Acute physiological responses to high-intensity interval exercise in patients with coronary artery disease.

PURPOSE: Time spent closer to maximal effort during exercise is a potent stimulus for cardiorespiratory adaptations. The primary purpose was to determine which high-intensity interval exercise (HIIE) protocol provided the greatest physiological stimulus by comparing time spent ≥ 90% peak oxygen consumption (V̇O2peak) and heart rate reserve (HRR) in patients with coronary artery disease (CAD) in response to 3 HIIE protocols and the exercise standard of care, moderate-intensity continuous exercise (MICE). A secondary purpose was to assess protocol preference. METHODS: Fifteen patients with CAD (6 females, 67 ± 6 years) underwent measurements of V̇O2 and heart rate during MICE and three HIIE protocols all performed on a treadmill. The HIIE protocols included one with long intervals (4 × 4-min), short intervals (10 × 1-min), and an adapted version of the 4 × 4 [Toronto Rehabilitation Institute Protocol, (TRIP)]. Time spent ≥ 90% V̇O2peak and HRR were compared. RESULTS: Time spent ≥ 90% V̇O2peak was higher during 4 × 4 (6.3 ± 8.4 min) vs. MICE (1.7 ± 3.9 min; P = 0.001), while time spent ≥ 90% HRR was higher during 4 × 4 (6.0 ± 5.3 min) vs. MICE (0.1 ± 0.2 min; P < 0.001) and 10 × 1 (0.7 ± 0.8 min; P = 0.016). TRIP had similar responses as 10 × 1 and MICE. The 10 × 1 was the most preferred protocol and the 4 × 4 was the least preferred protocol. CONCLUSION: Longer intervals (4 × 4) provided the greatest physiological stimulus compared to the exercise standard of care and shorter intervals. However, this protocol was least preferred which may impact exercise adherence. Although the physiological stimulus is important to maximize training adaptations, exercise preferences and attitudes should be considered.

Differential negative effects of acute exhaustive swim exercise on the right ventricle are associated with disproportionate hemodynamic loading.

Acute exhaustive endurance exercise can differentially impact the right ventricle (RV) versus the left ventricle (LV). However, the hemodynamic basis for these differences and its impact on postexercise recovery remain unclear. Therefore, we assessed cardiac structure and function along with hemodynamic properties of mice subjected to single bouts (216 ± 8 min) of exhaustive swimming (ES). One-hour after ES, LVs displayed mild diastolic impairment compared with that in sedentary (SED) mice. Following dobutamine administration to assess functional reserve, diastolic and systolic function were slightly impaired. Twenty-four hours after ES, LV function was largely indistinguishable from that in SED. By contrast, 1-h post swim, RVs showed pronounced impairment of diastolic and systolic function with and without dobutamine, which persisted 24 h later. The degree of RV impairment correlated with the time-to-exhaustion. To identify hemodynamic factors mediating chamber-specific responses to ES, LV pressure was recorded during swimming. Swimming initiated immediate increases in heart rates (HRs), systolic pressure, dP/dtmax and -dP/dtmin, which remained stable for ∼45 min. LV end-diastolic pressures (LVEDP) increased to ≥45 mmHg during the first 10 min and subsequently declined. After 45 min, HR and -dP/dtmin declined, which correlated with gradual elevations in LVEDP (to ∼45 mmHg) as mice approached exhaustion. All parameters rapidly normalized postexercise. Consistent with human studies, our findings demonstrate a disproportionate negative impact of acute exhaustive exercise on RVs that persisted for at least 24 h. We speculate that the differential effects of exhaustive exercise on the ventricles arise from a ∼2-fold greater hemodynamic load in the RV than in LV originating from profound elevations in LVEDPs as mice approach exhaustion.NEW & NOTEWORTHY Acute exhaustive exercise differentially impacts the right ventricle (RV) versus left ventricle (LV), yet the underlying hemodynamic basis remains unclear. Using pressure-volume analyses and pressure-telemetry implantation in mice, we confirmed a marked disproportionate and persistent negative impact of exhaustive exercise on the RV. These differences in responses of the ventricles to exhaustive exercise are of clinical relevance, reflecting ∼2-fold greater hemodynamic RV loads versus LVs arising from massive (∼45 mmHg) increases in LV end-diastolic pressures at exhaustion.

Exercise in hypertrophic cardiomyopathy: restrict or rethink.

