Effect of prolonged exercise in a hypoxic environment on cardiac function and cardiac troponin T

Background: Exercise induced cardiac fatigue has recently been observed after prolonged exercise. A moderate to high altitude has been suggested as a possible stimulus in the genesis of such cardiac fatigue. Objective: To investigate if exercise induced cardiac fatigue and or cardiac damage occurs after prolonged exercise in a hypoxic environment. Methods: Eight trained male triathletes volunteered for the study. Each completed two 50 mile cycle trials, randomly assigned from normobaric normoxia and normobaric hypoxia (15% FIO2). Echocardiographic assessment and whole blood collection was completed before, immediately after, and 24 hours after exercise. Left ventricular systolic and diastolic functional variables were calculated, and serum was analysed for cardiac troponin T. Results were analysed using a two way repeated measures analysis of variance, with α set at 0.05. Results: No significant differences were observed in either systolic or diastolic function across time or between trials. Cardiac troponin T was detected in one subject immediately after exercise in the normobaric hypoxic trial. Conclusions: A 50 mile cycle trial in either normobaric normoxia or normobaric hypoxia does not induce exercise induced cardiac fatigue. Some people, however, may exhibit minimal cardiac damage after exercise in normobaric hypoxia. The clinical significance of this is yet to be elucidated

The cardiospecificity of the third-generation cTnT assay after exercise-induced muscle damage

Purpose The purpose of the present study was to examine the cardiospecificity of cTnI and the new third-generation cTnT assay, in the presence of exercise-induced muscle damage in highly trained individuals, and to examine the impact of a maximal-ramping treadmill test on cardiac function. Methods Eight highly trained male triathletes (mean ± SD; age: 29 ± 9 yr; height: 1.79 ± 0.10 m; body mass: 77 ± 10 kg; V̇O2max: 67.4 ± 6.3 mL·kg−1·min−1) completed two bouts of exercise. On the first occasion, subjects completed a maximal-ramping treadmill test. On a separate occasion, the subjects completed 30 min of downhill running (15% gradient) at a speed equivalent to 70% of maximal running velocity attained during the maximal-ramping treadmill test. All subjects were assessed using ECG, echocardiography, and blood analysis. Measurements were taken at rest, immediately after, and 48 h postexercise for each bout of exercise. Echocardiographic analysis was used to determine left ventricular systolic and diastolic function. Blood samples were analyzed for markers of myocyte damage. Results Echocardiographic results indicated normal left ventricular function before and after both exercise bouts. Total CK and CKMB were significantly elevated 48 h after the downhill run. cTnT and cTnI were not elevated at any stage of the study. Conclusions Neither the maximal-ramping treadmill test nor the 30-min downhill run produced cardiac dysfunction or myocardial damage in young, healthy trained subjects. The elevated total CK and CKMB within the downhill study are noncardiac in origin as demonstrated by the lack of cTnT and cTnI. The cTnI and new third-generation cTnT assays may be used to detect cardiac damage in the presence of elevated total CK and CKMB associated with exercise-induced skeletal muscle damage

Cardiac troponin T in female athletes during a two-day mountain marathon

Background: Equivocal studies exist on the potential of cardiac damage following prolonged endurance exercise. Aims: The aim of the study was to examine humoral markers of cardiac damage in female athletes during a 2-day mountain endurance race. Methods: Venous blood samples were drawn from seven female competitors prior to, and immediately following day-1 and day-2 of the event. The serum was analysed for total creatine kinase (CK), creatine kinase isoenzyme MB (CKMB), and cardiac troponin T (cTnT). Results: Elevations in CK and CKMB were apparent following day-1 of the event (mean ± SD; CK 84.1±54.6 mg/L vs. 387±276.7 mg/L, CKMB 2±1.7 mg/L vs. 5.9±1.7 mg/L) and subsequently rose further following race completion (CK 743±500 mg/L, CKMB 11.9±4.9 mg/L). Elevations in cTnT were noted in three competitors following day-1 cTnT (range 0.013–0.044 mg/L) and remained elevated in two competitors following day-2 (range 0.014–0.017 mg/L). Conclusions: The elevations in cTnT likely represent release from the cytosolic fraction. The mechanism responsible for such release is yet to be elucidated

