|
Reprinted with permission from “Seminars In Neurology” 2000;20(2).
Thieme Medical Publishers, Inc.
Migraine in the athlete may occur secondary to effort, prolonged exertion,
trauma, or as a posttraumatic event. The chemistry is probably akin to that
of spontaneous migraine. The purpose of this discussion is to outline the
differential diagnosis of the athlete presenting with headache. Appropriate
treatment can enhance athletic performance and enable the migraineur to
participate in athletic endeavors.
Introduction. Headache associated with exertion was described by Hippocrates
who admonished his students to “be able to recognize those who have
headache from gymnastic exercises, running, walking, or
any seasonal labor.”1 In modern times the writer Stephen King wrote about
exertional headache in his book called "The Running Man." “Lobsterlike,
Richard humped backwards on his knees and forearms.
His breath came in sharp, doglike gasps.
The air was hot, full of the slick taste of oil, uncomfortable to breathe. A
headache surfaced within his skull and began to push daggers into the backs
of his eyes.”2
In the decade of the 80’s and 90’s, an explosion of understanding about
the chemical causes of migraine has occurred. Given a multitude of new
treatment options, this is an exciting time to treat headache suffers. As
migraine primarily afflicts young people, it is not surprising that many
people participating in sports have migraines.
Almost everybody has a headache on occasion. Many of the headaches that
people assume are “normal” actually represent migraine. There is a great
deal of controversy if it is appropriate to divide headaches into tension
type and migraine type. It is thought by many headache specialists,
including myself, that tension type headache is a variation of migraine.
Migraine is not an illness, but rather an episodic brain disorder. Anyone,
given an appropriate trigger, can develop a migraine type headache. It is
the ongoing occurrence of such headache that sets the migraineur apart.
Scope of the Problem. Sport and exercise related headaches have been
recognized over the last 20 years, but the prevalence is unknown.
Approximately, 1/3 of university students have experienced such headaches.3
The prevalence of childhood migraine increases with age. We know that 3% of
children have migraine. In adolescents, the rate is estimated to be 7% to
11%.4 At puberty, migraine incidence increases in women. By adulthood, 18%
of women and 6% of men have migraine. Incidence is greatest in the 20 to
40-year-old population. Migraine decreases over the age of 60. It is my
intent to discuss how headache may affect the athlete and how athletes may
be treated for headache in ways that will enhance their athletic
performance.
What Is Migrane? The International Headache Society (IHS) established
diagnostic criteria for the adult in 1988. The criteria are: 1) at least 5
attacks lasting 4 to 72 hours (untreated or unsuccessfully treated); 2) 2 of
the following characteristics: unilateral, throbbing, moderate to severe
intensity, aggravated by routine activity; 3) one of the following
associated symptoms: nausea, vomiting, or phonophobia and photophobia.5
However, most headache specialists agree that any episodic bad headache
should be considered migraine, by default. One-third
of patients with migraine have aura. Aura implies a neurologic change, most
often visual, that is present before or during migraine. In children
headache is often bilateral and shorter in duration.
Pathophysiology. To further understand how athletics might affect migraine,
a brief review of the pathophysiology of the migraine attack is warranted.
Our understanding of the migraine attack has increased greatly and continues
to evolve. There is no simple mechanism to explain the migraine attack. Two
theories are accepted: 1) neurovascular inflammation, and 2) serotonin
dysregulation. The first mechanism implies the presence of an irritable pain
generator in the brain stem. When the pain generator is triggered the
trigeminal nerve releases inflammatory chemicals into the brain. The
chemical release causes the associated symptoms of migraine. According to
the second theory, when an adequate trigger is received, serotonin platelet
levels drop, and headache ensues.
In addition, research shows that there is brain hyper-excitability between
migraine attacks. The cause of the hyper-excitability may be magnesium
deficiency or mitochondrial dysfunction. As many as 30% of patients with
migraine have low levels of intra-cerebral magnesium. During a migraine
attack, it is thought that the magnesium level decreases acutely.6
Mitochondrial energy may be enhanced by riboflavin. Studies in migraineurs
who take riboflavin supplements have shown a decrease in the incidence of
migraine attacks by as much as 50% compared to a decrease of 15% in the
placebo group.7
Sports Related Headache. In my practice, which includes both professional
and amateur athletes with headaches, I think of sports headache similarly to
the framework proposed by Williams and Nukada. (Table 1) The 4 categories of
sports headache as described by Williams and Nukada are:
1) effort-exertional headache, 2) effort migraine (in this paper referred to
as prolonged exertion as a trigger for migraine), 3) trauma-triggered
migraine, and 4) posttraumatic headache.8 I have modified this framework
because I think any bad episodic headache as migraine. Keep in mind that
headache sufferers often experience headaches in one or more of these
categories.
