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Can You Train With COPD? The Air-Hungry Barbell Audit: Where the ATS Issued a Strong Recommendation Standing on a 65-RCT Cochrane That Moved the Six-Minute Walk +43.93 m Against a 26-m MID and Closed With 'Further RCTs Are Not Warranted', the Mechanism File Watched Training Cut Lactate 7.2→4.5 mEq/L and Ventilation 55→48 L/min at Identical Work Rates While FEV₁ Stood Still at 56% Predicted, 18 Trials of Pure Resistance Training Moved Dyspnea +0.59 and FEV₁% +6.88 With Zero Adverse Events Reported, the Strength-Add-On RCT Built Quad Force +20% Against +8%, the Dosage File Watched High Load Beat Low-Moderate at +21.90 Nm, Quadriceps Strength Predicted Mortality at HR 0.91 Where FEV₁ Could Not, the Flare Cochrane Cut Readmissions to OR 0.44, and São Paulo Reads 15.8% Prevalence With 70% of New Cases Underdiagnosed, Train the Muscle, Not Just the Lungs

By RightRep AI Assistant · · 21 min read

COPD is the condition this library has already opened from the treatment side — does exercise help COPD is the file where medicine itself prescribes the gym — and the neighbor door can you train with asthma answers the reversible twin. This file answers the diagnosed lifter's version: what happens to a training program when the air itself is rationed — a condition whose global file reads 213.4 million prevalent cases and 1.69 million deaths in 2021, with smoking driving 38–55% of DALYs [1], and whose Brazilian file reads 15.8% of adults over 40 in São Paulo on post-bronchodilator spirometry [2] with 70% of new cases underdiagnosed at nine-year follow-up [3]. The default scripts fail in opposite directions. The scared script treats breathlessness as a damage signal — every set that leaves you air-hungry is read as proof the gym is over, training stops, and the deconditioning spiral begins in a disease where limb muscle dysfunction is an official systemic consequence that reduces exercise tolerance, quality of life and survival [8]. The reckless script trains straight through exacerbations — while the flare is a medical event whose post-hospital window is, precisely, the moment medicine says to start supervised training [13]. The reframe that carries the whole file is one line: the disease is in the lungs, the leverage is in the muscle — the airway obstruction is barely trainable, and almost everything downstream of it is [6][8]. Which puts the fences in order. First: the diagnosis fence. This file assumes COPD named by spirometry under a clinician's eye; breathlessness that has never been spirometried is a pulmonology appointment, not a self-diagnosis — in São Paulo, seven of ten new cases went years without the name [3]. Second: the flare fence. An exacerbation — worsening breathlessness, new sputum, fever — is a medical event treated by the prescriber; the program pauses, and the sick rules of this library defer to the pulmonologist here [13]. Third: the oxygen and inhaler shelf belongs to the prescriber — this file's job is the program that runs alongside it, and the guideline file says that program is not optional [4]. With the fences standing, the operational file is unusually complete for a condition the gym fears: the permission question has a strong recommendation from the American Thoracic Society [4], the dose question has a 65-trial Cochrane that closed with the verdict that further trials "are not warranted" [5], the mechanism question has the trial that watched trained muscles cut their lactate and ventilation while FEV₁ stood still [6], the prognosis question has the thigh that outpredicted the spirometer [7], the barbell question has an 18-trial meta with zero adverse events [10], the dosage question has a high-vs-low-load meta [12], the flare question has its own 20-trial Cochrane [13], the real-world question has a 2,386-person cohort where any regular activity cut admissions and mortality [14], and the honesty shelf is priced down to the breathing trainer [15].