Evidence of exercise induced cardiac dysfunction and elevated cTnT in separate cohorts competing in an ultra-endurance mountain marathon race

Cardiac damage has recently been implicated in the aetiology of "exercise induced cardiac dysfunction". The humoral markers of cardiac damage that have been utilised to date are not sufficiently cardio-specific to investigate this hypothesis. The aim of the present study was to examine cardiac function following prolonged exercise, and investigate the contention of cardiac damage utilising a new highly cardio-specific marker. Thirty-seven competitors in the 2-day Lowe Alpine Mountain Marathon 2000 volunteered for the study. Competitors were sub-divided into 2 groups. Group 1 (n = 11) were examined using echocardiography pre and post the event, examining left ventricular diastolic and systolic function. Group 2 (n = 26) had venous blood samples drawn prior to the event and immediately following day-1 and day-2. Blood samples were analysed for total creatine kinase activity (CK), creatine kinase isoenzyme MB(mass) (CK-MB(mass)), and cardiac troponin T. Echocardiographic results indicated left ventricular diastolic and systolic dysfunction following cessation of exercise. CK and CK-MB(mass) were both elevated following day-1, and immediately following race completion. Cardiac troponin T levels were below the 99th percentile (0.01 microg/L) in all subjects prior to the event, following day-1 cTnT was elevated above 0.01 microg/L in 13 subjects, but returned to below 0.01 microg/L following race completion on day-2. However, no individual data reached clinical cut-off levels for acute myocardial infarction (AMI) (0.1 microg/L). Two days arduous exercise over mountainous terrain resulted in cardiac dysfunction, and significant skeletal muscular degradation. The elevation of cTnT above the 99th percentile in the present study is suggestive of minimal myocardial damage. The clinical significance of and exact mechanism responsible for such damage remains to be elucidated

Cardiac troponin T in female athletes during a two-day mountain marathon

Background: Equivocal studies exist on the potential of cardiac damage following prolonged endurance exercise. Aims: The aim of the study was to examine humoral markers of cardiac damage in female athletes during a 2-day mountain endurance race. Methods: Venous blood samples were drawn from seven female competitors prior to, and immediately following day-1 and day-2 of the event. The serum was analysed for total creatine kinase (CK), creatine kinase isoenzyme MB (CKMB), and cardiac troponin T (cTnT). Results: Elevations in CK and CKMB were apparent following day-1 of the event (mean ± SD; CK 84.1±54.6 mg/L vs. 387±276.7 mg/L, CKMB 2±1.7 mg/L vs. 5.9±1.7 mg/L) and subsequently rose further following race completion (CK 743±500 mg/L, CKMB 11.9±4.9 mg/L). Elevations in cTnT were noted in three competitors following day-1 cTnT (range 0.013–0.044 mg/L) and remained elevated in two competitors following day-2 (range 0.014–0.017 mg/L). Conclusions: The elevations in cTnT likely represent release from the cytosolic fraction. The mechanism responsible for such release is yet to be elucidated

Left ventricular systolic function and diastolic filling after intermittent high intensity team sports

Background: Prolonged steady state exercise can lead to a decrease in left ventricular (LV) function as well as promote the release of cardiac troponin T (cTnT). There is limited information on the effect of intermittent high intensity exercise of moderate duration. Objectives: To determine the effect of intermittent high intensity exercise of moderate duration on LV function. Methods: Nineteen male rugby and football players (mean (SD) age 21 (2) years) volunteered. Assessments, before, immediately after, and 24 hours after competitive games, included body mass, heart rate (HR), and systolic blood pressure (sBP) as well as echocardiography to assess stroke volume (SV), ejection fraction (EF), systolic blood pressure/end systolic volume ratio (sBP/ESV), and global diastolic filling (E:A) as well as to indirectly quantify preload (LV internal dimension at end diastole (LVIDd)). Serum cTnT was analysed using a 3rd generation assay. Changes in LV function were analysed by repeated measures analysis of variance. cTnT data are presented descriptively. Results: SV (91 (26) v 91 (36) v 90 (35) ml before, after, and 24 hours after the game respectively), EF (71 (8) v 70 (9) v 71 (7)%), and sBP/ESV (4.2 (1.8) v 3.8 (1.9) v 4.1 (1.6) mm Hg/ml) were not significantly altered (p>0.05). Interestingly, whereas LVIDd was maintained after the game (50 (5) v 50 (6) mm), sBP was transiently but significantly reduced (131 (3) v 122 (3) mm Hg; p<0.05). E:A was moderately (p<0.05) reduced after the game (2.0 (0.4) v 1.5 (0.4)) but returned to baseline within 24 hours. No blood sample contained detectable levels of cTnT. Conclusions: In this cohort, LV systolic function was not significantly altered after intermittent activity. A transient depression in global diastolic filling was partially attributable to a raised HR and could not be explained by myocyte disruption as represented by cTnT release

