Blake and Larrabee (6) used the 1900-1902 races to comprehensively examine marathon physiology but were assisted by others physicians not listed as primary authors. The findings were remarkably insightful for their time.
Increases in heart rate after the race were "often surprisingly small" and depended primarily on how hard the athletes ran "particularly in the last few minutes of the race" (6). Similar observations that lactate levels increased primarily with a finishing sprint would not be made for another 66 yr (11). The best-trained runners had the slowest prerace heart rates, a concept not widely known until 1940 when White reported bradycardia in four distance runners (65). This report (6) was among the first to note that oral temperature was "not a reliable factor" and that rectal temperatures usually increased after the race (6).
Prerace samples in 1901 were transported to Boston for examination, whereas the 1902 samples were examined in Ashland, and the researchers took a "later train" back to Boston (6). This detail highlights that Ashland was the initial Boston start because trains could transport competitors from the city (13). Ashland remained the starting point and the race was only 40 km long, until 1924 when Boston served as the American Olympic Marathon Trial and the course increased to the Olympic distance of 42 km or 26.2 miles (13). There was marked leukocytosis with white blood cell counts of 14,200-27,700 after the race (6). Most of the increases were caused by an increase in polymorphonuclear cells (PMN), but seven of nine subjects demonstrated myelocytes, a potentially clairvoyant observation given recent evidence that circulating stem cells increase after exercise (63). Leukocytosis was correctly attributed to PMN demargination or release of leukocytes from their "rest in the great internal veins" (6).
Urine contained albumin in only 4 of the 30 specimens before, but in all after, the race. Postrace samples also contained hyaline, granular, and epithelial cell casts and blood expanding the findings of athletic pseudonephritis.
Ten runners examined using the percussion/tracing technique showed symmetrical cardiac enlargement, an early recognition that endurance training enlarges all four cardiac chambers (64). There was further cardiac enlargement after exercise, attributed to cardiac decompensation and "cardiac fatigue." "Bleeding from the mouth or nose did not occur" (6), a reference to the absence of pulmonary edema and an indicator of the authors' concern about cardiac failure (6). This concept of cardiac fatigue would reappear 84 yr later with echocardiographic evidence of impaired cardiac function after triathlons (15). Because of concern about acute cardiac failure, Paul Dudley White obtained arterial pulse tracings on runners in the 1916 race (68) and was reassured by the absence of pulsus alternans, a sign of severe heart failure.
Gordon et al. (24) measured vital capacity (VC) and cardiac dimensions in the 1923 race. VC decreased 17% after the race. VC in the runners was similar to normative values, and there was no relationship between VC and performance, indicating that training did not increase VC and that performance was limited "by the legs rather than by the wind" (24). Radiographs were obtained immediately after the race using a portable machine placed in the BAA clubhouse 100 yards from the finish. Cardiac size was determined by cutting out the cardiac silhouette and weighing the resultant x-ray film (21). There was no cardiac dilatation after exercise, and postrace cardiac size was small, probably because of venous vasodilatation from the exercise and the upright posture required for the x-ray studies.
The first serological study was performed in 1924 (36). Blood glucose fell in most of the 11 runners (36), and their condition at the finish correlated with their blood glucose. Levine et al. (23,36) noted that those "with low blood sugar presented a picture of shock not unlike that produced by an overdose of insulin." This report appeared soon after Banting and Best's discovery of insulin in 1921. They speculated that the "state of shock…could either have been prevented or at least ameliorated if a larger supply of carbohydrate had been taken in the diet the night before or the morning of the race" (36). According to personal notes provided by Dr. Samuel Levine's son, Dr. Herbert Levine, Professor of Medicine at Tufts, these studies interested Dr. Elliott Joslin because they supported Joslin's belief that exercise could help overcome insulin deficiency. Much later studies would show that exercise decreases blood glucose by both insulin-dependent and -independent mechanisms (28).
STUDIES 1930 TO 1960
Only three reports appeared during this period possibly because the Great Depression and World War II diverted medical attention from the event (5,20,22). Gordon (22) reported that runners followed for 6 yr after the marathon did not develop cardiac problems. On the other hand, in a comment that would presage studies on the acute cardiovascular risks of exercise, he noted that among individuals of the "well-developed 'angina type" … athletic competition should be undertaken cautiously."
