We report the case of an experienced, highly trained marathon runner who died suddenly while running. On post-mortem examination, left ventricle hypertrophy and idiopathic interstitial myocardial fibrosis was found. We believe that life-long, repetitive bouts of arduous physical activity resulted in fibrous replacement of the myocardium, causing a pathological substrate for the propagation of fatal arrhythmias.

PURPOSE:Research on intermittent training has mainly focused on the effects of exercise intensity while overlooking the specific effect of the modulations associated with alternating exercise and recovery. This study investigated how the frequency of modulations during moderate-intensity exercise affects postexercise vagal reactivation. METHODS:Healthy, active females and males 18-39 yr old were recruited for the study. Participants completed three treadmill running sessions on separate days. Each moderate-intensity session accumulated 30 min at 90% of the intensity associated with the second ventilatory threshold and was performed as either high-frequency intermittent (HiFi; 15 × [2 min + 2 min recovery]), low-frequency intermittent (LoFi; 5 × [6 min + 2 min recovery]), or moderate-intensity continuous training (MICT; 1 × 30 min). Heart rate recovery (HR rec ) at 1 min and heart rate variability recovery (HRV rec ; lnRMSSD) were assessed in response to submaximal constant-speed tests performed before (CST1) and after (CST2) each of the exercise sessions. HR rec , HRV rec , blood lactate (BLa), and blood pressure were also collected during the exercise sessions. RESULTS:Twenty-one individuals (8 females, 13 males) participated in the study. HR rec from CST2 was faster in HiFi versus MICT ( P < 0.001), whereas HRV rec post-CST2 was higher after HiFi versus both LoFi ( P = 0.024) and MICT ( P < 0.001). BLa increased in all conditions ( P = 0.007) but remained lower during HiFi compared with LoFi and MICT (both P < 0.001). Diastolic blood pressure did not change during exercise with HiFi ( P = 0.939) but decreased during LoFi ( P = 0.006) and MICT ( P = 0.008). CONCLUSIONS:Exercise pattern influences the physiologic response to exercise. Higher frequencies of modulations can preserve vagal activity and expedite postexercise recovery, suggesting moderate-intensity intermittent exercise as a potential strategy to mitigate autonomic impact and acute physiological stress while maintaining total work performed.

Exercise training requires the careful application of training dose to maximize adaptation while minimizing the risk of illness and injury. High-intensity interval training (HIIT) is a potent method for improving health and fitness but generates substantial autonomic imbalance. Assuming a supine posture between intervals is a novel strategy that could enhance physiological readiness and training adaptations. This study aimed to establish the safety and feasibility of supine recovery within a HIIT session and explore its acute effects. Fifteen healthy, active males (18–34 years) underwent assessment of cardiopulmonary fitness. Participants completed two identical HIIT treadmill sessions (4 x [3 min at 95

BACKGROUND:Growing evidence indicates that chronic high-intensity endurance exercise predisposes male, middle-aged athletes to increased risk of atrial fibrillation (AF). The aetiology of AF in endurance athletes is multifactorial and remains incompletely understood. Despite their unique training demands, AF care in athletes remains largely based on evidence derived from the general population. Understanding the experiences of athletes with AF provides a necessary foundation for addressing challenges in managing their condition and identifying gaps in care.AIM:The purpose of this interpretive descriptive qualitative study was to describe the experiences and perspectives of endurance athletes living with AF.METHOD:Masters athletes diagnosed with AF and aged between 35 and 60 years were recruited internationally through cardiology practices and social media. Ten middle-aged, male endurance athletes with AF and >1,500 lifetime training hours participated in individual, semi-structured interviews. Data were analysed using inductive thematic analysis.RESULTS:Three key themes were constructed: (1) tensions with training, (2) tensions with treatment plans, and (3) tensions with clinicians. Participants experienced a wide range of symptoms from AF that significantly affected their ability to train, and reacted negatively to medical treatment strategies that affected their exercise capacity and training performance. Athletes experienced tensions with providers who failed to acknowledge their athletic needs.CONCLUSIONS:Our results highlight the unique difficulties that male athletes with AF face in navigating between training and their disease, treatment, and clinicians. Shared decision-making between the athlete and provider is likely necessary for effective management of athletic AF.

