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

Recent evidence indicates that hypoxia enhances the generation of oxidants. Little is known about the role of free radicals in contractility of the rat diaphragm during hypoxia. We hypothesized that antioxidants improve contractility of the hypoxic rat diaphragm and that xanthine oxidase (XO) is an important source of free radicals in the hypoxic diaphragm. The effects of N-acetylcysteine (NAC; 18 mM), Tiron (10 mM), and the XO inhibitor allopurinol (250 microM) were studied on isometric and isotonic force generation during hypoxia (PO(2) approximately 7 kPa). NAC and Tiron decreased maximal force generation, slowed the shortening velocity, and decreased the power output. Fatigue rate was decreased in the presence of either NAC or Tiron. Allopurinol did not alter the contractility or fatigability of the diaphragm. During hyperoxia (PO(2) approximately 85 kPa), neither NAC nor allopurinol affected the contractility or fatigability of the diaphragm. Thus free radicals play a significant role in diaphragm contractility during hypoxia. Whether antioxidants exert a beneficial or harmful effect on muscle performance depends on the contraction pattern of the muscle. Free radicals generated by XO do not play a role in diaphragm contractility during either hypoxia or hyperoxia.
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PMID:Free radicals in hypoxic rat diaphragm contractility: no role for xanthine oxidase. 1170 36

Hypoxia is known to reduce isometric contractile properties of isolated rat diaphragm bundles. Its effect on isotonic contractile properties (i.e. force-velocity relationship and power output) has not been studied. We hypothesized that hypoxia reduces velocity of shortening and consequently power output of the unfatigued muscle, and shortens endurance time during isotonic contractions. Force-velocity relationship, power output, and fatigue resistance of rat diaphragm muscle bundles were measured during hypoxia (PO2: 6.6 +/- 0.2 kPa) and compared with hyperoxia (PO2: 91.8 +/- 0.7 kPa). Force was clamped from 1 to 100% of maximal tetanic force (Po). Fatigue during isotonic contractions was induced by repeated stimulation every 2 s at a clamp level of 33% of Po. Hypoxia did not affect isometric force generation compared with hyperoxia, nor contraction or relaxation time. In contrast, maximum shortening velocity decreased significantly (hypoxia: 4.2 +/- 0.3, hyperoxia: 6.0 +/- 0.2 Lo/s, P < 0.05). The force-velocity curve shifted downwards (P < 0.05). Hypoxia lowered power output at each load compared with hyperoxia (P < 0.05). The isotonic endurance time was shorter during hypoxia compared with hyperoxia (80 +/- 2 vs. 130 +/- 3 s, P < 0.05). These data show that hypoxia depresses isotonic contractile properties and power output, and reduces endurance time during repeated isotonic contractions.
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PMID:The effect of hypoxia on shortening contractions in rat diaphragm muscle. 1173 93

It is well established that altering O2 delivery to contracting skeletal muscle affects human performance. In this respect, a reduced O2 supply (e.g., hypoxia) increases the rate of muscle fatigue, whereas increasing O2 supply (e.g., hyperoxia) reduces the rate of fatigue. Interestingly, the faster onset of fatigue in moderate hypoxia does not appear to be a consequence of mitochondrial O2 limitation because these effects occur at submaximal rates of O2 consumption for these conditions and at O2 tensions well above that which impairs mitochondrial O2 uptake in vitro. Alterations in O2 supply modulate the regulation of cellular respiration and may affect the onset of impaired Ca2+ handling with fatigue. Specifically, changes in O2 supply alter the coupling between phosphocreatine hydrolysis and O2 uptake in contracting muscles, which by determining the rate of inorganic phosphate (Pi) accumulation may affect Ca2+ release. Partial ischemia differs somewhat in that the reduction in force could be due to reduced O2 supply and/or impaired removal of metabolic by-products secondary to insufficient blood flow. Nonetheless, recent evidence shows a parallel decline and restoration of force with alterations in O2 supply but not blood flow alone during submaximal contractions. Furthermore, the causes of fatigue are similar when O2 is plentiful and when it is reduced.
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PMID:The role of O2 supply in muscle fatigue. 1188 Jun 91

We tested the hypothesis that positive inotropic factors decrease fatigue and improve recovery from fatigue in mammalian skeletal muscle in vitro. To induce fatigue, we stimulated mouse soleus and extensor digitorum longus (EDL) to perform isometric tetanic contractions (50 impulses x s(-1) for 0.5 s) at 6 contractions x min(-1) for 60 min in soleus and 3 contractions x min(-1) for 20 min in EDL. Muscles were submerged in Krebs-Henseleit bicarbonate solution (Krebs) at 27 degrees C gassed with 95% nitrogen - 5% carbon dioxide (anoxia). Before and for 67 min after the fatigue period, muscles contracted at 0.6 contractions x min(-1) in 95% oxygen - 5% carbon dioxide (hyperoxia). We added a permeable cAMP analog (N6, 2'-O-dibutyryladenosine 3':5'-cyclic monophosphate at 10(-3) mol x L(-1) (dcAMP)), caffeine (2 x 10(-3) mol x L(-1), or Krebs as vehicle control at 25 min before, during, or at the end of the fatigue period. In soleus and EDL, both challenges added before fatigue significantly increased developed force but only caffeine increased developed force when added during the fatigue period. At the end of fatigue, the decrease in force in challenged muscles was equal to or greater than in controls so that the force remaining was the same or less than in controls. EDL challenged with dcAMP or caffeine at any time recovered more force than controls. In soleus, caffeine improved recovery except when added before fatigue. With dcAMP added to soleus, recovery was better after challenges at 10 min and the end of the fatigue period. Thus, increased intracellular concentrations of cAMP and (or) Ca2+ did not decrease fatigue in either muscle but improved recovery from fatigue in EDL and, in some conditions, in soleus.
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PMID:Positive inotropism in mammalian skeletal muscle in vitro during and after fatigue. 1518 63

