Effect of hyperoxia on substrate utilization during intense submaximal exercise

Adams, R. P.; Cashman, P. M. M.; Young, John C.

doi:10.1152/jappl.1986.61.2.523

Cited by 14 publications

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“…We observed a decrease in lactate concentrations at rest and during exercise in hyperoxia. This is in agreement with previous studies (1,9,18) where hyperoxia decreased blood and muscle lactate accumulation during exercise. The decreased lactate production did not, however, restrain metaboreflex activation during isometric handgrip.…”

Section: Discussionsupporting

confidence: 94%

“…First, hyperoxia decreases blood and muscle lactate accumulation (1,9,18), which stimulates group III and IV chemosensitive afferents. This phenomenon is observed despite evidence that high levels of oxygen are present in the cytosol of lactate producing muscles (9) and that oxygen-limited metabolism is not the main mechanism responsible for blood lactate (BL) increase during exercise.…”

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confidence: 99%

“…This phenomenon is observed despite evidence that high levels of oxygen are present in the cytosol of lactate producing muscles (9) and that oxygen-limited metabolism is not the main mechanism responsible for blood lactate (BL) increase during exercise. Decreased lactate levels with hyperoxia may be due to decreased lactate production, secondary to reduced glycogenolysis, glycolysis and pyruvate production, and/or increased lactate clearance (1,18).…”

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Hyperoxia enhances metaboreflex sensitivity during static exercise in humans

Houssière

Najem²,

Cuylits³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Houssière, Anne, Boutaina Najem, Nicolas Cuylits, Sophie Cuypers, Robert Naeije, and Philippe van de Borne. Hyperoxia enhances metaboreflex sensitivity during static exercise in humans. Am J Physiol Heart Circ Physiol 291: H210 -H215, 2006; doi:10.1152/ajpheart.01168.2005.-Peripheral chemoreflex inhibition with hyperoxia decreases sympathetic nerve traffic to muscle circulation [muscle sympathetic nerve activity (MSNA)]. Hyperoxia also decreases lactate production during exercise. However, hyperoxia markedly increases the activation of sensory endings in skeletal muscle in animal studies. We tested the hypothesis that hyperoxia increases the MSNA and mean blood pressure (MBP) responses to isometric exercise. The effects of breathing 21% and 100% oxygen at rest and during isometric handgrip at 30% of maximal voluntary contraction on MSNA, heart rate (HR), MBP, blood lactate (BL), and arterial O 2 saturation (SaO 2 ) were determined in 12 healthy men. The isometric handgrips were followed by 3 min of postexercise circulatory arrest (PE-CA) to allow metaboreflex activation in the absence of other reflex mechanisms. Hyperoxia lowered resting MSNA, HR, MBP, and BL but increased Sa O 2 compared with normoxia (all P Ͻ 0.05). MSNA and MBP increased more when exercise was performed in hyperoxia than in normoxia (MSNA: hyperoxic exercise, 255 Ϯ 100% vs. normoxic exercise, 211 Ϯ 80%, P ϭ 0.04; and MBP: hyperoxic exercise, 33 Ϯ 9 mmHg vs. normoxic exercise, 26 Ϯ 10 mmHg, P ϭ 0.03). During PE-CA, MSNA and MBP remained elevated (both P Ͻ 0.05) and to a larger extent during hyperoxia than normoxia (P Ͻ 0.05). Hyperoxia enhances the sympathetic and blood pressure (BP) reactivity to metaboreflex activation. This is due to an increase in metaboreflex sensitivity by hyperoxia that overrules the sympathoinhibitory and BP lowering effects of chemoreflex inhibition. This occurs despite a reduced lactic acid production.handgrip; muscle sympathetic nerve activity; metaboreceptors; chemoreceptors MUSCLE METABORECEPTORS regulate sympathetic activation during exercise (19,25). This reflex is activated by metabolites released from exercising skeletal muscle. Several substances, such as lactic acid, phosphate, K ϩ , H ϩ , adenosine, prostaglandins, and bradykinin, are now identified as stimulators of this pressor reflex (35,37,40).These metabolites stimulate group III and IV chemosensitive afferents in the working muscles (32). These afferent fibers can also be activated by injection of lactic acid or a hyperosmolar solution of potassium chloride, and their activity is modulated by endogenous nitric oxide in resting and contracting muscle (3,6,11,13,16). This activation in both nonexercising and exercising limbs (32) provokes a rise in cardiac output and vasoconstriction of the nonischemic vascular beds. As a result, blood pressure (BP) and perfusion pressure increase and correct blood flow deficits during exercise (32,35,40,43).There are several reasons to believe that hyperoxia may affect sympathetic regulation during exercise.First, hyp...