New Findings What is the central question of this study? Endurance athletes demonstrate altered regional right ventricular (RV) wall mechanics, characterized by lower basal deformation, in comparison to non-athletic control subjects at rest. We hypothesized that regional adaptations at the RV base reflect an enhanced functional reserve capacity in response to haemodynamic volume loading. What is the main finding and its importance? Free wall RV longitudinal strain is elevated in response to acute volume loading in both endurance athletes and control subjects. However, the RV basal segment longitudinal strain response to acute volume infusion is greater in endurance athletes. Our findings suggest that training-induced cardiac remodelling might involve region-specific adaptation in the RV functional response to volume manipulation. Eccentric remodelling of the right ventricle (RV) in response to increased blood volume and repetitive haemodynamic load during endurance exercise is well established. Structural remodelling is accompanied by decreased deformation at the base of the RV free wall, which might reflect an enhanced functional reserve capacity in response to haemodynamic perturbation. Therefore, in this study we examined the impact of acute blood volume expansion on RV wall mechanics in 16 young endurance-trained men (aged 24 +/- 3 years) and 13 non-athletic male control subjects (aged 27 +/- 5 years). Conventional echocardiographic parameters and the longitudinal strain and strain rate were quantified at the basal and apical levels of the RV free wall. Measurements were obtained at rest and after 7 ml/kg i.v. Gelofusine infusion, with and without a passive leg raise. After infusion, blood volume increased by 12 +/- 4 and 14 +/- 5% in endurance-trained individuals versus control subjects, respectively (P = 0.264). Both endurance-trained individuals (8 +/- 10%) and control subjects (7 +/- 9%) experienced an increase in free wall strain from baseline, which was also similar following leg raise (7 +/- 10 and 6 +/- 10%, respectively; P = 0.464). However, infusion evoked a greater increase in basal longitudinal strain in endurance-trained versus control subjects (16 +/- 14 vs. 6 +/- 11%; P = 0.048), which persisted after leg raise (16 +/- 18 vs. 3 +/- 11%; P = 0.032). Apical longitudinal strain and RV free wall strain rates were not different between groups and remained unchanged after infusion across all segments. Endurance training results in a greater contribution of longitudinal myocardial deformation at the base of the RV in response to a haemodynamic volume challenge, which might reflect a greater region-specific functional reserve capacity.

We are grateful for the interest and comments provided by Jensen and Wang (1) related to our recent paper (2). As previously noted, obtaining true resting blood pressure (BP) measurements in chimpanzees is challenging, if not impossible (1). In our study, and as described in detail in the SI Appendix of ref. 2, BP was measured at least three times in each animal, and the average of these measures was used for analysis (2). We specifically excluded measurements taken within the 20-min period immediately following anesthetic delivery, in order to minimize the effects of the stress associated with anesthetic induction and the initial hypertensive response … [↵][1]1To whom correspondence may be addressed. Email: rob.shave{at}ubc.ca. [1]: #xref-corresp-1-1

