Rob Shave

Exercise-Induced Cardiac Troponin Elevation Evidence, Mechanisms, and Implications

Regular physical exercise is recommended for the primary prevention of cardiovascular disease. Although the high prevalence of physical inactivity remains a formidable public health issue, participation in exercise programs and recreational sporting events, such as marathons and triathlons, is on the rise. Although regular exercise training reduces cardiovascular disease risk, recent studies have documented elevations in cardiac troponin (cTn) consistent with cardiac damage after bouts of exercise in apparently healthy individuals. At present, the prevalence, mechanism(s), and clinical significance of exercise-induced cTn release remains incompletely understood. This paper will review the biochemistry, prevalence, potential mechanisms, and management of patients with exercise-induced cTn elevations.

Elevation in cerebral blood flow velocity with aerobic fitness throughout healthy human ageing

It is known that cerebral blood flow declines with age in sedentary adults, although previous studies have involved small sample sizes, making the exact estimate of decline imprecise and the effects of possible moderator variables unknown. Animal studies indicate that aerobic exercise can elevate cerebral blood flow; however, this possibility has not been examined in humans. We examined how regular aerobic exercise affects the age‐related decline in blood flow velocity in the middle cerebral artery (MCAv) in healthy humans. Maximal oxygen consumption, body mass index (BMI), blood pressure and MCAv were measured in healthy sedentary (n= 153) and endurance‐trained (n= 154) men aged between 18 and 79 years. The relationships between age, training status, BMI and MCAv were examined using analysis of covariance methods. Mean ±s.e.m. estimates of regression coefficients and 95% confidence intervals (95% CI) were calculated. The age‐related decline in MCAv was −0.76 ± 0.04 cm s−1 year−1 (95% CI =−0.69 to −0.83, r2= 0.66, P < 0.0005) and was independent of training status (P= 0.65). Nevertheless, MCAv was consistently elevated by 9.1 ± 3.3 cm s−1 (CI = 2.7–15.6, P= 0.006) in endurance‐trained men throughout the age range. This ∼17% difference between trained and sedentary men amounted to an approximate 10 year reduction in MCAv ‘age’ and was robust to between‐group differences in BMI and blood pressure. Regular aerobic‐endurance exercise is associated with higher MCAv in men aged 18–79 years. The persistence of this finding in older endurance‐trained men may therefore help explain why there is a lower risk of cerebrovascular disease in this population.

State-of-the-Art PaperExercise-Induced Cardiac Troponin Elevation: Evidence, Mechanisms, and Implications

Regular physical exercise is recommended for the primary prevention of cardiovascular disease. Although the high prevalence of physical inactivity remains a formidable public health issue, participation in exercise programs and recreational sporting events, such as marathons and triathlons, is on the rise. Although regular exercise training reduces cardiovascular disease risk, recent studies have documented elevations in cardiac troponin (cTn) consistent with cardiac damage after bouts of exercise in apparently healthy individuals. At present, the prevalence, mechanism(s), and clinical significance of exercise-induced cTn release remains incompletely understood. This paper will review the biochemistry, prevalence, potential mechanisms, and management of patients with exercise-induced cTn elevations.

Influence of tart cherry juice on indices of recovery following marathon running

This investigation determined the efficacy of a tart cherry juice in aiding recovery and reducing muscle damage, inflammation and oxidative stress. Twenty recreational Marathon runners assigned to either consumed cherry juice or placebo for 5 days before, the day of and for 48 h following a Marathon run. Markers of muscle damage (creatine kinase, lactate dehydrogenase, muscle soreness and isometric strength), inflammation [interleukin‐6 (IL‐6), C‐reactive protein (CRP) and uric acid], total antioxidant status (TAS) and oxidative stress [thiobarbituric acid reactive species (TBARS) and protein carbonyls] were examined before and following the race. Isometric strength recovered significantly faster (P=0.024) in the cherry juice group. No other damage indices were significantly different. Inflammation was reduced in the cherry juice group (IL‐6, P<0.001; CRP, P<0.01; uric acid, P<0.05). TAS was ∼10% greater in the cherry juice than the placebo group for all post‐supplementation measures (P<0.05). Protein carbonyls was not different; however, TBARS was lower in the cherry juice than the placebo at 48 h (P<0.05). The cherry juice appears to provide a viable means to aid recovery following strenuous exercise by increasing total antioxidative capacity, reducing inflammation, lipid peroxidation and so aiding in the recovery of muscle function.

