Aim: To investigate the effect of carbon monoxide (CO) in the inspired air as anticipated during peak hours of traffic in polluted megalopolises on cerebral, respiratory and leg muscle oxygenation during a constant-power test (CPT). 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. Methods: Nine men participated in three trials: (i) 3-h air exposure followed by a control CPT, (ii) 1-h air and 2-h CO (18.9 ppm) exposure succeeded by a CPT under CO conditions (CPTCOA), and (iii) 2-h CO and 1-h 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 (Δ[O2Hb]), deoxygenated (Δ[HHb]) and total (Δ[tHb]) haemoglobin in cerebral, intercostal and vastus lateralis muscles were monitored with near-infrared spectroscopy throughout the CPTs. Results: Performance time did not vary between trials. However, the vastus lateralis and intercostal Δ[O2Hb] and Δ[tHb] were lower in CPTCOA than in CPT. During the CPTCOB, the intercostal Δ[O2Hb] and Δ[tHb] were higher than in the CPTCOA. There were no differences in cerebral oxygenation between the trials. Conclusion: Inspiration of 18.9 ppm CO decreases oxygenation in the vastus lateralis and serratus anterior muscles, but does not affect performance. Breathing normobaric O2 moderates the CO-induced reductions in muscle oxygenation, mainly in the intercostals, but does not affect endurance.
COBISS.SI-ID: 25109799
Introduction: It has been speculated that short (~1-h) exposures to intermittent normobaric hypoxia at rest can enhance subsequent exercise performance. Thus, the present study investigated the effect of daily resting intermittent hypoxic exposures (IHE) on peak aerobic capacity and performance under both normoxic and hypoxic conditions. Methods: Eighteen subjects were equally assigned to either a control (CON) or IHE group and performed a 4-wk moderate intensity cycling exercise training (1 h · d−1, 5 d · wk−1). The IHE group additionally performed IHE (60 min) prior to exercise training. IHE consisted of seven cycles alternating between breathing a hypoxic gas mixture (5 min; FIo2 = 0.12-0.09) and room air (3 min; FIo2 = 0.21). Normoxic and hypoxic peak aerobic capacity ((inline-graphic xlink:href="942inf1.gif"/)o2peak) and endurance performance were evaluated before (PRE), during (MID), upon completion (POST), and 10 d after (AFTER) the training period. Results: Similar improvements were observed in normoxic (inline-graphic xlink:href="942inf1.gif"/)o2peak tests in both groups [IHE: (POST-PRE) = 10%; CON: (POST-PRE) = 14%], with no changes in the hypoxic condition. Both groups increased performance time in the normoxic constant power test only [IHE: (POST-PRE) = 108%; CON: (POST-PRE) = 114%], whereas only the IHE group retained this improvement in the AFTER test. Higher levels of minute ventilation were noted in the IHE compared to the CON group at the POST and AFTER tests. Conclusion: Based on the results of this study, the IHE does not seem to be beneficial for normoxic and hypoxic performance enhancement.
COBISS.SI-ID: 26168871
Recent findings suggest that besides renal tissue hypoxia, relative decrements in tissue oxygenation, using a transition of the breathing mixture from hyperoxic to normoxic, can also stimulate erythropoietin (EPO) production. To further clarify the importance of the relative change in tissue oxygenation on plasma EPO concentration [EPO], we investigated the effect of a consecutive hyperoxic and hypoxic breathing intervention. Eighteen healthy male subjects were assigned to either IHH (N = 10) or CON (N = 8) group. The IHH group breathed pure oxygen (FiO2 ~ 1.0) for 1 h, followed by a 1-h period of breathing a hypoxic gas mixture (FiO2 ~ 0.15). The CON group breathed a normoxic gas mixture (FiO2 ~ 0.21) for the same duration (2 h). Blood samples were taken just before, after 60 min, and immediately after the 2-h exposure period. Thereafter, samples were taken at 3, 5, 8, 24, 32, and 48 h after the exposure. During the breathing interventions, subjects remained in supine position. There were significant increases in absolute [EPO] within groups at 8 and 32 h in the CON and at 32 h only in the IHH group. No significant differences in absolute [EPO] were observed between groups following the intervention. Relative (∆[EPO]) levels were significantly lower in the IHH than in the CON group, 5 and 8 h following exposure. The tested protocol of consecutive hyperoxic-hypoxic gas mixture breathing did not induce [EPO] synthesis stimulation. Moreover, the transient attenuation in ∆[EPO] in the IHH group was most likely due to a hyperoxic suppression. Hence, our findings provide further evidence against the “normobaric O2 paradox” theory.
COBISS.SI-ID: 25007911
This study investigated the effects of four exposures to normobaric hypoxia (SIH group; FIO2=0.120,N = 10) or placebo-control normoxia (Control group; FIO2=0.209,N = 9) on cardio-respiratory responses to hypoxic exercise. Before and after the exposures all subjects performed a constant power test (CP) to exhaustion in hypoxia (FIO2=0.120) at a work load corresponding to 75% of previously determined normoxic . Arterial oxygen saturation (SpO2) and minute ventilation were measured continuously. NIRS was used to monitor regional changes in oxygenated, de-oxygenated and total hemoglobin concentrations of the frontal cortex, vastus lateralis and serratus anterior. Although neither group improved CP time, the SIH group exhibited increases in both (+15%; P ( 0.05) and SpO2 (+4%; P ( 0.05) after intermittent hypoxia. No physiologically significant differences were observed during exercise in vastus lateralis, serratus anterior and cerebral oxygenation between groups and testing periods. These data suggest that normobaric SIH enhances hypoxic exercise and SpO2, without affecting regional oxygenation or time to exhaustion.
COBISS.SI-ID: 25708839
Aim: The purpose of the present study was to evaluate the ‘normobaric oxygen paradox’ theory by investigating the effect of a 2-h normobaric O2 exposure on the concentration of plasma erythropoietin (EPO). Methods: 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 h, and 1 and 2 weeks after the exposure to determine EPO concentration. Results: The concentration of plasma erythropoietin increased markedly 8 and 32 h after the NOR exposure (approx. 58% and approx. 52%, respectively, P £ 0.05) as a consequence of its natural diurnal variation. Conversely, the O2 breathing was followed by approx. 36% decrement of EPO 3 h after the exposure (P £ 0.05). Moreover, EPO concentration was significantly lower in HYPER than in the NOR condition 3, 5 and 8 h after the breathing intervention (P £ 0.05). Conclusion: In contrast to the ‘normobaric oxygen paradox’ theory, the present results indicate that a short period of normobaric O2 breathing does not increase the EPO concentration in aerobically fit healthy males. Increased O2 tension suppresses the EPO concentration 3 and 5 h after the exposure; thereafter EPO seems to change in a manner consistent with natural diurnal variation.
COBISS.SI-ID: 24589095