Gastrointestinal cell injury and perceived symptoms after running the Boston Marathon.

Gastrointestinal (GI) disturbances are a prevalent cause of marathon related complaints, and in extreme cases can promote life-threatening conditions such as exertional heat stroke. Our aim was to study intestinal cell injury [via intestinal fatty acid binding protein (I-FABP)] and perceived GI distress symptoms among marathon runners. We also examined potential risk factors (e.g., inadequate sleep) that could exacerbate GI disturbances in healthy, trained endurance runners. This was a parallel mixed-methods study design. 2019 Boston Marathon participants were recruited via email and subjects completed surveys before the race describing demographics and training history. Participants completed a GI questionnaire to assess presence and severity of symptoms, a survey regarding risk factors (e.g., recent illness, medications) that could promote GI disturbances, and provided a urine sample at three time points (immediately pre-race, post-race, and 24-h post-race). Due to weather, blood samples were only collected immediately and 24-h post-race. A total of 40 runners (males: n = 19, age = 44.9 ± 10.8 years; females: n = 21, age = 44.8 ± 10.6 years) completed this study. I-FABP significantly decreased from post-race (3367.5 ± 2633.5 pg/mL) to 24-h post-race (1657.3 ± 950.7 pg/mL, t (39) = -4.228, p < .001, d = -.669). There was a significant difference in overall GI symptom scores across the three time points (F (2, 39) = 41.37, p < .001). The highest average score occurred post-race (.84 ± .68), compared to pre-race (.09 ± .12) and 24-h post-race (.44 ± .28). Post-race I-FABP (r = .31, p = .048) and post-race urine specific gravity (r = .33, p = .041) were significantly correlated with post-race GI symptom scores. Our study provides further support to the individualized nature of GI disturbances, with participants experiencing a wide range of risk factors that can influence the extent of GI damage and perceived symptoms during and after exercise.

Compression Socks Worn During Flight and Hemostatic Balance in Boston Marathon Runners on Oral Contraceptives.

OBJECTIVE: To investigate the effect of oral contraceptive (OC) use and compression socks on hemostatic activation in women flying cross-country to and from a marathon. DESIGN: Prospective study. SETTING: 2015 Boston Marathon. PARTICIPANTS: Women were divided into non-OC using (CONTROL; n = 12), OC-using (OC; n = 15), and OC-using plus compression sock (OC + SOCK; n = 14) groups. INTERVENTION: Women in OC + SOCK wore compression socks during flights to and from the marathon. MAIN OUTCOME MEASURES: Venous blood samples were collected within 24 hours of arriving in Boston (EXPO), immediately after the marathon (RUN), and within 24 hours after a return flight home (Post-Flight) for analysis of thrombin-antithrombin complex (TAT), d-dimer, and tissue plasminogen activator (t-PA). RESULTS: TAT did not increase with exercise (P = 0.48) and was not affected by group (P = 0.08) or the interaction between these 2 factors (P = 0.80). Group, time, and their interaction were significant for d-dimer (all P < 0.05) such that d-dimer increased with acute exercise to a greater extent (Δ d-dimer from expo to postrace = 909.5 ± 1021.9 ng/mL) in the OC + SOCK group relative to OC (Δ d-dimer = 240.0 ± 178.5 ng/mL; P = 0.02) and CONTROL (Δ d-dimer = 230.3 ± 120.3 ng/mL; P = 0.02). There was a significant effect of time, group, and the interaction on t-PA (all P < 0.01) such that t-PA increased with acute exercise to a greater extent (Δ t-PA from expo to postrace = 19.6 ± 10.0 ng/mL) in the CONTROL group relative to OC (Δ t-PA = 4.0 ± 1.8 ng/mL; P < 0.01) and OC + SOCK (Δ t-PA = 3.3 ± 1.2 ng/mL; P < 0.01). CONCLUSIONS: Female runners using OCs did not exhibit disproportionately increased coagulation. The use of compression socks in women on OCs, surprisingly, resulted in a greater increase in d-dimer after exercise.

Myocardial adaptations to recreational marathon training among middle-aged men.

