Aerobic capacity predict skeletal but not cardiac muscle damage after triathlon - the Iron(WO)man study.

This study examines the association between aerobic capacity and biomarkers of skeletal- and cardiac muscle damage among amateur triathletes after a full distance Ironman. Men and women (N = 55) were recruited from local sport clubs. One month before an Ironman triathlon, they conducted a 20 m shuttle run test to determine aerobic capacity. Blood samples were taken immediately after finishing the triathlon, and analyzed for cardiac Troponin T (cTnT), Myosin heavy chain-a (MHC-a), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), Creatin Kinas (CK), and Myoglobin. Regression models examining the association between the biomarkers and aerobic capacity expressed in both relative terms (mLO2*kg-1*min-1) and absolute terms (LO2*min-1) controlled for weight were fitted. A total of 39 subjects (26% females) had complete data and were included in the analysis. No association between aerobic capacity and cardiac muscle damage was observed. For myoglobin, adding aerobic capacity (mLO2*kg-1*min-1) increased the adjusted r2 from 0.026 to 0.210 (F: 8.927, p = 0.005) and for CK the adjusted r2 increased from -0.015 to 0.267 (F: 13.778, p = 0.001). In the models where aerobic capacity was entered in absolute terms the adjusted r2 increased from 0.07 to 0.227 (F: 10.386, p = 0.003) for myoglobin and for CK from -0.029 to 0.281 (F: 15.215, p < 0.001). A negative association between aerobic capacity and skeletal muscle damage was seen but despite the well-known cardio-protective health effect of high aerobic fitness, no such association could be observed in this study.

Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death.

OBJECTIVE: It has been suggested that the mechanism behind cardiac troponin elevation after strenuous exercise is passage through a cell membrane with changed permeability rather than myocardial cell death. We hypothesised that an increase of cardiac specific myosin heavy chain-alpha (MHC-α; 224 kDa compared with cardiac troponin T's (cTnT) 37 kDa) could hardly be explained by passage through a cell membrane. METHODS: Blood samples were collected from 56 athletes (15 female, age 42.5±9.7, range 24-70 years) before, directly after and on days 1-8 after an Ironman. Biomarkers (C reactive protein (CRP), cTnT, creatine kinase (CK), MHC-α, myoglobin (MG), creatinine (C) and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) were measured. RESULTS: The course of MHC-α concentration (µg/L) was 1.33±0.53 (before), 2.57±0.78 (directly after), 1.51±0.53 (day 1), 2.74±0.55 (day 4) and 1.83±0.76 (day 6). Other biomarkers showed a one-peaked increase with maximal values either directly after the race or at day 1: cTnT 76 ± 80 ng/L (12-440; reference<15), NT-proBNP 776±684 ng/L (92-4700; ref.<300), CK 68±55 µkat/L (5-280; ref.<1.9), MG 2088±2350 µg/L (130-17 000; ref.<72) and creatinine 100±20 µmol/L (74-161; ref.<100), CRP 49±23 mg/L (15-119; ref.<5). CONCLUSION: MHC-α exhibited a two-peaked increase which could represent a first release from the cytosolic pool and later from cell necrosis. This is the first investigation of MHC-α plasma concentration after exercise.

Blood biomarkers in male and female participants after an Ironman-distance triathlon.

BACKGROUND: While overall physical activity is clearly associated with a better short-term and long-term health, prolonged strenuous physical activity may result in a rise in acute levels of blood-biomarkers used in clinical practice for diagnosis of various conditions or diseases. In this study, we explored the acute effects of a full Ironman-distance triathlon on biomarkers related to heart-, liver-, kidney- and skeletal muscle damage immediately post-race and after one week's rest. We also examined if sex, age, finishing time and body composition influenced the post-race values of the biomarkers. METHODS: A sample of 30 subjects was recruited (50% women) to the study. The subjects were evaluated for body composition and blood samples were taken at three occasions, before the race (T1), immediately after (T2) and one week after the race (T3). Linear regression models were fitted to analyse the independent contribution of sex and finishing time controlled for weight, body fat percentage and age, on the biomarkers at the termination of the race (T2). Linear mixed models were fitted to examine if the biomarkers differed between the sexes over time (T1-T3). RESULTS: Being male was a significant predictor of higher post-race (T2) levels of myoglobin, CK, and creatinine levels and body weight was negatively associated with myoglobin. In general, the models were unable to explain the variation of the dependent variables. In the linear mixed models, an interaction between time (T1-T3) and sex was seen for myoglobin and creatinine, in which women had a less pronounced response to the race. CONCLUSION: Overall women appear to tolerate the effects of prolonged strenuous physical activity better than men as illustrated by their lower values of the biomarkers both post-race as well as during recovery.

[Biochemical changes after strenuous exercise ­ data from the Kalmar Ironman]. / Hjärtmarkörer ökar efter intensiv motion - oklar klinisk betydelse - Data från förstudie av Kalmar IronWoman-studien visar på troponin T-värden som vid hjärtinfarkt.

Biochemical changes after strenuous exercise - data from the Kalmar Ironman Strenuous and prolonged exercise like marathon, ultra running and triathlon can lead to changes in biomarkers of cardiac, muscle and kidney functional damage. We present the data of 30 (15 men, 15 women) participants of the Kalmar Ironman 2015. Pre-race electrocardiograms and echocardiograms showed a high frequency of abnormalities. Post race elevations of troponin T, creatine kinase, myoglobin, N-terminal prohormone of brain natriuretic peptide, and creatinine returned to normal in almost all cases within 5-8 days. In all but one participant the troponin T pattern was compatible with the diagnosis of myocardial infarction. It is an up-to-date unanswered question whether the increase of troponin represents myocardial damage or just is a benign consequence of an intermittent change of the permeability of myocardial cell membranes.