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

This study comprised 2 main experiments: one was to determine the oxidative DNA damage under hyperbaric hyperoxia (HBO), and the other was to evaluate the effects of pre-exposure to HBO on high-intensity exercise performance. Healthy subjects (n = 8) inspired 100% O2 in an experimental chamber at a pressure of 1.3 atmospheres absolute (ATA) for 50 minutes once per week for 2 weeks. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) was measured as a marker of DNA oxidative damage on day 0 and on days 1, 3, and 5 after each HBO exposure. To investigate the effects of pre-exposure to HBO on high-intensity exercise performance, subjects (n = 6) performed maximal isometric knee extensor exercise (30 repetitions x 2 sets) with and without HBO pre-exposure (100% O2 at 1.3 ATA for 50 minutes). Urinary 8-OHdG did not show any significant change after HBO exposure. Isometric knee extensor torque was significantly lower during the first half of the first set of exercises after HBO pre-exposure compared with the normobaric normoxia (NBO) trial. The decreased torque was associated with the lower integrated electromyography with respect to time. Changes in the degree of ischemia-reperfusion in the vastus lateralis muscle during exercise were larger in the HBO pre-exposure trial than in the NBO trial. Muscle fatigue index, serum lactate concentration, heart rate, and systolic blood pressure showed no differences between the 2 trials. These results indicated that HBO exposure was harmless to DNA, and HBO pre-exposure did not enhance high-intensity exercise performance. As a practical application, athletes who require maximal muscle strength should not inspire high-concentration of O2 just before their competitions because it might, as the case may be, impair their performance.
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PMID:Effects of pre-exposure to hyperbaric hyperoxia on high-intensity exercise performance. 1829 57

We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O(2) fractions (FIO2) of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each FIO2 (63 +/- 1, 78 +/- 1 and 87 +/- 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 +/- 4.8%, significantly (P < 0.05) more than after both normoxic (25.6 +/- 3.5% reduction) and hyperoxic (26.6 +/- 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 +/- 1.2 l min(-1) and 100.4 +/- 8.7 ml (100 ml)(-1) min(-1), respectively) were significantly different compared with normoxia (28.4 +/- 1.9 l min(-1) and 94.4 +/- 5.2 ml (100 ml)(-1) min(-1), respectively) and hyperoxia (27.8 +/- 1.6 l min(-1) and 95.1 +/- 7.8 ml (100 ml)(-1) min(-1), respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 +/- 8.5, 49.9 +/- 5.9 and 52.9 +/- 5.9 ml (100 ml)(-1) min(-1), respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in PaO2, thus further compromising O(2) supply to the respiratory muscles.
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PMID:Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists. 1883 19

We evaluated the rate of fatigue development in the inspiratory muscles of healthy trained individuals during graded bicycle exercise and high resistive resistance to breath under conditions of normoxia and hyperoxia. Fatigue of the respiratory muscles was assessed by tension-time index (TT(m)=P(m)I/P(m)I(maxx)T(I)/T(T)), by the dynamics of changes in the ratio of respiratory volume to inspiratory muscles force, and by ratio of the mean amplitudes of electrical activity in high and low frequency ranges. It was found that the limit of extreme working capacity in humans during heavy resistive load is related to fatigue of the inspiratory muscles developing with the same rate under conditions of normoxia or hyperoxia.
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PMID:Effects of normoxia and hyperoxia on the rate of fatigue development in human respiratory muscles under conditions of intensive resistive load. 1952 89

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

Immersion pulmonary edema (IPE) can occur in otherwise healthy swimmers and divers, likely because of stress failure of pulmonary capillaries secondary to increased pulmonary vascular pressures. Prior studies have revealed progressive increase in ventilation [minute ventilation (Ve)] during prolonged immersed exercise. We hypothesized that this increase occurs because of development of metabolic acidosis with concomitant rise in mean pulmonary artery pressure (MPAP) and that hyperoxia attenuates this increase. Ten subjects were studied at rest and during 16 min of exercise submersed at 1 atm absolute (ATA) breathing air and at 4.7 ATA in normoxia and hyperoxia [inspired P(O(2)) (Pi(O(2))) 1.75 ATA]. Ve increased from early (E, 6th minute) to late (L, 16th minute) exercise at 1 ATA (64.1 +/- 8.6 to 71.7 +/- 10.9 l/min BTPS; P < 0.001), with no change in arterial pH or Pco(2). MPAP decreased from E to L at 1 ATA (26.7 +/- 5.8 to 22.7 +/- 5.2 mmHg; P = 0.003). Ve and MPAP did not change from E to L at 4.7 ATA. Hyperoxia reduced Ve (62.6 +/- 10.5 to 53.1 +/- 6.1 l/min BTPS; P < 0.0001) and MPAP (29.7 +/- 7.4 to 25.1 +/- 5.7 mmHg, P = 0.002). Variability in MPAP among subjects was wide (range 14.1-42.1 mmHg during surface and depth exercise). Alveolar-arterial Po(2) difference increased from E to L in normoxia, consistent with increased lung water. We conclude that increased Ve at 1 ATA is not due to acidosis and is more consistent with respiratory muscle fatigue and that progressive pulmonary vascular hypertension does not occur during prolonged immersed exercise. Wide variation in MPAP among healthy subjects is consistent with variable individual susceptibility to IPE.
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PMID:Effects of hyperoxia on ventilation and pulmonary hemodynamics during immersed prone exercise at 4.7 ATA: possible implications for immersion pulmonary edema. 2043 Oct 20


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