Inspiratory muscle training enhances pulmonary O(2) uptake kinetics and high-intensity exercise tolerance in humans.
Fatigue of the respiratory muscles during intense exercise might compromise leg blood flow, thereby constraining oxygen uptake (Vo(2)) and limiting exercise tolerance. We tested the hypothesis that inspiratory muscle training (IMT) would reduce inspiratory muscle fatigue, speed Vo(2) kinetics and enhance exercise tolerance. Sixteen recreationally active subjects (mean + or - SD, age 22 + or - 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 Vo(2) 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 vs. Post: 155 + or - 22 vs. 181 + or - 21 cmH(2)O; P < 0.001), and the degree of inspiratory muscle fatigue was reduced after severe- and maximal-intensity exercise. During severe exercise, the Vo(2) slow component was reduced (Pre vs. Post: 0.60 + or - 0.20 vs. 0.53 + or - 0.24 l/min; P < 0.05) and exercise tolerance was enhanced (Pre vs. Post: 765 + or - 249 vs. 1,061 + or - 304 s; P < 0.01). Similarly, during maximal exercise, the Vo(2) slow component was reduced (Pre vs. Post: 0.28 + or - 0.14 vs. 0.18 + or - 0.07 l/min; P < 0.05) and exercise tolerance was enhanced (Pre vs. Post: 177 + or - 24 vs. 208 + or - 37 s; P < 0.01). Four weeks of IMT, which reduced inspiratory muscle fatigue, resulted in a reduced Vo(2) 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 Vo(2) dynamics, presumably as a consequence of increased blood flow to the exercising limbs.
Bailey
Stephen J
SJ
School of Sport and Health Sciences, St. Luke's Campus, Univ. of Exeter, Heavitree Road, Exeter, Devon EX1 2LU, UK.
Romer
Lee M
LM
Kelly
James
J
Wilkerson
Daryl P
DP
DiMenna
Fred J
FJ
Jones
Andrew M
AM
D000222:Adaptation, Physiological; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001945:Breathing Exercises; D004417:Dyspnea / Q000503:physiopathology; D005080:Exercise Test; D017079:Exercise Tolerance; D005260:Female; D006339:Heart Rate; D006801:Humans; D001239:Inhalation; D007700:Kinetics; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009119:Muscle Contraction; D018763:Muscle Fatigue; D018482:Muscle, Skeletal / Q000098:blood supply / Q000502:physiology*; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption; D011659:Pulmonary Gas Exchange; D012039:Regional Blood Flow; D012132:Respiratory Muscles / Q000502:physiology*; D055815:Young Adult
D015415:Biomarkers; D019344:Lactic Acid; D010100:Oxygen