Table 1. Sports Related Headache
Exertion or Effort Headache
Prolonged Exertion as a Trigger for Migraine
Trauma Triggered Migraine
Posttraumatic Headache |
Exertion or Effort Headache. Exertion or effort headache is a benign
headache precipitated by any form of exercise. The headache typically occurs
de novo in an otherwise healthy person who has not been prone to headaches.8
According to IHS criteria, the headache is bilateral, throbbing
at onset and may develop migrainous features in those predisposed to
migraine. Duration is 5 minutes to 24 hours. The headache may be prevented
by avoiding excessive exertion, particularly in hot weather.6
Evaluation of exertion headache includes a thorough patient history. The
physician should inquire: What effort or activity triggers headache? Does
the headache increase in intensity along with the effort? How quickly does
the headache peak? How long does the headache last after effort stops?
Is the headache associated with other symptoms? Are migraine features
present?
Is there anything unusual or concerning in presentation? Was there recent
trauma or illness? Is there a history of altitudinal headache? Does
coughing, sneezing, Valsalva, or sex trigger headache?
Effort migraine has been reported in various settings. Several cases were
reported during the 1977 Olympic Games in Mexico City. Young,
well-conditioned athletes developed scotoma, severe retro-orbital pain,
nausea, and vomiting. The rather unusually high incidence of this condition
during the Mexico City games suggested that high altitude may have been a
contributing factor.9
In new onset headache after the age
of 50, cardiac evaluation is indicated. A particularly important cause of
exertion headache has been reviewed in the older athlete. Lipton and
associates suggested the term “cardiac cephalgia” in patients who
presented with exertional headache as the most prominent manifestation of
myocardial ischemia. In response to exertion, 2 men aged 57 and 67 quickly
developed severe bilateral head pain. One patient reported nausea. Neither
had a known history of heart disease. Neither man complained of chest
discomfort, diaphoresis, or palpitations. During treadmill testing, head
pain recurred and cardiac ischemia was seen. Myocardial ischemia is a
treatable cause of exertional headache. Accurate diagnosis is critical to
prevent myocardial infarction as well as to offer headache control.10
Basoglu, et al, reported a case of a
15-year-old boy who suffered exclusively with exercise induced headache and
had migraine like accompanying symptoms. A single photo emission
computerized tomography (SPECT) was done during a typical attack.
Perfusion-related pathology was demonstrated. Asymmetrical decreased
regional cerebral blood flow was seen in both frontal cortices. The SPECT
scan was thought to support a pathogenetic relationship to migraine.11
In patients with effort headache, the
physical exam, including neurologic exam, is typically normal. Examination
should include blood pressure measurement and auscultation of the head and
neck to detect bruits. If one suspects an intracranial mass lesion (ie,
tumor, aneurysm, AV malformation, Arnold Chiari malformation) then MRI or CT
scanning is indicated. MRI can be done in conjunction with a Valsalva
maneuver to assess the presence of tonsillar herniation. If a subarachnoid
hemorrhage is suspected, further studies, such as MR angiogram and
arteriography or an lumbar puncture (LP) to rule out intracranial blood may
be needed. Prior to LP, imaging is necessary to rule out increased
intracranial pressure. In new onset headache after age 50, cardiac
evaluation is indicated.
The exertional activity should be discontinued until diagnosis is
established. Often pharmacological therapy helps these patients. If the
attacks occur predictably, treatment can be administered just before
exertion. For attacks that are frequent and not always predictable,
preventative therapy may be the best choice.
Indomethacin is the “gold standard” for exertional headache. For
infrequent and predictable headache it can be taken 1 to 2 hours before
exertion. If headaches are more frequent, it can be taken daily at 25 to 50
mg TID. Because of the probable relation to migraine, migraine prevention
medication are often beneficial.
Prolonged Exertion as a Trigger to Migrane. Athletes with predisposition to
migraine may have prolonged exertion as one trigger for a typical migraine.
