on record

Counter-evidence and confounding Respiration and energy expenditure are not ATP measurements. The three energy-expenditure studies were small and used different formoterol doses and routes. Framing caution No evidence of lowered ATP synthesis; this entry gives no basis for energy or mitochondrial supplements.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

Potassium "depletion" reading of hypokalemia
Where it comes from: Consumer drug pages list hypokalemia as a side effect: Mayo Clinic says hypokalemia may occur and lists its symptoms, and Medical News Today lists hypokalemia as a serious side effect and says diuretics may lower potassium further [29][30]. Neither separates redistribution from loss, which invites the depletion reading. Neither recommends supplements.
Why it fails: The measured change is a transient shift of potassium into cells (see the orange potassium entry), not a loss of body potassium. The label says the decrease is usually transient and does not require supplementation [1][2]. The serum fall is real and graded orange as a dose-bounded disturbance; the reading that it is a deficiency to be supplemented fails.
Mitochondrial boost or exercise-mimetic benefit in people
Where it comes from: Preclinical literature describing formoterol as stimulating mitochondrial biogenesis in kidney and heart cells and mice, and as an "exercise mimetic" in cultured human muscle cells [19][20][21].
Why it fails: Not borne out in the one human trial: 6 weeks of inhaled formoterol lowered maximal muscle mitochondrial respiration (-14% and -16%) and maximal oxygen uptake (-5%) in endurance-trained adults [15]. The preclinical work used cells, mouse injections or 3-hour exposures of cultured cells, with gene expression or respiration readouts and no inhaled human dosing. The preclinical signal is carried as reverse-direction context in the mitochondrial and ATP entries.

How the body handles this medication

Metabolism and enzymes: "Formoterol is metabolized primarily by direct glucuronidation at either the phenolic or aliphatic hydroxyl group" (UGT1A1, 1A8, 1A9, 2B7, 2B15 in vitro); O-demethylation involves CYP2D6, CYP2C19, CYP2C9 and CYP2A6. "Formoterol did not inhibit CYP450 enzymes at therapeutically relevant concentrations," and no induction is described. "Some patients may be deficient in CYP2D6 or 2C19 or both."[1][2] Perforomist and Foradil labels sec 12.3; read through a summarizing fetch
Elimination: After oral radiolabeled formoterol, 59 to 62% of radioactivity was in urine and 32 to 34% in feces over 104 hours. After inhalation, 1.1 to 1.7% of a nebulized dose (about 3.4% of a dry-powder comparison) was excreted unchanged in urine; renal clearance was about 150 to 157 mL/min. Mean terminal half-life was 7 hours (Perforomist, 244 mcg) and 10 hours (Foradil). About 8% of the delivered budesonide/formoterol dose was recovered unchanged in urine in asthma patients.[1][2][3] sec 12.3
Absorption and exposure: In the budesonide/formoterol label, the majority of inhaled formoterol delivered is swallowed and then absorbed from the gastrointestinal tract, so the gut sees drug exposure. No absorption transporter is named in the label sections read. Systemic exposure is the route to the potassium, glucose and lactate effects.[3] Symbicort label sec 12.3 (retrieved text truncated; first 100,000 characters read)
Renal handling of electrolytes: No effect on renal tubular handling of water or electrolytes is described. The Foradil label attributes the potassium fall to cellular uptake: beta-agonists "may produce significant hypokalemia in some patients, possibly through intracellular shunting," usually transient and "not requiring supplementation."[1][2] sec 5.7 and 5.9
Drug and food interactions: Xanthines, steroids and non-potassium-sparing diuretics (loop or thiazide) may potentiate the hypokalemic and ECG effects, especially above the recommended dose. Use with MAO inhibitors, tricyclic antidepressants or QTc-prolonging drugs calls for extreme caution; beta-blockers may cause severe bronchospasm in COPD. No food, mineral or antacid interaction is listed in the labels read; the Drugs.com food page lists caffeine only (additive blood pressure and heart rate).[1][31] Perforomist sec 7.1 to 7.5; Drugs.com food interactions
Hepatic or renal impairment: "The pharmacokinetics of formoterol fumarate has not been studied in subjects with hepatic or renal impairment." Accumulation in impairment is therefore unknown from the labels.[1][2] sec 12.3

What the research says is worth watching

General information from the medication label and the studies above. It is not personal medical advice, and any change belongs with your prescriber.