The detailed physiological consequences of aerobic training, in patients with hypertrophic cardiomyopathy (HCM), are not well understood. In athletes and nonathletes with HCM, there are two hypothetical concerns with respect to exercise: exercise-related worsening of the phenotype (e.g., promoting hypertrophy and fibrosis) and/or triggering of arrhythmia. The former concern is unproven and animal studies suggest an opposite effect, where exercise has been shown to be protective. The main reason for exercise restriction in HCM is fear of exercise-induced arrhythmia. Although the safety of sports in HCM has been reviewed, even more recent data suggest a substantially lower risk for sudden cardiac death (SCD) in HCM than previously thought, and there is an ongoing debate about restrictions of exercise imposed on individuals with HCM. This review outlines the pathophysiology of HCM, the impact of acute and chronic exercise (and variations of exercise intensity, modality, and athletic phenotype) in HCM including changes in autonomic function, blood pressure, cardiac dimensions and function, and cardiac output, and the underlying mechanisms that may trigger exercise-induced lethal arrhythmias. It provides a critical evaluation of the evidence regarding risk of SCD in athletes and the potential benefits of targeted exercise prescription in adults with HCM. Finally, it provides considerations for personalized recommendations for sports participation based on the available data.

Cardiac remodeling in middle-aged endurance athletes: relation between signal-averaged electrocardiogram and LV mass.

The relationship between structural and electrical remodeling in the heart, particularly after long-standing endurance training, remains unclear. Signal-averaged electrocardiogram (SAECG) may provide a more sensitive method to evaluate cardiac remodeling than a 12-lead electrocardiogram (ECG). Accurate measures of electrical function (SAECG filtered QRS duration (fQRSd) and late potentials (LP) and left-ventricular (LV) mass (cardiac magnetic resonance, CMR) can allow an assessment of structural remodeling and QRS prolongation. Endurance athletes (45-65 yr old, >10 yr of endurance sport), screened to exclude cardiac disease, had standardized 12-lead ECG, SAECG, resting echocardiogram (ECHO), and CMR performed. SAECG fQRSd was correlated with QRS duration on the 12-lead ECG, and ECHO and CMR-derived LV mass. Participants (n = 82, 67% male, mean age: 54 ± 6 yr, mean V̇o2max: 50 ± 7 mL/kg/min) had a CMR-derived LV mass of 118 ± 28 g/m2 and a fQRSd of 112 ± 8 ms (46% had abnormal fQRSd (>114 ms), and 51% met clinical threshold for abnormal SAECG). fQRSd was positively correlated with the 12-lead ECG QRS duration (r = 0.83), ECHO-derived LV mass (r = 0.60), CMR-derived LV mass (r = 0.58) and LV end-diastolic volume (r = 0.63, P < 0.001 for all). fQRSd had higher correlations with ECHO and CMR-derived LV mass than 12-lead ECG (P < 0.0008 and P < 0.0005, respectively). In conclusion, in a healthy cohort of middle-aged endurance athletes, the SAECG is often abnormal by conventional criteria, and is correlated with structural remodeling, but CMR evaluation does not indicate pathologic structural remodeling. SAECG fQRSd is superior to the 12-lead ECG for the electrocardiographic evaluation of LV mass.NEW & NOTEWORTHY Study findings indicate that a positive correlation exists between electrical (SAECG fQRSd) and structural indices (LV mass) in middle-aged endurance athletes with normal physiological LV adaptation, in the absence of known cardiac pathology. SAECG fQRSd may also provide an alternative, superior method for identifying increased LV mass compared to other 12-lead ECG criteria.

Indexes of aortic wave reflection are not augmented in estrogen-deficient physically active premenopausal women.

BACKGROUND: Hypoestrogenemia due to menopause is associated with increased cardiovascular disease risk, in part due to elevated indexes of aortic wave reflection (AWRI) and central (aortic) blood pressure. We sought to investigate whether AWRI and central blood pressure are also augmented in hypoestrogenic exercise-trained premenopausal women with functional hypothalamic amenorrhea (ExFHA). METHODS: In age- (pooled mean ± SEM, 24 ± 1 years), BMI- (21 ± 1 kg/m2 ), and cardiorespiratory fitness-matched (45 ± 2 ml/kg/min) eumenorrheic ovulatory (ExOv; n = 11) and ExFHA women (n = 10), we assessed aortic blood pressure and waveform characteristics (augmentation index and wave reflection amplitude) obtained from radial pressure waves (applanation tonometry). Doppler ultrasound determined cardiac output (CO) and total peripheral resistance (TPR). Measures were recorded before and 1 hour after 45 minutes of moderate intensity exercise to determine the influence of exercise-induced increases in nitric oxide. RESULTS: Pre-exercise, AIx75, central systolic BP (SBPc), and CO were lower (P < .05) and TPR higher (P < .05) in ExFHA. Post-exercise, AIx75 was unchanged (P > .05) in ExFHA but was lowered (P < .05) in ExOv. Both groups demonstrated increased CO, and lowered SBPc and TPR, yet TPR remained higher (P < .05), and CO and SBPc lower (P < .05) in ExFHA. CONCLUSIONS: Despite hypoestrogenemia, functional compliance of the central arteries and central BP is not augmented, yet TPR is higher, in ExFHA versus ExOv. An acute bout of dynamic exercise did not alter AIx75 in ExFHA, suggesting blunted vascular responsiveness to exercise-induced increases in nitric oxide, possibly due to augmented vascular tone. These findings have relevance in understanding the vascular consequences of hypoestrogenemia during the premenopausal years.

