Role of nitric oxide in isometric contraction properties of rat diaphragm during hypoxia

Zhu, Xiaoping; Heunks, Leo; Ennen, Leo; Machiels, Herwin A.; Dekhuijzen, P.N.R.

doi:10.1007/s00421-002-0719-9

Cited by 10 publications

(17 citation statements)

References 43 publications

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“…It is also unlikely that the duration of exposure to hypoxia plays a role as a decline in force was already detected after 2 min of hypoxia, 6 whereas others found no change in MVC even after a 40-day simulated climb. 10 Whereas in vivo force-generating capacity of the muscle tissue itself seems to be maintained during hypoxia, in vitro studies generally show a decline in force-generating capacity 2,17,20,26 and a downward shift of the force-frequency relation. 18 We did not find such a depression of force or shift in the forcefrequency relation in the in vivo situation.…”

Section: Discussionmentioning

confidence: 96%

“…20 Indeed, hemoglobin, a scavenger of nitric oxide (NO), in the incubation medium alleviated the effects of an NO donor on in vitro diaphragm contractility during hypoxia. 26 As myoglobin not only plays a role in O 2 storage and facilitated diffusion but also as an intracellular scavenger of NO and reactive oxygen species (ROS), 19 it is possible that in vivo the hemoglobin in the blood and the intracellular myoglobin scavenge the NO and ROS to such an extent that during acute hypoxia for a limited period their detrimental effect on in vivo skeletal muscle function is attenuated. Indeed, it has been reported that acute hypoxemia does not induce oxidative stress in muscle in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…The PaO 2 was similar or even lower than that obtained in many in vitro studies. 2,17,26 To compensate for the reduced supply of O 2 to the tissues, the heart rate was elevated in order to increase cardiac output.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, hypoxia is thought to be a contributing factor to skeletal muscle dysfunction and remodeling during chronic heart failure and chronic obstructive pulmonary disease. 3,13,25 Moreover, the accelerated production of reactive oxygen species during acute hypoxia affects the contractile properties of the diaphragm in vitro, 14,18,20,26 but little is known about the effects of acute hypoxia on the in vivo contractile properties of skeletal muscle.Most human studies on in vivo skeletal muscle function during hypoxia are performed with voluntary contractions. 8,9 Skeletal muscle function, howAbbreviations: ATP, adenosine 5Ј-triphosphate; FIO 2 , fraction of inspired air consisting of oxygen; MVC, maximal voluntary contraction; NO, nitric oxide; P/Po, for the fatigue test, force at a certain time point as a percentage of the force at the onset of the fatigue test; P/Po, for the force-frequency relation, force at a given stimulation frequency as a percentage of the force generated during 100-HZ stimulation; PaO 2 , arterial oxygen partial pressure; ROS, reactive oxygen species; SaO 2 , oxygen saturation of hemoglobin…”

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confidence: 99%

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Acute hypoxia limits endurance but does not affect muscle contractile properties

2005

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Acute hypoxia causes skeletal muscle dysfunction in vitro, but little is known about its effect on muscle function in vivo. In 10 healthy male subjects, isometric contractile properties and fatigue resistance of the quadriceps muscle were determined during normoxia and hypoxia using electrically evoked and voluntary contractions. The oxygen saturation (SaO(2); 96.9 +/- 0.7 vs. 79.9 +/- 3.0%; P < 0.001) was reduced during hypoxia. The maximal voluntary contraction (MVC), force-frequency relation, and contraction and relaxation times were unaffected by hypoxia. The endurance time of a sustained 30% MVC was reduced in hypoxia (248 +/- 104 vs. 217 +/- 76 s; P < 0.05), but not that of a sustained 70% MVC. Fatigue induced by electrically evoked intermittent contractions was unaltered. Thus, acute hypoxia has no significant impact on contractile properties of skeletal muscle in vivo but causes reduced endurance during low-level sustained voluntary contractions. This indicates that skeletal muscle dysfunction during conditions associated with prolonged hypoxemia, except for limited endurance, is not due to acute effects of hypoxemia.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Acute hypoxia limits endurance but does not affect muscle contractile properties

2005

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“…Another possibility is a mechanism similar to that described by Maréchal & Beckers-Bleukx (1998) and Zhu et al (2003), associated with the production of NO.…”

Section: Changes In V Max and Powermentioning

confidence: 99%

Change in contractile properties of human muscle in relationship to the loss of power and slowing of relaxation seen with fatigue

