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Inspiratory muscle training enhances pulmonary O2 uptake kinetics and high-intensity exercise tolerance in humans
Bailey SJ, Romer LM, Kelly J, Wilkerson DP, di Menna FJ, Jones AM
Journal of Applied Physiology 2010 Aug;109(2):457-468
clinical trial
4/10 [Eligibility criteria: No; Random allocation: Yes; Concealed allocation: No; Baseline comparability: Yes; Blind subjects: No; Blind therapists: No; Blind assessors: No; Adequate follow-up: No; Intention-to-treat analysis: No; Between-group comparisons: Yes; Point estimates and variability: Yes. Note: Eligibility criteria item does not contribute to total score] *This score has been confirmed*

Fatigue of the respiratory muscles during intense exercise might compromise leg blood flow, thereby constraining oxygen uptake (VO2) and limiting exercise tolerance. We tested the hypothesis that inspiratory muscle training (IMT) would reduce inspiratory muscle fatigue, speed VO2 kinetics and enhance exercise tolerance. Sixteen recreationally active subjects (mean +/- SD age 22 +/- 4 yr) were randomly assigned to receive 4 wk of either pressure threshold IMT (30 breaths twice daily at approximately 50% of maximum inspiratory pressure (MIP)) or sham treatment (60 breaths once daily at approximately 15% of MIP). The subjects completed moderate-, severe- and maximal-intensity "step" exercise transitions on a cycle ergometer before (pre) and after (post) the 4-wk intervention period for determination of VO2 kinetics and exercise tolerance. There were no significant changes in the physiological variables of interest after Sham. After IMT, baseline MIP was significantly increased (pre versus post 155 +/- 22 versus 181 +/- 21 cmH2O; p < 0.001), and the degree of inspiratory muscle fatigue was reduced after severe- and maximal-intensity exercise. During severe exercise, the VO2 slow component was reduced (pre versus post 0.60 +/- 0.20 versus 0.53 +/- 0.24 l/min; p < 0.05) and exercise tolerance was enhanced (pre versus post 765 +/- 249 versus 1,061 +/- 304 s; p < 0.01). Similarly, during maximal exercise, the VO2 slow component was reduced (pre versus post 0.28 +/- 0.14 versus 0.18 +/- 0.07 l/min; p < 0.05) and exercise tolerance was enhanced (pre versus post 177 +/- 24 versus 208 +/- 37 s; p < 0.01). Four weeks of IMT, which reduced inspiratory muscle fatigue, resulted in a reduced VO2 slow-component amplitude and an improved exercise tolerance during severe- and maximal-intensity exercise. The results indicate that the enhanced exercise tolerance observed after IMT might be related, at least in part, to improved VO2 dynamics, presumably as a consequence of increased blood flow to the exercising limbs.

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