Pulmonary hemodynamic and right ventricular responses to brief and prolonged exercise in middle-aged endurance athletes.

Right ventricular (RV) function is closely coupled to pulmonary arterial (PA) hemodynamics and is believed to decline with prolonged exercise. A linear pressure-flow relationship is thought to exist between PA pressures and increasing exercise intensity in athletes, yet a paucity of directly measured pulmonary hemodynamic data exists supporting this contention. We sought to describe the PA pressure, PA wedge pressure (PAWP), and RV functional responses to brief and prolonged exercise in endurance-trained athletes. Twenty-one healthy athletes (54 ± 5 yr) underwent right heart catheterization to assess pulmonary hemodynamics during graded, submaximal exercise. Measurements were made at rest and during three stages of steady-state, semiupright cycle ergometry at heart rates of 100 beats/min (EX1), 130 beats/min (EX2), and 150 beats/min (EX3). Five athletes completed an additional 34 min at 130 beats/min for a total exercise time of 60 min [prolonged exercise (PLG)]. PA pressures and PAWP increased significantly at EX1 without a further rise at EX2, EX3, or PLG. PAWP adjusted for absolute work rate demonstrated a significant decline as exercise intensity increased from EX1 to EX2. The resistance compliance time constant decreased at EX1 without further changes at EX2, EX3, and prolonged exercise. RV function did not decline during PLG. After an initial rise in PA pressure and PAWP during early, nonsteady-state exercise, values remained constant despite increases in exercise intensity and duration. These data indicate that in healthy, middle-aged endurance-trained athletes, the PA and pulmonary venous/left atrial compartments rapidly accommodate high conduit flows produced during intensive and prolonged exercise while maintaining RV function. NEW & NOTEWORTHY The right ventricular (RV)-pulmonary arterial (PA) circulatory unit has not been well studied during prolonged exercise, and this study provides an ecological approach that reflects a typical bout of endurance training integrating a transition from rest to exercise with successive increases in intensity, progressing to steady-state, sustained exercise. We demonstrated a remarkably constant response of the PA and PA wedge pressure during incremental, steady-state exercise and that no changes occur in pulmonary pressures throughout prolonged exercise, concomitant to a preservation of RV performance.

The relationship of pulmonary vascular resistance and compliance to pulmonary artery wedge pressure during submaximal exercise in healthy older adults.

KEY POINTS: A consistent inverse hyperbolic relationship has been observed between pulmonary vascular resistance and compliance, although changes in pulmonary artery wedge pressure (PAWP) may modify this relationship. This relationship predicts that pulmonary artery systolic, diastolic and mean pressure maintain a consistent relationship relative to the PAWP. We show that, in healthy exercising human adults, both pulmonary vascular resistance and compliance decrease in relation to exercise-associated increases in PAWP. Pulmonary artery systolic, diastolic and mean pressures maintain a consistent relationship with one another, increasing linearly with increasing PAWP. Increases in PAWP in the setting of exercise are directly related to a decrease in pulmonary vascular compliance, despite small decreases in pulmonary vascular resistance, thereby increasing the pulsatile afterload to the right ventricle. ABSTRACT: The resistive and pulsatile components of right ventricular afterload (pulmonary vascular resistance, Rp; compliance, Cp) are related by an inverse hyperbolic function, expressed as their product known as RpCp-time. The RpCp-time exhibits a narrow range, although it may be altered by the pulmonary artery wedge pressure (PAWP). Identifying the determinants of RpCp-time should improve our understanding of the physiological behaviour of pulmonary arterial systolic (PASP), diastolic (PADP) and mean (mPAP) pressures in response to perturbations. We examined the effect of exercise in 28 healthy non-athletic adults (55 ± 6 years) who underwent right heart catheterization to assess haemodynamics and calculate Rp and Cp. Measurements were made at rest and during two consecutive 8-10 min stages of cycle ergometry, at targeted heart-rates of 100 beats min(-1) (Light) and 120 beats min(-1) (Moderate). Cardiac output increased progressively during exercise. PASP, PADP, mPAP and PAWP increased for Light exercise, without any further rise for Moderate exercise. RpCp-time decreased for Light exercise (0.39 ± 0.08 to 0.25 ± 0.08, P < 0.001) without any further change for Moderate exercise, and the decrease in RpCp-time was related to changes in PAWP (r(2)  = 0.26, P < 0.001). Changes in PASP (r(2)  = 0.43, P < 0.001), PADP (r(2)  = 0.47, P < 0.001) and mPAP (r(2)  = 0.50, P < 0.001) were linearly correlated with changes in PAWP, although they were not significantly related to changes in cardiac output. In healthy adults, exercise is associated with decreases in Cp and a resultant decline in RpCp-time, indicating increased pulsatile right ventricular afterload. Changes in RpCp-time, PASP, PADP and mPAP were systematically related to increases in PAWP.

