Impact of marathon running on cardiac structure and function in recreational runners

Abstract

The present study examined the relationship between LV (left ventricular) function, markers of cardiac-specific damage and markers of oxidative stress in recreational runners following a marathon. Runners (n=52; 43 male and nine female; age, 35+/-10 years; height, 1.74+/-0.08 m; body mass, 75.9+/-8.9 kg) were assessed pre- and immediately post-marathon. LV function was assessed using standard M-mode two-dimensional Doppler echocardiography and TDI (tissue-Doppler imaging) echocardiography. Serum was analysed for cTnT (cardiac troponin-T), TEAC (Trolox equivalent antioxidant capacity; a measure of total antioxidant capacity), MDA (malondealdehyde) and 4-HNE (4-hydroxynonenal). A strong relationship was observed between standard and TDI echocardiography for all functional measures. Diastolic function was altered post-marathon characterized by a reduction in E (peak early diastolic filling: 0.79+/-0.11 compared with 0.64+/-0.16 cm/s; P<0.001), an increase in A (peak late diastolic filling: 0.48+/-0.11 compared with 0.60+/-0.12 cm/s; P<0.001) and a resultant decrease in E/A (ratio of E to A; 1.71+/-0.48 compared with 1.10+/-0.31; P<0.001). Ejection fraction remained unchanged post-marathon. Thirty-two runners presented with cTnT values above the lower limit of detection for the assay (0.01 microg/l), and 20 runners presented post-marathon with cTnT values above the acute myocardial infarction cut-off value (0.05 microg/l). No significant correlations were observed between cTnT and any functional measurements. MDA (2.90+/-1.58 compared with 3.59+/-1.47 micromol/l) and TEAC (1.80+/-0.12 compared with 1.89+/-0.21 mmol/l) were significantly increased post-marathon, but were unrelated to changes in function or cTnT. In conclusion, the present study demonstrated a reduction in diastolic function and widespread evidence of minimal cardiac damage following a marathon in recreational runners. The mechanism(s) underpinning the altered function and appearance of cTnT appear unrelated to reactive oxygen species.

Progressive and biphasic cardiac responses during extreme mountain ultramarathon

“…At midrace (148 km; 47 Ϯ 7 h), SV was greater than at prerace, an observation in accordance with one of our previous studies after 38 h of running (39). Conversely, after shorter-duration exercises, SV was generally decreased (26,29,35,42). Of note, consequently to the higher SV, we observed a greater cardiac output at mid-and posttest.…”

“…These findings strongly support the role of diastolic filling in the increase of SV. They contrast with the adaptation observed after shorter-duration races where diastolic filling was usually depressed (26,29,30,35,42).…”

“…Although previous studies evaluated cardiac function following endurance exercise such as marathons, ironman triathlons, or MUMs (7,20,22,28,42), the present study is the first to investigate alterations in cardiac function induced by a MUM Ͼ100 h (i.e., during several days) and the first to include a measurement performed during the event. We observed that a MUM run over 4 -7 days induced 1) a specific and progressive increase of SV from pre-to postrace concomitant with an increase in diastolic filling and 2) a biphasic adaptation of HR, LV strain rates, with an initial increase from pre-to midrace and a return to baseline values from mid-to postrace.…”

“…An extreme MUM induced a biphasic pattern of heart rate in parallel with specific cardiac responses characterized by a progressive increase in diastolic filling, biventricular volumes, and SV. IT IS WELL DOCUMENTED THAT prolonged intense exercise, such as a marathon or Ironman triathlon, transitorily alters cardiac function (7,13,20,22,23,28,42). A range of 3-15 h exercising induces transient left ventricular (LV) global systolic (20, 42) and diastolic (7,23,28) dysfunctions.…”

“…A range of 3-15 h exercising induces transient left ventricular (LV) global systolic (20,42) and diastolic (7,23,28) dysfunctions. This phenomenon, named exercise-induced cardiac fatigue (EICF), is generally associated with the release of biochemical markers of myocardial damage (13,22).…”