BACKGROUND: Myocardial adaptations to exercise have been well documented among competitive athletes. To what degree cardiac remodeling occurs among recreational exercisers is unknown. We sought to evaluate the effect of recreational marathon training on myocardial structure and function comprehensively. METHODS AND RESULTS: Male runners (n=45; age, 48±7 years; 64% with ≥1 cardiovascular risk factor) participated in a structured marathon-training program. Echocardiography, cardiopulmonary exercise testing, and laboratory evaluation were performed pre and post training to quantify changes in myocardial structure and function, cardiorespiratory fitness, and traditional cardiac risk parameters. Completion of an 18-week running program (25±9 miles/wk) led to increased cardiorespiratory fitness (peak oxygen consumption, 44.6±5.2 versus 46.3±5.4 mL/kg per minute; P<0.001). In this setting, there was a significant structural cardiac remodeling characterized by dilation of the left ventricle (end-diastolic volume, 156±26 versus 172±28 mL, P<0.001), right ventricle (end-diastolic area=27.0±4.8 versus 28.6±4.3 cm(2); P=0.02), and left atrium (end-diastolic volume, 65±19 versus 72±19; P=0.02). Functional adaptations included increases in both early (E'=12.4±2.5 versus 13.2±2.0 cm/s; P=0.007) and late (A'=11.5±1.9 versus 12.2±2.1 cm/s; P=0.02) left ventricular diastolic velocities. Myocardial remodeling was accompanied by beneficial changes in cardiovascular risk factors, including body mass index (27.0±2.7 versus 26.7±2.6 kg/m(2); P<0.001), total cholesterol (199±33 versus 192±29 mg/dL; P=0.01), low-density lipoprotein (120±29 versus 114±26 mg/dL; P=0.01), and triglycerides (100±52 versus 85±36 mg/dL; P=0.02). CONCLUSIONS: Among middle-aged men, recreational marathon training is associated with biventricular dilation, enhanced left ventricular diastolic function, and favorable changes in nonmyocardial determinants of cardiovascular risk. Recreational marathon training may, therefore, serve as an effective strategy for decreasing incident cardiovascular disease.

Influence of chronic exercise on carotid atherosclerosis in marathon runners.

OBJECTIVES: The effect of habitual, high-intensity exercise training on the progression of atherosclerosis is unclear. We assessed indices of vascular health (central systolic blood pressure (SBP) and arterial stiffness as well as carotid intima-medial thickness (cIMT)) in addition to cardiovascular risk factors of trained runners versus their untrained spouses or partners to evaluate the impact of exercise on the development of carotid atherosclerosis. SETTING: field study at Boston Marathon. PARTICIPANTS: 42 qualifiers (mean age±SD: 46±13 years, 21 women) for the 2012 Boston Marathon and their sedentary domestic controls (46±12 years, n=21 women). OUTCOMES: We measured medical and running history, vital signs, anthropometrics, blood lipids, C reactive protein (CRP), 10 years Framingham risk, central arterial stiffness and SBP and cIMT. RESULTS: Multiple cardiovascular risk factors, including CRP, non-high-density lipoprotein cholesterol, triglycerides, heart rate, body weight and body mass index (all p<0.05), were reduced in the runners. The left and right cIMT, as well as central SBP, were not different between the two groups (all p>0.31) and were associated with age (all r≥0.41; p<0.01) and Framingham risk score (all r≥0.44; p<0.01) independent of exercise group (all p>0.08 for interactions). The amplification of the central pressure waveform (augmentation pressure at heart rate 75 bpm) was also not different between the two groups (p=0.07) but was related to age (p<0.01) and group (p=0.02) in a multiple linear regression model. CONCLUSIONS: Habitual endurance exercise improves the cardiovascular risk profile, but does not reduce the magnitude of carotid atherosclerosis associated with age and cardiovascular risk factors.

Statins Attenuate the Increase in P-Selectin Produced by Prolonged Exercise.

