Effects of intravenous <i>N</i>-acetylcysteine infusion on time to fatigue and potassium regulation during prolonged cycling exercise

Medved, Ivan; Brown, Malcolm J.; Bjorksten, Andrew R.; McKenna, Michael J.

doi:10.1152/japplphysiol.00458.2003

Cited by 82 publications

(101 citation statements)

References 45 publications

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“…Whole blood GSH measurements appear to be more effective than plasma GSH (Medved et al, 2003;Medved et al, 2004a). These authors explain that whole blood GSH measurements may be more responsive than plasma GSH measurements.…”

Section: Limitationsmentioning

confidence: 99%

“…In another study, NAC increased red blood cell GSH during hand grip exercise (50% maximal voluntary contraction, 3 seconds on, 3 seconds off) (Matuszczak et al, 2005). To ensure NAC was responsible for these increases in total blood GSH, Medved et al (2004a) measured total NAC, whole blood NAC, and whole blood GSH pre-and post-submax cycling exercise. Significant changes were found in total NAC, whole blood NAC, and whole blood GSH suggesting NAC is responsible for the increase in whole blood GSH (Medved et al, 2004a).…”

Section: Plasma Glutathionementioning

confidence: 99%

“…To ensure NAC was responsible for these increases in total blood GSH, Medved et al (2004a) measured total NAC, whole blood NAC, and whole blood GSH pre-and post-submax cycling exercise. Significant changes were found in total NAC, whole blood NAC, and whole blood GSH suggesting NAC is responsible for the increase in whole blood GSH (Medved et al, 2004a). To accurately account for NAC supplementation in the body, it may perhaps be best to use whole blood assays versus plasma only assays.…”

Section: Plasma Glutathionementioning

confidence: 99%

“…This respiratory muscle fatigue has been hypothesized to be a primary determinant in pulmonary performance, as well as exercise performance (Dempsey, Romer, Rodman, Miller, & Smith, 2006). Respiratory muscle fatigue has been shown to be associated with hydrogen ion production, glycogen depletion, and, recently, the production of reactive oxygen species (ROS) within the respiratory and locomotor muscles (Barreiro et al, 2006;Davies, Quintanilha, Brooks, & Packer, 1982;Juel, 2006;Kerksick & Willoughby, 2005;McKenna et al, 2006;Medved et al, 2004b;Medved, Brown, Bjorksten, & McKenna, 2004a;Reid, Stokic, Koch, Khawli, & Leis, 1994;Reid, 2001a;Supinski, 1998). At the cellular level, ROS can alter chemical balances, blood flow, damage cell membranes, and cause DNA morphing (Davies et al, 1982;Kerksick & Willoughby, 2005;Medved et al, 2004a).…”

Section: Chapter 1 -Introductionmentioning

confidence: 99%

“…However, the mechanism of how NAC delays this fatigue has not been examined (Juel, 2006;McKenna et al, 2006;Medved et al, 2003;Medved et al, 2004a;Mishima, Yamada, Matsunaga, & Wada, 2005;Sen & Packer, 2000;Shindoh et al, 1990). It is presently unknown whether an acute oral doses of NAC will reduce respiratory muscle fatigue and/or improve exercise performance in humans.…”

Section: Chapter 1 -Introductionmentioning

confidence: 99%

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The Effects of N-Acetylcysteine on Respiratory Muscle Fatigue During Heavy Exercise

