Intense exercise may cause heart remodeling to compensate increases in blood pressure or volume by increasing muscle mass. Cardiac changes do not involve only the left ventricle, but all heart chambers. Physiological ...Intense exercise may cause heart remodeling to compensate increases in blood pressure or volume by increasing muscle mass. Cardiac changes do not involve only the left ventricle, but all heart chambers. Physiological cardiac modeling in athletes is associated with normal or enhanced cardiac function, but recent studies have documented decrements in left ventricular function during intense exercise and the release of cardiac markers of necrosis in athlete's blood of uncertain significance. Furthermore, cardiac remodeling may predispose athletes to heart disease and result in electrical remodeling, responsible for arrhythmias. Athlete's heart is a physiological condition and does not require a specific treatment. In some conditions, it is important to differentiate the physiological adaptations from pathological conditions, such as hypertrophic cardiomyopathy, arrhythmogenic dysplasia of the right ventricle, and non-compaction myocardium, for the greater risk of sudden cardiac death of these conditions. Moreover, some drugs and performance-enhancing drugs can cause structural alterations and arrhythmias, therefore, their use should be excluded.展开更多
Abstract： This study investigated the effects of three sport-specific high-intensity training units on cardiac biomarker alteration in elite athletes of dragon boating. Thirty six male （age 33 ± 9） and twenty ...Abstract： This study investigated the effects of three sport-specific high-intensity training units on cardiac biomarker alteration in elite athletes of dragon boating. Thirty six male （age 33 ± 9） and twenty nine female （age 31 ±8） elite athletes, members of the German national team, were examined in their final training camp preparing for world championship. At two time points blood panels （pre-training and one hour post-training） were collected and concentrations of high sensitive troponin T, N-terminal pro brain natriuretic peptide （NT-pro BNP）, ereatine phosphokinase （CPK）, MB-creatine kinase （CKMB） and myoglobin were assessed. After exercise, serum levels ofNT-pro BNP, CPK, myoglobin and CKMB increased significantly （P 〈 0.01 for each） with only few values exceeding the upper reference limits. High sensitive troponin T remained below the limit of detection both before and after exercise in all athletes. Significant gender-related differences were found with a higher increase ofNT-pro BNP levels in female athletes （P 〈 0.01） compared to males. In contrast, male athletes displayed a significant higher increase of CPK （P 〈 0.01） and myoglobin （P 〈 0.01） compared to female athletes. In conclusion, three high-intensity training units did not lead to elevated high sensitive troponin T concentrations in elite athletes of dragon boating but to significant increases ofNT-pro BNP, CPK and myoglobin levels. This suggests that high-intensity training units do not lead to a cardiac injury in these athletes.展开更多
Yi-Qi-Fu-Mai(YQFM) is extensively used clinically to treat cardiovascular diseases in China. To explore the anti-hypoxia effect of the extract of YQFM preparation(EYQFM), the EYQFM(1.4, 2.8, and 5.5 g·kg-1·d...Yi-Qi-Fu-Mai(YQFM) is extensively used clinically to treat cardiovascular diseases in China. To explore the anti-hypoxia effect of the extract of YQFM preparation(EYQFM), the EYQFM(1.4, 2.8, and 5.5 g·kg-1·d-1) was assessed for its heart-protective effect in a chronic intermittent hypoxia(CIH) animal model(oxygen pressure 7%-8%, 20 min per day) for 28 days of treatment. Betaloc(0.151 6 g·kg^(-1)·d^(-1)) was used as a positive control. The histopathological analyses of heart in CIH mice were conducted. Several cardiac state parameters, such as left ventricular ejection fractions(EF), stroke volume(SV), expression of creatine kinase(CK), lactate dehydrogenase(LDH), superoxide dismutase(SOD), and malondialdehyde(MDA) were measured. The results showed that treatment with EYQFM markedly reversed swelling of the endothelial cells and vacuolization in the heart when compared with the model group. Further study demonstrated that EYQFM significantly improved ventricular myocardial contractility by increasing EF and SV. In addition, EYQFM inhibited the activity of CK, LDH, decreased the level of MDA and improved SOD activity. The results demonstrated that EYQFM significantly improved the tolerability of myocardium to hypoxia and ameliorated the cardiac damage in the CIH model.展开更多