Strenuous endurance exercise increases inflammatory markers and acutely increases cardiovascular risk; however, statins may mitigate this response. We measured serum levels of p-selectin in 37 runners treated with statins and in 43 nonstatin treated controls running the 2011 Boston Marathon. Venous blood samples were obtained the day before (PRE) as well as within 1 hour after (FINISH) and 24 hours after (POST) the race. The increase in p-selectin immediately after exercise was lower in statin users (PRE to FINISH: 20.5 ± 19.4 ng/mL) than controls (PRE to FINISH: 30.9 ± 27.1 ng/mL; P < 0.001). The increase in p-selectin 24 hours after exercise was also lower in statin users (PRE to POST: 21.5 ± 26.6 ng/mL) than controls (PRE to POST: 29.3 ± 31.9 ng/mL; P < 0.001). Furthermore, LDL-C was positively correlated with p-selectin at FINISH and POST (P < 0.01 and P < 0.05, resp.), irrespective of drug treatment, suggesting that lower levels of LDL-C are associated with a reduced inflammatory response to exercise. We conclude that statins blunt the exercise-induced increase in p-selectin following a marathon and that the inflammatory response to a marathon varies directly with LDL-C levels.

Effect of marathon run and air travel on pre- and post-run soluble d-dimer, microparticle procoagulant activity, and p-selectin levels.

D-dimer, microparticles, and p-selectin are venous thrombotic risk markers. Elevated p-selectin is associated with increased cardiovascular events. We examined the effects of exercise and air travel on the markers of vascular risk in marathon runners. Forty-one persons participating in the 114th Boston Marathon (April 19, 2010) were divided into travel (n = 23) and nontravel "control" (n = 18) groups according to whether they lived more than a 4-hour plane flight or less than a 2-hour car trip from Boston. The subjects provided venous blood samples the day before, immediately after, and after returning home the day after the marathon. The blood was analyzed for soluble d-dimer, microparticle procoagulant activity, and p-selectin. D-dimer levels increased more before to immediately after (142 ± 83 to 387 ± 196 ng/mL) in the travel group than in the controls (85 ± 26 to 233 ± 95 ng/mL; p = 0.02). Moreover, 6 travel subjects versus 0 controls had d-dimer values >500 ng/mL after returning home the day after the marathon, the clinical threshold for excluding venous thrombosis (p = 0.03). P-selectin increased with exercise (p <0.01) regardless of travel (p = 0.09) but age was related to p-selectin (p = 0.01) such that older subjects exhibited greater p-selectin values before (r(2) = 0.14; p = 0.02) and after returning home the day after the marathon (r(2) = 0.16, p = 0.01). In conclusion, the combination of exercise and travel increases venous and arterial thrombotic risk. Moreover, the p-selectin levels at rest and after exercise were greater with age. These results might explain the reports of venous thrombosis with air travel after athletic events and the reports of cardiac events in older participants running marathons.

Effect of statins on creatine kinase levels before and after a marathon run.

We measured the serum levels of myoglobin, total creatine kinase (CK), and the CK myocardial (CK-MB), muscle (CK-MM), and brain (CK-BB) isoenzymes in 37 subjects treated with statins and 43 nonstatin-treated controls running the 2011 Boston Marathon. Venous blood samples were obtained the day before (PRE) and within 1 hour (FINISH) and 24 hours after (POST) the race. The hematocrit and hemoglobin values were used to adjust for changes in the plasma volume. The CK distribution was normalized using log transformation before analysis. The exercise-related increase in CK 24 hours after exercise, adjusted for changes in plasma volume, was greater in the statin users (PRE to POST 133 ± 15 to 1,104 ± 150 U/L) than in the controls (PRE to POST 125 ± 12 to 813 ± 137 U/L; p = 0.03 for comparison). The increase in CK-MB 24 hours after exercise was also greater in the statin users (PRE to POST 1.1 ± 3.9 to 8.9 ± 7.0 U/L) than in the controls (PRE to POST 0.0 ± 0.0 to 4.2 ± 5.0 U/L; p <0.05 for comparison). However, the increases in muscle myoglobin did not differ at any point between the 2 groups. Increases in CK at both FINISH and POST race measurements were directly related to age in the statin users (r(2) = 0.13 and r(2) = 0.14, respectively; p <0.05) but not in the controls (r(2) = 0.02 and r(2) = 0.00, respectively; p >0.42), suggesting that susceptibility to exercise-induced muscle injury with statins increases with age. In conclusion, our results show that statins increase exercise-related muscle injury.