Augmented vagal heart rate modulation in active hypoestrogenic pre-menopausal women with functional hypothalamic amenorrhoea.

Compared with eumenorrhoeic women, exercise-trained women with functional hypothalamic amenorrhoea (ExFHA) exhibit low heart rates (HRs) and absent reflex renin-angiotensin-system activation and augmentation of their muscle sympathetic nerve response to orthostatic stress. To test the hypothesis that their autonomic HR modulation is altered concurrently, three age-matched (pooled mean, 24 ± 1 years; mean ± S.E.M.) groups of women were studied: active with either FHA (ExFHA; n=11) or eumenorrhoeic cycles (ExOv; n=17) and sedentary with eumenorrhoeic cycles (SedOv; n=17). Blood pressure (BP), HR and HR variability (HRV) in the frequency domain were determined during both supine rest and graded lower body negative pressure (LBNP; -10, -20 and -40 mmHg). Very low (VLF), low (LF) and high (HF) frequency power spectra (ms(2)) were determined and, owing to skewness, log10-transformed. LF/HF ratio and total power (VLF + LF + HF) were calculated. At baseline, HR and systolic BP (SBP) were lower (P<0.05) and HF and total power were higher (P<0.05) in ExFHA than in eumenorrhoeic women. In all groups, LBNP decreased (P<0.05) SBP, HF and total power and increased (P<0.05) HR and LF/HF ratio. However, HF and total power remained higher (P<0.05) and HR, SBP and LF/HF ratio remained lower (P<0.05) in ExFHA than in eumenorrhoeic women, in whom measures did not differ (P>0.05). At each stage, HR correlated inversely (P<0.05) with HF. In conclusion, ExFHA women demonstrate augmented vagal yet unchanged sympathetic HR modulation, both at rest and during orthostatic stress. Although the role of oestrogen deficiency is unclear, these findings are in contrast with studies reporting decreased HRV in hypoestrogenic post-menopausal women.

Short-term high-intensity interval and continuous moderate-intensity training improve maximal aerobic power and diastolic filling during exercise.

PURPOSE: This study examined the effects of short-term high-intensity interval training (HIT) and continuous moderate-intensity training (CMT) on cardiac function in young, healthy men. METHODS: Sixteen previously untrained men (mean age of 25.1 ± 4.1 years) were randomly assigned to HIT and CMT (n = 8 each) and assessed before and after six sessions over a 12-day training period. HIT consisted of 8-12 intervals of cycling for 60 s at 95-100% of pre-training maximal aerobic power (VO(2max)), interspersed by 75 s of cycling at 10% VO(2max). CMT involved 90-120 min of cycling at 65% pre-training VO(2max). Left ventricular (LV) function was determined at rest and during submaximal exercise (heart rate ~105 bpm) using two-dimensional and Doppler echocardiography. RESULTS: Training resulted in increased calculated plasma volume (PV) in both groups, accompanied by improved VO(2max) in HIT (HIT: from 39.5 ± 7.1 to 43.9 ± 5.5 mL kg(-1) min(-1); CMT: from 39.9 ± 5.9 to 41.7 ± 5.3 mL kg(-1) min(-1); P < 0.001). Resting LV function was not altered. However, increased exercise stroke volume (P = 0.02) and cardiac output (P = 0.02) were observed, secondary to increases in end-diastolic volume (P < 0.001). Numerous Doppler and speckle tracking indices of diastolic function were similarly enhanced during exercise in both training groups and were related to changes in PV. CONCLUSION: Short-term HIT and CMT elicit rapid improvements in VO2max and LV filling without global changes in cardiac performance at rest.

Left atrial functional changes following short-term exercise training.

BACKGROUND: Exercise-induced adaptations of the human atria remain understudied, particularly early in the training process. We examined the effects of short-term high-intensity interval training (HIT) and continuous moderate-intensity training (CMT) on left atrial (LA) systolic and diastolic function, relative to left ventricular (LV) function in young, healthy men, by speckle tracking echocardiography (STE). METHODS: Fourteen untrained men (mean age = 25 ± 4 years) were randomized to HIT or CMT, and assessed before and after six training sessions over a 12-day period. HIT included 8-12 intervals of cycling for 60 s at 95-100% of maximal aerobic power (VO2MAX), interspersed by 75 s of cycling at 10 % VO2MAX. CMT consisted of 90-120 min of cycling at 65% VO2MAX. RESULTS: VO2MAX increased following HIT and CMT by 11.5 and 5.5%, respectively (p < 0.05). Calculated plasma volume expanded 11 % following HIT and 10% following CMT (p < 0.005). Resting LV volumes and ejection fraction were unaltered following training. Peak atrial longitudinal strain increased following HIT (41.8 ± 5.2%-47.1 ± 3.7%, p < 0.01) and CMT (38.5 ± 4.6%-41.7 ± 6.0%, p < 0.01). Atrial systolic strain rate increased following HIT (1.6 ± 0.2%/s-2.0 ± 0.3%/s, p < 0.01) and CMT (1.6 ± 0.2%/s-1.9 ± 0.2%/s, p < 0.01). CONCLUSIONS: LA function assessed by STE improves rapidly during short-term intensive exercise training.

