CYCLING PERFORMANCE TIPS
The Athlete and the GI Tract
by R. Rafoth MD
Sun Mountain Lodge - 1/2004
Gastrointestinal Physiology During Exercise
The etiology of digestive system symptoms with exercise is almost certainly multifactorial.
The most two significant factors are felt to be mechanical trauma (esp in running)
and changes in blood flow most likely moderated by changes in the autonomic nervous
system (sympathetic tone increase). In contrast to the cardiovascular and musculoskeletal
systems, the gastrointestinal system does not change or adapt to exercise "loading".
Instead, any decrease in symptoms with training is thought to be indirect and related
to the fact that the %VO2max for a given level of performance decreases with training and
is associated with a decrease in sympathetetic (autonomic nervous system) activity and
a decrease in the shift of blood flow away from abdominal viscera to heart and
muscles. The result is less physiologic change in digestive system activity. In other
words, for a given level of exercise, blood flow to the gut is much less reduced with
training. Mechanical trauma to the abdominal viscera, however, remains unchanged.
Direct mechanical effects of exercise on intra abdominal organs are significant
factors affecting functioning of gastrointestinal system organs. The effects may be:
- direct trauma (such as rapid descent of the diaphragm on inspiration
traumatizing the stomach and transverse colon or psoas muscle hypertrophy pressing on
the sigmoid colon)
- mechanical "jostling" (the up and down movement of viscera - more evident in
running sports with cecal slap syndrome and cecal volvulus)
- indirect effects related to increased intraabdominal pressure with diaphragmatic
A mechanical etiology is supported by the observation that GI symptoms are much more
common in the running portion of a triathlon than the swimming or cycling portions.
A controlled study in which athletes alternated running and cycling demonstrated symptoms
increasing from cycling (the first leg) to running, but then decreasing again when
switching back to cycling as the third leg while the intensity (measured by % VO2max)
Another studies with an abdominal wall accelerometer documented twice the
accel/deceleration with running compared to cycling (again compatible with the
mechanical hypothesis as significant in the etiology of those symptoms which are more
common in runners).
- 6 subjects
- standardized, measured asphalt paved course
- piezo electric monitor on the abd wall
- compared subject to themselves
- measured episodes per minute of acceleration/deceleration
- when expressed relative to time - twice as frequent with running as cycling
It has been speculated (but unproven) the jarring of small intestine may lead to
an increase in the release of small bowel hormones. As levels have been shown (not
reproduced) to be higher in runners, this could be related to the increase in symptoms
in runners as well.
Next we'll review
- changes in GI "support systems" with exercise
- then the effect of exercise on GI tract functions
- and finally the specific effects of exercise on each of the 4 sections of the GI
tract - esophagus, stomach, small intestine, and colon.
Gastrointestinal System Changes with Exercise
1). Autonomic nervous system
In the resting state, digestion is accompanied by high parasympathetic neural activity and
low sympathetic activity. During exercise, sympathetic activity is increased. How this
relates to change in splanchnic blood flow is unknown (i.e. is there a cause and effect
relationship?). We do know that there are lower basal and exercise catecholamine levels
for any specific level of performance with the adaptation of training, and this
has been proposed as a possible explanation as to why training leads to fewer GI
Changes in autonomic nervous system activity are most likely the culprit in the pre exercise
stress response. 57% of athletes in one questionnaire based study noted pre
competition symptoms, generally cramps and diarrhea, which were similar to symptoms they
experienced when emotionally stressed at other times in their lives.
2) Splanchnic Blood Flow
Intestinal blood has been demonstrated to decrease by up to 80% with exercise. Although
this was based on a single study (with questionable methodology) other studies support
at least a 20 - 50 % decrease. Visceral blood flow decreases with
The teleological explanation is that a decrease in visceral blood flow preserves blood
flow to the muscles, heart, and brain.
