Left Atrial Electromechanical Remodeling Following 2 Years of High-Intensity Exercise Training in Sedentary Middle-Aged Adults.

BACKGROUND: Moderate intensity exercise is associated with a decreased incidence of atrial fibrillation. However, extensive training in competitive athletes is associated with an increased atrial fibrillation risk. We evaluated the effects of 24 months of high intensity exercise training on left atrial (LA) mechanical and electric remodeling in sedentary, healthy middle-aged adults. METHODS: Sixty-one participants (53±5 years) were randomized to 10 months of exercise training followed by 14 months of maintenance exercise or stretching/balance control. Fourteen Masters athletes were added for comparison. Left ventricular (LV) and LA volumes underwent 3D echocardiographic assessment, and signal-averaged electrocardiographs for filtered P-wave duration and atrial late potentials were completed at 0, 10, and 24 months. Extended ambulatory monitoring was performed at 0 and 24 months. Within and between group differences from baseline were compared using mixed-effects model repeated-measures analysis. RESULTS: Fifty-three participants completed the study (25 control, 28 exercise) with 88±11% adherence to assigned exercise sessions. In the exercise group, both LA and LV end diastolic volumes increased proportionately (19% and 17%, respectively) after 10 months of training (peak training load). However, only LA volumes continued to increase with an additional 14 months of exercise training (LA volumes 55%; LV end diastolic volumes 15% at 24 months versus baseline; P<0.0001 for all). The LA:LV end diastolic volumes ratio did not change from baseline to 10 months, but increased 31% from baseline in the Ex group ( P<0.0001) at 24 months, without a change in controls. There were no between group differences in the LA ejection fraction, filtered P-wave duration, atrial late potentials, and premature atrial contraction burden at 24 months and no atrial fibrillation was detected. Compared with Masters athletes, the exercise group demonstrated lower absolute LA and LV volumes, but had a similar LA:LV ratio after 24 months of training. CONCLUSIONS: Twenty-four months of high intensity exercise training resulted in LA greater than LV mechanical remodeling with no observed electric remodeling. Together, these data suggest different thresholds for electrophysiological and mechanical changes may exist in response to exercise training, and provide evidence supporting a potential mechanism by which high intensity exercise training leads to atrial fibrillation. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02039154.

Does High-Intensity Endurance Training Increase the Risk of Atrial Fibrillation? A Longitudinal Study of Left Atrial Structure and Function.

BACKGROUND: Exercise mitigates many cardiovascular risk factors associated with atrial fibrillation. Endurance training has been associated with atrial structural changes which can increase the risk for atrial fibrillation. The dose of exercise training required for these changes is uncertain. We sought to evaluate the impact of exercise on left atrial (LA) mechanical and electrical function in healthy, sedentary, middle-aged adults. METHODS: Sixty-one adults (52±5 years) were randomized to either 10 months of high-intensity exercise training or yoga. At baseline and post-training, all participants underwent maximal exercise stress testing to assess cardiorespiratory fitness, P-wave signal-averaged electrocardiography for filtered P-wave duration and atrial late potentials (root mean square voltage of the last 20 ms), and echocardiography for LA volume, left ventricular end-diastolic volume, and mitral inflow for assessment of LA active emptying. Post-training data were compared with 14 healthy age-matched Masters athletes. RESULTS: LA volume, Vo2 max, and left ventricular end-diastolic volume increased in the exercise group (15%, 17%, and 16%, respectively) with no change in control (P<0.0001). LA active emptying decreased post-exercise versus controls (5%; P=0.03). No significant changes in filtered P-wave duration or root mean square voltage of the last 20 ms occurred after exercise training. LA and left ventricular volumes remained below Masters athletes. The athletes had longer filtered P-wave duration but no difference in the frequency of atrial arrhythmia. CONCLUSIONS: Changes in LA structure, LA mechanical function, and left ventricular remodeling occurred after 10 months of exercise but without significant change in atrial electrical activity. A longer duration of training may be required to induce electrical changes thought to cause atrial fibrillation in middle-aged endurance athletes. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique Identifier: NCT02039154.

Reversing the Cardiac Effects of Sedentary Aging in Middle Age-A Randomized Controlled Trial: Implications For Heart Failure Prevention.

