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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relation between VO2 and work rate (WR) was examined in seven male subjects who performed ramp (1 W.3s-1) two-legged cycle ergometry to exhaustion while inspiring either hypoxic (12% O2), normoxic (21% O2), or hyperoxic (40% O2) air. The anaerobic threshold was estimated from respiratory gas exchange threshold (RGET). Prior to the RGET, the delta VO2/delta WR was greater under normoxic [mean (SD); 10.19(1.04) ml O2.min-1.W-1] and hyperoxic [10.44 (0.72)] conditions compared with hypoxia [9.34 (0.89)]. Above the RGET, the delta VO2/delta WR for hypoxia [8.91 (0.63)], normoxia [10.40 (0.77)], and hyperoxia [11.08 (0.48)] were all significantly different from each other. These data indicated that for two-legged, cycle, ramp ergometry in normoxia below the RGET, both the delta VO2/delta WR and response time was constant. Above the RGET, the normoxic VO2 response was the net result of a declining delta VO2/delta WR and a longer response time to the unsteady state character of a ramp exercise protocol.
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PMID:The influence of inspired oxygen on the oxygen uptake response to ramp exercise. 878 73

This study analysed the effectiveness of an on-demand system of supplying pre-mixed inspiratory gases to subjects under working conditions. A supply of pre-mixed inspiratory gas is often required in order to study the effects of acute hypoxia/hyperoxia on numerous physiological variables whilst normobaric pressure is maintained. The principle aim of this investigation was to determine if the introduction of the on-demand system resulted in any changes in minute ventilation (VE), oxygen consumption (VO2), respiratory rate (RR), tidal volume (VT) or endurance performance during incremental cycle ergometry to exhaustion. Trained male subjects participated in the study (n = 9). The subjects completed two incremental trials on a Monark cycle ergometer. The trials commenced at a power output of 60W implementing a 30 W.4 min-1 work increment. In one trial the subjects inspired ambient room air as per normal VO2max testing, whilst in the other trial the subjects inspired compressed air supplied from high pressure cylinders using a demand valve. Trial order was randomised. Raw data (time, heart rate, VI[ATPS], respiratory rate, tidal volume, FEO2 and FECO2) were recorded on line every 15 seconds. No differences in gas exchange variables were apparent at rest (VO2 VE RR, VT) nor during submaximal work between normal and on-demand trials. VO2max, VEmax and physical performance were also not significantly different between trials. On the basis of these findings, it was suggested that the on-demand system of supplying inspiratory gas resulted in minimal changes in gas exchange variables and performance during incremental work. Using this system of gas supply researchers can effectively supply subjects with premixed gas for little financial expense.
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PMID:An on-demand system of delivering pre-mixed inspiratory gas for use during physical activity. 893 62

The hyperoxia-improved tolerance to maximal aerobic performance was studied in relation to exercising muscle metabolic state. Five students were submitted to four different tests on a cycle ergometer, each being conducted under normoxia and hyperoxia (60% FiO2) on separate days: Test 1, a progressive exercise until exhaustion to determine the maximal work load (Wmax) which was unchanged by hyperoxia; Test 2, an exercise at Wmax (287 +/- 12 W) until exhaustion to determine the performance time (texh) which was elevated by 38% under hyperoxia but exhaustion occurred at the same arterial proton and lactate concentrations; Test 3 (S-Exercise test) consisted of cycling at Wmax for 90% normoxic-texh (4.8 +/- 0.5 min under both O2 conditions) then followed by a 10-s sprint bout during which the total work output (Wtot) was determined; Wtot was elevated by 15% when exercising under hyperoxia; Test 4 (M-Exercise test) consisted also of cycling at Wmax for 4.8 +/- 0.5 min with blood and muscle samples taken at rest and at the end of the exercise to compare the level of different metabolites. During hyperoxic M-Exercise test, glycogen was twice more depleted whereas glucose-6-phosphate and lactate were less accumulated when compared with normoxia. No significant differences were observed for pyruvate, phosphocreatine and muscle/blood lactate ratio between the two conditions. Conversely to normoxia, levels of ATP, ADP and total NADH were maintained at their resting level under 60% FiO2. These data lead us to suppose a higher oxidation rate for pyruvate and NADH in mitochondria, thereby lowering the metabolic acidosis and allowing a better functioning of the glycolytic and contractile processes to delay the time to exhaustion.
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PMID:Effect of hyperoxia on aerobic and anaerobic performances and muscle metabolism during maximal cycling exercise. 1071 78