Cardiac Troponin T Release Is Stimulated by Endurance Exercise in Healthy Humans

To the Editor: Post-exercise release of cardiac troponin (cTn)T and cTnI has been previously reported after prolonged bouts of exercise ([1][1]). However, this release has only been observed in a limited number of subjects ([2][2]). It is unclear whether post-exercise release of cTn represents

Exercise-associated increases in cardiac biomarkers.

At present, the risk of myocardial damage by endurance exercise is under debate because of reports on exercise-associated increases in cardiac biomarkers troponin and B-type natriuretic peptide (BNP); these markers are typically elevated in patients with acute myocardial infarction and chronic heart failure, respectively. Exercise-associated elevations of cardiac biomarkers can be present in elite and in recreational athletes, especially after prolonged and strenuous endurance exercise bouts (e.g., marathon and ultratriathlon). However, in contrast to cardiac patients, it is still unclear if the exercise-associated appearance or increase in cardiac biomarkers in obviously healthy athletes represents clinically significant cardiac insult or is indeed part of the physiological response to endurance exercise. In addition, elevations in cardiac biomarkers in athletes after exercise may generate difficulties for clinicians in terms of differential diagnosis and may result in inappropriate consequences. Therefore, the aim of this article is to provide an overview of exercise-associated alterations of the cardiac biomarkers troponin T and I, ischemia-modified albumin, BNP, and its cleaved inactive fragment N-terminal pro BNP for the athlete, coach, scientist, and clinician.

Changes in vascular and cardiac function after prolonged strenuous exercise in humans

Prolonged exercise has been shown to result in an acute depression in cardiac function. However, little is known about the effect of this type of exercise on vascular function. Therefore, the purpose of the present study was to investigate the impact of an acute bout of prolonged strenuous exercise on vascular and cardiac function and the appearance of biomarkers of cardiomyocyte damage in 15 male (32 +/- 10 yr) nonelite runners. The subjects were tested on two occasions, the day before and within an hour of finishing the London marathon (229 +/- 38 min). Function of the brachial and femoral arteries was determined using flow-mediated dilatation (FMD). Echocardiographic assessment of cardiac strain, strain rate, tissue velocities, and flow velocities during diastole and systole were also obtained. Venous blood samples were taken for later assessment of cardiac troponin I (cTnI), a biomarker of cardiomyocyte damage. Completion of the marathon resulted in a depression in femoral (P = 0.04), but not brachial (P = 0.96), artery FMD. There was no change, pre- vs. postmarathon, in vascular shear, indicating that the impaired femoral artery function was not related to hemodynamic changes. The ratio of peak early to atrial radial strain rate, a measure of left ventricular diastolic function, was reduced postmarathon (P = 0.006). Postrace cTnI was elevated in 12 of 13 runners, with levels above the recognized clinical threshold for damage in 7 of these. In conclusion, when taken together, these data suggest a transient depression in cardiac and leg vascular function following prolonged intensive exercise.

Dilatation and Dysfunction of the Right Ventricle Immediately After Ultraendurance Exercise Exploratory Insights From Conventional Two-Dimensional and Speckle Tracking Echocardiography