The headache does not typically resolve when the activity is discontinued.
The headache may occur minutes or hours into the activity, or after
cessation of activity.
Effort migraine was seen in 9% of 128 subjects reported by Williams and
Nukada.
In the study population, such headaches often began in childhood or
adolescence with the average age of onset 15. Aura was noticed by all,
nausea by the majority, and vomiting and neck stiffness were frequent. The
headache was generally throbbing, moderate to severe, and lasted for hours.
Spontaneous migraine, which did not relate to sport or exercise, was
experienced in 55% of subjects, with a positive family history in 64%. The
authors suggested that low oxygen tension may trigger effort migraine by an
as yet unknown mechanism.8
For a headache to occur with prolonged exertion, additional triggers may be
required. Such triggers include heat, altitude, bright light, dehydration,
or low blood sugar. Swain and Kaplan reported headache development after use
of certain types of athletic equipment. Poorly fitting mouth guards, tight
helmets, and goggles were noted as potential triggers for the athlete with
migraine.12
“Goggle” migraine has been described by neurologist Alan Pestronk. He
developed a migraine headache beginning 1 to 2 hours after exercise and
occurring only on days when he swam. His father, a retailer of sporting
goods, noted anecdotally that his customers frequently complained of
headache associated with the use of ill-fitting swim goggles. When Dr.
Pestronk changed to a goggle not requiring a tight head strap, he had no
further migraine headaches.13
Another interesting case report in the literature is of a 48-year-old woman
who consistently developed migraine after completing aerobic exercise class.
Switching from a “high impact” to a “low impact” exercise regimen
was not beneficial. A change in her estrogen replacement therapy was
observed to be the responsible second trigger. She had changed from pill
form to a patch prior to the development of headache. The patch, along with
exercise-associated vasodilatation, increased absorption of estrogen. The
estrogen “bolus” then precipitated a vascular headache. Removal of the
patch during exercise solved the problem.14
The evaluation of the athlete with exertion as one trigger for migraine is
the
same as for that of any patient presenting
with headache. Special emphasis on triggers related to the athletic event
should be reviewed. This might include use of equipment, environmental
factors, (ie, sunlight, altitude, or diet).
Some athletes with prolonged exertion
as a trigger for migraine will respond to pretreatment with Indocin. Other
anti-inflammatory medications could be tried as well. These and other treatments are
discussed below.
Trauma Triggered Migrane. Trauma triggered migraine is typically seen in
children, adolescents, and young adults. It represents a complex temporary
disturbance
of brain function precipitated by a mild blow to the head. The attack may
begin with visual disturbance, such as temporary blindness, change in level
of consciousness, or with hemiparesis or brain-stem symptoms. A severe
headache, nausea, and vomiting follow. Symptoms begin 1 to 10 minutes after
a blow to the head, but are not triggered by blows to the rest of the body.
The attack usually resolves within a few to 24 hours. Rarely, neurologic
deficits do not totally clear. These post-traumatic attacks may be mistaken
for cerebral concussions, contusions, or acute epidural or subdural
hematoma.15-17
Trauma triggered migraines have been reported with soccer, football,
volleyball, and wrestling. Because of the involvement in contact sports,
these headaches are more typical in boys and young men. Except that the
trigger is trauma, the presentation is similar to other migraine attacks.
The incidence of spontaneous migraine is much higher in children with trauma
migraine. A positive family history of migraine is seen in 77% of children
with this variety of headache.
In 1980, Bennett of the University of Nebraska reviewed 3 members of a
university football team, aged 18 to 21 years old, who were evaluated
because of migraine symptoms precipitated by head trauma. The head trauma
was usually minor and not associated with amnesia. Visual, motor, sensory,
or confusional signs and symptoms began after a short symptom-free interval.
