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Abstract

The aim of the present thesis was to examine the effect of acute and long-term
normobaric hyperoxic exposure on selected haemodynamic and haematological responses
during resting and exercise conditions in healthy aerobically well-trained males. This
purpose was evaluated in four separate studies, and each of them had a specific aim listed
below:
Study I evaluated the effect of a 2-hour normobaric O2 exposure on the concentration
of plasma erythropoietin (EPO). Ten healthy males were studied twice in a single blinded
counterbalanced crossover study protocol. On one occasion they breathed air (NOR) and
on the other 100% normobaric O2 (HYPER). Blood samples were collected Pre, Mid and
Post exposure; and thereafter, 3, 5, 8, 24, 32, 48, 72 and 96 hours, and 1 and 2 weeks after
the exposure to determine [EPO]. [EPO] increased markedly 8 and 32 hours after the
NOR exposure (~58% and ~52%, respectively, P ! 0.05) as a consequence of its natural
diurnal variation. Conversely, the O2 breathing was followed by a ~36% decrement of
EPO 3 hours after the exposure (P ! 0.05). Moreover, [EPO] was significantly lower in
HYPER than in the NOR condition 3, 5 and 8 hours after the breathing intervention (P !
0.05). Accordingly, the present results indicate that a short period of normobaric O2
breathing does not increase EPO in aerobically fit healthy males. Increased O2 tension
suppresses EPO 3 and 5 hours after the exposure; thereafter EPO seems to change in a
manner consistent with natural diurnal variation.
Study II investigated the effect of ten daily short-term exposures to normobaric O2 over
a 2-week period on the plasma EPO in healthy individuals. Twenty males were assigned
to either an experimental (HYPER) or to a control (NOR) group. The HYPER group
breathed 100% normobaric O2 for 2 hours every weekday over a 2-week period. The
NOR group breathed air within the same time protocol. Blood samples were collected the
Pre, Mid and Post intervention period to determine EPO. EPO of the HYPER group was
significantly lower than in the NOR group during the Mid and Post periods (P < 0.001).
EPO of the HYPER group showed a slight, albeit statistically non-significant, decrease
during the Mid (~11%) and Post (~16%) periods. Accordingly, daily short-term exposures
to normobaric hyperoxia do not increase EPO. The increased O2 tension suppresses EPO.
Hence, administration of pure O2 to enhance erythropoiesis is not warranted.
Study III mapped the cerebral, intercostal and leg muscle oxygenation of young
healthy males during an acute short-term normobaric O2 administration at rest. Ten
healthy males were studied twice in a single blinded counterbalanced crossover study
protocol. On one occasion they breathed air and on the other 100% normobaric O2 for a 2-
hour time period. Oxygenated ("[O2Hb]), deoxygenated ("[HHb] and total ("[tHb])
haemoglobin in the cerebral, intercostal and vastus lateralis tissues were simultaneously
monitored with near-infrared spectroscopy. The hyperoxic stimulus promptly increased
the "[O2Hb] (~2 μM) and decreased the "[HHb] (~3.6 μM) in the frontal cortex. These
cerebral responses were directly and fully countered by the return to a normoxic
environment. On the contrary, in both intercostal and vastus lateralis muscles only
"[HHb] was significantly decreased by pure O2. The aforementioned muscle changes
transpired slower compared to those in the cerebral area; and they were partially
recovered during the 15-min normoxic-recovery period. Accordingly, the acute
supplementation of normobaric O2 at rest influences the cerebral, leg and respiratory
muscle oxygenation of healthy individuals, but not in the same manner. The cerebral
tissue appears to be more sensitive to the O2-induced changes compared to the muscle
region; a fact which is characterized by the heterogeneous vasoconstrictive response to
pure O2 and the dissimilar return to baseline levels upon the transition to normoxic
environment.
Study IV investigated the effect of carbon monoxide (CO) in the inspired air as
anticipated during peak hours of traffic in higly polluted urban areas on cerebral,
respiratory and leg muscle oxygenation during a constant-power cyce ergometer exercise.
In addition, since O2 breathing is used to hasten elimination of CO from the blood, we
examined the effect of breathing O2 following exposure to CO on cerebral and muscle
oxygenation during a subsequent exercise test under CO conditions. Nine healthy males
participated in three trials: (a) 3-hr air exposure followed by a control constant-power test
(CPT), (b) 1-hour air and 2-hour CO (18.9 ppm) exposure succeeded by a CPT under CO
conditions (CPTCOA), and (c) 2-hour CO and 1-hour 100% normobaric O2 exposure
followed by a CPT under CO conditions (CPTCOB). All exercise tests were performed at
85% of peak power output to exhaustion. Oxygenated (![O2Hb]), deoxygenated
(![HHb]) and total (![tHb]) haemoglobin in cerebral, intercostal and vastus lateralis
muscles were monitored with near-infrared spectroscopy (NIRS) throughout the constantpower
tests. Performance time did not vary between exercise trials. However, the vastus
lateralis and intercostal ![O2Hb] and ![tHb] were lower in CPTCOA than in the CPT (P "
0.05). During the CPTCOB, the intercostal ![O2Hb] and ![tHb] were higher than in the
CPTCOA (P " 0.05). There were no differences in cerebral oxygenation between the trials.
Accordingly, inspiration of 18.9 ppm CO decreases the oxygenation in the vastus lateralis
and serratus anterior muscles, but does not affect endurance during cycle ergometry.
Breathing normobaric O2 moderates the CO-induced reductions in muscle oxygenation,
mainly in the intercostals, but does not affect exercise endurance.