• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • transferases br Discussion Intriguingly in a


    Discussion Intriguingly, in a case report about elevation of skeletal enzymes in ultramarathon runners, the CK level reached its peak value one day after the run, had a ∼4-day plateau, and began to decline after a few more days. The sustained increase of plasma CK in this athlete was quite different from the peak pattern seen in patients with myocardial infarction. We do not know whether the athletes in this study follow the same kinetics, as more plasma samples collected at different time points need to be analyzed. Because it is likely that proteins leaked from stressed muscle cells, rather than being released from damaged tissues, these results together suggest that endurance exercises probably transferases have a prolonged effect on membrane permeability, which is manifested as a multiple-day plateau for the CK or CK-MB level. We examined how cTnI levels changed in ultramarathon runners. Our findings are very similar to those reported for one marathon athlete. The cTnI level of this runner reached its peak value at 8–17 hours after the run, and returned to baseline within 48 hours. Thus, the cTnI level in endurance exercises dropped fairly quickly, which is in sharp transferases to the known cTnI profiles seen in myocardial injury. For patients with myocardial infarction, cTnI, among tested cardiac biomarkers, is supposed to be the last one to reach its peak level as well as to return to its baseline level. Thus, our results seem to confirm that the plasma cTnI profiles due to exertion-induced rhabdomyolysis are different from those caused by myocardial injury. Furthermore, HBV latent infection appeared to cause some aberration in troponin kinetics in ultramarathon athletes. Our data suggest that the recovery of plasma cTnI levels is somehow delayed in ultramarathon runners with HBVc. Multiple linear regression analyses were performed to identify whether any factors were associated with this higher postrace cTnI level, which identified age, previous running experience, training, and 4-hour running distance as independent predictors for HBV carriers. By contrast, those parameters were not significantly different from those of non-HBVc runners, with an excellent correlation coefficient (r2=0.8) for the overall prediction model. We examined the potential independent factors previously reported to relate to postrace cTnI levels using linear regression analysis. We found that age, 4-hour running distance, previous running experience, and postrace cTnI levels demonstrated an inverse relationship in HBVc runners. This observation is in line with those of other studies. Previously, Shave et al had investigated whether higher cTnI release might relate to higher exercise intensity, and to higher work of the heart muscle, suggesting an age-dependent relationship. Eijsvogels et al, however, reported an opposite relationship between postrace cTnI levels and exercise duration. However, in the present study, we observed that the 4-hour running distance was related to increase of cTnI levels. This is consistent with the model that longer exercise duration is usually related to exercise intensity-induced cTnI levels. In addition, we also observed a positive relationship between training (β=0.37, p=0.02) and postrace cTnI levels in HBVc runners. This finding is in line with Shave et al group’s report that exercise-induced cTnI release was strongly related to training experience. Thus, factors such as age, intensity of exercise, training, and running experience might be a potential relation to be explained by the exercise mode in the present study. Taken together, 100-km ultramarathon seems not to have been the trigger for myocardial damage in our study. Meanwhile, our exercise model\'s predictive value is high (r2=0.8), which indicates that a portion of cTnI levels can be explained due to those potential factors in the HBVc runners’ group. However, a recent study by He et al investigated whether autophagy is induced by exercise, which resulted in biochemical evidence of skeletal and cardiac muscle autophagy. In addition, exercise-induced autophagy in liver and heart involved glucose and energy homeostasis. Thus, exercise is a newly defined stimulus that induces autophagy in vivo.