Symptoms lasted for 15 to 30 minutes and were followed by a headache
frequently accompanied by nausea and vomiting. In 9 of 11 cases the attacks
reoccurred with subsequent head trauma.18
The differential diagnosis includes concussion, focal brain injury, seizure,
or stroke. By the time the patient presents to the neurologist, an imaging
study has often been done. If the neurologic evaluation is nonfocal, and the
spell appears to be consistent with migraine, imaging studies may not be
necessary. Matthews noted that because of
the widespread and erroneous belief that complicated migraine is associated
with vascular anomalies, patients often fear that they have a more serious
condition. He believed that if there were no physical abnormalities or
sequelae, elaborate investigations may not be required. Rather,
in children participating in routine physical activities, observation may be
sufficient.17
In the athlete who plays football, an additional concern is the possibility
of traumatic intracranial hemorrhage. According to Bennett, participation
should be continued only after a thorough neurological evaluation. The
athlete should be apprized of his condition and any abnormalities found on
examination. The neurologist should warn the patient to report to the team
physician or trainer if neurological symptoms recur.18
Post-traumatic Headache. Post-traumatic headache implies a new onset
headache after injury. To be directly attributable to the trauma, no
precursors for migraine were present prior to the onset of the headache. The
assumption is that the trauma caused the headache by altering brain function
or structure.19 Trauma can also provoke the first episode of migraine in a
predisposed individual or exacerbate a pre-existing headache condition.
Onset usually occurs within 14 days after head trauma. Solomon gives the
following analogy for trauma triggering the first attack of migraine in the
predisposed individual: “Trauma,” shaking a branch of the tree will
cause the fruit to fall, but even without “trauma” the ripe fruit
will soon fall.19
I have seen several patients who developed a chronic headache after a
seemingly minor blow to the head with a basketball or volleyball. Such
headaches may present as migraine, tension type headache, or daily headache
with varying degrees of migraine symptomatology. Post-traumatic headache is
more likely to occur in a predisposed individual than in an individual with
no history of headache and no family history of headache.
Williams and Nukada reviewed 29 subjects with post-traumatic headache as a
result of head trauma in a contact sport. The headaches were not classified
as migraine. The trauma was usually minor. Associated symptoms included
stiff neck, confusion, and loss of concentration. Some subjects were unable
to continue the sport or exercise because of severe headache. A number of
the subjects appeared to have susceptible migrainous features, such as a
family history
of migraine or prior spontaneous migraine. The post-traumatic headache was
often associated with concussion.8
If the examination is normal, it is unlikely that an imaging study will add
further information. The decision to order further studies is at the
discretion of the evaluating physician. Swain and Kaplan note that
medical-legal concerns often necessitate laboratory studies be done although
studies are unlikely to be helpful.12
Treatment. The treatment plan can
be divided into nonpharmacologic and pharmacologic approaches. Treatment
plans should include education focusing on lifestyle changes and nutritional
factors. The physician should be encouraged to involve the patient, parents,
school coaches, and athletic trainers. Environmental and behavioral triggers
should be identified and, as possible, reduced. (Table 2)
Table 2. Headache Triggers
Estrogen fluctuations
Stress or “let down”
Chemicals in foods:
MSG, artificial sweeteners, caffeine, alcohol, preserved meats, aged cheese
Behaviors:
skipping meals, exertion, odors/perfume, changes in sleep pattern, bright
light
|
Biofeedback and stress management strategies have been helpful in some
athletes, especially young athletes.
Athletes are often interested in nutritional factors (well-balanced diet and
supplements). Supplements that might
reduce the severity and frequency of
migraine include:
- Magnesium (chelated or citrate), 200 mg b.i.d. Foods high in magnesium
include nuts, legumes, vegetables, whole-grain cereals and breads, and
seafood; some of these foods may be migraine triggers.
- Riboflavin, 200 mg b.i.d. Foods high in riboflavin are dairy products,
liver, meat, green vegetables, eggs, and dried beans, and peas. The maximum
effect of riboflavin on reducing headache frequency was seen at 3 months of
treatment.7
When nonpharmacological approaches fail to control headaches, medications
are required. Ideally, they should have minimal
or no impact on athletic performance. Medications can be divided into the
following groups:
- Preventive medicines: chosen if headache frequency is more than 2 days a
week or if headaches are not easily aborted. Headache specialists differ in
their recommendations. I favor the following approach:
- Calcium channel blockers. Rationale for use: these drugs decrease the
irritability of the pain generator. I start with nicardipine sustained
release, which has few side effects. Starting dose: 30 mg SR daily. Increase
to twice-daily in one week. Another option is verapamil. Side effect:
constipation. If headaches persist, I add a selective serontonin reuptake
inhibitor (SSRI).
- SSRI’s. Rationale for use: it is now known that migraineurs have an
abnormality in serotonin function. I generally start with paroxetine or
sertraline. A starting dose of paroxetine is 10 mg daily; sertraline 25 mg
daily, increasing to 50 mg daily in one week. Side effects: nausea and
decreased libido.
