2007, Piran, Slovenia

Environmental Ergonomics XII
Igor B. Mekjavic, Stelios N. Kounalakis & Nigel A.S. Taylor (Eds.), © BIOMED, Ljubljana 2007
This single-blinded, placebo controlled study involved a baseline cycle test to
volitional exhaustion, followed 2 days later by a 10-day period of IHE or placebo
breathing, and a post-intervention maximal cycle test 2 days after intervention.
Hypoxic and placebo exposures: Exposures involved breathing through a hand-held
face mask while sitting at rest for 90 min . day -1 on 10 consecutive days. The IHE
group breathed normobaric hypoxic air for 7 min followed by ambient air for 3 min,
whereas ambient air was substituted for the hypoxic air in the placebo group
(GO2Altitude® hypoxicator). The oxygen concentration of the hypoxic gas was
automatically adjusted by the hypoxicator using automatic-biofeedback control to
maintain a SaO2 of ~80 %.
Maximal cycle test: Maximal incremental cycle tests were performed on an
electronically braked cycle ergometer (Lode, Groningen, Netherlands) starting at an
intensity equivalent to 3.33 W . kg -1 body mass. All stages were 150 s duration with
the first increase in load being 50 W for male and 25 W for female athletes.
Subsequent load increases were 25 W for all athletes until exhaustion. Throughout the
test expired gases were collected (automated system) and heart rate (ECG), arterial
oxygenation saturation (SaO2, pulse oximeter), and muscle (right vastus lateralis) and
brain (left forehead) oxygenation (near-infrared spectroscopy, NIRS) were measured.
Oxyhaemoglobin (oxy-Hb), deoxyhaemoglobin (deoxy-Hb) and total-haemoglobin (t-
Hb) were expressed as the magnitude of the change from the initial value at rest. Total
oxygenation index (TOI% = oxy-Hb/t-Hb × 100) was calculated by the NIRS system.
Statistical analyses: Repeated-measures analyses were performed with a mixedmodeling
procedure (Proc Mixed) in the Statistical Analysis System. Data are
presented as mean (SD), and alpha was set at P ≤ 0.05.
RESULTS
Intervention: During the last minute of the 7 min breathing sessions, SaO2 was lower
(P < 0.01) and HR was higher (P = 0.03) for the IHE participants. Hypoxic breathing
resulted in a similar reduction in SaO2 (day 1 SaO2 = 80.4%, day 10 SaO2 = 80.6%; P
= 0.8) and increase in HR (day 1 HR = 80 beats . min -1 , day 10 HR = 78 beats . min -1 ; P
= 0.6) throughout the exposures.
Incremental exercise: There was no change in V & O2peak or peak power output in either
the IHE or placebo group. Compared with baseline, IHE participants showed a
significant increase in SaO2 at maximal exercise (Figure 1), and reduction in end-tidal
CO2 (PETCO2) (P < 0.01) despite little change in ventilation. The placebo group
showed no change in these variables.
SaO2 (%)
102
100
98
96
94
92
90
88
IHE
0 20 40 60 80 100
Exercise Intensity (% VO2peak)
*
Placebo
0 20 40 60 80 100
. .
Exercise Intensity (% VO2peak)
Figure 1. Arterial oxygen
saturation (SaO2) during
incremental exercise at
baseline (closed circles)
and 2-days post
intervention (open
circles). * difference from
baseline (P < 0.01).
Values are mean (SD).