The short answer: yes — train the muscle, not just the lungs

Strip the file to its spine. The permission is official: the 2023 American Thoracic Society clinical practice guideline issues a strong recommendation for pulmonary rehabilitation in stable COPD, a second strong one after exacerbations, and a strong grade for center-based or tele-rehabilitation as equal choices — this is medicine's own strength-and-conditioning prescription [4]. The dose file behind it is closed: the flagship Cochrane pooled 65 RCTs and 3,822 participants and found the six-minute walk up 43.93 m (95% CI 32.64–55.21) against a minimal important difference of about 26 m, the SGRQ quality-of-life score down 6.89 points against a 4-point MID, dyspnea and fatigue and mastery each past their MID on the CRQ, maximal cycle work up 6.77 W against a 4 W MID — and the authors wrote that further rehab-versus-usual-care RCTs "are not warranted" [5]. The barbell file stands on its own: across 18 trials and 750 subjects, resistance training versus non-exercise control improved dyspnea by +0.59 CRQ points (0.26–0.93, I²=0%), skeletal muscle strength, and even percent-predicted FEV₁ by +6.88 points — with no adverse events related to resistance training reported in any trial [10]. The mechanism explains why: in the classic training trial, eight weeks of high-work-rate cycling cut blood lactate at identical work rates from 7.2 to 4.5 mEq/L and minute ventilation from 55 to 48 L/min, raised constant-work endurance +73% against +9% — and left FEV₁ at 56% predicted exactly where it started: you were never training the airways [6]. The prognosis file prices the muscle: quadriceps maximal voluntary contraction predicted mortality at HR 0.91 (0.83–0.99) in 162 patients, outpredicting age, BMI and FEV₁ — the strongest single instrument in this file is a leg exercise [7]. What the file does not promise: exercise does not reopen the airways [6], a flare is never trained through [13], and no program replaces the inhaler shelf — those sentences belong to the fences, not the barbell [4]. The honest split, named: the pulmonologist owns the spirometry, the prescriptions and the flare; the program owns the muscle, the breath budget and the continuity [4][13][14].

The reframe: air-hungry, not fragile

Everything operational in this file hangs on one honest division of labor. What training does: it lowers the ventilatory price of every watt of daily life — less lactate at the same work means less CO₂ to blow off, less ventilation, less breathlessness per task [6]; it rebuilds the limb muscle the disease and disuse waste, the dysfunction the ATS/ERS statement names as a systemic consequence that predicts survival itself [8]; and it compounds into the outcomes the Cochrane measured — walking, breathlessness, quality of life [5]. What training does not do: it does not reverse airflow obstruction, it does not treat a flare, and it does not outrank the prescriber [6][13]. The two sentences must be carried together, because each alone produces a broken program. The lifter who believes the lung is fragile quits the gym, and the disuse arithmetic runs against them in a disease where the muscle is already the weak link [8]. The lifter who believes breathlessness is just weakness leaving the body trains through an exacerbation — the one event in this disease with a mortality file of its own, and the one event whose aftermath is the highest-value training window medicine has measured (readmissions cut to OR 0.44 when rehabilitation starts after the flare) [13]. The reframe also settles the identity of the program: COPD fluctuates — good weeks, bad weeks, flare weeks — so the program is built flare-tolerant, the way this library builds around deloads and a frequency that survives a lost fortnight: sustainable weekly set budgets, loads climbed by progressive overload as the breath budget expands — because the program only works while it keeps running [5][14].

The mechanism file: you are training the engine's fuel economy, not the airways

The most clarifying experiment in respiratory training medicine is also one of the oldest. Nineteen patients with obstructive lung disease trained eight weeks on cycles — one arm at high work rates, one at low, total work matched — and the investigators then measured what happened at identical work rates before and after [6]. In the high-intensity arm, blood lactate at the same external work fell from 7.2 to 4.5 mEq/L, and minute ventilation fell from 55 to 48 L/min; constant-work-rate endurance time rose +73% against +9% in the low-intensity arm [6]. And the spirometer — the instrument that defines this disease — measured FEV₁ at 56±12% predicted and watched it not change [6]. The sentence written in 1991 has not needed revision since: the training effect in COPD is peripheral, not pulmonary. For the lifter this is the whole permission structure in one experiment: the obstruction is the fixed bottleneck, but the demand side of breathing is trainable — every kilogram of muscle that clears lactate better is a lower CO₂ load, a lower minute ventilation, a lower breath price on every set of squats and every flight of stairs [6]. The ATS/ERS statement formalizes the flip side: limb muscle dysfunction is not a lifestyle footnote to COPD but a key systemic consequence — it reduces exercise tolerance and quality of life, tracks with survival even after adjustment for airflow limitation, and exercise training is its most potent intervention [8]. The disease is in the lungs; the leverage is in the muscle [6][8].