- Indomethacin. Rationale for use: acts as an anti-inflammatory and also as
a nitric oxide antagonist. It can reduce intracranial pressure.20 Dose: for
frequent headache: 25 mg to 50 mg 3 times daily. For infrequent headache, or
headache only with exertion: 25 mg to 50 mg 1 to 2 hours before exerting.
Side effects: can compromise renal function and potentiate the risk of
developing acute renal failure. More likely to occur with dehydration or
increased stress.23 Athletes should be warned of the potential danger of any
anti-inflammatory drug to compromise renal function. Monitor renal function
prior to use and at approximately 6 month intervals. Additional side
effects: gastritis or ulcers.
- Abortive medications. Many of the new medications are migraine specific.
This means that they inhibit neurovascular inflammation and vasoconstrict
dilated cerebral vessels. New medications are rapidly being added to our
armamentarium. Do not use the medications for the first time during an
athletic endeavor.
- One of the oldest is dihydroergotamine (DHE). My initial recommendation
is to use the nasal spray. Pain relief is often seen within 1/2 hour. Side
effects of the nasal spray are minimal with nasal congestion as the most
frequent.
- Triptans are an important addition to the therapeutic cabinet. The first
one released was sumatriptan. I would again recommend starting with the
nasal spray form. Dose: 20 mg. May be repeated in 1 hour. Side effects:
include chest tightness. Two newer triptans: zolmatriptan and rizatriptan
are well absorbed in pill form and may be effective in less than 30 minutes.
Typical dose of zolmatriptan is 5 mg, repeating in 2 hours if necessary.
Maximum dose 10 mg per day. For rizatriptan, 10 mg at onset, repeating in 2
hours for a maximum dose of 30 mg per day. Side effects: drowsiness.
Prior to use of the migraine specific medications, DHE or the triptans, the
patient’s medical history is reviewed. Men over the age of 40 and
postmenopausal women should be screened for risk of cardiovascular disease.
Because of vasoconstrictive effects, these medications are never used in the
presence of coronary artery disease, uncontrolled hypertension, or with
pregnancy. In addition, these agents are contraindicated with hemi-paretic
migraine. Use of sumatriptan is being studied in children and criteria are
being established for pediatric use.
- Oxygen is sometimes useful abortively. It may be particularly useful at
higher altitudes. It is administered by a mask, preferably non-rebreathing,
at 100%.
Its use can be combined with one of the abortive medications above.
Mechanism
of benefit is not clear.
- Lidocaine 4% nasal drops are sometimes of benefit. Dose: full dropperful
into nostril on the same side as headache. Repeat one time after 5 minutes
if needed. No more than 3 doses per day. Side effect: possible burning
sensation. Mechanism: may inhibit the trigeminal nerve.
- Anti-inflammatories. In addition to indomethacin, useful ones to try
include diclofenac potassium 50 mg to 100 mg
at onset, oxzprozin 600 mg to 1200 mg
at onset, or etodolac 500 mg at onset. Gastrointestinal side effects are
common, but these choices are typically well tolerated.
- Isometheptene. Two at onset, 2 in one hour. Combination of a mild
vasoconstrictor, mild sedative, and a mild pain suppressant. Side effects:
sleepiness for some.
Conclusion. To illustrate the discussion above, I will close with some brief
cases. Five patients come to you complaining of sports related headache. The
first patient is a 10-year-old girl who plays soccer. She describes an
insignificant blow to her head with a subsequent change in vision, loss of
sensation in her left arm, and a bilateral headache of moderate level. The
second patient is a 24-year-old Army specialist. He describes the onset of
severe headache to maneuvers. The headache resolves within one hour when he
discontinues strenuous physical activities. The third patient, a 30-year old
woman, describes development of headache after playing 2 sets of tennis. The
headache does not resolve when she stops playing, however, resembles one of
her typical migraine headaches. The fourth patient is an 18-year-old high
school athlete. After being hit in the head with a basketball, she develops
a persistent moderate to severe daily headache. The fifth patient is a
55-year-old man. After going for his usual swim he develops a one-sided
throbbing headache. He has no history of prior headache.