Chimpanzees and gorillas, when not inactive, engage primarily in short bursts of resistance physical activity (RPA), such as climbing and fighting, that creates pressure stress on the cardiovascular system. In contrast, to initially hunt and gather and later to farm, it is thought that preindustrial human survival was dependent on lifelong moderate-intensity endurance physical activity (EPA), which creates a cardiovascular volume stress. Although derived musculoskeletal and thermoregulatory adaptations for EPA in humans have been documented, it is unknown if selection acted similarly on the heart. To test this hypothesis, we compared left ventricular (LV) structure and function across semiwild sanctuary chimpanzees, gorillas, and a sample of humans exposed to markedly different physical activity patterns. We show the human LV possesses derived features that help augment cardiac output (CO) thereby enabling EPA. However, the human LV also demonstrates phenotypic plasticity and, hence, variability, across a wide range of habitual physical activity. We show that the human LV's propensity to remodel differentially in response to chronic pressure or volume stimuli associated with intense RPA and EPA as well as physical inactivity represents an evolutionary trade-off with potential implications for contemporary cardiovascular health. Specifically, the human LV trades off pressure adaptations for volume capabilities and converges on a chimpanzee-like phenotype in response to physical inactivity or sustained pressure loading. Consequently, the derived LV and lifelong low blood pressure (BP) appear to be partly sustained by regular moderate-intensity EPA whose decline in postindustrial societies likely contributes to the modern epidemic of hypertensive heart disease.

Exercise-induced cardiac remodeling (EICR) and the attendant myocardial adaptations characteristic of the athlete's heart may regress during periods of exercise reduction or abstinence. The time course and mechanisms underlying this reverse remodeling, specifically the impact of concomitant plasma volume (PV) contraction on cardiac chamber size, remain incompletely understood. We therefore studied recreational runners ( n = 21, age 34 ± 7 yr; 48% male) who completed an 18-wk training program (~7 h/wk) culminating in the 2016 Boston Marathon after which total exercise exposure was confined to <2 h/wk (no single session >1 h) for 8 wk. Cardiac structure and function, exercise capacity, and PV were assessed at peak fitness (10-14 days before) and at 4 wk and 8 wk postmarathon. Mixed linear modeling adjusting for age, sex, V̇o2peak, and marathon finish time was used to compare data across time points. Physiological detraining was evidenced by serial reductions in treadmill performance. Two distinct phases of myocardial remodeling and hematological adaptation were observed. After 4 wk of detraining, there were significant reductions in PV (Δ -6.0%, P < 0.01), left ventricular (LV) wall thickness (Δ -8.1%, <0.05), LV mass (Δ -10.3%, P < 0.001), and right atrial area (Δ -8.2%, P < 0.001). After 8 wk of detraining, there was a significant reduction in right ventricle chamber size (end-diastolic area Δ = -8.0%, P < 0.05) without further concomitant reductions in PV or LV wall thickness. Abrupt reductions in exercise training stimulus result in a structure-specific time course of reverse cardiac remodeling that occurs largely independently of PV contraction. NEW & NOTEWORTHY Significant reverse cardiac remodeling, previously documented among competitive athletes, extends to recreational runners and occurs with a distinct time course. Initial reductions in plasma volume and left ventricular (LV) mass, driven by reductions in wall thickness, are followed by contraction of the right ventricle. Consistent with data from competitive athletes, LV chamber volumes appear less responsive to detraining and may be a more permanent adaptation to sport.

Background: Deliberate exercise abstinence, “prescribed detraining”, has been proposed as means to differentiate the athlete's heart from occult cardiomyopathy. At present, data defining the myocardial response to detraining among healthy athletes are sparse. Methods: Marathon runners

Fourteen captive Livingstone's fruit bats ( Pteropus livingstonii) were anesthetized for routine veterinary health checks, including echocardiography, using sevoflurane. In addition, three specimens suffering from cardiac disease and a pregnant specimen were anesthetized for clinical assessment. No anesthetic complications were observed in any of the specimens. Significant differences in the core body temperature were found between the esophageal and rectal measurements. A significant decrease in blood glucose was noted through the anesthesia, suspected to be related to an extended fasting period prior to the procedure.