Replicative senescence of human diploid fibroblasts (HDFs) or melanocytes is caused by the exhaustion of their proliferative potential. Stress-induced premature senescence (SIPS) occurs after many different sublethal stresses including H(2)O(2), hyperoxia, or tert-butylhydroperoxide. Cells in replicative senescence share common features with cells in SIPS: morphology, senescence-associated beta-galactosidase activity, cell cycle regulation, gene expression and telomere shortening. Telomere shortening is attributed to the accumulation of DNA single-strand breaks induced by oxidative damage. SIPS could be a mechanism of accumulation of senescent-like cells in vivo. Melanocytes exposed to sublethal doses of UVB undergo SIPS. Melanocytes from dark- and light- skinned populations display differences in their cell cycle regulation. Delayed SIPS occurs in melanocytes from light-skinned populations since a reduced association of p16(Ink-4a) with CDK4 and reduced phosphorylation of the retinoblastoma protein are observed. The role of reactive oxygen species in melanocyte SIPS is unclear. Both replicative senescence and SIPS are dependent on two major pathways. One is triggered by DNA damage, telomere damage and/or shortening and involves the activation of the p53 and p21(waf-1) proteins. The second pathway results in the accumulation of p16(Ink-4a) with the MAP kinase signalling pathway as possible intermediate. These data corroborate the thermodynamical theory of ageing, according to which the exposure of cells to sublethal stresses of various natures can trigger SIPS, with possible modulations of this process by bioenergetics.
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PMID:Cellular and molecular mechanisms of stress-induced premature senescence (SIPS) of human diploid fibroblasts and melanocytes. 1112 81

The purpose of this study was to examine the influence of hyperoxic gas (50% O2 in N2) inspiration on pulmonary oxygen uptake (V(O2)) kinetics during step transitions to moderate, severe and supra-maximal intensity cycle exercise. Seven healthy male subjects completed repeat transitions to moderate (90% of the gas exchange threshold, GET), severe (70% of the difference between the GET and V(O2) peak) and supra-maximal (105% V(O2) peak) intensity work rates while breathing either normoxic (N) or hyperoxic (H) gas before and during exercise. Hyperoxia had no significant effect on the Phase II V(O2) time constant during moderate (N: 28+/-3s versus H: 31+/-7s), severe (N: 32+/-9s versus H: 33+/-6s) or supra-maximal (N: 37+/-9s versus H: 37+/-9s) exercise. Hyperoxia resulted in a 45% reduction in the amplitude of the V(O2) slow component during severe exercise (N: 0.60+/-0.21 L min(-1) versus H: 0.33+/-0.17 L min(-1); P < 0.05) and a 15% extension of time to exhaustion during supra-maximal exercise (N: 173+/-28 s versus H: 198+/-41 s; P < 0.05). These results indicate that the Phase II V(O2) kinetics are not normally constrained by (diffusional) O2 transport limitations during moderate, severe or supra-maximal intensity exercise in young healthy subjects performing upright cycle exercise.
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PMID:Influence of hyperoxia on pulmonary O2 uptake kinetics following the onset of exercise in humans. 1630 78