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Section: Discussionsupporting

confidence: 94%

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confidence: 99%

mentioning

confidence: 99%

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Hyperoxia enhances metaboreflex sensitivity during static exercise in humans

Houssière

Najem²,

Cuylits³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…In man, performance capacity can be influenced by acutely varying the oxygen concentration of inspired air, resulting in impairment during hypoxia and improvement during hyperoxia (Linnarsson et al 1974;Eiken and Tesch 1984). At similar submaximal works levels, lactate concentrations in blood and muscle are higher during acute hypoxia and lower during acute hyperoxia in comparison with normoxia (Linnarsson et al 1974;Hogan et al 1983;Adams et al 1986). Ammonia concentrations in muscle and blood are not influenced by hyperoxia, but increase with time during submaximal exercise (Graham et al 1987).…”

Section: Introductionmentioning

confidence: 99%

Muscle and blood metabolic responses to intense exercise during acute hypoxia and hyperoxia

Essén‐Gustavsson

Nyman

Wagner

1995

Equine Veterinary Journal

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Summary Three horses performed exercise on a treadmill under normoxic conditions (F1O2–0.21) and during exposure to acute hypoxia (F1O2–0.17) and hyperoxia (F1O2–0.35) achieved by addition of nitrogen and oxygen to inspired air by means by an open flow system. The gases were added after the horses had walked and trotted at 2 submaximal speeds (2 and 4 m/s for 7–15 min). Thereafter, the treadmill speed was increased in 3 steps to attain near maximal oxygen uptake within 5–8 min (8–10.5 m/s for normoxia and hyperoxia and 7–10 m/s for hypoxia). Heart rate and oxygen uptake were recorded continuously. By use of indwelling catheters in the pulmonary and carotid arteries, blood samples were drawn at rest and immediately after exercise. Muscle biopsies (m. gluteus) were taken before and immediately after exercise. In all horses, at the end of exercise, heart rates were lower and oxygen uptake, arterial and venous PO2, haemoglobin saturation and oxygen content were higher following hyperoxia than following hypoxia. At the end of exercise, all horses had lower concentrations of lactate, ammonia and potassium in plasma and lower lactate in muscle after hyperoxia than after hypoxia and normoxia. Concentrations of ATP were higher and of G‐6‐P lower after hyperoxia than after normoxia. Significant correlations were observed between post exercise concentrations of lactate and ammonia (r=0.80) and between lactate and potassium (r=0.96) in plasma. There was also a correlation between muscle and plasma lactate (r=0.92). Post exercise ATP concentrations were correlated with IMP (r=0.85), ammonia (r=0.94) and potassium (r=0.84) concentrations in plasma. The results indicate that acute hypoxia and hyperoxia during intense exercise influence the production and/or removal of lactate.

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“…The only greater oxidation of fatty acids during hyperoxia proposed by several authors appears here to be insufficient to explain the whole _ V O 2 excess. Moreover, studies from Howley et al (1983), Adams et al (1986) and Linossier et al (2000) concluded that blood levels of free fatty acids were similar and that there was no glycogen sparing during exercise in hyperoxia. Thus, there should be another mechanism responsible for the O 2 overconsumption in hyperoxia.…”

Section: Discussionmentioning

confidence: 99%

A high blood lactate induced by heavy exercise does not affect the increase in submaximal $$\dot V{\text{O}}_2 $$ with hyperoxia

et al. 2005

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Few studies evidenced an enhancement in oxygen uptake (VO2) during submaximal exercise in hyperoxia. This O2 "overconsumption" seems to increase above the lactate threshold. The aim of this study was to determine whether the hyperoxia-induced enhancement in VO2 may be related to a higher metabolism of lactate. Nine healthy males (aged 23.1 years, mean VO2 max= 53.8 ml min-1 kg-1) were randomized to two series of exercise in either normoxia or hyperoxia corresponding to an inspired O2 fraction (FIO2) of 30%. Each series consisted of 6 min cycling at 50% VO2 max (Moderate1), 5 min cycling at 95%VO2 max (Near Max) and then 6 min at 50% VO2 max (Moderate2). In both series Near Max was performed in normoxia. VO2 was significantly greater under hyperoxia than in normoxia during Moderate1 (2192 +/- 189 vs. 2025 +/- 172 ml min-1) and during Moderate2 (2352 +/- 173 vs. 2180+ /- 193 ml min-1). However, the effect of the high FIO2 was not significantly different on VO2Moderate2 (+172+/-137 ml min-1 with [La] approximately 6 mmol l-1) compared to VO2Moderate1 (+166 +/- 133 ml min-1 with [La] approximately 2.4 mmol l-1). [La] at the onset of Moderate2 was not different between normoxia and hyperoxia (10.1 +/- 2.2 vs. 10.9 +/- 1.6 mmol l-1). The results show that VO2 is significantly increased during moderate exercise in hyperoxia. But this O2 overconsumption was not modified by a high [La] induced by a prior heavy exercise. It could be concluded that lactate accumulation is not directly responsible for the increase in O2 overconsumption with intensity during exercise in hyperoxia.

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Effect of hyperoxia on substrate utilization during intense submaximal exercise

Cited by 14 publications

References 0 publications

Hyperoxia enhances metaboreflex sensitivity during static exercise in humans

Hyperoxia enhances metaboreflex sensitivity during static exercise in humans

Muscle and blood metabolic responses to intense exercise during acute hypoxia and hyperoxia

A high blood lactate induced by heavy exercise does not affect the increase in submaximal $$\dot V{\text{O}}_2 $$ with hyperoxia

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