Effect of acetazolamide on respiratory muscle fatigue in humans

Joaquin Gonzales, Barry W Scheuermann

Research output: Contribution to journalArticlepeer-review


Previous studies have demonstrated that carbonic anhydrase inhibition with acetazolamide reduces exercise capacity. The mechanism responsible for this early fatigue is unclear, but may be partly mediated by impaired respiratory muscle function. Inspiratory muscle strength and endurance were assessed in seven healthy men (age 28 ± 5 yrs, ± SD) by measuring maximal inspiratory pressure (PImax) and time to task failure during a constant-load breathing test (CLBT), respectively, under control and acetazolamide (500 mg/8 h po for 3 days) conditions that were separated by two weeks and randomized between subjects. In addition, PImax was measured before and after moderate-intensity cycling exercise to fatigue while pulmonary gas exchange, plasma pH, and ventilation were measured during exercise. Acetazolamide did not alter pulmonary function (FVC, FEV1.0, MVV) or PImax measured at rest (control, -157 ± 47 vs. acetazolamide, -154 ± 45 cmH2O), but decreased time to task failure during the
Original languageEnglish
Pages (from-to)386-392
JournalRespiratory Physiology and Neurobiology
StatePublished - Jan 15 2013


Dive into the research topics of 'Effect of acetazolamide on respiratory muscle fatigue in humans'. Together they form a unique fingerprint.

Cite this