This article was published in Journal of Zoo and Aquarium Research on 30 April 2016 (online), available at http://www.jzar.org/jzar/article/view/172

PURPOSE: While vigorous exercise is well known to stimulate erythropoiesis, the hematological response to exercise detraining remains incompletely understood. We sought to characterize red blood cell (RBC) mediated determinants of oxygen carry capacity, including RBC population dynamics, during a period of detraining. METHODS: Recreational marathon runners participated in a structured 18-week training program (~7-8 h/w) then completed the 2016 Boston Marathon. Participants then reduced total exercise exposure to <2 h/w (no single session >1 hour) for 8 weeks. Exercise testing, carbon monoxide rebreathing tests and venous blood draws were performed 10-14 days before, and at 4 and 8 weeks after the marathon. Mixed linear modeling adjusting for age and marathon finish time was used to compare data across time points. RESULTS: Twenty-two runners (age = 34.5 ± 7.5 y, 50% men) completed the study protocol. Detraining was confirmed by serial reductions in time to exhaustion during treadmill testing (p<0.01, Figure 1). Plasma volume significantly declined by 4 weeks. In contrast, total hemoglobin mass (tHbmass) and serum ferritin remained stable. By 4 weeks, glycated hemoglobin was significantly elevated while RBC mean corpuscular volume was significantly reduced, indicating an increase in mean RBC age. By 8 weeks, there was a significant decrease in the RBC clearance threshold (Vc). CONCLUSION: tHbmass, a primary determinant of oxygen carrying capacity, appears to be stable during 8 weeks of exercise detraining. We speculate that this phenomenon is mediated by a subtle decrease in RBC production rate, and that an extended Vc after 8 weeks occurs to defend tHbmass in the absence of a sufficient erythropoietic stimulus.Figure 1: Changes in exercise capacity and hematologic parameters in response to 8 weeks of exercise detraining following completion of the Boston Marathon.

OBJECTIVETo generate reference intervals for ECG variables in clinically normal chimpanzees (Pan troglodytes).ANIMALS100 clinically normal (51 young [< 10 years old] and 49 adult [≥ 10 years old]) wild-born chimpanzees.PROCEDURESElectrocardiograms collected between 2009 and 2013 at the Tchimpounga Chimpanzee Rehabilitation Centre were assessed to determine heart rate, PR interval, QRS duration, QT interval, QRS axis, P axis, and T axis. Electrocardiographic characteristics for left ventricular hypertrophy (LVH) and morphology of the ST segment, T wave, and QRS complex were identified. Reference intervals for young and old animals were calculated as mean ± 1.96•SD for normally distributed data and as 5th to 95th percentiles for data not normally distributed. Differences between age groups were assessed by use of unpaired Student t tests. RESULTS Reference intervals were generated for young and adult wild-born chimpanzees. Most animals had sinus rhythm with small or normal P wave morphology; 24 of 51 (47%) young chimpanzees and 30 of 49 (61%) adult chimpanzees had evidence of LVH as determined on the basis of criteria for humans.CONCLUSIONS AND CLINICAL RELEVANCECardiac disease has been implicated as the major cause of death in captive chimpanzees. Species-specific ECG reference intervals for chimpanzees may aid in the diagnosis and treatment of animals with, or at risk of developing, heart disease. Chimpanzees with ECG characteristics outside of these intervals should be considered for follow-up assessment and regular cardiac monitoring.

Carbohydrate (CHO) mouth-rinsing, rather than ingestion, is known to improve performance of high-intensity (>75% maximal oxygen uptake) short-duration (≤1 h) cycling exercise. Mechanisms responsible for this improvement, however, are unclear. The present study aimed to investigate the effect of a CHO mouth-rinse on cycling time-trial (TT) performance and mechanisms of fatigue. On 2 separate occasions, 9 male cyclists (mean ± SD; maximal oxygen uptake, 61 ± 5 mL·kg(-1)·min(-1)) completed 45 min at 70% maximum power output (preload) followed by a 15-min TT. At 7.5-min intervals during the preload and TT, participants were given either a tasteless 6.4% maltodextrin mouth-rinse (CHO) or water (placebo (PLA)) in a double-blind, counterbalanced fashion. Isometric knee-extension force and electromyographic responses to percutaneous electrical stimulation and transcranial magnetic stimulation were measured before, after the preload, and after the TT. There were greater decreases in maximal voluntary contraction after the TT in PLA (20% ± 10%) compared with the CHO (12% ± 8%; P = 0.019). Voluntary activation was reduced following exercise in both trials, but did not differ between conditions (PLA -10% ± 8% vs. CHO -5% ± 4%; P = 0.150). The attenuation in the manifestation of global fatigue did not translate into a TT improvement (248 ± 23 vs. 248 ± 39 W for CHO and PLA, respectively). Furthermore, no differences in heart rate or ratings of perceived exertion were found between the 2 conditions. These data suggest that CHO mouth-rinsing attenuates neuromuscular fatigue following endurance cycling. Although these changes did not translate into a performance improvement, further investigation is required into the role of CHO mouth-rinse in alleviating neuromuscular fatigue.