Changing arterial oxygen content (C(aO(2))) has a highly sensitive influence on the rate of peripheral locomotor muscle fatigue development. We examined the effects of C(aO(2)) on exercise performance and its interaction with peripheral quadriceps fatigue. Eight trained males performed four 5 km cycling time trials (power output voluntarily adjustable) at four levels of C(aO(2)) (17.6-24.4 ml O(2) dl(-1)), induced by variations in inspired O(2) fraction (0.15-1.0). Peripheral quadriceps fatigue was assessed via changes in force output pre- versus post-exercise in response to supra-maximal magnetic femoral nerve stimulation (DeltaQ(tw); 1-100 Hz). Central neural drive during the time trials was estimated via quadriceps electromyogram. Increased C(aO(2)) from hypoxia to hyperoxia resulted in parallel increases in central neural output (43%) and power output (30%) during cycling and improved time trial performance (12%); however, the magnitude of DeltaQ(tw) (-33 to -35%) induced by the exercise was not different among the four time trials (P > 0.2). These effects of C(aO(2)) on time trial performance and DeltaQ(tw) were reproducible (coefficient of variation = 1-6%) over repeated trials at each F(IO(2)) on separate days. In the same subjects, changing C(aO(2)) also affected performance time to exhaustion at a fixed work rate, but similarly there was no effect of Delta C(aO(2)) on peripheral fatigue. Based on these results, we hypothesize that the effect of C(aO(2)) on locomotor muscle power output and exercise performance time is determined to a significant extent by the regulation of central motor output to the working muscle in order that peripheral muscle fatigue does not exceed a critical threshold.
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PMID:Arterial oxygenation influences central motor output and exercise performance via effects on peripheral locomotor muscle fatigue in humans. 1796 24

The 100% oxygen (O(2)) technique has been used to detect and quantify right-to-left shunt for more than 50 years. The goal of this study was to determine if breathing 100% O(2) affected intrapulmonary arteriovenous pathways during exercise. Seven healthy subjects (3 females) performed two exercise protocols. In Protocol I subjects performed an incremental cycle ergometer test (60 W + 30 W/2 min; breathing room air, FIO2 = 0.209) and arteriovenous shunting was evaluated using saline contrast echocardiography at each stage. Once significant arteriovenous shunting was documented (bubble score = 2), workload was held constant for the remainder of the protocol and FIO2 was alternated between 1.0 (hyperoxia) and 0.209 (normoxia) as follows: hyperoxia for 180 s, normoxia for 120 s, hyperoxia for 120 s, normoxia for 120 s, hyperoxia for 60 s and normoxia for 120 s. For Protocol II, subjects performed an incremental cycle ergometer test until volitional exhaustion while continuously breathing 100% O(2). In Protocol I, shunting was seen in all subjects at 120-300 W. Breathing oxygen for 1 min reduced shunting, and breathing oxygen for 2 min eliminated shunting in all subjects. Shunting promptly resumed upon breathing room air. Similarly, in Protocol II, breathing 100% O(2) substantially decreased or eliminated exercise-induced arteriovenous shunting in all subjects at submaximal and in 4/7 subjects at maximal exercise intensities. Our results suggest that alveolar hyperoxia prevents or reduces blood flow through arteriovenous shunt pathways.
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PMID:Hyperoxia prevents exercise-induced intrapulmonary arteriovenous shunt in healthy humans. 1868 13

We tested the hypothesis that the combination of 2 oxidant stressors (hyperoxia and fatiguing exercise) might reduce or suppress the oxidative stress. We concomitantly measured the plasma concentration of heat shock proteins (Hsp) that protect the cells against the deleterious effects of reactive oxygen species. Healthy humans breathed pure oxygen under normobaric condition for 50-minute periods during which they stayed at rest or executed maximal static handgrip sustained until exhaustion. They also repeated handgrip bouts in normoxic condition. We performed venous blood measurements of 2 markers of the oxidative stress (thiobarbituric acid reactive substances and reduced ascorbic acid) and Hsp27. Under normoxic condition, the handgrip elicited an oxidative stress and a modest increase in plasma Hsp27 level (+7.1 +/- 5.4 ng/mL). Under hyperoxic condition, (1) at rest, compared with the same time schedule in normoxic condition, we measured an oxidative stress (increased thiobarbituric acid reactive substances and decreased reduced ascorbic acid levels) and the plasma Hsp27 level increased (maximal variation, +12.5 +/- 6.0 ng/mL); and (2) after the handgrip, the oxidative stress rapidly disappeared. The combination of both hyperoxia and handgrip bout doubled the Hsp27 response (maximal variation, +24.8 +/- 9.2 ng/mL). Thus, the combination of 2 hits eliciting an oxidative stress seems to induce an adaptive Hsp27 response that might counterbalance an excessive production of reactive oxygen species.
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PMID:Combination of two oxidant stressors suppresses the oxidative stress and enhances the heat shock protein 27 response in healthy humans. 2000 45