The survival file: the thigh that outpredicted the spirometer

If the mechanism file explains why training works, the prognosis file explains why it matters this much. The Royal Brompton cohort measured quadriceps maximal voluntary contraction in 184 patients with moderate-to-severe COPD and followed them a median 38 months [7]. Only two variables survived the multivariate model: age, at hazard ratio 1.72 — and quadriceps strength, at HR 0.91 per unit (95% CI 0.83–0.99, p=0.036), with the authors' conclusion that this simple force measurement provided more powerful prognostic information than age, body mass index and FEV₁ [7]. Sit with that ordering: in the disease defined by FEV₁, the leg extensor force outpredicted the spirometer. The real-world cohort completes the arc — 2,386 people with COPD in the Copenhagen City Heart Study, register follow-up: those reporting any regular physical activity against the very-low group carried hospital admission IRR 0.72 (0.53–0.97) and all-cause mortality HR 0.76 (0.65–0.90), with no subgroup — sex, age, severity, ischemic heart disease — exempted from the effect [14]. Neither file is a randomized trial of barbell training, and this file prices them honestly as they price themselves: observational, prognostic, directionally unanimous [7][14]. But they explain why a lung-disease guideline issues strong recommendations for exercise [4]: the mortality-relevant machinery sits disproportionately below the waist [7][8].

The barbell file: what pure resistance training does in a lung disease

Now the sentence this library exists to write: for the lifter with COPD, the iron has its own meta-analysis — not as conditioning's poor cousin but as the standalone intervention. The RT-alone meta: 18 trials, 750 subjects, resistance training versus non-exercise control — dyspnea improved +0.59 on the CRQ (0.26–0.93, I²=0%), skeletal muscle strength improved, percent-predicted FEV₁ improved +6.88 (0.41–13.35), and across every trial zero adverse events related to the resistance training [10]. The combination meta: stacking resistance onto endurance versus endurance alone improved the SGRQ total −7.44 (−12.62 to −2.25) and strength further — the barbell adds what the bike cannot [10]. The strength-add-on RCT: 45 patients, 12 weeks — aerobic plus strength versus aerobic alone: quadriceps force +20±12% against +8±10%, thigh cross-sectional area +8±13% in the combined arm — actual tissue, built in a lung disease [9]. The RT-function meta: 23 studies, 690 patients — resistance training moved the six-minute walk +37.3 m (9.8–64.8) pre-post and quadriceps strength SMD 2.9 (1.1–4.7), heterogeneity honestly priced and the conclusion unambiguous: walking itself is trainable with iron [11]. The dosage file is where the lifter's question gets its direct answer: seven RCTs, 188 individuals, high-load versus low-moderate-load lower-limb training — high load won knee-extensor strength at MD 21.90 Nm (17.46–26.34) and leg press at 5.80 kg (3.87–7.73), VO₂peak favored the heavy arm (+3.10 ml/kg/min), while the six-minute walk favored the lighter arm (−16.90 m) [12]. Both doses built strength; the heavy one built more of it — the program does not require retirement into pink dumbbells, it requires the same progressive overload this library teaches everyone else, paced inside the breath budget [6][12].

The breath budget: how the lifter actually runs a set

The practical translation of the mechanism file is that a training session with COPD is an exercise in spending ventilation deliberately. The rest between sets is not weakness — it is the interval in which the trained system's lower lactate and lower ventilatory demand do their compounding work [6]. The operating rules this file can honestly give: favor multi-joint work at moderate rep ranges you can breathe around, exhale on the effort rather than holding it down, lengthen rest clocks until the breath settles rather than until a stopwatch says go, and structure conditioning as intervals — work/recover — which is exactly how the rehabilitation programs that produced the +43.93 m walked [5]. The warm-up matters more here than in any other file in this library: the first minutes of exercise are the most air-hungry, and graduated loading buys the ventilation time to settle [4][6]. And the honest adjacency: supervised pulmonary rehabilitation is not the alternative to the gym — it is the on-ramp; the ATS grades it strongly for a reason, and the lifter who has never trained post-diagnosis earns the most per session inside one [4]. What this file will not do is hand you a Valsalva verdict or an SpO₂ threshold from a literature it did not cite — oxygen decisions belong to the prescriber, and breathlessness that suddenly changes character belongs to the pulmonologist this week, not next block [3][13].

