Nitric oxide effects on shortening velocity and power production in the rat diaphragm

Morrison, Robert; Miller, Charles C.; Reid, Michael B.

doi:10.1152/jappl.1996.80.3.1065

Cited by 61 publications

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“…Our control data regarding P o , V max , and the curvature of the force-velocity relationship correspond with published values for isolated diaphragm muscle at the same experimental setup (21,48), but differ from those of Morisson et al (36) and Metzger et al (33). Factors that contribute to this variability could include difference in the temperature, animal species, and incubation time.…”

Section: Effects Of Hypoxia On Isotonic Contractile and Fatigue Propesupporting

confidence: 68%

“…A previous study reported that NOS inhibition depressed velocity of shortening and power generation of the rat diaphragm under hyperoxic conditions in vitro (36). The NOS inhibitor N G -nitro-L-arginine, at a concentration of 10 mM, reduced V max and peak power ϳ16 and ϳ18%, respectively.…”

Section: Effects Of No On Isotonic Contractile and Fatigue Propertiesmentioning

confidence: 86%

“…These alterations are reversed by NO donors (26), suggesting that NO inhibits excitation-contraction coupling in unfatigued muscle. On the other hand, NO is essential for optimal myofilament function in the rat diaphragm during active shortening in vitro (36). Inhibition of NOS decreases the shortening velocity and power generation of the rat diaphragm under hyperoxic conditions (36).…”

mentioning

confidence: 99%

“…On the other hand, NO is essential for optimal myofilament function in the rat diaphragm during active shortening in vitro (36). Inhibition of NOS decreases the shortening velocity and power generation of the rat diaphragm under hyperoxic conditions (36). These findings of NOS inhibition on force generation and velocity of shortening indicate multiple possible targets for NO in skeletal muscle.…”

mentioning

confidence: 99%

“…This could result in an increase of intracellular Ca 2ϩ concentration levels ([Ca 2ϩ ] i ) and may, in turn, potentiate NO production by Ca 2ϩ -dependent NOS (19). Based on previous studies showing that NO facilitates the shortening velocity and preserves muscle function (36,38), we hypothesized that NO has a protective role in hypoxia-mediated modulation of muscle contraction in the rat diaphragm in vitro. Accordingly, the aim of the present study was to investigate the effects of the NOS inhibitor N G -monomethyl-L-arginine (L-NMMA), the NO scavenger hemoglobin, and the NO donor spermine NONOate (Sp-NO) on the shortening velocity, power generation, and fatigue endurance of rat diaphragm during hypoxia in vitro.…”

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confidence: 99%

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Effects of modulation of nitric oxide on rat diaphragm isotonic contractility during hypoxia

Zhu

Heunks

Machiels

et al. 2003

Journal of Applied Physiology

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Effects of modulation of nitric oxide on rat diaphragm isotonic contractility during hypoxia. J Appl Physiol 94: 612-620, 2003. First published October 18, 2002 10.1152/ japplphysiol.00441.2002 is essential for optimal myofilament function of the rat diaphragm in vitro during active shortening. Little is known about the role of NO in muscle contraction under hypoxic conditions. Hypoxia might increase the NO synthase (NOS) activity within the rat diaphragm. We hypothesized that NO plays a protective role in isotonic contractile and fatigue properties during hypoxia in vitro. The effects of the NOS inhibitor N G -monomethyl-L-arginine (L-NMMA), the NO scavenger hemoglobin, and the NO donor spermine NONOate on shortening velocity, power generation, and isotonic fatigability during hypoxia were evaluated (PO 2 ϳ 7 kPa). L-NMMA and hemoglobin slowed the shortening velocity, depressed power generation, and increased isotonic fatigability during hypoxia. The effects of L-NMMA were prevented by coadministration with the NOS substrate L-arginine. Spermine NONOate did not alter isotonic contractile and fatigue properties during hypoxia. These results indicate that endogenous NO is needed for optimal muscle contraction of the rat diaphragm in vitro during hypoxia.N G -monomethyl-L-arginine; hemoglobin; spermine NONOate SKELETAL MUSCLE, INCLUDING the diaphragm, continuously produces nitric oxide (NO) (3,26). NO is produced in biological systems via the enzymatic action of NO synthase (NOS) (32). NO generation by the constitutive NOS isoforms (neuronal NOS and endothelial NOS) is calcium dependent (16). NO production within skeletal muscle is enhanced during contractile activity (5).NO has been shown to modulate contractile properties of skeletal muscle in vitro. The overall effect depends on the experimental paradigm. Inhibition of NOS increases twitch and submaximal tetanic force of the rat diaphragm. These alterations are reversed by NO donors (26), suggesting that NO inhibits excitation-contraction coupling in unfatigued muscle. On the other hand, NO is essential for optimal myofilament function in the rat diaphragm during active shortening in vitro (36). Inhibition of NOS decreases the shortening velocity and power generation of the rat diaphragm under hyperoxic conditions (36). These findings of NOS inhibition on force generation and velocity of shortening indicate multiple possible targets for NO in skeletal muscle. In fatiguing contractions, supplementation with exogenous NO slowed the decline of maximal force in mouse soleus muscle (38). This finding suggests that NO preserves skeletal muscle function in vitro during strenuous contractile activity.Hypoxia impairs force generation and accelerates skeletal muscle fatigue in vitro (21, 48). To date, no study has investigated the role of NO in shortening velocity or isotonic fatigability during hypoxia. This is of particular interest because NO affects excitationcontraction coupling in striated muscle (26), and O 2 tension is an important factor in regulating NOS in an...

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Section: Effects Of Hypoxia On Isotonic Contractile and Fatigue Propesupporting

confidence: 68%

Section: Effects Of No On Isotonic Contractile and Fatigue Propertiesmentioning

confidence: 86%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of modulation of nitric oxide on rat diaphragm isotonic contractility during hypoxia

Zhu

Heunks

Machiels

et al. 2003

Journal of Applied Physiology

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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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Muscle Mass and Weight Gain Nutritional Supplements

Campbell

2008

Nutritional Supplements in Sports and Exercise

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Nitric oxide effects on shortening velocity and power production in the rat diaphragm

Cited by 61 publications

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Effects of modulation of nitric oxide on rat diaphragm isotonic contractility during hypoxia

Effects of modulation of nitric oxide on rat diaphragm isotonic contractility during hypoxia

Nitric oxide modulates neuromuscular transmission during hypoxia in rat diaphragm

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