Following on from the original articles featured last month –
“Association between collapse and serum creatinine and electrolyte concentrations in marathon runners: a 9-year retrospective study”
“High‐sensitivity troponin T in marathon runners, marathon runners with heart disease and collapsed marathon runners”
More research was conducted which resulted in another paper being published recently –
Marathon running and cell-cycle arrest biomarkers of acute kidney injury
Todd Leckie | Daniel Fitzpatrick | Alan J. Richardson | Alex Hunter | Sonia Bains | Rachael Grimaldi | Rob Galloway | Lui G. Forni | Luke E. Hodgson
Link to published article – Click here.
Objective:
Raised serum creatinine levels are frequently seen in both healthy and collapsed marathon runners following a race. However, it isn’t known whether this represents true renal cell stress, or if it’s the result of increased production from muscles along with reduced renal clearance due to physiological reduced renal perfusion during marathons.
Insulin Like Growth Factor Binding Protein 7 (IGFBP7) and Tissue Inhibitor of Metalloprotinases-2 (TIMP-2) are two markers of renal cell cycle arrest found in urine. They have previously been shown to be strongly predictive of the development of Acute Kidney Injury (AKI) in hospital, but have not previously been used in the context of marathon running.
This study aimed to investigate the change in IFGBP7 and TIMP-2 in marathon running and compare it to changes in serum and urinary creatinine in order to determine whether there is a true renal insult associated with marathon running.
What difference could the outcomes of the research make to treatment / prevention?
We found that there are significant increases in both IFGBP7 and TIMP-2 in healthy marathon runners, but that these return to near normal levels after 24 hours. There were also increases in creatinine, but when the IFGBP7 and TIMP-2 results were corrected for creatinine, there were still significant increases. This suggests there is a true renal insult and increases in creatinine routinely seen cannot be explained by increased production and reduced renal perfusion alone.
This suggests we need to consider the possible impact of people running serial marathons on long term renal function and investigate whether this puts runners at increased risk of Chronic Kidney Disease (CKD). Renal cell cycle arrest is associated with fibrosis and CKD development. In addition, it’s known that high volumes of endurance exercise can predispose to other chronic conditions such as atrial fibrillation. There haven’t been any studies into long term endurance exercise and the development of CKD but it should likely now be considered.
How would a medical practitioner use this information?
Medical practitioners who may see a marathon runner in the period after a race can use this information to be aware that a raised creatinine is likely representative of a true renal insult. They may want to consider following up individuals with altered renal function who have taken part in endurance exercise for a large number of years, to ensure it has returned to the previous baseline.
Would the public gain anything from knowing this information and if so, what would that be?
Members of the public should understand that there isn’t any current evidence showing that long term endurance exercise causes CKD. However, we do know that there is there is likely an ‘inverted U’ curve for the dose of exercise and health benefits, and so doing too much may be detrimental to health. Although not directly showing this, this study does add some further weight to the argument that there is such a thing as too much exercise.
Commentary written by:
Dan FitzPatrick (He/Him)
Sport and Exercise Medicine Registrar (ST3), Charing Cross Hospital
Honorary Research Fellow, SASME, University of Brighton
First Team Doctor, Rosslyn Park FC
Independent Match Day Doctor, Premiership Rugby
Council Member, Royal Society of Medicine Sport and Exercise Medicine Section