exercise-induced leucocyte margination, and
that exogenous and endogenous GSH can regu-
late exercise-induced priming of neutrophil for
oxidative burst response (Atalay et al. 1996).
In another human study, the effect of oral NAC
on exercise-associated rapid blood GSH oxida-
tion in healthy adult males who performed two
identical maximal bicycle ergometer exercises 3
weeks apart was investigated. Before the second
maximal exercise test, the men took effervescent
NAC tablets (4¥200 mg · day–1) for 2 days, and an
additional 800 mg on the morning of the test. The
NAC supplementation protocol used in the
study (i) increased the net peroxyl radical scav-
enging capacity of the plasma, and (ii) spared
exercise-induced blood GSH oxidation (Fig. 22.3)
(Senet al. 1994d).
Reid and associates have shown that antioxi-
dant enzymes are able to depress contractility of
unfatigued diaphragm fibre bundles and inhibit
development of acute fatigue. NAC has been
tested for similar effects. Fibre bundles were
removed from diaphragms and stimulated
directly using supramaximal current intensity.
Studies of unfatigued muscle showed that 10 mm
NAC reduced peak twitch stress, shortened time
to peak twitch stress, and shifted the stress-
frequency curve down and to the right. Fibre
bundles incubated in 0.1–10 mmNAC exhibited a
dose-dependent decrease in relative stresses
developed during 30-Hz contraction with no
change in maximal tetanic (200 Hz) stress. NAC
(10 mm) also inhibited acute fatigue. In a later
experiment, this effect of NAC was tested in
humans. Healthy volunteers were studied on
two occasions each. Subjects were pretreated
with NAC 150 mg · kg–1or 5% dextrose in water
by intravenous infusion. It was evident that NAC
pretreatment can improve performance of
human limb muscle during fatiguing exercise,
suggesting that oxidative stress plays a causal
role in the fatigue process and identifying anti-
oxidant therapy as a novel intervention that may
be useful clinically (Khawli & Reid 1994; Reid et
al.1994).
The first study testing the efficacy of a-lipoate
supplementation in exercise-induced oxidative
stress has been just reported. Khanna et al. (1997)
studied the effect of intragastric lipoate supple-
mentation (150 mg · kg–1 body weight for 8
weeks) on lipid peroxidation and GSH-
dependent antioxidant defences in liver, heart,oxidative stress and antioxidant nutrients 309
Glutathione (μmol–1.l
blood)200015010050Pre
Exercise2 min 24 h
(a)200015010050Pre
Exercise2 min 24 h
(b)Fig. 22.3Human blood-oxidized
glutathione levels 5 min before,
2 min after and 24 h after
continuous progressive cycle
ergometer exercise. (a) Maximal
oxygen uptake capacity
determination test (max. test).
(b) Max. test following NAC
supplementation. NAC
supplementation spared exercise-
induced blood glutathione
oxidation in humans. From Sen
et al. (1994d), with permission.