sive training session but that numbers of lym-
phocytes in the circulation decrease below pre-
exercise levels during the recovery period and
lymphocyte proliferation is impaired (seeFryet
al. 1992; Haq et al.1993; Nieman 1994a, 1994b;
Castell & Newsholme 1998). There is now also
considerable evidence that prolonged, exhaus-
tive exercise is associated with adverse effects on
immune function (for reviews, see Brenner et al.
1994; Shinkai et al.1994; Nieman 1997; Pedersen
et al. 1998).
These effects include:
- decreased cytolytic activity of natural killer
cells; - lower circulating numbers of T-lymphocytes
for 3– 4 h after exercise; - a decrease in the proliferative ability of
lymphocytes; - impaired antibody synthesis;
- decreased immunoglobulin levels in blood
and saliva; - a decreased ratio of CD4 to CD8 cells.
In contrast, it has been suggested that low-
intensity exercise is beneficial for the immune
system (Fitzgerald 1988; Nieman 1994a, 1994b).
Nehlsen-Cannarella et al. (1991) reported a
20% increase in serum immunoglobulins and a
decrease in circulating T-cell numbers in mildly
obese women after 6 weeks of brisk walking.
Natural killer cell activity is enhanced by moder-
ate exercise (Pedersen & Ullum 1994).
Hack et al. (1997) reported a correlation
between a decreased plasma glutamine concen-
tration and circulating levels of CD4 cells after 8
weeks of anaerobic training. Rohde et al.(1996),
inin vitrostudies on T-cell derived cytokines,
found that glutamine influenced the production
of the cytokines interleukin 2 and g-interferon. In
a study on triathletes, they also found that a time
course of changes in serum glutamine correlated
with changes in lymphokine-activated killer cell
activities.
If, as indicated above, glutamine is important
for the immune system, then provision of gluta-
mine might be beneficial for athletes at particular
times during their training.
164 nutrition and exercise
glutamine feeding after
prolonged exhaustive exercise
Since the plasma concentration of glutamine is
decreased by approximately 25% in endurance
runners after a marathon as well as in clinical
conditions, a series of studies was undertaken in
which glutamine was administered. The first
study established a suitable glutamine dose and
timing in resting, normal subjects (Castell &
Newsholme 1997). The results showed that
glutamine (at concentrations of 0.1 g · kg–1body
weight and 5 g per subject), given as a drink, sig-
nificantly increased the plasma glutamine con-
centration within 30 min in healthy humans. This
level returned to close to baseline levels after
approximately 2 h.
The effect of giving glutamine or a placebo
after exercise was subsequently investigated in
full and ultramarathon runners. Glutamine (5 g
l-glutamine (GlutaminOx5, Oxford Nutrition
Ltd) in 330 ml mineral water) or placebo (mal-
todextrin) was given to athletes on a double-
blind basis after prolonged, exhaustive exercise.
Athletes were asked to take two drinks (gluta-
mine/placebo), the first drink immediately after
exercise and the second drink 1 or 2 h after exer-
cise. This timing was chosen as a result of infor-
mation obtained from the glutamine feeding
studies in normal subjects. Blood samples were
also taken after exercise, before and after a gluta-
mine or placebo drink. In addition to meas-
urement of plasma glutamine and cytokine
concentrations and acute phase markers,
numbers of leucocytes and lymphocytes (for
details, see Castell et al.1996) were measured
before and after the drinks, as well as CD4
and CD8 cells (Castell & Newsholme 1997).
The plasma concentrations of glutamine and
branched-chain amino acids were decreased
(23% and 26%, respectively) 1 h after the
marathon but had returned to normal the next
morning (Castell et al.1997). The number of leu-
cocytes tripled in the blood samples taken from
runners immediately after the marathon. This
leucocytosis, due mainly to a substantial increase