Lab / high-dose or acute care
Serum potassium
Worth checking when formoterol is given at high cumulative doses (emergency or inpatient use), in children receiving cumulative dosing, and in anyone also on a loop or thiazide diuretic, a xanthine or a corticosteroid, which the label says may potentiate the effect [1][5][7]. Expect the fall to be transient. The Perforomist label advises caution with non-potassium-sparing diuretics, especially above the recommended dose [1].
ECG / cardiac
Rhythm and QTc context
The labels list flattened T waves, QTc prolongation and ST depression as reported beta-agonist ECG changes of unknown significance, and call for extreme caution with MAO inhibitors, tricyclics and QTc-prolonging drugs [1][2]. Low potassium adds to that concern.
Lab / diabetes
Blood glucose
People with diabetes may see a small, brief rise after dosing, larger at high doses [1][5][9][29].
Lab / unexplained acidosis
Lactate
Consider a lactate level when a patient on high-dose beta-agonist therapy develops unexplained rapid breathing or acidosis. The label lists metabolic acidosis with overdose [2][3]; the one numeric formoterol rise was moderate [5].
Function / athletes
Aerobic capacity
In endurance-trained adults, 6 weeks of inhaled formoterol lowered maximal oxygen uptake by 5% [15]. This is a performance observation, not a lab test, and no nutrient is implicated. Magnesium has no formoterol-specific evidence, so no formoterol-specific magnesium monitoring is supported.
Timing
Supplement separation
No separation interval is required: no vitamin, mineral or antacid interaction is listed in the labels read, and the Drugs.com food page lists caffeine only [31]. No supplement dose is recommended or appears anywhere in this dossier, so no upper-limit comparison was needed. Potassium, glucose and lactate shifts reverse on their own, so supplementation is not advised from this evidence.
Special populations
Children, impairment, pregnancy
Children given cumulative dosing reached a mean minimum potassium of 2.98 mmol/L [5]. Formoterol kinetics have not been studied in renal or hepatic impairment, and some patients lack CYP2D6 or CYP2C19 activity [1][2]. Pregnancy was not assessed in the sources read. In combination products (for example budesonide/formoterol) the steroid component carries its own effects that are not attributed to formoterol here [3].

Overlap map, to prevent double counting

Potassium
Shares evidence with: Blood glucose; Lactate; Magnesium
Note: Kaae 2004 [5] measured potassium, glucose and lactate in the same 20 children; Singh 2008 [9] measured potassium, glucose and lactate in the same adults; Rosenborg [10] and Ankerst [11] list the same trio. The beta-2 receptor action is the shared mechanism. These are one pharmacologic event seen at different analytes, not independent confirmations. The magnesium entry rests on salbutamol [28] and adds nothing to the formoterol count.
Mitochondrial burden
Shares evidence with: ATP production; Oxygen delivery/utilization
Note: Jessen 2023 [15] is the only human source behind all three: muscle respiration, citrate synthase and maximal oxygen uptake come from one trial. It supports the orange mitochondrial grade once; in the ATP and oxygen entries it is cited only as a surrogate or context and is not counted as independent confirmation.
Mitochondrial burden
Shares evidence with: Oxidative stress; ATP production
Note: The reverse-direction preclinical set (Wills [19], Jesinkey [20], Gordon [21], Salazar-Degracia [22]) feeds the context rows of the mitochondrial, ATP and oxidative-stress entries. It is one body of preclinical work, not three.
Potassium
Shares evidence with: QTc outcome (not an entry)
Note: The QTc data in the potassium entry come from the same trials [1][2][5][7] as the potassium measurements; QTc is a clinical outcome and is not graded separately.
Oxygen delivery/utilization
Shares evidence with: Iron (yellow)
Note: The unchanged hemoglobin mass in [15] sits in the oxygen entry. It is not iron evidence and is not counted toward the iron entry, which rests only on the rat study of other agonists [35].
Oxidative stress
Shares evidence with: Iron (yellow)
Note: Teng 2025 [23] (formoterol as a ferroptosis inhibitor, independent of iron chelation) is cited in the oxidative-stress entry and as a no-chelation note in the iron entry; it is one source, not two lines of evidence, and measures no iron status.
Copper; Gut microbiome risk
Shares evidence with: None
Note: Ungraded entries rest on no evidence and share nothing with graded entries.

All references used above

Formoterol

Findings for this medication

What the research found

Potassium: transient serum fall by cellular redistribution, clinically sized at high cumulative or acute-care doses (not store depletion)

Blood glucose: small transient rise after dosing, larger at high doses (excess direction)

Lactate: rise during high cumulative dosing in children, one numeric trial (excess direction)

Magnesium: plasma fall shown with intravenous salbutamol; no formoterol measurement found (CLASS EXTRAPOLATION)

The five body-system areas

⚡Mitochondrial Burden

Mitochondrial burden: lower muscle mitochondrial respiratory capacity after 6 weeks of inhaled formoterol in endurance-trained adults (one trial; opposite to the preclinical biogenesis signal)

💥Oxidative Stress

Oxidative stress: reverse direction (protective) in a rat disease model and a mouse liver-injury model; no human formoterol redox data

⚖️Copper and Iron Balance

Iron: lower serum iron in rats given other beta-agonists and methylxanthines at necrosis-inducing doses; formoterol not tested (CLASS EXTRAPOLATION, animal toxicology)

Copper

🌿Gut Microbiome Risk

Gut microbiome risk

💨Oxygen and ATP Output

Oxygen delivery/utilization: hemoglobin mass and oxygen saturation unchanged; lower maximal oxygen uptake in trained adults is a drug effect shared with the mitochondrial entry

ATP production: not measured in people or animals with formoterol; surrogates point in opposite directions (human muscle respiration down, cell and mouse markers up)

Claims checked and not supported

Potassium "depletion" reading of hypokalemia

Mitochondrial boost or exercise-mimetic benefit in people

How the body handles this medication

What the research says is worth watching

Overlap map, to prevent double counting

Mitochondrial Burden

Oxidative Stress

Copper and Iron Balance

Gut Microbiome Risk

Oxygen and ATP Output