- increasing heart rate
- increasing oxygen utilization
- increasing plasma noradrenalin levels
- one study in cycling demonstrated an average 49% decrease at one hour when
exercising at 70% VO2max but with significant variability between subjects
- another found that an asymptomatic runner had minimal changes in splanchnic blood
flow while another symptomatic runner was at 20% of baseline. This strongly suggested
that the degree of decrease in blood flow correlated with symptoms.
- And a third study suggested that a meal may blunt, but not eliminate, the drop in
visceral flow with exercise suggesting a possible strategy to minimize the effects of
exercise on splanchnic blood flow.
Several studies have demonstrted that splanchnic blood flow is inversely
proportional to the intensity of exercise or %VO2max. This would support the concept that
for any set level of activity, GI symptoms decrease with training as one functions at a
Blood viscosity changes with exercise which is accentuated with dehydration. this is
presumed to explain why marathoners with a weight loss of >3.5% of body weight have
more symptoms than those with less weight change. Interestingly, when stratified,
a weight change of <2 %, 2-3 %, 3 - 3.5% demonstrated no significant difference in symptoms,
indicating this may be a threshhold phenomena.
How can a decrease in blood flow cause symptoms? One speculation is that the
countercurrent exchange process in the villi leads to a disproportionate anoxia at the
tip of the villus with the hypoxia of slow flow. This idea is supported by a histologic
picture of ischemic damage.
3) Immune System
While there is suggestive evidence that recreational/leisure exercise may improve immune
system functioning, endurance exercise appears to decrease immune resistance. The
incidence of URIs increases in direct proportion to training and in the post marathon
periods. Although it has been theorized that these changes could impact GI system
function (an increase in cramps and diarrhea from a break in the immunological barrier),
there is no proof.
Changes in intestinal motility are generally felt to be moderated via an increase in
sympathetic nervous system tone with a resultant decrease in GI motility as exercise
increases. But other factors may play a role as well:
- intrinsic GI hormones
- Gastrin, motilin, somatostatin, glucagons, pancreatic polypeptide, VIP - all
increase with exercise.
- However, they have a variable effect on GI activity with some increasing it
while others decrease it. The net effect (i.e. their final role as an etiology in
motility changes throughout the GI tract) is unclear.
- prostaglandins are increased with exercise - they can decrease esophageal LES
pressure and cause defecation in a dog model, both of which are seen in athletes
- endogenous opiates (considered but unproven) may decrease GI motility
- mechanical effects - physically causing colonic material to move down the sigmoid
colon for example
- dietary modifications of training and exercise - more unabsorbed bulk delivered to
the colon in a "healthy" diet
But even though motility effects can be individually measured with each of the
above factors, attempts to correlate them with an overall change in orocecal or total
GI transit time have been equivocal.
One careful study done at 70% VO2 max on a treadmill demonstrated no change in small bowel
(where most absorption takes place) water/glucose/electrolyte solution absorption. Other
studies have provided mixed results. Realistically, one would speculate that there is so
much excess absorptive capacity in the small bowel, there would have to be a significant
change in absorption to be clinically significant. But on the other hand, measures of
breath hydrogen levels (formed from the bacterial fermentation of unabsorbed carbohydrate
that passes into the colon) rise with exercise. The authors of that study speculated
that this might be explain a significant proportion of the flatulence and cramps
associated with exercise.
There has been no hard evidence of changes in secretion of digestive enzymes or evidence
of abnormal secretion of water.
II. Effects of Exercise on the Esophagus, Stomach, Small Intestine, & Colon
1) The Esophagus (UES, body, & LES)
The lower esophageal sphincter serves as the primary barrier between the stomach and
esophagus and a decrease in pressure with exercise has been documented with manometry in
healthy subjects. There has been the suggestion that the tendency to reflux is
- an increase in transient relaxations (i.e. normal pressures but more frequent
episodes of relaxation)
- a increase in the intrathoracic - abdominal pressure gradient with diaphragm movement
(decrease in intrathoracic pressure & increase in intraabdominal pressure)
- documented changes in esophageal body motility - duration, freq, amplitude - which
normally clear any refluxed material back into the stomach (felt to be a back up to the LES)
- delayed gastric emptying (see below) resulting in more material available to reflux
- air swallowing secondary to the increased respiration of exercise resulting in more
gastric distention and subsequently reflux.