Left atrial reservoir pressure-volume relations during exercise in healthy older adults.

The left atrium (LA) mediates cardiopulmonary interactions. During ventricular systole, the LA functions as a compliant reservoir that is coupled to the left ventricle (LV) and offloads volume from the pulmonary vasculature. We aimed to describe LA reservoir function using phasic relationships between pulmonary artery wedge pressure (PAWP) and LA volume events. We included healthy adults (7 M/6 F, 56 ± 8 yr) who were studied at rest and during semirecumbent cycle ergometry at a target of 100 beats/min heart rate. Right heart catheterization was performed to record the PAWP and two-dimensional (2-D) echocardiography was used to measure LA and LV volumes. We manually measured A-wave, x-trough, V-wave, and y-trough PAWP beat-by-beat, as well as minimal, maximal, and precontraction biplane LA volumes. Heart rate increased by 40 ± 7 beats/min with exercise; stroke volume and cardiac output also rose. Although all phasic PAWP measurements increased with exercise, the x-V pressure pulse during LA filling doubled from 4 ± 2 to 8 ± 4 mmHg (P = 0.001). LA minimal volume was unchanged but maximal volume increased from 39 ± 9 to 48 ± 9 mL (P < 0.001) with exercise, and so reservoir volume increased from 24 ± 5 to 32 ± 8 mL (P < 0.001). As such, calculated LA compliance decreased from 6.8 ± 3.4 to 4.8 ± 2.6 mL/mmHg (P = 0.029). The product of V-wave PAWP and LA maximal volume, a surrogate for LA wall stress, increased from 486 ± 193 to 953 ± 457 mmHg·mL (P < 0.001). In healthy older adults during submaximal exercise, the PAWP waveform shifts upward and its amplitude widens, LA filling increases, LA compliance decreases modestly, and LA wall stress may augment substantially.NEW & NOTEWORTHY We combined invasive estimates of left atrial pressure with noninvasive left atrial volume measurements made at rest and during exercise in healthy humans. Left atrial pressure and volume both increased with exercise, though the pressure increase was relatively greater, and calculated compliance decreased modestly while estimated peak wall stress nearly doubled. Our results demonstrate left atrial loading during exercise in healthy older adults and provide insight into how the left atrium mediates cardiopulmonary interactions.

The effect of chronic exercise training and acute exercise on power spectral analysis of heart rate variability.

Moderate to vigorous physical activity performed regularly is cardioprotective and reduces all-cause mortality, concomitant with increased resting heart rate variability (HRV). However, there are contradictory reports regarding the effects of chronic and acute exercise on nocturnal HRV in those performing exercise well-beyond physical activity guidelines. Therefore, the purpose of this study was to compare the power spectral analysis components of HRV in middle-aged endurance athletes (EA) and recreationally active individuals (REC) and explore acute exercise effects in EA. A total of 119 EA (52, 49-57 years) and 32 REC (56, 52-60 years) were recruited to complete 24 h Holter monitoring (GE SEER 1000) in the absence of exercise. Fifty one EA (52, 49-57 years) then underwent 24 h Holter monitoring following an intense bout of endurance exercise. Power spectral HRV analysis was completed hourly and averaged to quantify morning (1000-1200 h), evening (1900-2100 h), and nocturnal (0200-0400 h) HRV. EA had greater very low frequency (VLF) and low frequency (LF) (both p < 0.001) compared to REC. LF/high frequency (HF) was greater in EA at 0200-0400 h (p = 0.04). Among all participants, the change in HR and HF from 1000-1200 to 0200-0400 h was negatively correlated (r = -0.47, p < 0.001). Following acute exercise in EA, only nocturnal HRV was assessed. VLF (p < 0.001) and HF (p = 0.008) decreased, while LF/HF increased (p = 0.02). These results suggest that in EA, both long-term and acute exercises increase nocturnal sympathovagal activity through an increase in LF and decrease in HF, respectively. Further work is required to understand the mechanism underlying reduced nocturnal HRV in middle-aged EA and the long-term health implications.

Atrial fibrillation in middle-aged athletes: Impact on left atrial, ventricular and exercise performance.