The flare file: the event that pauses the program and then restarts it

The exacerbation is COPD's tax, and the training question around it has a randomized answer with a specific shape. The post-exacerbation Cochrane pooled 20 RCTs and 1,477 patients who began pulmonary rehabilitation after a flare: hospital readmissions cut to OR 0.44 (95% CI 0.21–0.91), the six-minute walk up +62 m (38–86), SGRQ down −7.80 (−12.12 to −3.47), four of five studies reporting adverse events counting zero — and the one outcome that refused to move, honestly labeled: mortality, OR 0.68 (0.28–1.67), low-quality evidence [13]. Read the ledger as the program runs it: the flare itself is a medical event — worsening breathlessness, more or purulent sputum, fever — and the program's job is to pause without apology, exactly the way this library pauses for illness, because the disuse arithmetic prices a fortnight in days, not months. Then the counterintuitive order: the weeks after the flare are the highest-value training window medicine has measured in this disease — readmissions nearly halved when structured training starts there [13]. So the flare protocol runs: treat first, resume at the deload door when the prescriber clears activity, and let the restarted program collect the OR 0.44 dividend instead of paying the readmission [13]. The tragedy the twin file documents — post-hospital attendance at rehabilitation running in single digits against the strongest evidence window in this disease — is the door this protocol tells you to walk through [13].

The adjunct honesty file: the breathing trainer priced exactly as narrow

The shelf of breathing gadgets deserves its own pricing paragraph, because the diagnosed reader will meet it first. The Cochrane on inspiratory muscle training pooled 55 RCTs and split the question in two [15]. Stacked on pulmonary rehabilitation, IMT bought nothing honest: Borg dyspnea at submaximal work unchanged (MD 0.19, −0.42 to 0.79), mMRC unchanged, 6MWD +5.95 m — below the 26 m MID — SGRQ flat, CAT flat [15]. Standalone against sham, in the patients who train nothing else, it bought something small and real: 6MWD +35.71 m (25.68–45.74, moderate-certainty), transition dyspnea +2.98, CAT −2.97, with zero adverse events in 32 RCTs of PImax reporting [15]. The translation for the lifter who already trains: the breathing trainer is the shelf for the weeks you cannot reach the bar, not a stackable upgrade to a real program [5][15]. The same honesty applies to the mode question — telerehabilitation graded an equal choice by the guideline itself [4], so the supervised on-ramp has a front door for every geography.

The Brazil anchors: who the pt-BR twin serves

The pt-BR lane's reader holds a specific position in this disease, and it is the reason this file ships bilingually. The PLATINO study spirometred a population-based sample of Greater Metropolitan São Paulo, adults over 40, and read COPD prevalence at 15.8% (95% CI 13.5–18.1) on the post-bronchodilator fixed ratio — rising with age and smoking, inversely with BMI [2]. Nine years later the follow-up read the diagnosis ledger: 70% of new COPD cases were underdiagnosed — real obstruction on the spirometer, no name on the chart, the undiagnosed showing fewer symptoms but the same disease [3]. "DPOC" is becoming mainstream Brazilian gym vocabulary exactly as its parent population fills the academias — one in six adults over 40 in the largest city of the pt-BR lane's home market [2]. What the pt-BR twin replaces is the two default scripts Brazilian gym culture runs on this diagnosis — "pare de se esforçar" from the scared side and "treina que é frescura" from the reckless side — with the priced line: a doença está no pulmão, a alavanca está no músculo — o espirômetro dá o nome, a coxa dá o prognóstico, e a barra tem meta-análise própria com zero eventos adversos [7][10].

So what do you actually do? The practical file

Six rules, every one sourced from the files above:

  1. Name the diagnosis before you program it. Spirometry defines COPD; in São Paulo 70% of new cases went undiagnosed — breathlessness that has never been spirometried is a pulmonology appointment first, a training question second [3].
  2. Enter through the supervised door when it exists. The ATS grades pulmonary rehabilitation strongly in stable disease and again after flares [4]; it is the on-ramp that produced the +43.93 m walk, not the alternative to your gym [5].
  3. Keep the barbell, keep it progressive. Pure resistance training moved dyspnea, strength and even FEV₁% across 18 trials with zero adverse events [10]; high load beat low-moderate at +21.90 Nm on the knee extensors [12]; strength stacking built quad force +20% against +8% for endurance alone [9] — this is a lift-and-add file, not a swap-to-walking file.
  4. Spend the breath budget deliberately. Rest clocks until the breath settles, exhale on effort, interval the conditioning, warm up longer than you think you need — the mechanism file promises the ventilatory price of every unit of work falls with training [6].
  5. Flare weeks are pause-and-refer weeks — then restart through the highest-value window in the disease. The exacerbation is a medical event; when the prescriber clears activity, the post-flare start cut readmissions to OR 0.44 [13].
  6. Price the shelf honestly. Training does not reopen airways — FEV₁ stood still while lactate fell [6]; the inhaler and oxygen prescriptions are the pulmonologist's; the breathing trainer is narrow — standalone +35.71 m, stacked-on-rehab null [15]; and the strongest prognostic instrument you can move is the quadriceps, HR 0.91 [7].

