N-Acetylcysteine is a strong antioxidant, and athletes take it to protect their muscles from the negative effects of extreme exertion, such as soreness and inflammation. But it also inhibits their muscle recovery, sports scientists at the Democritus University of Thrace in Greece discovered.
N-Acetylcysteine is a strong antioxidant, and athletes take it to protect their muscles from the negative effects of extreme exertion, such as soreness and inflammation. But it also inhibits their muscle recovery, sports scientists at the Democritus University of Thrace in Greece discovered.
The peptide glutathione helps enzymes in muscle cells to carry out their protective functions. If you take N-acetylcysteine, your cells use this amino acid as a precursor for glutathione.
N-Acetylcysteine is a strong antioxidant, and athletes take it to protect their muscles from the negative effects of extreme exertion, such as soreness and inflammation. But it also inhibits their muscle recovery, sports scientists at the Democritus University of Thrace in Greece discovered.
The more glutathione your muscle cells contain, the worse the transcription factor NF-kB works. As a result, post-workout supplementation using N-acetylcysteine can weaken inflammatory reactions initiated by immune cells clearing up damaged muscle cells.
Is that performance enhancing or not? This is the question the researchers posed. To answer it they did an experiment with 10 recreational sportsmen, who did two extreme quadriceps training sessions: they performed 20 sets of 15 reps on a leg extension machine.
On one occasion the men took 20 mg N-acetylcysteine per kg bodyweight after their workout every day for eight days. The subjects’ dose was divided over three daily intakes. On the other occasion the men were given a placebo.
During the eight days after the training session the supplementation boosted the concentration of glutathione in the muscles and reduced the concentration of TBARS – an indicator of free radical activity.
Sounds good, but in the days after the workout, the torque [strength] recovery was less good when the subjects had taken N-acetylcysteine. On the other hand, N-acetylcysteine did reduce muscle soreness [DOMS].
N-Acetylcysteine reduced the secretion of inflammatory proteins such as CRP, interleukin 1-beta [below left] and interleukin-6. In addition, N-acetylcysteine also reduced the activity of anabolic signalling molecules such as Akt, mTOR [below right] and MyoD in the muscle cells.
“Our results corroborate those of previous studies suggesting that heavy use of antioxidants may have an adverse effect on muscle performance and recovery, probably by altering signaling pathways mediating muscle inflammation and recovery and potentially mitochondrial biogenesis and subsequent energy metabolism”, the researchers write.
Perhaps athletes who are training to enhance their performance level should be given pro-oxidants instead of antioxidants.
Thiol-based antioxidant supplementation alters human skeletal muscle signaling and attenuates its inflammatory response and recovery after intense eccentric exercise.
Michailidis Y, Karagounis LG, Terzis G, Jamurtas AZ, Spengos K, Tsoukas D, Chatzinikolaou A, Mandalidis D, Stefanetti RJ, Papassotiriou I, Athanasopoulos S, Hawley JA, Russell AP, Fatouros IG.
Source
Democritus University of Thrace, Department of Physical Education and Sport Sciences, Komotini, Greece.
Abstract
BACKGROUND:
The major thiol-disulfide couple of reduced glutathione (GSH) and oxidized glutathione is a key regulator of major transcriptional pathways regulating aseptic inflammation and recovery of skeletal muscle after aseptic injury. Antioxidant supplementation may hamper exercise-induced cellular adaptations.
OBJECTIVE:
The objective was to examine how thiol-based antioxidant supplementation affects skeletal muscle’s performance and redox-sensitive signaling during the inflammatory and repair phases associated with exercise-induced microtrauma.
DESIGN:
In a double-blind, crossover design, 10 men received placebo or N-acetylcysteine (NAC; 20 mg · kg(-1) · d(-1)) after muscle-damaging exercise (300 eccentric contractions). In each trial, muscle performance was measured at baseline, after exercise, 2 h after exercise, and daily for 8 consecutive days. Muscle biopsy samples from vastus lateralis and blood samples were collected before exercise and 2 h, 2 d, and 8 d after exercise.
RESULTS:
NAC attenuated the elevation of inflammatory markers of muscle damage (creatine kinase activity, C-reactive protein, proinflammatory cytokines), nuclear factor ?B phosphorylation, and the decrease in strength during the first 2 d of recovery. NAC also blunted the increase in phosphorylation of protein kinase B, mammalian target of rapamycin, p70 ribosomal S6 kinase, ribosomal protein S6, and mitogen activated protein kinase p38 at 2 and 8 d after exercise. NAC also abolished the increase in myogenic determination factor and reduced tumor necrosis factor-? 8 d after exercise. Performance was completely recovered only in the placebo group.
CONCLUSION:
Although thiol-based antioxidant supplementation enhances GSH availability in skeletal muscle, it disrupts the skeletal muscle inflammatory response and repair capability, potentially because of a blunted activation of redox-sensitive signaling pathways. This trial was registered at clinicaltrials.gov as NCT01778309.
PMID: 23719546 [PubMed – indexed for MEDLINE]