The 10-year-old girl had a trauma triggered migraine. She was found to have
a positive family history of migraine. Brain image done prior to your
evaluation was normal. Her examination was unremarkable. She now wears a
helmet during soccer games. She could be treated abortively with a
medication such as isometheptene mucate/dichloralphenazone/acetaminophen.
It is likely that she will have further episodes. The Army specialist
describes exertional headache. There was no evidence of posterior fossa
structural abnormality on his brain MRI. Pretreatment with indomethacin 50
mg,
1 hour before strenuous activity was successful. The 3rd patient describes
prolonged exertion as one trigger for her typical migraine. If pretreatment
with an anti-inflammatory is not beneficial, or if the headache only occurs
occasionally when playing tennis, one of the migraine specific abortive
medications is appropriate. The 18-year-old athlete has developed
post-traumatic headache characterized by a chronic daily picture. It is most
likely that she will benefit from preventive medications in the form of a
calcium channel blocker and possibly with the addition of a serotonin
reuptake inhibitor. If the headache cycle can be broken, preventive
medications can be tapered and discontinued. The 55-year-old man is
discovered to have coronary artery disease masquerading as migraine. His
headaches resolve with successful treatment of his heart disease.
|
References
1. Braun A, Klawans H. Headaches associated with exercise and sexual
activity. In: Rose FC, ed. Handbook of Clinical Neurology.VB
Elsevier,
1986:373-382.
2. King S. The Running Man. New York, NY: New American Library; 1982:78.
3. Williams S, Nukada,
H. Sports and exercise headache: Part 1. Prevalence among university
students.
Br J Sp Med. 1994;28(2):90-95.
4. Scheller J. The history, epidemiology, and classification of headaches in
childhood. Semin Pediatr Neurol. 1995;2(2):102-108.
5. Headache Classification Committee of the International Headache Society.
Classification and diagnostic criteria for headache disorders, cranial
neuralgias and face pain. Cephalalgia. 1988;8(suppl 7):1-96.
6. Welch K. Synthesis of mechanisms. 49th Annual Meeting, American Academy
of Neurology, April 12 to 19, 1997.
7. Schoenen J, Jacquy,
J, Lenaerts M. Effectiveness of high-dose riboflavin in migraine
prophylaxis. Neurology. 1998;50:466-470.
8. Williams S, Nukada
H. Sports and exercise headache: Part 2. Diagnosis and classification. Br J Sp Med. 1994;28(2):96-100.
9. Hazelrigg R. Discussion: exertional headache. Headache Quarterly, Current
Treatment and Research. 1990;1(3):244-250.
10. Lipton R, Lowenkopf T, Bajwa Z, et al. Cardiac cephalgia: a treatable
form of exertional headache. Neurology.1997;49:813-816.
11. Basoglu T, Ozbenli T, Bernay I, et al. Demonstration of frontal
hypoperfusion in benign exertional headache by technetium-99 m-HMPAO SPECT.
J Nucl Med. 1996;37(7):1172-1174.
12. Swain R, Kaplan B. Diagnosis, prophylaxis, and treatment of headache in
the athlete. South Med J. 1997;90(9):878-888.
13. Pestronk A. Goggle migraine. N Engl J Med. 1983;308(4):226-227.
14. North K, Davies L. Postexercise headache in menapausal women. Lancet.
1993;341:972.
15. Haas D, Pineda G, Lourie H. Juvenile head trauma syndromes and their
relationships to migraine. Arch Neurol. 1975;32:727-730.
16. Haas D, Lourie H. Trauma-triggered migraine: an explanation for common
neurological attacks after mild head injury. J Neurosurg. 1988;68:181-188.
17. Matthews W. Footballer’s migraine. Br Med J. 1972;2:326-327.
18. Bennett D, Fuenning S, Sullivan G, Weber J. Migraine precipitated by
head trauma in athletes. Am J Sports Med. 1980;8(3):202-205.
19. Solomon S. Posttraumatic migraine. Headache 1998;38:772-778.
20. Dodick D. Indomethacin responsive headache syndromes: a hypothesis on
the mechanisms underlying the efficacy of indomethacin in these disorders. Neurology.
1999;52(6)(suppl): Abstract.
21. Walker R, Fawcett J, Flannery E, Gerrard D. Indomethacin potentiates
exercise-induced reduction in renal hemodynamics in athletes. Med Sci Sports
Exer. 1994;26:1302- 1306.
|
|