文摘Intense exercise may cause heart remodeling to compensate increases in blood pressure or volume by increasing muscle mass. Cardiac changes do not involve only the left ventricle, but all heart chambers. Physiological cardiac modeling in athletes is associated with normal or enhanced cardiac function, but recent studies have documented decrements in left ventricular function during intense exercise and the release of cardiac markers of necrosis in athlete's blood of uncertain significance. Furthermore, cardiac remodeling may predispose athletes to heart disease and result in electrical remodeling, responsible for arrhythmias. Athlete's heart is a physiological condition and does not require a specific treatment. In some conditions, it is important to differentiate the physiological adaptations from pathological conditions, such as hypertrophic cardiomyopathy, arrhythmogenic dysplasia of the right ventricle, and non-compaction myocardium, for the greater risk of sudden cardiac death of these conditions. Moreover, some drugs and performance-enhancing drugs can cause structural alterations and arrhythmias, therefore, their use should be excluded.
文摘Abstract： This study investigated the effects of three sport-specific high-intensity training units on cardiac biomarker alteration in elite athletes of dragon boating. Thirty six male （age 33 ± 9） and twenty nine female （age 31 ±8） elite athletes, members of the German national team, were examined in their final training camp preparing for world championship. At two time points blood panels （pre-training and one hour post-training） were collected and concentrations of high sensitive troponin T, N-terminal pro brain natriuretic peptide （NT-pro BNP）, ereatine phosphokinase （CPK）, MB-creatine kinase （CKMB） and myoglobin were assessed. After exercise, serum levels ofNT-pro BNP, CPK, myoglobin and CKMB increased significantly （P 〈 0.01 for each） with only few values exceeding the upper reference limits. High sensitive troponin T remained below the limit of detection both before and after exercise in all athletes. Significant gender-related differences were found with a higher increase ofNT-pro BNP levels in female athletes （P 〈 0.01） compared to males. In contrast, male athletes displayed a significant higher increase of CPK （P 〈 0.01） and myoglobin （P 〈 0.01） compared to female athletes. In conclusion, three high-intensity training units did not lead to elevated high sensitive troponin T concentrations in elite athletes of dragon boating but to significant increases ofNT-pro BNP, CPK and myoglobin levels. This suggests that high-intensity training units do not lead to a cardiac injury in these athletes.
基金supported by the National Natural Science Foundations of China(Nos.81274004,81473317)
文摘Yi-Qi-Fu-Mai(YQFM) is extensively used clinically to treat cardiovascular diseases in China. To explore the anti-hypoxia effect of the extract of YQFM preparation(EYQFM), the EYQFM(1.4, 2.8, and 5.5 g·kg-1·d-1) was assessed for its heart-protective effect in a chronic intermittent hypoxia(CIH) animal model(oxygen pressure 7%-8%, 20 min per day) for 28 days of treatment. Betaloc(0.151 6 g·kg^(-1)·d^(-1)) was used as a positive control. The histopathological analyses of heart in CIH mice were conducted. Several cardiac state parameters, such as left ventricular ejection fractions(EF), stroke volume(SV), expression of creatine kinase(CK), lactate dehydrogenase(LDH), superoxide dismutase(SOD), and malondialdehyde(MDA) were measured. The results showed that treatment with EYQFM markedly reversed swelling of the endothelial cells and vacuolization in the heart when compared with the model group. Further study demonstrated that EYQFM significantly improved ventricular myocardial contractility by increasing EF and SV. In addition, EYQFM inhibited the activity of CK, LDH, decreased the level of MDA and improved SOD activity. The results demonstrated that EYQFM significantly improved the tolerability of myocardium to hypoxia and ameliorated the cardiac damage in the CIH model.