Effect of air travel on exercise-induced coagulatory and fibrinolytic activation in marathon runners.

OBJECTIVE: Air travel and exercise change hemostatic parameters. This study investigated the effect of air travel on exercise-induced coagulation and fibrinolysis in endurance athletes. DESIGN: A prospective longitudinal study. SETTING: The 114th Boston Marathon (April 19, 2010). PARTICIPANTS: Forty-one adults were divided into travel (T: 23 participants, living >4-hour plane flight from Boston) and nontravel (C: 18 participants, living <2-hour car trip from Boston) groups. INDEPENDENT VARIABLES: Age, anthropometrics, vital signs, training mileage, and finishing time were collected. MAIN OUTCOME MEASURES: Subjects provided venous blood samples the day before (PRE), immediately after (FINISH), and the day following the marathon after returning home (POST). Blood was analyzed for thrombin-antithrombin complex (TAT), tissue plasminogen activator (t-PA), hematocrit (Hct), and the presence of Factor V Leiden R506Q mutation. RESULTS: Thrombin-antithrombin complex increased more in T subjects in PRE to FINISH samples (5.0 ± 4.0 to 12.9 ± 15.6 µg/L) than in C subjects (4.0 ± 1.2 to 6.1 ± 1.2 µg/L; P = 0.02 for comparison). The t-PA increased in both the T (5.4 ± 2.3 to 25.1 ± 12.2 ng/mL) and C (5.6 ± 2.0 to 27.7 ± 11.3 ng/mL) groups in PRE to FINISH samples, and this response did not differ between groups (P = 0.23 for comparison). Both groups exhibited similar t-PA and TAT values at POST that were not different than PRE (all P > 0.35). Age was related to the FINISH TAT values in T (r = 0.19; P = 0.04) but not in C (r = 0.03; P = 0.53) subjects. CONCLUSIONS: Results suggest that the combination of air travel and marathon running induces an acute hypercoaguable state; this hemostatic imbalance is exaggerated with increasing age.

Cold-water dousing with ice massage to treat exertional heat stroke: a case series.

INTRODUCTION: We sought to determine the rate of cooling via a novel water ice therapy (WIT) as an alternative to cold-water immersion for the acute treatment of exertional heat stroke (EHS). METHODS: Observations were made at the 2004-2008 Marine Corps Marathons (mean +/- SD: 16.3 +/- 4.9 degrees C dry bulb, 32 +/- 6% RH). Nine (seven men, two women) EHS patients (33 +/- 6 yr of age; 268 +/- 54 min average race time for six who finished) were observed during on-site treatment. Patients were treated while lying supine on a porous stretcher resting on a tub filled with cold water (approximately 10-12 degrees C). Medical personnel monitored T(re), doused the patient with water and massaged major muscle groups with ice bags until T(re) decreased to 38.9 degrees C. Patients were not immersed in water. Serial T(re) and time were used to calculate cooling rates. RESULTS: Final T(re) (39.12 +/- 0.63 degrees C) was significantly lower than initial T(re) (41.43 +/- 0.71 degrees C, P < 0.05). Cooling rates were 0.13 +/- 0.04 degrees C min(-1). The decrease in T(re) for the initial 6 min of WIT (0.38 +/- 0.13 degrees C) was significantly less than for the subsequent 6-min time period (1.31 +/- 0.34 degrees C, P < 0.001). Cooling rates for these time periods were significantly different (0.06 +/- 0.02 degrees C x min(-1) and 0.22 +/- 0.06 degrees C x min(-1), respectively, P < 0.05). Initial T(re) was not correlated with overall cooling rate (r = 0.434, P = 0.244), or total cooling time required (17 +/- 4 min; r = 0.207, P = 0.593). Survival rate was 100%. CONCLUSION: WIT provided cooling rates that were 70% as effective as those published for cold-water immersion with 8 degrees C water (0.19 degrees C x min(-1)) and resulted in 100% patient survival.