PO2 cycling reduces diaphragm fatigue by attenuating ROS formation

Li Zuo, Philip T. Diaz, Michael T. Chien, William J. Roberts, Juliana Kishek, Thomas Best, Peter D. Wagner

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Prolonged muscle exposure to low PO2 conditions may cause oxidative stress resulting in severe muscular injuries. We hypothesize that PO2 cycling preconditioning, which involves brief cycles of diaphragmatic muscle exposure to a low oxygen level (40 Torr) followed by a high oxygen level (550 Torr), can reduce intracellular reactive oxygen species (ROS) as well as attenuate muscle fatigue in mouse diaphragm under low PO2. Accordingly, dihydrofluorescein (a fluorescent probe) was used to monitor muscular ROS production in real time with confocal microscopy during a lower PO2 condition. In the control group with no PO2 cycling, intracellular ROS formation did not appear during the first 15 min of the low PO2 period. However, after 20 min of low PO2, ROS levels increased significantly by ,30% compared to baseline, and this increase continued until the end of the 30 min low PO2 condition. Conversely, muscles treated with PO2 cycling showed a complete absence of enhanced fluorescence emission throughout the entire low PO2 period. Furthermore, PO2 cycling-treated diaphragm exhibited increased fatigue resistance during prolonged low PO2 period compared to control. Thus, our data suggest that PO2 cycling mitigates diaphragm fatigue during prolonged low PO2. Although the exact mechanism for this protection remains to be elucidated, it is likely that through limiting excessive ROS levels, PO2 cycling initiates ROS-related antioxidant defenses.

Original languageEnglish (US)
Article numbere109884
JournalPLoS One
Volume9
Issue number10
DOIs
StatePublished - Oct 9 2014
Externally publishedYes

Fingerprint

diaphragm
Diaphragms
Diaphragm
Fatigue
reactive oxygen species
Reactive Oxygen Species
Fatigue of materials
Muscle
muscle fatigue
Oxygen
oxygen
Muscles
muscles
Muscle Fatigue
Oxidative stress
Confocal microscopy
Fluorescent Dyes
Confocal Microscopy
Oxidative Stress
oxidative stress

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Cite this

Zuo, L., Diaz, P. T., Chien, M. T., Roberts, W. J., Kishek, J., Best, T., & Wagner, P. D. (2014). PO2 cycling reduces diaphragm fatigue by attenuating ROS formation. PLoS One, 9(10), [e109884]. https://doi.org/10.1371/journal.pone.0109884

PO2 cycling reduces diaphragm fatigue by attenuating ROS formation. / Zuo, Li; Diaz, Philip T.; Chien, Michael T.; Roberts, William J.; Kishek, Juliana; Best, Thomas; Wagner, Peter D.

In: PLoS One, Vol. 9, No. 10, e109884, 09.10.2014.

Research output: Contribution to journalArticle

Zuo, L, Diaz, PT, Chien, MT, Roberts, WJ, Kishek, J, Best, T & Wagner, PD 2014, 'PO2 cycling reduces diaphragm fatigue by attenuating ROS formation', PLoS One, vol. 9, no. 10, e109884. https://doi.org/10.1371/journal.pone.0109884
Zuo L, Diaz PT, Chien MT, Roberts WJ, Kishek J, Best T et al. PO2 cycling reduces diaphragm fatigue by attenuating ROS formation. PLoS One. 2014 Oct 9;9(10). e109884. https://doi.org/10.1371/journal.pone.0109884
Zuo, Li ; Diaz, Philip T. ; Chien, Michael T. ; Roberts, William J. ; Kishek, Juliana ; Best, Thomas ; Wagner, Peter D. / PO2 cycling reduces diaphragm fatigue by attenuating ROS formation. In: PLoS One. 2014 ; Vol. 9, No. 10.
@article{df3f1e79affc40f59d196a3b9dd14df9,
title = "PO2 cycling reduces diaphragm fatigue by attenuating ROS formation",
abstract = "Prolonged muscle exposure to low PO2 conditions may cause oxidative stress resulting in severe muscular injuries. We hypothesize that PO2 cycling preconditioning, which involves brief cycles of diaphragmatic muscle exposure to a low oxygen level (40 Torr) followed by a high oxygen level (550 Torr), can reduce intracellular reactive oxygen species (ROS) as well as attenuate muscle fatigue in mouse diaphragm under low PO2. Accordingly, dihydrofluorescein (a fluorescent probe) was used to monitor muscular ROS production in real time with confocal microscopy during a lower PO2 condition. In the control group with no PO2 cycling, intracellular ROS formation did not appear during the first 15 min of the low PO2 period. However, after 20 min of low PO2, ROS levels increased significantly by ,30{\%} compared to baseline, and this increase continued until the end of the 30 min low PO2 condition. Conversely, muscles treated with PO2 cycling showed a complete absence of enhanced fluorescence emission throughout the entire low PO2 period. Furthermore, PO2 cycling-treated diaphragm exhibited increased fatigue resistance during prolonged low PO2 period compared to control. Thus, our data suggest that PO2 cycling mitigates diaphragm fatigue during prolonged low PO2. Although the exact mechanism for this protection remains to be elucidated, it is likely that through limiting excessive ROS levels, PO2 cycling initiates ROS-related antioxidant defenses.",
author = "Li Zuo and Diaz, {Philip T.} and Chien, {Michael T.} and Roberts, {William J.} and Juliana Kishek and Thomas Best and Wagner, {Peter D.}",
year = "2014",
month = "10",
day = "9",
doi = "10.1371/journal.pone.0109884",
language = "English (US)",
volume = "9",
journal = "PLoS One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "10",