Mechanical factors (jostling) are definitely part of the pathophysiology. Using 24
hour ambulatory pH monitoring, 12 trained, asymptomatic athletes were
evaluated during running, weight lifting, and cycling. Runners showed the most reflux,
weight lifters an intermediate amount, while cyclists had the least. All were worse when
exercising after eating demonstrating that gastric distention plays a contributing role.
2) The Stomach
Gastric emptying is stimulated at low exercise levels but is definitely prolonged at
higher %VO2max - with the cross over point is about 70% VO2max . In addition to
fluid osmolarity and fat content, the following can be important factors in the exercise
- emotional and mental stress of competition can decrease the gastric emptying rate.
- oral intake with exercise (volumes > 600 - 1000 cc/hour and hyperosmotic
solutions - more than 139 mg/100ml) can delay gastric emptying
- dehydration has been shown to decrease gastric emptying.
Vascular changes may have a more direct effect as a hemorrhagic gastritis has been
described in association with vigorous exercise.
- prospective endoscopic study of 16 runners (competitive) in a 20 Km race -
16 of 16 dx as having gastritis by endoscopic criteria
- a case report of a runner who died from bleeding gastritis
- prospective observational study to compare the effect of cimetidine usage
immediately before and during a 100-mile running race on the frequency of detectable
gastrointestinal bleeding and relate these data to the frequency and intensity of
gastrointestinal symptoms and to training data collected from pre- and post race
questionnaires. Nine of 25 runners in the 1989 Old Dominion 100-mile Endurance Race
took 800 mg of cimetidine 1 hr before the start and at 50 miles. Sixteen other runners
acted as controls and were not different in age, gender, or training data. All runners
also submitted three stool specimens from the week before the race and from the first
three bowel movements after the race on standard Hemoccult cards. All runners were
Hemoccult negative before the race. One of the 9 (11%) cimetidine runners and 14 of the
16 (87.5%) control runners were Hemoccult positive afterwards (P less than or equal
to 0.05). Nausea and vomiting were less in those runners taking cimetidine
(P less than or equal to 0.05). There was no difference in the race performance as
related to the ability to finish or in the number of miles run during the race. This
study may help to define the etiology of this common gastrointestinal bleeding in these
ultra distance runners and may be useful in preventing some of the symptoms associated
with long-distance running.
3) The Small Intestine (duodenum, jejunum, and ileum)
Of the four parts of the GI tract, the small intestine is the least, if at all, clinically
affected by exercise. To date, only equivocal effects on small bowel transit have been
demonstrated and overall stomach to cecal transit times of 4 to 8 hours remain in the
normal range. No definitive effects on absorption or secretion have been proven.
4) The Colon (ascending, transverse, descending, sigmoid, and rectum)
As opposed to the small intestine, the effects of exercise on the colon are marked and the
results (diarrhea, urgency, and incontinence) readily evident.
- There is a change in motility. There are two types of motility in the colon -
segmenting activity and propulsive waves. As elsewhere in the GI system, there is a
decrease in segmenting contractions (which usually act to delay transit through the colon)
and propulsive or phasic waves are then unopposed. The result is a decrease in oral -
rectal transit time.
- mechanical effects, especially with the jostling of running, may contribute
to the more rapid movement of fecal material down the descending colon with the
result being rectal urgency - which is most common in running events and
directly correlates with the duration of the running event.
- There is a change in colonic mucosal integrity with exercise. It is unclear whether
this is related to mechanical effects on an organ which has a long mesentery or is
a result of mucosal damage from a decrease in visceral blood flow. Evidence includes:
- an increase in endotoxemia (measured in blood samples)
- there is a significant correlation between endotoxin levels and
symptoms of nausea, vomiting, and diarrhea,
- colonoscopic evidence of ischemic colitis picture (confirmed by biopsy)
- an increase in occult GI blood loss that directly correlates with exercise
Next section - Exercise Related Gastrointestinal Symptoms
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