Behrman (5) observed an increase in albumin in 19 of 20 runners from before to after the 1941 race. Gilligan et al. (20), undoubtedly influenced by the war effort, studied "march hemoglobinuria" in the 1941 race. Plasma hemoglobin levels were increased after the race in 18 of 22 runners. Spectrophotometric studies confirmed that this was hemoglobin and not myoglobin. Red cell fragility studies on six runners, five with hemoglobinemia and one with hemoglobinuria, were normal. The concept of exercise hemolysis would be popularized years later by Dr. Randy Eichner. The authors (20) were assisted by Dr. Paul Zoll, subsequently a pioneer of cardiac pacing and defibrillation.
STUDIES 1960 TO 1970
There were only three studies published during this period (8,11,47). Buskirk and Beetham (8) measured body weight and rectal and skin temperatures in an unspecified Boston race, the Brighton 18-mile race, and a training run. Data from Boston are provided for seven marathoners, but for unspecified reasons, finishing times are provided for only four. Marathoners lost 6% of their body weight and increased their rectal temperatures by 1.9°C. The highest rectal temperature was 39.8°C or 103.7°F. Weight loss for all three events was directly related to the increase in temperature (r = 0.58), a relationship demonstrated in other studies (8).
Costill and Fox (11) determined maximal oxygen uptake (V˙O2max) in six runners before the 1968 race to estimate their intensity of effort. The subjects included Amby Burfoot (1968 winner), Ed Winrow (11th place), Tom Osler (23rd place), Tom Corbitt (43rd place and future President of the Road Runners Club of America), Lou Castagnaldo (45th place) (13), and Hal Higdon (author of Boston: A Century of Running). Their average V˙O2max was 71.4 mL·kg−1·min−1, and they used 74.8% of their maximum running the race. Lactate increased only at the end of the race, and generally in response to a finishing sprint. This contradicted conventional view that fatigue during marathons was related to lactic acid accumulation.
Three other reports (7,12,14) during this period were not performed using the race itself, but its most famous participant, Clarence DeMar. DeMar won seven Boston races (12). He had undergone six separate physiologic examinations (14) at the Harvard Fatigue Laboratory, the premier exercise physiology laboratory of this time. DeMar died of metastatic rectal carcinoma at age 70. His autopsy, reported by Currens and White (12), demonstrated coronary arteries two to three times the normal diameter. This report is often cited as evidence that exercise increases coronary caliber. Examination of the heart was difficult because the embalming trocar had pierced the heart in several places (12). This suggests that the necropsy was an afterthought and likely occurred because of Dr. White's interest in exercise.
STUDIES 1970 TO 1980
Publications (25,29,40,42,44,45,49,52) in this period are noteworthy for four reasons. First, Dr. Kenneth Cooper coauthored an article on serum electrolytes (49) and another documenting a threefold increase in cortisol and a nearly sixfold increase in aldosterone levels (42).
Second, Green et al. (25) published the first report at Boston of a cardiac arrest, anterior myocardial infarction, and subsequent death in the 1973 race. The autopsy showed only minimal coronary artery atherosclerosis. These findings predated the present knowledge that most acute cardiac events occur at non-flow-limiting atherosclerotic plaques and that autolysis of obstructing thromboses can occur.
Third, Dr. Terrance Kavanaugh et al. (29) reported on eight male cardiac patients from the Toronto Cardiac Rehabilitation Program who ran the 1973 race. They were escorted by resuscitation teams in cars. Seven men finished. That cardiac patients could run a marathon was a revolutionary concept at the time.
Fourth, Dr. Arthur Siegel et al. (52) published the first of multiple publications using members of the American Medical Joggers Association (AMJA), the predecessor of the American Medical Athletic Association (AMAA). Fifty participants provided urine samples before and 2 h after the 1978 race. Nine showed gross (n = 1) or microscopic hematuria after the race. Eight had cleared all blood by 48 h, whereas one physician had persistent slight hematuria demonstrating that athletic pseudonephritis is generally self-limited and benign.
Perhaps the most important event during the 1970s, the 1976 race or the "Run for the Hoses," was barely addressed in the medical literature. The temperature at the start was 37.2°C (45). The number of heat-injured runners prompted the formation of a more formal medical coverage team in 1978 (3). Dr. Marvin Adner has served as medical race director since 1978, assisted with many of the Boston medical studies, and retired as director after the 2006 event. (Dr. Adner, personal communication). In the only medical report of the event, Dr. Thomas O'Donnell (45) noted that heat stroke could be present despite continued sweating, a concept not widely recognized previously (45).