How RightRep fits into this

The air-hungry program runs on one currency this app counts better than any notebook — the dosed, dated, camera-verified session:

  • The 8–12 week compliance ledger, kept honestly. The rehabilitation dose that moved the six-minute walk +43.93 m is weeks of accumulated sessions [5] — a camera that counts every rep of every set is the compliance instrument that ledger requires.
  • The breath budget needs a training log, not a memory. Which loads, which rest clocks, which exercises left you settled versus spent — the dose-decision this program makes weekly is exactly what a dated, rep-counted log renders visible [6].
  • Flare-tolerant continuity. The program that survives the flare is the one that works — the visible streak, with pauses logged rather than hidden, is the cheapest continuity device in this file [13][14].
  • Progressive overload honesty at sub-maximal doses. High load beat low-moderate for strength [12] — but only if the load actually climbs; the camera keeps the climb honest without the guesswork [10][12].
  • The pulmonologist-visit artifact. "What have you been able to do since the last visit?" — the question every respiratory consult asks is answered by the camera-counted log you hand over [3][13].

The bottom line

  • The permission file: the 2023 ATS guideline issues a strong recommendation for pulmonary rehabilitation in stable COPD, another after exacerbations, and grades center versus tele an equal choice [4].
  • The dose file: 65 RCTs, 3,822 participants — 6MWD +43.93 m against a 26 m MID, SGRQ −6.89 against 4, every CRQ domain past MID — and the authors' verdict that further rehab-vs-usual-care RCTs "are not warranted" [5].
  • The mechanism file: at identical work rates, trained muscles cut lactate 7.2→4.5 mEq/L and ventilation 55→48 L/min, endurance +73% vs +9% — while FEV₁ at 56% predicted did not move. You train the engine's fuel economy, not the airways [6].
  • The barbell file: 18 trials, 750 subjects — resistance training alone improved dyspnea +0.59, strength and FEV₁% +6.88, with zero adverse events reported [10]; stacked on endurance, SGRQ −7.44 [10]; RT alone moved the 6MWT +37.3 m [11].
  • The strength-add-on RCT: aerobic+strength built quad force +20±12% against +8±10% for aerobic alone, thigh cross-sectional area +8±13% [9].
  • The dosage file: high load beat low-moderate on knee-extensor strength MD 21.90 Nm and leg press 5.80 kg — both doses built strength; the lifter's instinct survives the file [12].
  • The survival file: quadriceps strength predicted mortality at HR 0.91 (0.83–0.99), outpredicting age, BMI and FEV₁ [7]; in the real world, any regular activity cut admissions IRR 0.72 and all-cause mortality HR 0.76 across 2,386 people [14].
  • The flare file: rehabilitation started after an exacerbation cut hospital readmissions to OR 0.44 (0.21–0.91), 6MWD +62 m, with the mortality null honestly labeled [13].
  • The honesty shelf: IMT stacked on rehab bought nothing past noise; standalone it bought +35.71 m — the breathing trainer is the can't-reach-the-bar shelf, not an upgrade [15].
  • The Brazil file: PLATINO São Paulo — 15.8% of adults 40+ (13.5–18.1), and 70% of new cases underdiagnosed at nine-year follow-up; the pt-BR twin's audience is one in six adults over 40 [2][3].

Train the muscle, not just the lungs — and let the camera keep the ledger honest while the pulmonologist keeps the fences, at rightrep.app.

This post was written by the RightRep AI Assistant — the same AI that counts and scores your reps at rightrep.app.

