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The Effect of Acute Simulated Altitude on the Lactate Thresholds of Well-Trained Cyclists: 923 Board #102 May 31 200 PM - 330 PM

Bourdon, Pitre C.1; Clark, Sally A.2; Aughey, Robert J.3; Stanef, Tom4; Woolford, Sarah M.4; Schmidt, Walter5; Gore, Christopher J. FACSM2

Medicine & Science in Sports & Exercise: May 2017 - Volume 49 - Issue 5S - p 243
doi: 10.1249/01.mss.0000517517.13886.68
B-63 Free Communication/Poster - Altitude/Hypoxia Wednesday, May 31, 2017, 1:00 PM - 6:00 PM Room: Hall F

1ASPIRE Academy, Doha, Qatar. 2Australian Institute of Sport, Canberra, Australia. 3Victoria University, Melbourne, Australia. 4South Australian Sports Institute, Adelaide, Australia. 5Bayreuth University, Bayreuth, Germany. (Sponsor: Christopher J Gore, FACSM)

(No relationships reported)

PURPOSE: Endurance cyclists often race or train at altitudes ranging from 1,000-3,000 m above sea level. It is well known that peak oxygen consumption (VO2peak) and mean power output (PO) decrease with increasing altitude. However, factors such as lactate thresholds are also important for endurance performance. Research investigating the response of the lactate thresholds to acute hypoxia is however scarce. The aim of this study was to quantify and titrate the acute effect of simulated altitude on the lactate thresholds of well-trained cyclists.

METHODS: Ten well-trained, non-altitude acclimatized male cyclists and triathletes completed a graded cycling exercise test in a hypobaric chamber at each of four simulated altitudes (200, 1,200, 2,200, 3,200 m). The test protocol comprised 5 x 5-min submaximal efforts (50, 100, 150, 200 and 250 W), to determine VO2, heart rate (HR) and blood lactate concentration ([La-]) responses. Following a 10 min passive rest, a 5-min maximal time-trial (5-minTT) was performed to determine peak physiological and performance responses. Combining these measures allowed a modified 2-in-1 protocol to be applied to calculate the lactate thresholds (LT1, LT2) using customized software (ADAPT).

RESULTS: VO2 decreased by 5.5 ± 1.1%, 15.9 ± 1.5% and 26.3 ± 1.4% at LT1 and by 6.5 ± 1.2%, 13.4 ± 1.3% and 23.2 ± 1.8% at LT2 at 1,200, 2,200 and 3,200 m compared with 200 m respectively, P<0.05. Mean PO declined by 5.4 ± 1.1%, 17.7 ± 1.7% and 30.3 ± 1.9% for LT1 and by 5.2 ± 1.3%, 13.9 ± 1.4% and 25.7 ± 1.8% at LT2 at 1,200, 2,200 and 3,200 m compared with 200 m respectively, P<0.05. HR and [La-] at these thresholds remained unchanged. 5-minTT VO2peak and PO both followed the same pattern of decline with increasing altitude, P<0.05.

CONCLUSIONS: A dose response effect of acute hypobaric hypoxia on VO2 and PO was found at both submaximal (LT1 and LT2) and maximal (5-minTT) intensities. No such effects were seen for HR or [La-] at any intensity.

© 2017 American College of Sports Medicine