STUDIES 1980 TO 1990
The availability of research subjects from the AMJA, the support provided by formal medical race coverage, and the growth of marathoning as a participation sport facilitated the 41 Boston medical studies (63% of total) from 1980 onward.
Dr. Adner and Dr. William Castelli of the Framingham Heart Study (1) confirmed Dr. Peter Wood's original observation (72) of higher levels of HDL cholesterol (HDL-C) in endurance athletes. A subsequent study showed additional increases in HDL-C with modest alcohol intake (70).
Siegel et al. (58) examined creatine kinase (CK) levels in the 1979 race. Average CK levels increased further from 161 (normal < 100 U·L−1) before to 3424 U·L−1 the day after the race. Results from Boston may not be readily applicable to other endurance events. The Boston course, despite its infamous Newton and "Heartbreak" hills, actually declines a total of 448 ft (13). Downhill running is an "eccentric exercise," in which the muscle contracts while being stretched and is especially damaging to the skeletal muscle. Skeletal muscle-derived CK increases may be greater at Boston than in other events because of this eccentric component. Another study demonstrated that 8.3% of the CK was caused by the myocardial isoform (CK-MB) suggesting myocardial injury (56). Technetium 99m pyrophosphate myocardial scans 24 to 48 h after the race (56) and myocardial imaging in runners who were injected with thallium at the finish line and promptly transported to the Brigham and Women's Hospital for imaging (57) failed to show myocardial ischemia. CK-MB is the developmental form of CK and is expressed in embryonal muscle (56,66) and may be produced in satellite cells that repair muscle. Skeletal muscle CK-MB increases during marathon training and CK-MB is present in distance runners' skeletal muscle (66). Consequently, it is likely that exercise training injures skeletal muscle (as evidenced by the increased pre-exercise CK ) and that the repair process recruits satellite repair cells containing CK-MB, which is released when muscle is injured by the marathon.
McMahon et al. (38) demonstrated guaiac-positive stools after the race in 7 of 32 AMJA marathoners. This was attributed to splanchnic vasoconstriction and intestinal ischemia, a suggestion supported by subsequent Boston case reports of ischemic colitis in Boston runners (33,37,51). Runners with positive samples were younger and ran faster suggesting that the sympathetic vasoconstriction and blood flow redistribution required for more intense effort produced intestinal ischemia and fecal blood loss. "Runners' anemia" had previously been attributed to plasma volume expansion and march hemolysis.
STUDIES 1990 TO 2000
There were only six studies in this decade (9,37,54,55,60,62). Most notably, Siegel et al. (54) used antimyosin imaging to confirm normal myocardial scintigraphic images in runners with increases in cardiac troponin T (cTnT) and I (cTnI) after the race.
STUDIES 2000 TO PRESENT
Reports from the last 7 yr have addressed ischemic colitis in female runners (33,51), climatic factors affecting marathon performance (17,18,48), and changes in prostate-specific antigen (PSA) levels (31). Because cycling is known to increase PSA levels, AMAA marathoners were used to examine the effect of prolonged exercise on PSA without direct prostate trauma. Average PSA levels did not change, but 2 of the 18 subjects had elevated PSA levels (>4 ng·mL−1) at 4 and 24 h after the race, suggesting that endurance exercise can increase PSA levels in some individuals. The most important articles since 2000, however, examined exercise-associated hyponatremia (EAH) and possible cardiac injury.
EAH was first reported in 1985 in runners in the Comrades 90-km ultramarathon and the Durban Triathlon (43). Rapid-onset hyponatremia can produce pulmonary and cerebral edema, coma, and seizures (43), and it has caused death in two female marathoners in the 2002 Boston and Marine Corps races (61). Almond et al. (4) in 2002 analyzed postrace serum samples in 488 participants. EAH (serum sodium values ≤135 mmol·L−1) was found in 13% of the runners after the race. Three (0.6%) had values ≤120 mmol·L−1. On multivariate analysis, EAH was directly related to weight gain, increased race time, and BMI <20 kg·m−2. The authors suggested that excessive fluid intake was primarily responsible.
