N-acetylcysteine fails to modulate the in vitro function of sarcoplasmic reticulum of diaphragm in the final phase of fatigue.
OBJECTIVE
In the present study, we tested the hypothesis whether N-acetylcysteine (NAC), a non-specific antioxidant, might influence fatigue by modulating Ca2+-handling capacity by the sarcoplasmic reticulum (SR).


METHODS
In the presence (10 mm) or absence of NAC, bundles of rat diaphragm were stimulated with tetanic trains (350 ms, 30-40 Hz) at 1 train every 2 s for 300 s. SR functions, as assessed by SR Ca2+-uptake and release rates and SR Ca2+-ATPase activity, were measured in vitro on muscle homogenates.


RESULTS
Following the 300-s stimulation, the force developed by NAC-treated muscles is approximately 1.8-fold higher (P < 0.05) than that of muscles without NAC treatment. Stimulation elicited an 18-30% depression in SR function (P < 0.05). Despite the differing degrees of fatigue between NAC-treated and non-treated muscles, SR functions in these muscles were reduced to similar extents.


CONCLUSIONS
These results suggest that modulation of SR function measured in vitro may not be a major contributor to inhibition of diaphragmic fatigue with antioxidant, at least, in the final phase of fatigue where force output is remarkably reduced.
Mishima
T
T
Graduate School of Biosphere Science, Hiroshima University, Higashihiroshima-shi, Hiroshima, Japan.
Yamada
T
T
Matsunaga
S
S
Wada
M
M
D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D003964:Diaphragm / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D008297:Male; D018763:Muscle Fatigue / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012519:Sarcoplasmic Reticulum / Q000187:drug effects* / Q000502:physiology
D000975:Antioxidants; D000252:Calcium-Transporting ATPases; D002118:Calcium; D000111:Acetylcysteine