The impact of prolonged exercise in a cold environment upon cardiac function

Purpose: The purpose of the present study was to examine the impact of cold exposure coupled with prolonged exercise upon postexercise left ventricular (LV) function and markers of myocardial damage. Methods: colon; Eight highly trained male athletes (mean +/- SD; age: 28.2 +/- 8.8 yr; height: 1.78 +/- 0.07 m; body mass: 74.9 +/- 7.6 kg; VO2max: 65.6 +/- 7.0 mL x kg(-1) x min(-1)) performed two 100-mile cycle trials, the first in an ambient temperature of 0 degrees C, the second in an ambient temperature of 19 degrees C. Echocardiographic assessment was completed and blood samples drawn before, immediately postexercise, and 24-h postexercise. Left ventricular systolic (stroke volume [SV], ejection fraction [EF], and systolic blood pressure/end systolic volume ratio [SBP/ESV]) and diastolic (early [E] to late [A] filling ratio [E:A]) parameters were calculated. Serum was analyzed for creatine kinase isoenzyme MB (CK-MBmass) and cardiac troponin T (cTnT). cTnT was analyzed descriptively whereas other variables were assessed using two-way repeated-measures ANOVA. Results: No significant change was observed in systolic function across time or between trials. A significant difference between trials was observed in E:A immediately after exercise (1.4 +/- 0.4 [19 degrees C] vs 1.8 +/- 0.3 [0 degrees C]) (P < 0.05). CK-MBmass was significantly elevated immediately after exercise in both trials (P < 0.05). Positive cTnT concentrations were observed in two subjects immediately after the 19 degrees C trial (0.012 microg x L(-1) and 0.034 microg x L(-1)). Conclusions: Cycling 100 miles in an ambient temperature of 19 degrees C is associated with an acute change in diastolic filling that is not observed after prolonged exercise at 0 degrees C. Prolonged exercise is associated with minimal cardiac damage in some individuals; it appears that this is a separate phenomenon to the change in diastolic filling

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;

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

Cardiac drift during prolonged exercise with echocardiographic evidence of reduced diastolic function of the heart

This study examined whether, in 16 male subjects, a continuous increase in heart rate (HR) during 4 h of ergometry cycling relates to cardiac fatigue or cardiomyocyte damage. Serum cardiac troponin T (cTnT) was determined and echocardiographic assessment was carried out prior to and after 2 h of exercise, within 15 min of completing exercise and after 24 h. Left ventricular contractile function (end-systolic blood pressure–volume relationship [SBP/ESV]) and diastolic filling (ratio of early to late peak left ventricular filling velocities [E:A]) were calculated. During exercise HR was 132±5 beats min−1 after 2 h and increased to 141±5 beats min−1 (mean ± SD; P<0.05), but there was no evidence of altered LV contractile function (SBP/ESV 39.0±5.1 mmHg cm−1 to 36.5±5.2 mmHg cm−1 and SBP/ESV was not correlated to maximal oxygen uptake (r2=0.363). In contrast, E:A decreased (1.82±0.32 to 1.48±0.30; P<0.05) and returned towards baseline after 24 h (1.78±0.28), and individual changes were correlated to maximal oxygen uptake (r2=0.61; P<0.05). Low levels of cTnT were detected in two subjects after 4 h of exercise that had normalised by 24 h of recovery. During prolonged exercise cardiovascular drift occurred with echocardiographic signs of a reduced diastolic function of the heart, especially in those subjects with a high maximal oxygen uptake