BACKGROUND: Poor fitness in middle age is a risk factor for heart failure, particularly heart failure with a preserved ejection fraction. The development of heart failure with a preserved ejection fraction is likely mediated through increased left ventricular (LV) stiffness, a consequence of sedentary aging. In a prospective, parallel group, randomized controlled trial, we examined the effect of 2 years of supervised high-intensity exercise training on LV stiffness. METHODS: Sixty-one (48% male) healthy, sedentary, middle-aged participants (53±5 years) were randomly assigned to either 2 years of exercise training (n=34) or attention control (control; n=27). Right heart catheterization and 3-dimensional echocardiography were performed with preload manipulations to define LV end-diastolic pressure-volume relationships and Frank-Starling curves. LV stiffness was calculated by curve fit of the diastolic pressure-volume curve. Maximal oxygen uptake (Vo2max) was measured to quantify changes in fitness. RESULTS: Fifty-three participants completed the study. Adherence to prescribed exercise sessions was 88±11%. Vo2max increased by 18% (exercise training: pre 29.0±4.8 to post 34.4±6.4; control: pre 29.5±5.3 to post 28.7±5.4, group×time P<0.001) and LV stiffness was reduced (right/downward shift in the end-diastolic pressure-volume relationships; preexercise training stiffness constant 0.072±0.037 to postexercise training 0.051±0.0268, P=0.0018), whereas there was no change in controls (group×time P<0.001; pre stiffness constant 0.0635±0.026 to post 0.062±0.031, P=0.83). Exercise increased LV end-diastolic volume (group×time P<0.001), whereas pulmonary capillary wedge pressure was unchanged, providing greater stroke volume for any given filling pressure (loading×group×time P=0.007). CONCLUSIONS: In previously sedentary healthy middle-aged adults, 2 years of exercise training improved maximal oxygen uptake and decreased cardiac stiffness. Regular exercise training may provide protection against the future risk of heart failure with a preserved ejection fraction by preventing the increase in cardiac stiffness attributable to sedentary aging. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT02039154.

The Cardiovascular Physiology of Sports and Exercise.

Athletes represent the extremes of human performance. Many of their remarkable abilities stem from a cardiovascular system that has adapted to meet the metabolic needs of exercising muscle. A large and compliant heart is a hallmark feature of athletes who engage in highly aerobic events. Despite high fitness levels, athletes may present with symptoms that limit performance. Understanding and dissecting these limitations requires a strong background in sports science and the factors that determine sports capabilities. This article reviews the basic principles of exercise physiology, cardiovascular adaptations unique to the "athlete's heart," and the utility of exercise testing in athletes.

C-reactive protein and erythrocyte sedimentation rate discordance: frequency and causes in adults.

C-reactive protein (CRP) levels and the erythrocyte sedimentation rate (ESR) are widely used tests of inflammation that sometimes show opposite results. We performed a retrospective cohort study to clarify the frequency and causes of CRP/ESR discordance in adults. Between January and December of 2011, the laboratories of Texas Health Presbyterian Hospital performed 2150 paired CRP/ESR measurements in 1753 patients, 1731 of whom were nonpregnant adults aged ≥ 18 years. Initial CRP and ESR results for each patient were divided into quartiles. CRP/ESR discordance, predefined as results differing by 2 or 3 quartiles, occurred in 212 patients (12%), 105 of whom had high CRP/low ESR discordance (6%) and 107 of whom had high ESR/low CRP discordance (6%). The 212 patients in the CRP/ESR-discordant group (128 women and 84 men) were subdivided into 1 of 6 diagnostic categories, and the causes of discordances were compared. The high CRP/low ESR-discordant group had more patients with infections than the high ESR/low CRP-discordant group (P = 0.001), particularly infections in the urinary tract (P = 0.03), gastrointestinal tract (P = 0.001), lungs (P = 0.005), and bloodstream (P = 0.03). However, they had fewer bone and joint infections than the high ESR/low CRP-discordant group (P = 0.001). Connective tissue diseases, such as systemic lupus erythematosus, were less common in the high CRP/low ESR-discordant group than in the high ESR/low CRP-discordant group (P = 0.001). Ischemic strokes or transient ischemic attacks almost invariably occurred in the high ESR/low CRP-discordant group (P = 0.001), whereas myocardial infarction or venous thromboembolism was limited to the high CRP/low ESR-discordant group (P = 0.001). Our findings provide information to physicians who order these 2 tests together and receive discordant results, which occurs in approximately 1 in 8 patients.