Jones

Ruiter

Haan

2006

The Journal of Physiology

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Slow relaxation from an isometric contraction is characteristic of acutely fatigued muscle and is associated with a decrease in the maximum velocity of unloaded shortening (V max ) and both these phenomena might be due to a decreased rate of cross bridge detachment. We have compared the change in relaxation rate with that of various parameters of the force-velocity relationship over the course of an ischaemic series of fatiguing contractions and subsequent recovery using the human adductor pollicis muscle working in vivo at approximately 37• C in nine healthy young subjects. Maximal isometric force (F 0 ) decreased from 91.0 ± 1.9 to 58.3 ± 3.5 N (mean ± S.E.M.). Maximum power decreased from 53.6 ± 4.0 to 17.7 ± 1.2 (arbitrary units) while relaxation rate declined from −10.3 ± 0.38 to −2.56 ± 0.29 s −1 . V max showed a smaller relative change from 673 ± 20 to 560 ± 46 deg s −1 and with a time course that differed markedly from that of slowing of relaxation, showing very little change until late in the series of contractions. Curvature of the force-velocity relationship increased (a/F 0 decreasing from 0.22 ± 0.02 to 0.11 ± 0.02) with fatigue and with a time course that was similar to that of the loss of power and the slowing of relaxation. It is concluded that for human muscle working at a normal physiological temperature the change in curvature of the force-velocity relationship with fatigue is a major cause of loss of power and may share a common underlying mechanism with the slowing of relaxation from an isometric contraction.

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Nitric oxide modulates neuromuscular transmission during hypoxia in rat diaphragm

Zhu¹,

Heunks²,

Ennen³

et al. 2005

Muscle and Nerve

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Hypoxia impairs neuromuscular transmission in the rat diaphragm. In previous studies, we have shown that nitric oxide (NO) plays a role in force modulation of the diaphragm under hypoxic conditions. The role of NO, a neurotransmitter, on neurotransmission in skeletal muscle under hypoxic conditions is unknown. The effects of the NO synthase (NOS) inhibitor nomega-nitro-L-arginine (L-NNA, 1 mM) and the NO donor spermine NONOate (Sp-NO, 1 mM) were evaluated on neurotransmission failure during nonfatiguing and fatiguing contractions of the rat diaphragm under hypoxic (PO 2 ϳ 5.8 kPa) and hyperoxic conditions (PO 2 ϳ 64.0 kPa). Hypoxia impaired force generated by both muscle stimulation at 40 HZ (P 40 M) and by nerve stimulation at 40 HZ (P 40 N). The effect of hypoxia in the latter was more pronounced. L-NNA increased P 40 N whereas Sp-NO decreased P 40 N during hypoxia. In contrast, neither L-NNA nor Sp-NO affected P 40 N during hyperoxia. L-NNA only slightly reduced neurotransmission failure during fatiguing contractions under hyperoxic conditions. Consequently, neurotransmission failure assessed by comparing force loss during repetitive nerve simulation and superimposed direct muscle stimulation was more pronounced in hypoxia, which was alleviated by L-NNA and aggravated by Sp-NO. These data provide insight in the underlying mechanisms of hypoxia-induced neurotransmission failure. This is important as respiratory muscle failure may result from hypoxia in vivo. Respiratory muscle fatigue, especially that of the diaphragm, is a possible contributor to the development of respiratory failure-for instance, in patients with chronic obstructive pulmonary disease (COPD). 24 Diaphragm fatigue may be the result of a failure of the muscle tissue itself to generate force (contractile fatigue) or failure in neuromuscular transmission. 3 In vitro studies indicate that the contribution of neurotransmission failure to muscle fatigue ranges from 18% 17 to as much as 75%. 1 The importance of neuromuscular transmission failure in the development of respiratory failure has also been demonstrated in intact animals. 5 Hypoxia, a common feature in several respiratory diseases including COPD, adult respiratory distress syndrome, and pneumonia, impairs neuromuscular transmission in the rat diaphragm. 4 However, little is known about the underlying mechanisms of hypoxiainduced neurotransmission failure in the respiratory muscles. In skeletal muscle, nitric oxide (NO) plays a role in the regulation of neural transmission. 31,47 Skeletal muscle is a major source for NO in the body 32 and neuronal NO synthase (nNOS) is present in high concentrations at the postsynaptic surface of the neuromuscular junction of both fast-and slowtwitch fibers. 7,21 Furthermore, NO appears to influence acetylcholine release from presynaptic terminals in several types of neuromuscular junction models, including skeletal muscle. 31,37 We have previously shown that hypoxia-induced impairment in rat diaphragm contractile performance is associated with el...

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Role of nitric oxide in isometric contraction properties of rat diaphragm during hypoxia

Cited by 10 publications

References 43 publications

Acute hypoxia limits endurance but does not affect muscle contractile properties

Acute hypoxia limits endurance but does not affect muscle contractile properties

Change in contractile properties of human muscle in relationship to the loss of power and slowing of relaxation seen with fatigue

Nitric oxide modulates neuromuscular transmission during hypoxia in rat diaphragm

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