NUTRITION IN SPORT

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(r=–0.54,P<0.01; Iwao et al. 1995). In this study,
however, exercise was performed on a treadmill,
but measurements were made after exercise
ceased, with subjects in a supine position. A
similar inverse correlation between portal
venous flow and plasma noradrenaline concen-
tration in man was observed (r=– 0.65, P<0.01)
when data were collected at rest and during
cycling exercise at 70% of V


.
o2max.with and
without glucose ingestion, inhibitory and stimu-
latory influences, respectively (Rehrer et al. 1993).
Neuropeptide Y is also known to be released
from nerve endings with sympathetic activation
and has been observed to be increased during
exercise (Ahlborg et al. 1992). As it also is a vaso-
constrictor in the blood vessels of the kidneys
and splanchnic region, it may be implicated in
the redistribution of blood flow during exercise.
Other hormones implicated in the regulation
of intestinal blood flow include cholecystekinin
(CCK) and secretin, both having been observed
to increase blood flow within the SMA (Fara &
Madden 1975). Although these hormones are of
particular relevance with respect to blood supply
to the digestive organs after the ingestion of a
meal, it is doubtful that they play a role in the
regulation of blood flow in response to exercise.
Angiotensin II, however, is increased during
exercise and it causes vasoconstriction of
splanchnic and renal blood vessels (Stebbins &
Symons 1995). Similarly, endothelin-1 (ET-1)
increases during exercise and an infusion of ET-1
has been shown to decrease the splanchnic blood
flow to levels lower than those observed during
exercise without ET-1 infusion (Ahlborg et al.
1995).


Gastrointestinal transit


Regular exercise has been observed to increase
the rate of gastrointestinal transit. Cordain et al.
(1986) observed an increased transit as a result of
participation in a running training programme.
It was thought that the mechanical jarring oc-
curring during running may have caused the
increased transit. However, in another study,
Koffler et al. (1992) have demonstrated that


strength training also increases gastrointestinal
transit in elderly and middle-aged men. Further
in support of these findings is a study showing
that a brief period (2 weeks) of relative inactivity
decreases transit in elderly individuals (Liu
et al. 1993). The mechanism responsible for the
decreased transit time with exercise is uncertain.
Changes in hormones and/or parasympathetic
tone, an increased food intake and mechanical
effects have been speculated upon.
A positive health effect may be related to this
adjustment in gastrointestinal transit time
observed with regular exercise. A number of
studies indicate an inverse relationship between
physical activity and colorectal cancer; among
these, one of the most comprehensive is a cohort
study of 104 485 Norwegians (Thune & Lund
1996). These authors speculate that it is the
increase in gastrointestinal transit, reducing
exposure of the gut to potentially carcinogenic
components of the diet, which may account for
the decrease in colorectal cancer seen with
increased levels of exercise participation.

Exercise and

gastrointestinal dysfunction

A number of gastrointestinal symptoms have
long been linked to various forms of moderate
exercise (Larson & Fisher 1987; Green 1992;
Brukner & Kahn 1993). Surveys of runners and
multisport athletes have confirmed the fre-
quency with which prolonged physical exertion
precipitates significant digestive tract problems
which may interrupt training and hinder perfor-
mance (Moses 1990). Fortunately, such symp-
toms are most often self-limiting rather than
life-threatening, but it is increasingly more
common for sports physicians to evaluate gas-
trointestinal symptoms.
Common explanations for these clinical symp-
toms include dehydration, altered gastrointesti-
nal blood flow, changes in gut permeability,
disturbed gastrointestinal tract motility, psycho-
logical influences (‘stress’) and pharmacological
agents (Table 18.1) (Brukner & Khan 1993). Ir-
respective of the cause, exercise-induced al-

gastrointestinal function and exercise 247

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