Sources

  1. Liu D, Zhao L, Chen L, et al. Demographic time bomb in COPD (1990-2050): A joinpoint-APC-BAPC modeling study on diverging risk factor attributions across age and SDI spectrums. Medicine (Baltimore), 2026;105(33):e50162. pubmed.ncbi.nlm.nih.gov
  2. Menezes AMB, Jardim JR, Pérez-Padilla R, Camelier A, Rosa F, Nascimento O, Hallal PC. Prevalence of chronic obstructive pulmonary disease and associated factors: the PLATINO Study in São Paulo, Brazil. Cadernos de Saúde Pública, 2005;21(5):1565–1573. pubmed.ncbi.nlm.nih.gov
  3. Moreira GL, Manzano BM, Gazzotti MR, Nascimento OA, Perez-Padilla R, Menezes AM, Jardim JR. PLATINO, a nine-year follow-up study of COPD in the city of São Paulo, Brazil: the problem of underdiagnosis. Jornal Brasileiro de Pneumologia, 2014;40(1):30–37. pubmed.ncbi.nlm.nih.gov
  4. Nici L, Mammen MJ, Charbek E, et al. Pulmonary Rehabilitation for Adults with Chronic Respiratory Disease: An Official American Thoracic Society Clinical Practice Guideline. American Journal of Respiratory and Critical Care Medicine, 2023;208(4):e7–e26. pubmed.ncbi.nlm.nih.gov
  5. McCarthy B, Casey D, Lohan P, Brassington W, Martina OM, Broderick BM. Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews, 2015;(2):CD003793. pubmed.ncbi.nlm.nih.gov
  6. Maltais F, LeBlanc P, Simard C, et al. Reductions in exercise lactic acidosis and ventilation as a result of exercise training in patients with obstructive lung disease. American Review of Respiratory Disease, 1991;143(1):115–121. pubmed.ncbi.nlm.nih.gov
  7. Swallow EB, Reyes D, Hopkinson NS, Man WD-C, Porcher R, Cetti EJ, Moore AJ, Moxham J, Polkey MI. Quadriceps strength predicts mortality in patients with moderate to severe chronic obstructive pulmonary disease. Thorax, 2007;62(2):115–120. pubmed.ncbi.nlm.nih.gov
  8. Barreiro E, Gea J. An official American Thoracic Society/European Respiratory Society statement: update on limb muscle dysfunction in chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine, 2014;189(9):e15–e62. pubmed.ncbi.nlm.nih.gov
  9. Bernard S, LeBlanc P, Whittom F, et al. Aerobic and strength training in patients with chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine, 1999;159(3):896–901. pubmed.ncbi.nlm.nih.gov
  10. Liao WH, Chen JW, Chen X, Lin L, Yan HY, Zhou YQ, Chen R. Impact of Resistance Training in Subjects With COPD: A Systematic Review and Meta-Analysis. Respiratory Care, 2015;60(8):1130–1145. pubmed.ncbi.nlm.nih.gov
  11. Ferté JB, Boyer FC, Taiar R, Pineau C, Barbe C, Rapin A. Impact of resistance training on the 6-minute walk test in individuals with chronic obstructive pulmonary disease: A systematic review and meta-analysis. Annals of Physical and Rehabilitation Medicine, 2022;65(3):101582. pubmed.ncbi.nlm.nih.gov
  12. Topcuoğlu C, Sağlam M, Yağlı NV. Comparison of the effects of high and low-moderate load lower limb resistance training on muscle strength and exercise capacity in individuals with COPD: A systematic review and meta-analysis. Heart & Lung, 2024;64:107–116. pubmed.ncbi.nlm.nih.gov
  13. Puhan MA, Gimeno-Santos E, Cates CJ, Troosters T. Pulmonary rehabilitation following exacerbations of chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews, 2016;(12):CD005305. pubmed.ncbi.nlm.nih.gov
  14. Garcia-Aymerich J, Lange P, Benet M, Schnohr P, Antó JM. Regular physical activity reduces hospital admission and mortality in chronic obstructive pulmonary disease: a population-based cohort study. Thorax, 2006;61(9):772–778. pubmed.ncbi.nlm.nih.gov
  15. Ammous O, Feki W, Lotfi T, Khamis AM, Gosselink R, Rebai A, Kammoun S. Inspiratory muscle training, with or without concomitant pulmonary rehabilitation, for chronic obstructive pulmonary disease (COPD). Cochrane Database of Systematic Reviews, 2023;1(1):CD013778. pubmed.ncbi.nlm.nih.gov