}

TY - JOUR

T1 - PO2 cycling reduces diaphragm fatigue by attenuating ROS formation

AU - Zuo, Li

AU - Diaz, Philip T.

AU - Chien, Michael T.

AU - Roberts, William J.

AU - Kishek, Juliana

AU - Best, Thomas

AU - Wagner, Peter D.

PY - 2014/10/9

Y1 - 2014/10/9

N2 - Prolonged muscle exposure to low PO2 conditions may cause oxidative stress resulting in severe muscular injuries. We hypothesize that PO2 cycling preconditioning, which involves brief cycles of diaphragmatic muscle exposure to a low oxygen level (40 Torr) followed by a high oxygen level (550 Torr), can reduce intracellular reactive oxygen species (ROS) as well as attenuate muscle fatigue in mouse diaphragm under low PO2. Accordingly, dihydrofluorescein (a fluorescent probe) was used to monitor muscular ROS production in real time with confocal microscopy during a lower PO2 condition. In the control group with no PO2 cycling, intracellular ROS formation did not appear during the first 15 min of the low PO2 period. However, after 20 min of low PO2, ROS levels increased significantly by ,30% compared to baseline, and this increase continued until the end of the 30 min low PO2 condition. Conversely, muscles treated with PO2 cycling showed a complete absence of enhanced fluorescence emission throughout the entire low PO2 period. Furthermore, PO2 cycling-treated diaphragm exhibited increased fatigue resistance during prolonged low PO2 period compared to control. Thus, our data suggest that PO2 cycling mitigates diaphragm fatigue during prolonged low PO2. Although the exact mechanism for this protection remains to be elucidated, it is likely that through limiting excessive ROS levels, PO2 cycling initiates ROS-related antioxidant defenses.

AB - Prolonged muscle exposure to low PO2 conditions may cause oxidative stress resulting in severe muscular injuries. We hypothesize that PO2 cycling preconditioning, which involves brief cycles of diaphragmatic muscle exposure to a low oxygen level (40 Torr) followed by a high oxygen level (550 Torr), can reduce intracellular reactive oxygen species (ROS) as well as attenuate muscle fatigue in mouse diaphragm under low PO2. Accordingly, dihydrofluorescein (a fluorescent probe) was used to monitor muscular ROS production in real time with confocal microscopy during a lower PO2 condition. In the control group with no PO2 cycling, intracellular ROS formation did not appear during the first 15 min of the low PO2 period. However, after 20 min of low PO2, ROS levels increased significantly by ,30% compared to baseline, and this increase continued until the end of the 30 min low PO2 condition. Conversely, muscles treated with PO2 cycling showed a complete absence of enhanced fluorescence emission throughout the entire low PO2 period. Furthermore, PO2 cycling-treated diaphragm exhibited increased fatigue resistance during prolonged low PO2 period compared to control. Thus, our data suggest that PO2 cycling mitigates diaphragm fatigue during prolonged low PO2. Although the exact mechanism for this protection remains to be elucidated, it is likely that through limiting excessive ROS levels, PO2 cycling initiates ROS-related antioxidant defenses.

UR - http://www.scopus.com/inward/record.url?scp=84907741280&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84907741280&partnerID=8YFLogxK

U2 - 10.1371/journal.pone.0109884

DO - 10.1371/journal.pone.0109884

M3 - Article

C2 - 25299212

AN - SCOPUS:84907741280

VL - 9

JO - PLoS One

JF - PLoS One

SN - 1932-6203

IS - 10

M1 - e109884

ER -