Acute cardiorespiratory responses to low-load blood-flow restriction vs high-load resistance exercise in COPD: a randomised crossover trial.

Authors

Manuel Kuhn, Christian F Clarenbach, Adrian Kläy, Malcolm Kohler, Diego M Baur, Oliver Senn, Thomas Radtke, Sarah R Haile, Laura C Mayer, Noriane A Sievi, Dario Kohlbrenner

Published in

Thorax. Aug 26, 2026. Epub Aug 26, 2026.

Abstract

Dyspnoea is a major barrier to effective pulmonary rehabilitation in patients with chronic obstructive pulmonary disease (COPD). Low-load blood flow restriction (LL-BFR) resistance exercise may reduce ventilatory demand and dyspnoea burden compared with traditional high-load resistance exercise (HL-TRA). However, its acute physiological and perceptual effects in COPD remain unclear. We compared the acute physiological and perceptual responses to LL-BFR and HL-TRA in patients with COPD.
In a randomised crossover trial, 24 patients with moderate to severe COPD performed LL-BFR (30% of one-repetition maximum (1RM); four sets separated by three rest periods) and HL-TRA (70% of 1RM; three sets separated by two rest periods). Ventilation (V̇E), tidal volume (VT), oxygen uptake (V̇O₂), carbon dioxide output (V̇CO₂), heart rate and ratings of perceived exertion (RPE) were measured throughout. Linear mixed models with participant-level random intercepts were used to compare responses between conditions.
LL-BFR resulted in lower V̇E (-2.2 L/min), VT (-0.08 L), V̇O₂ (-0.04 L/min) and V̇CO₂ (-0.07 L/min) compared with HL-TRA. Heart rate and breathing rate were similar across both conditions. Dyspnoea was significantly reduced (RPE -0.7), while leg effort increased (RPE +0.7). LL-BFR was well tolerated, with no adverse events.
Compared with HL-TRA, LL-BFR was associated with lower ventilatory and metabolic demands and lower perceived dyspnoea despite higher perceived leg exertion. These findings suggest that LL-BFR may represent a useful resistance training strategy for patients with COPD who are primarily limited by dyspnoea during exercise.
NCT05163600.

PMID:
42648900
Bibliographic data and abstract were imported from PubMed on 27 Aug 2026.

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