High volume endurance training may increase the risk of paroxysmal atrial fibrillation (AF) in middle-aged athletes. Limited data are available describing the cardiovascular phenotype of middle-aged endurance athletes, or the impact of AF on atrial function and exercise performance performed in sinus rhythm. The purpose of this study was to characterize LA phasic function at rest and during exercise in athletes with paroxysmal AF, and to determine its impact on exercise performance. Fifteen endurance trained males (EA) (56 ± 5 years) without AF and 14 endurance trained males with paroxysmal AF (EA-AF) (55 ± 8 years) underwent echocardiography during cycle-ergometry at light and moderate intensities. Resting LA maximal volumes were similar between EA and EA-AF (30 ± 4 vs. 29 ± 8 ml/m2, p = 0.50), and there were no differences in atrial electromechanical delay (AEMD). During moderate intensity exercise, EA-AF had reduced LA conduit (30 ± 6 vs. 40 ± 5 ml/m2, p = 0.002) LA booster volumes (17 ± 5 vs. 21 ± 4 ml/m2, p = 0.021), and reduced LV stroke volumes (100 ± 12 vs. 117 ± 16 ml, p = 0.007). These results demonstrate that exercise testing in athletes with AF unmasks evidence of adverse functional cardiac remodelling that may contribute to impaired exercise performance. It is unclear whether these functional alterations are the consequence of AF. Reductions in LA conduit volume, LA booster volume, and LV stroke volume during exercise may be helpful in clinical management and distinguishing pathologic from physiologic remodelling.

Exercise-Dependent Modulation of Immunological Response Pathways in Endurance Athletes With and Without Atrial Fibrillation.

BACKGROUND: Atrial fibrillation (AF) is a common arrhythmia characterized by uncoordinated atrial electrical activity. Lone AF occurs in the absence of traditional risk factors and is frequently observed in male endurance athletes, who face a 2- to 5-fold higher risk of AF compared with healthy, moderately active males. Our understanding of how endurance exercise contributes to the pathophysiology of lone AF remains limited. This study aimed to characterize the circulating protein fluctuations during high-intensity exercise as well as explore potential biomarkers of exercise-associated AF. METHODS AND RESULTS: A prospective cohort of 12 male endurance cyclists between the ages of 40 and 65 years, 6 of whom had a history of exercise-associated AF, were recruited to participate using a convenience sampling method. The circulating proteome was subsequently analyzed using multiplex immunoassays and aptamer-based proteomics before, during, and after an acute high-intensity endurance exercise bout to assess temporality and identify potential markers of AF. The endurance exercise bout resulted in significant alterations to proteins involved in immune modulation (eg, growth/differentiation factor 15), skeletal muscle metabolism (eg, α-actinin-2), cell death (eg, histones), and inflammation (eg, interleukin-6). Subjects with AF differed from those without, displaying modulation of proteins previously known to have associations with incident AF (eg, C-reactive protein, insulin-like growth factor-1, and angiopoietin-2), and also with proteins having no previous association (eg, tapasin-related protein and α2-Heremans-Schmid glycoprotein). CONCLUSIONS: These findings provide insights into the proteomic response to acute intense exercise, provide mechanistic insights into the pathophysiology behind AF in athletes, and identify targets for future study and validation.

Atrial structure and function in middle-aged, physically-active males and females: A cardiac magnetic resonance study.

Recent studies have reported on an association between endurance sport, atrial enlargement and the development of lone atrial fibrillation in younger, male cohorts. The atrial morphology and function of middle-aged, physically-active males and females have not been well studied. We hypothesized that middle-aged males would demonstrate larger left atrium (LA) and right atrium (RA) volumes compared to females, but atrial function would not differ. LA and RA volume and function were evaluated at rest in healthy adults, using a standardized 3.0Tesla cardiac magnetic resonance protocol. Physical activity, medical history, and maximal oxygen consumption ( V ˙ O 2 peak ) were also assessed. Physically-active, middle-aged men (n = 60; 54 ± 5 years old) and women (n = 30; 54 ± 5 years old) completed this study. Males had a higher body mass index, systolic blood pressure, and V ˙ O 2 peak than females (p < .05 for all), despite similar reported physical activity levels. Absolute and BSA and height-indexed LA and RA maximum volumes were higher in males relative to females, despite no differences in ejection fractions (p < .05 for all). In multivariable regression, male sex p < .001) and V ˙ O 2 peak (p = .004) were predictors of LA volume (model R2  = 0.252), whereas V ˙ O 2 peak (p < .001), male sex (p = .03), and RV EF (p < .05) were predictors of RA volume (model R2  = 0.377). While middle-aged males exhibited larger atrial volumes relative to females, larger, prospective studies are needed to explore the magnitude of physiologic atrial remodeling and functional adaptations in relation to phenotypic factors.

A Novel Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) Biomarker-Anti-DSG2-Is Absent in Athletes With Right Ventricular Enlargement.