A subsequent report concluded that EAH was due to inappropriate arginine vasopressin (AVP) secretion (61). AVP was detectable in 7 of 16 runners with EAH, although AVP should be undetectable with hyponatremia and hypo-osmolality. Even with inappropriate AVP levels, hyponatremia could not develop without increased fluid intake. The opportunity for excessive fluid intake is increased in ultramarathons and in slower recreational runners. Both women who died at the Boston and Marine Corps races were running as charity fund-raisers (61). Such runners are not required to meet the qualifying times required at Boston. In the 2003 race, the first finisher with EAH finished in 4h35min (32), almost 2.5 h after the winner.
The mechanism for inappropriate AVP is unclear, but interleukin-6 (IL-6) is released from muscle during exercise (46) and can increase AVP secretion (61). Genetic factors may also contribute. One Boston runner with a sodium <120 mmol·L−1 had "mild cystic fibrosis" (2), a disease known to increase the sodium content of sweat, suggesting that some athletes may secrete "salty sweat" thereby increasing their risk for water intoxication. Inappropriate AVP could also explain why nonsteroidal anti-inflammatory drugs (NSAID) seem to be common among EAH victims (26,61) because NSAID enhance renal AVP activity (61). Intravenous 3% sodium chloride is now the standard treatment of acute EAH (61), in part because of research performed at Boston.
Nine of the 21 articles published after 2000 address serum and/or imaging markers of possible myocardial injury. C-reactive protein (CRP), von Willebrand factor, D-dimer, and fibrinolytic activity more than doubled 4 h after the 1996-2001 races, whereas fibrinogen levels decreased (59). Platelet aggregation also increased after exertion (59). Matrix metalloproteinase-9 (MMP-9) activity, a possible risk marker for acute coronary syndrome (ACS) and brain-type natriuretic peptide (BNP), a marker of heart failure severity increased immediately after the 2005 race (50). Myeloperoxidase (MPO) activity may identify patients at risk for ACS earlier than traditional markers (39). MPO levels increased in 22 of 24 subjects immediately after the 2005 race, and 14 subjects' values exceeded the manufacturer's recommended clinical threshold for diagnosing ACS (39). Both MMP and MPO are present in white blood cells, however, so increased levels may simply reflect the exercise leukocytosis noted by others (6,34) a century ago. Nevertheless, such results demonstrate the difficulty of diagnosing ACS in athletes after prolonged exertion.
Six articles examined cTn, the clinical standard for myocyte necrosis and ACS. Both cTnT (19,39,41,50,53) and cTnI (19,30,53) increased after the race. Among 482 runners in the 2002 race, 68% demonstrated elevated cTnT and cTnI levels, and 11% had values "diagnostic" of myocardial infarction, demonstrating elevations in cardiac markers in the absence of ACS. Runners with no prior marathon experience where three times more likely to increase cTn.
Neilan et al. (41) measured serological markers of myocardial injury and used echocardiographic markers of myocardial performance in the 2004-2005 races. Early transmitral filling velocities decreased and late filling increased immediately after the race, suggesting left ventricular diastolic dysfunction. The change in right ventricular area decreased, suggesting reduced right ventricular performance. cTnT increased above the 99th percentile after the race in 63% of the participants and 47% had cTnT levels consistent with myocardial necrosis. N-terminal pro-brain natriuretic peptide (NT-proBNP) concentrations doubled. The increases in myocardial serological markers correlated directly with measures of myocardial dysfunction and inversely with the number of miles run per week. Runners training <35 miles weekly had worse myocardial performance and higher serologic markers of myocardial injury. The authors suggested that runners with less training are more vulnerable to cardiac injury. An accompanying editorial cautioned against concluding that marathoning produces actual myocardial injury because there is no evidence that former endurance athletes experience more cardiac dysfunction (66).
The 66 Boston articles identified must be among the largest number from a single athletic event. Boston medical studies not only provide lessons applicable to medically managing modern athletes but also demonstrate the interests and concerns of researchers who have used the Boston Marathon for more than a century to study the effects of prolonged exercise. Advances in the understanding and treatment of marathon complications such as EAH are major accomplishments produced by medical researchers interested in the marathon and the runners who participated in these studies.
The results of the present review do not constitute endorsement by ACSM.
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Keywords:©2009The American College of Sports Medicine
ENDURANCE; EXERCISE; ATHLETE'S HEART; CARDIOMEGALY; TROPONIN