Background— Running an ultramarathon has been shown to have a transient negative effect on right ventricular (RV) and left ventricular (LV) function. Additionally, recent findings suggested that ultraendurance athletes may be more at risk of developing a RV cardiomyopathy. The standard echocardiographic assessment of RV function is problematic; however, the introduction of ultrasonic speckle tracking technology has the potential to yield a comprehensive evaluation of RV longitudinal function, providing new insights into this phenomenon. Thus, the primary aim of this exploratory study was to evaluate comprehensively RV structure and function after a 161-km ultramarathon and establish whether changes in the RV are associated with alterations in LV function. Methods and Results— Myocardial speckle tracking echocardiograms of the RV and LV were obtained before and immediately after a 161-km ultramarathon in 16 healthy adults. Standard echocardiography was used to determine RV size and function and LV eccentricity index. Speckle tracking was used to determine the temporal evaluation of indices of RV and LV function. RV size was significantly increased postrace (RV outflow, 32 to 35 mm, P =0.002; RV inflow, 42 to 45 mm, P =0.027) with an increase in LV eccentricity index (1.03 to 1.13, P =0.006). RV strain (e) was significantly reduced postrace (−27% to −24%, P =0.004), but there was no change in the rates of e. Peak e in all planes of LV motion were reduced postrace (longitudinal, −18.3 to −16.3%, P =0.012; circumferential, −20.2% to −15.7%, P =0.001; radial, 53.4% to 40.3%, P =0.009). Changes in RV size and function correlated with diastolic strain rates in the LV. Conclusions— This exploratory study demonstrates RV dilatation and reduction in function after an ultramarathon. Further research is warranted to elucidate the mechanisms responsible for these findings. It is not clear what clinical impact might result from consecutive bouts of postexercise RV dysfunction.Background— Running an ultramarathon has been shown to have a transient negative effect on right ventricular (RV) and left ventricular (LV) function. Additionally, recent findings suggested that ultraendurance athletes may be more at risk of developing a RV cardiomyopathy. The standard echocardiographic assessment of RV function is problematic; however, the introduction of ultrasonic speckle tracking technology has the potential to yield a comprehensive evaluation of RV longitudinal function, providing new insights into this phenomenon. Thus, the primary aim of this exploratory study was to evaluate comprehensively RV structure and function after a 161-km ultramarathon and establish whether changes in the RV are associated with alterations in LV function. Methods and Results— Myocardial speckle tracking echocardiograms of the RV and LV were obtained before and immediately after a 161-km ultramarathon in 16 healthy adults. Standard echocardiography was used to determine RV size and function and LV eccentricity index. Speckle tracking was used to determine the temporal evaluation of indices of RV and LV function. RV size was significantly increased postrace (RV outflow, 32 to 35 mm, P=0.002; RV inflow, 42 to 45 mm, P=0.027) with an increase in LV eccentricity index (1.03 to 1.13, P=0.006). RV strain (&egr;) was significantly reduced postrace (−27% to −24%, P=0.004), but there was no change in the rates of &egr;. Peak &egr; in all planes of LV motion were reduced postrace (longitudinal, −18.3 to −16.3%, P=0.012; circumferential, −20.2% to −15.7%, P=0.001; radial, 53.4% to 40.3%, P=0.009). Changes in RV size and function correlated with diastolic strain rates in the LV. Conclusions— This exploratory study demonstrates RV dilatation and reduction in function after an ultramarathon. Further research is warranted to elucidate the mechanisms responsible for these findings. It is not clear what clinical impact might result from consecutive bouts of postexercise RV dysfunction.

Mitral annular myocardial velocity assessment of segmental left ventricular diastolic function after prolonged exercise in humans

We assessed segmental and global left ventricular (LV) diastolic function via tissue‐Doppler imaging (TDI) as well as Doppler flow variables before and after a marathon race to extend our knowledge of exercise‐induced changes in cardiac function. Twenty‐nine subjects (age 18–62 year) volunteered to participate and were assessed pre‐ and post‐race. Measurements of longitudinal plane TDI myocardial diastolic velocities at five sites on the mitral annulus included peak early myocardial tissue velocity (E′), peak late (or atrial) myocardial tissue velocity (A′) and the ratio E′/A′. Standard pulsed‐wave Doppler transmitral and pulmonary vein flow indices were also recorded along with measurements of body mass, heart rate, blood pressures and cardiac troponin T (cTnT), a biomarker of myocyte damage. Pre‐ to post‐race changes in LV diastolic function were analysed by repeated measures ANOVA. Delta scores for LV diastolic function were correlated with each other and alterations in indices of LV loading. Diastolic longitudinal segmental and mean TDI data were altered post‐race such that the mean E′/A′ ratio was significantly depressed (1.51 ± 0.34 to 1.16 ± 0.35, P < 0.05). Changes in segmental and global TDI data were not related to an elevated post‐race HR, a decreased post‐race pre‐load or an elevated cTnT. The pulsed wave Doppler ratio of peak early transmitral flow velocity (E)/peak late (or atrial) flow velocity (A) was also significantly reduced post‐race (1.75 ± 0.46 to 1.05 ± 0.30, P < 0.05); however, it was significantly correlated with post‐race changes in heart rate. The lack of change in E/E′ from pre‐ to post‐race (3.4 ± 0.8 and 3.3 ± 0.7, respectively) suggests that the depression in diastolic function is likely to be due to altered relaxation of the left ventricle; however, the exact aetiology of this change remains to be determined.

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

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.