The aim of the present study was to determine the development of the inspiratory muscle fatigue in healthy human during incremental cycling to exhaustion under mild and heavy resistive loaded breathing in air and oxygen. Minute ventilation, tidal volume, respiratory rate, inspiratory mouth pressure, and parasternal EMG activities were recorded during an incremental cycling test under mild (12 cmH(2)O x l(-1) x s(-1)) and heavy (40 cmH(2)O x l(-1) x s(-1)) resistive loading in air and oxygen in 8 men. The degree of inspiratory muscle fatigue was evaluated by analysis of the dynamics of inspiratory mouth pressure, 'tension-time' index, and the fall of the high-to-low (H/L) ratio of the parasternal EMG. It was found that oxygen breathing slowed the development of inspiratory muscles fatigue evoked by incremental cycling only during mild resistive loading, whereas hyperoxia had not influence on inspiratory muscle endurance during heavy resistive loading.
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PMID:Effects of oxygen breathing on inspiratory muscle fatigue during resistive load in cycling men. 2013 50

We examined the effects of respiratory muscle work [inspiratory (W(r-insp)); expiratory (W(r-exp))] and arterial oxygenation (Sp(O(2))) on exercise-induced locomotor muscle fatigue in patients with chronic obstructive pulmonary disease (COPD). Eight patients (FEV, 48 +/- 4%) performed constant-load cycling to exhaustion (Ctrl; 9.8 +/- 1.2 min). In subsequent trials, the identical exercise was repeated with 1) proportional assist ventilation + heliox (PAV); 2) heliox (He:21% O(2)); 3) 60% O(2) inspirate (hyperoxia); or 4) hyperoxic heliox mixture (He:40% O(2)). Five age-matched healthy control subjects performed Ctrl exercise at the same relative workload but for 14.7 min ( approximately best COPD performance). Exercise-induced quadriceps fatigue was assessed via changes in quadriceps twitch force (Q(tw,pot)) from before to 10 min after exercise in response to supramaximal femoral nerve stimulation. During Ctrl, absolute workload (124 +/- 6 vs. 62 +/- 7 W), W(r-insp) (207 +/- 18 vs. 301 +/- 37 cmH(2)O x s x min(-1)), W(r-exp) (172 +/- 15 vs. 635 +/- 58 cmH(2)O x s x min(-1)), and Sp(O(2)) (96 +/- 1% vs. 87 +/- 3%) differed between control subjects and patients. Various interventions altered W(r-insp), W(r-exp), and Sp(O(2)) from Ctrl (PAV: -55 +/- 5%, -21 +/- 7%, +6 +/- 2%; He:21% O(2): -16 +/- 2%, -25 +/- 5%, +4 +/- 1%; hyperoxia: -11 +/- 2%, -17 +/- 4%, +16 +/- 4%; He:40% O(2): -22 +/- 2%, -27 +/- 6%, +15 +/- 4%). Ten minutes after Ctrl exercise, Q(tw,pot) was reduced by 25 +/- 2% (P < 0.01) in all COPD and 2 +/- 1% (P = 0.07) in healthy control subjects. In COPD, DeltaQ(tw,pot) was attenuated by one-third after each interventional trial; however, most of the exercise-induced reductions in Q(tw,pot) remained. Our findings suggest that the high susceptibility to locomotor muscle fatigue in patients with COPD is in part attributable to insufficient O(2) transport as a consequence of exaggerated arterial hypoxemia and/or excessive respiratory muscle work but also support a critical role for the well-known altered intrinsic muscle characteristics in these patients.
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PMID:Impact of pulmonary system limitations on locomotor muscle fatigue in patients with COPD. 2044 60


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