Biomarkers of organ stress and injury following the Boston Marathon

We examined the changes in blood and urine-based biomarkers of organ stress/injury and hydration before and after the 2024 Boston Marathon. Our primary aims were to compare responses between males and females, and euhydrated and hypohydrated runners. Seventy-two runners (34 males/38 females; 50 ± 11 yr; finish time 3:45 ± 0:32 h:min) had blood and/or urine samples taken before and after the race. Average temperature on a race day was 19 ± 3°C, and relative humidity was 47 ± 15%. Samples were assayed for markers of hydration, intestinal injury (intestinal fatty acid binding protein and soluble cluster of differentiation 14), skeletal muscle damage (creatine kinase), and acute kidney injury (tissue inhibitor of metalloproteinase 2, insulin-like growth factor binding protein 7, neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, creatinine). Markers of hydration were elevated from pre- to postrace, but only 25%-34% of runners were deemed hypohydrated postrace. All markers of organ stress/injury were increased postrace (fold change: 1.3-1455; <i>P</i> ≤ 0.007 for all indices); however, there were no differences based on sex or hydration status (<i>P</i> ≥ 0.099 for all indices). Our findings show that the Boston Marathon produces a significant level of stress on the gastrointestinal and renal organ systems and that these effects do not appear to be modulated by biological sex. In addition, our findings suggest that the substantial increases in markers of kidney and intestinal barrier injury persist even when severe hypohydration is prevented, suggesting that during the marathon, maintaining hydration cannot fully offset the risk for organ injury. These findings should be considered when designing interventions to minimize gastrointestinal and renal-related health complications associated with marathon running to promote both health and performance in recreational, but completive marathon runners.<b>NEW & NOTEWORTHY</b> We show that the Boston Marathon produces a significant level of stress on the gastrointestinal and renal organ systems, but these effects do not appear to be modulated by biological sex or age. Furthermore, the substantial rise in the markers of kidney and intestinal barrier injury persisted despite runners mitigating severe hypohydration. These findings may be useful for identifying interventions aimed at minimizing acute health complications associated with marathon running.

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Publication Details

Journal
Journal of Applied Physiology
Published
2025-10-17
DOI
https://doi.org/10.1152/japplphysiol.00775.2025
Citations
1
Primary Topic
Thermoregulation and physiological responses
Type
article
Field-Weighted Citation Impact
1.16
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article

Biomarkers of organ stress and injury following the Boston Marathon

Cory L. Butts, R.M. Álvarez Pérez, Whitley C. Atkins, Sarah Gustus et al.
1 citations
Journal of Applied Physiology
Thermoregulation and physiological responses
1.16
article

Biomarkers of organ stress and injury following the Boston Marathon

Cory L. Butts, R.M. Álvarez Pérez, Whitley C. Atkins, Sarah Gustus, Brendon P. McDermott, Zachary J. McKenna, Xiujing Zhao, Abigail K. Morris, Shawn C. Wierick
article en
1 citations

Abstract

We examined the changes in blood and urine-based biomarkers of organ stress/injury and hydration before and after the 2024 Boston Marathon. Our primary aims were to compare responses between males and females, and euhydrated and hypohydrated runners. Seventy-two runners (34 males/38 females; 50 ± 11 yr; finish time 3:45 ± 0:32 h:min) had blood and/or urine samples taken before and after the race. Average temperature on a race day was 19 ± 3°C, and relative humidity was 47 ± 15%. Samples were assayed for markers of hydration, intestinal injury (intestinal fatty acid binding protein and soluble cluster of differentiation 14), skeletal muscle damage (creatine kinase), and acute kidney injury (tissue inhibitor of metalloproteinase 2, insulin-like growth factor binding protein 7, neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, creatinine). Markers of hydration were elevated from pre- to postrace, but only 25%-34% of runners were deemed hypohydrated postrace. All markers of organ stress/injury were increased postrace (fold change: 1.3-1455; <i>P</i> ≤ 0.007 for all indices); however, there were no differences based on sex or hydration status (<i>P</i> ≥ 0.099 for all indices). Our findings show that the Boston Marathon produces a significant level of stress on the gastrointestinal and renal organ systems and that these effects do not appear to be modulated by biological sex. In addition, our findings suggest that the substantial increases in markers of kidney and intestinal barrier injury persist even when severe hypohydration is prevented, suggesting that during the marathon, maintaining hydration cannot fully offset the risk for organ injury. These findings should be considered when designing interventions to minimize gastrointestinal and renal-related health complications associated with marathon running to promote both health and performance in recreational, but completive marathon runners.<b>NEW & NOTEWORTHY</b> We show that the Boston Marathon produces a significant level of stress on the gastrointestinal and renal organ systems, but these effects do not appear to be modulated by biological sex or age. Furthermore, the substantial rise in the markers of kidney and intestinal barrier injury persisted despite runners mitigating severe hypohydration. These findings may be useful for identifying interventions aimed at minimizing acute health complications associated with marathon running.

Journal of Applied PhysiologyVol. 139(5)
University of New Mexico (US), Texas Health Dallas (US), Massachusetts General Hospital (US), Presbyterian Hospital (US), Institute for Exercise and Environmental Medicine (US), Exercise Science Consulting (GB), Southwestern Medical Center (US), University of Arkansas at Fayetteville (US), The University of Texas Southwestern Medical Center (US)
Openalex Percentile: Top 17%
Thermoregulation and physiological responses
1.16
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