BACKGROUND: Right ventricular (RV) enlargement is common in endurance athletes. It is usually considered to be physiological, but it is possible that this remodelling is adverse, manifesting as a variant of arrhythmogenic right ventricular cardiomyopathy (ARVC), termed "exercise-induced ARVC." A novel biomarker (anti-desmoglein-2 [anti-DSG2] antibody) has been shown to indicate ARVC with high sensitivity and specificity and may be an immune response to breakdown of RV desmosomes. It is not known if this antibody is present in endurance athletes with RV enlargement but without clinical ARVC. METHODS: Middle-aged, healthy endurance athletes with RV enlargement on cardiac magnetic resonance imaging had serum tested for the presence of the anti-DSG2 antibody. All athletes also underwent Holter monitoring, a signal-averaged electrocardiogram, and an exercise questionnaire. RESULTS: A total of 30 athletes (20 men, 10 women, average age 53 ± 6 years) were enrolled in this study with median RV end-diastolic volume indexes of 117.1 mL/m2 (men) and 103.5 mL/m2 (women). Athletes demonstrated other characteristics of endurance training, including depolarization abnormalities (abnormal signal-averaged electrocardiogram, 19 of 30) and incomplete right bundle branch block (8 of 30). No athlete met criteria for definite or probable ARVC. None of the athletes tested positive for anti-DSG2 antibody. CONCLUSIONS: Among middle-aged endurance athletes with RV enlargement, the anti-DSG2 antibody, a suggested ARVC biomarker, is absent in all and is highly specific in this cohort (95% confidence interval, 88%-100%). Despite significant RV remodelling, these athletes did not express a previously characterized pathologic biomarker known to be sensitive for ARVC. Physiological exercise remodelling and pathologic ARVC remodelling are likely separate processes.

INTRODUCTION: L'augmentation du volume du ventricule droit (VD) est fréquente chez les sportifs d'endurance. On considère habituellement que ce remodelage est physiologique, mais il est possible qu'il soit indésirable, c'est-à-dire qu'il révèle une variante de la cardiomyopathie arythmogène du ventricule droit (CAVD), appelée « CAVD induite par l'exercice ¼. Il a été démontré qu'un nouveau biomarqueur (l'anticorps anti-desmogléine 2 [anti-DSG2]) présente une sensibilité et une spécificité élevées pour dépister la CAVD et qu'il peut être une réponse immunitaire à la dégradation des desmosomes du VD. On ne sait pas si cet anticorps est présent chez les sportifs d'endurance qui ont une augmentation du volume du VD, sans CAVD clinique. MÉTHODES: Les sportifs d'endurance d'âge moyen en bonne santé qui ont une augmentation du volume du VD à l'imagerie cardiaque par résonance magnétique ont subi une épreuve pour vérifier la présence de l'anticorps anti-DSG2 dans le sérum. Tous les athlètes ont également eu une surveillance par la méthode de Holter, un électrocardiogramme à signaux moyennés et un questionnaire sur l'exercice. RÉSULTATS: Nous avons inscrit à cette étude un total de 30 athlètes (20 hommes, 10 femmes, âge moyen de 53 ± 6 ans) dont les indices volumiques télédiastoliques médians du VD des hommes étaient de 117,1 ml/m2 et des femmes, de 103,5 ml/m2. Les athlètes ont démontré d'autres caractéristiques de l'entraînement en endurance, notamment des anomalies de la dépolarisation (électrocardiogramme à signaux moyennés anormal, 19 sur 30) et un bloc de branche droit incomplet (8 sur 30). Aucun athlète n'a répondu aux critères de CAVD définie ou probable. Aucun des athlètes n'a eu de résultats positifs au test de dépistage des anticorps anti-DSG2. CONCLUSIONS: Chez tous les sportifs d'endurance d'âge moyen qui ont une augmentation du volume du VD, l'anticorps anti-DSG2, un biomarqueur proposé pour dépister la CAVD, est absent et est hautement spécifique dans cette cohorte (intervalle de confiance à 95 %, 88 %-100 %). En dépit d'un remodelage important du VD, les athlètes n'ont pas exprimé le biomarqueur pathologique, auparavant caractérisé, connu pour être sensible au dépistage de la CAVD. Le remodelage physiologique induit par l'exercice et le remodelage pathologique associé à la CAVD sont des processus probablement distincts.

COVID-19-Myocarditis and Return to Play: Reflections and Recommendations From a Canadian Working Group.

