Cardiac Damage Biomarkers Following a Triathlon in Elite and Non-elite Triathletes

The purpose of the present study was to investigate cardiac damage biomarkers after a triathlon race in elite and non-elite athlete groups. Fifteen healthy men participated in the study. Based on performance, they were divided into elite athlete group (EG: n=7) and non-elite athlete group (NEG: n=8). Participants' blood samples were obtained during four periods: before, immediately, 2 hours and 7 days after finishing the race. creatine kinase (CK), creatine kinase-myoglobin (CK-MB), myoglobin, and lactate dehydrogenase (LDH) were significantly increased in both groups immediately after, and 2 hours after finishing the race (p<.05). CK, CK-MB, and myoglobin were completely recovered after 7 days (p<.05). Hematocrit (Hct) was significantly decreased in both groups (p<.05) 7 days after the race. LDH was significantly decreased in the EG (p<.05) only 7 days after the race. Homoglobin (Hb) was significantly decreased in the NEG (p<.05) only 2 hours after the race. Although cardiac troponin T (cTnT) was significantly increased in the EG but not in the NEG 2hours after the race (p<.05), there was no group-by-time interaction. cTnT was completely recovered in both groups 7 days after the race. In conclusion, cardiac damage occurs during a triathlon race and, is greater in elite than in non-elite. However, all cardiac damage markers return to normal range within 1 week.

Combined effects of food and exercise on anaphylaxis

Food-dependent exercise-induced anaphylaxis (FDEIAn) is induced by different types and various intensities of physical activity, and is distinct from food allergies. It has been shown that consumption of allergenic food followed by exercise causes FDEIAn symptoms. Intake of allergenic food or medication before exercise is a major predisposing factor for FDEIAn. Urticaria and severe allergic reactions are general symptoms of FDEIAn. Dermatological tests and serum IgE assays are the typical prescreening methods, and have been used for several decades. However, these screening tests are not sufficient for detecting or preventing FDEIAn. It has been found that exercise may stimulate the release of mediators from IgE-dependent mast cells that can result in FDEIAn when a certain threshold level has been exceeded. Mast cell degradation might be a major factor to induce FDEIAn but this has not been determined. A number of foods have been reported to be involved in the onset of FDEIAn including wheat, eggs, chicken, shrimp, shellfish, nuts, fruits, and vegetables. It is also known that aspirin increases the occurrence of type I allergy symptoms when combined with specific foods. Moreover, high intensity and frequent exercise are more likely to provoke an attack than low intensity and less frequent exercise. In this paper, we present the current views of the pathophysiological mechanisms underlying FDEIAn within the context of exercise immunology. We also present a detailed FDEIAn definition along with etiologic factors and medical treatment for cholinergic urticaria (UC) and exercise-induced anaphylaxis (EIA).