Kelly

Wicker

Barstow

et al. 2008

Medicine &Amp; Science in Sports &Amp; Exercise

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Diaphragmatic fatigue is known to limit endurance performance during heavy exercise in humans. Previous reports have shown that diaphragmatic fatigue is reduced in rats with N-acetylcysteine (NAC; a nonspecific antioxidant) infusion, suggesting that oxidative stress contributes to this fatigue. However, it is not known if oral supplementation of NAC will reduce respiratory muscle fatigue during heavy exercise in humans. Therefore, the purpose of this study was to determine the effect of an acute oral dose of NAC on respiratory muscle fatigue during whole body heavy exercise. Eight healthy, non-smoking men (22+2 yrs), with no history of cardiovascular or lung disease, completed baseline pulmonary function tests followed by an incremental cycle VO 2peak test. A randomized, double blind crossover design was then used where subjects were given either placebo (PLA) or NAC (1800 mg) 45 min prior to a 30 minute constant load (85% VO 2peak ) discontinuous (six-five minute stages) or continuous (cycle until volitional exhaustion) exercise test. Tests were separated by approximately one week. Maximum pressures (inspiratory, P Imax ; expiratory, P Emax ) and venous blood samples (plasma lactate and total plasma glutathione) were made prior to-and following each 5-min of exercise in discontinuous tests and pre-and post-exercise in continuous tests. Subject's VO 2peak was 43+5 ml/kg/min. There was no difference (p>0.05) in P Imax between NAC (127.9+34.1 cmH 2 O) or PLA (134.1+28.1 cmH 2 O) at rest. During exercise, P Imax was significantly lower (~14%) in 6 of 8 subjects with PLA compared to NAC at minutes 25 and 30 of the discontinuous test indicating respiratory muscle fatigue. With NAC, P Imax did not change (p>0.05) from rest throughout exercise indicating no respiratory muscle fatigue. There was no difference (p>0.05) in P Emax , plasma glutathione, lactate, oxygen uptake (VO 2 ), ventilation (VE), heart rate (HR), or rating of perceived exertion between PLA and NAC at rest or during exercise. Time to exhaustion was not different (p>0.05) during the continuous tests (PLA: 1263 + 334 sec; NAC: 1047 + 136 sec). These results suggest that an acute dose of NAC reduces respiratory muscle fatigue during high intensity exercise but does not alter other ventilatory or metabolic indices. The significance of this reduced respiratory muscle fatigue with NAC on whole body exercise performance remains to be determined.

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Section: Limitationsmentioning

confidence: 99%

Section: Plasma Glutathionementioning

confidence: 99%

Section: Plasma Glutathionementioning

confidence: 99%

Section: Chapter 1 -Introductionmentioning

confidence: 99%

Section: Chapter 1 -Introductionmentioning

confidence: 99%

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The Effects of N-Acetylcysteine on Respiratory Muscle Fatigue During Heavy Exercise

Kelly

Wicker

Barstow

et al. 2008

Medicine &Amp; Science in Sports &Amp; Exercise

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Reactive Oxygen Species: Impact on Skeletal Muscle

Powers

Kavazis

et al. 2011

Comprehensive Physiology

376

371

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It is well established that contracting muscles produce both reactive oxygen and nitrogen species. Although the sources of oxidant production during exercise continue to be debated, growing evidence suggests that mitochondria are not the dominant source. Regardless of the sources of oxidants in contracting muscles, intense and prolonged exercise can result in oxidative damage to both proteins and lipids in the contracting myocytes. Further, oxidants regulate numerous cell signaling pathways and modulate the expression of many genes. This oxidant-mediated change in gene expression involves changes at transcriptional, mRNA stability, and signal transduction levels. Furthermore, numerous products associated with oxidant-modulated genes have been identified and include antioxidant enzymes, stress proteins, and mitochondrial electron transport proteins. Interestingly, low and physiological levels of reactive oxygen species are required for normal force production in skeletal muscle, but high levels of reactive oxygen species result in contractile dysfunction and fatigue. Ongoing research continues to explore the redox-sensitive targets in muscle that are responsible for both redox-regulation of muscle adaptation and oxidant-mediated muscle fatigue.

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Effects of N‐acetylcysteine on glutathione oxidation and fatigue during handgrip exercise

et al. 2005

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Fatigue of hand and forearm muscle groups can limit task performance by astronauts wearing space suits. Countermeasures to delay fatigue would therefore be useful to the space program. N-acetylcysteine (NAC) has been shown to inhibit fatigue during other tasks so we tested its effects during handgrip exercise. Volunteers practiced isometric handgrip maneuvers until performance was reproducible over three successive sessions (baseline). Performance then was retested after ingesting NAC (150 mg.kg(-1)) or saline. Drug administration increased NAC and cysteine blood levels (P < 0.001). Performance of sustained maximal efforts was unaffected. During repetitive submaximal efforts, NAC delayed fatigue (130% baseline) and inhibited glutathione oxidation. Saline did not alter glutathione status or performance of sustained maneuvers; repetitive task performance was increased by 15% (P < 0.05), a placebo effect. These data indicate that NAC supports glutathione homeostasis in exercising humans and may delay muscle fatigue during repetitive handgrip exercise. Our findings support oxidative stress as a causal factor in human muscle fatigue and argue for larger translational studies to define NAC effects on human performance.

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Effects of intravenous N-acetylcysteine infusion on time to fatigue and potassium regulation during prolonged cycling exercise

Cited by 82 publications

References 45 publications

The Effects of N-Acetylcysteine on Respiratory Muscle Fatigue During Heavy Exercise

The Effects of N-Acetylcysteine on Respiratory Muscle Fatigue During Heavy Exercise

Reactive Oxygen Species: Impact on Skeletal Muscle

Effects of N‐acetylcysteine on glutathione oxidation and fatigue during handgrip exercise

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