The COVID-19-related pandemic has resulted in profound health, financial, and societal impacts. Organized sporting events, from recreational to the Olympic level, have been cancelled to both mitigate the spread of COVID-19 and protect athletes and highly active individuals from potential acute and long-term infection-associated harms. COVID-19 infection has been associated with increased cardiac morbidity and mortality. Myocarditis and late gadolinium enhancement as a result of COVID-19 infection have been confirmed. Correspondingly, myocarditis has been implicated in sudden cardiac death of athletes. A pragmatic approach is required to guide those who care for athletes and highly active persons with COVID-19 infection. Members of the Community and Athletic Cardiovascular Health Network (CATCHNet) and the writing group for the Canadian Cardiovascular Society/Canadian Heart Rhythm Society Joint Position Statement on the Cardiovascular Screening of Competitive Athletes recommend that highly active persons with suspected or confirmed COVID-19 infection refrain from exercise for 7 days after resolution of viral symptoms before gradual return to exercise. We do not recommend routine troponin testing, resting 12-lead electrocardiography, echocardiography, or cardiac magnetic resonance imaging before return to play. However, medical assessment including history and physical examination with consideration of resting electrocardiography and troponin can be considered in the athlete manifesting new active cardiac symptoms or a marked reduction in fitness. If concerning abnormalities are encountered at the initial medical assessment, then referral to a cardiologist who cares for athletes is recommended.

Heart rate variability and recovery following maximal exercise in endurance athletes and physically active individuals.

The purpose of this study was to determine potential adverse cardiac effects of chronic endurance training by comparing sympathovagal modulation via heart rate variability (HRV) and heart rate recovery (HRR) in middle-aged endurance athletes (EA) and physically active individuals (PA) following maximal exercise. Thirty-six (age, 53 ± 5 years) EA and 19 (age, 56 ± 5 years) PA were recruited to complete a 2-week exercise diary and graded exercise to exhaustion. Time domain and power spectral HRV analyses were completed on recorded R-R intervals. EA had a greater HRR slope following exercise (95% confidence interval, 0.0134-0.0138 vs. 0.0101-0.0104 beats/s; p < 0.001). While EA had greater HRR at 1-5 min after exercise (all p < 0.01), PA and EA did not differ when expressed as a percentage of baseline heart rate (130 ± 19 vs. 139 ± 19; p = 0.2). Root mean square of successive differences in R-R intervals (rest and immediately after exercise) were elevated in EA (p < 0.05). Low-frequency (LF) and high-frequency (HF) spectral components were nonsignificantly elevated after exercise (p = 0.045-0.147) in EA while LF/HF was not different (p = 0.529-0.986). This data suggests greater HRR in EA may arise in part due to a lower resting HR. While nonsignificant elevations in HF and LF in EA produces a LF/HF similar to PA, absolute spectral component modulation differed. These observations require further exploration. Novelty Acute effects of exercise on HRV in EA compared with a relevant control group, PA, are unknown. EA had greater HRR and nonsignificant elevations in LF and HF compared with PA, yet LF/HF was not different. Future work should explore the implications of this observation.

Left Ventricular Fibrosis in Middle-Age Athletes and Physically Active Adults.

INTRODUCTION: Cardiac magnetic resonance (CMR) late gadolinium enhancement (LGE) and T1 mapping techniques enable the quantification of focal and diffuse myocardial LGE, respectively. Studies have shown evidence of fibrosis in middle-age athletes, but not relative to physically active (PA) adults who perform recommended physical activity levels. Therefore, we examined cardiac remodeling and presence of left ventricular (LV) LGE and T1 values in both recreational middle-age endurance athletes (EA) and PA adults. METHODS: Healthy EA and PA adults (45-65 yr) completed a standardized 3-T CMR protocol with ventricular volumetry, LV LGE, and T1 mapping. RESULTS: Seventy-two EA and 20 PA participants (mean age, 53 ± 5 vs 56 ± 4 yr; P < 0.01; V˙O2peak = 50 ± 7 vs 37 ± 9 mL·kg·min, P < 0.0001) were examined, with CMR data available in 89/92 participants. Focal LV LGE was observed in 30% of participants (n = 27/89): 33% of EA (n = 23/69; 33%) and 20% of PA (n = 4/20; 20%). LGE was present at the right ventricular hinge point (n = 21/89; 23.5%) or identified as ischemic (n = 2/89; 2%) or nonischemic (n = 4/89; 4%). Focal LV LGE was observed similarly in both EA and PA (P = 0.25). EA had larger LV chamber sizes and T1 native values (1169 ± 35 vs 1190 ± 26, P = 0.02) compared with PA, with similar LV ejection fraction. Global extracellular volume (ECV) was similar in both EA and PA (22.6% ± 3.5% vs 21.5% ± 2.6%, P = 0.26), with no relationship between global ECV and LV mass (r = -0.16, P = 0.19). CONCLUSIONS: Focal LGE at the right ventricular hinge point was detected at the same frequency in both groups, was unrelated to demographic or clinical indices, and was found without evidence of global ECV expansion in EA, suggesting a physiologic remodeling response. The long-term clinical implications of hinge-point LGE require clarification using prospective, long-term follow-up studies.