PURPOSE: The purpose of this study was to compare common carotid artery (CCA) stiffness at rest and immediately following brief aerobic exercise between young males of moderate and high cardiorespiratory fitness (CRF). METHODS: Accordingly, heart rate (HR), blood pressure (BP), arterial diameter, conventional parameters of arterial stiffness (Petersons’ elastic modulus [Ep], β1 stiffness index) and novel two-dimensional (2D) strain imaging indices (global circumferential strain, strain rate and β2 stiffness index) were assessed in the CCA pre and immediately post 5-min of aerobic exercise (40% peak exercise capacity) in twenty-two young healthy males (age: 21 ± 2 years). Moderate and high CRF groups demonstrated mean V†o2 peak data of 49 ± 8 and 66 ± 6 mL kg-1min-1, respectively (P .05). However, whilst there was a similar increase in CCA wall deformation as indicated by global circumferential strain following exercise (pre vs. post, moderate: 9.12 ± 2.6% vs. 9.36 ± 2.4%; high: 10.19 ± 2.9% vs. 11.34 ± 2.9%, both P > .05), CCA wall deformation was significantly faster in the high-fit group only, as reflected by increased systolic circumferential strain rate (moderate: 1.09 ± 0.3 vs. 1.17 ± 0.2 1/s, P > .05; high: 1.14 ± 0.2 vs. 1.35 ± 0.3 1/s, P = .049). CONCLUSION: Using novel 2D strain imaging, this study shows that young high-fit individuals may exhibit different arterial wall dynamics compared to their lower-fit counterparts following a short bout of aerobic exercise. The increase in global circumferential strain rate following exercise in high-fit individuals may reflect a greater ability to buffer the significant rise in pulse-pressure and blood flow that occurs in response to exercise.

PURPOSE:The purposes of this study were to describe resting cardiopulmonary function in highly trained athletes with cervical spinal cord injury (SCI) and to compare the data with able-bodied (AB) control subjects. METHODS:Twelve Paralympic wheelchair rugby players with cervical SCI (injury level = C5-C7) and 12 AB controls matched for age, stature, and body mass were assessed for pulmonary function using spirometry, body plethysmography, and maximal inspiratory and expiratory mouth pressures; diaphragm function using magnetic stimulation of the phrenic nerves; and cardiac function using transthoracic echocardiography. RESULTS:Total lung capacity, vital capacity, inspiratory reserve volume, and expiratory reserve volume were lower in SCI compared with AB (P < 0.01), whereas residual volume was elevated in SCI (P = 0.022). Airway resistance and maximal inspiratory mouth pressure were not different between groups (P > 0.41), whereas maximal expiratory mouth pressure, maximal transdiaphragmatic pressure, and twitch transdiaphragmatic pressure were lower in SCI (P < 0.01). Percent predicted total lung capacity was significantly correlated with maximal transdiaphragmatic pressure in SCI (r = 0.74), suggesting that the pulmonary restriction was a result of diaphragm weakness. Left ventricular mass, ejection fraction, stroke volume, and cardiac output were lower in SCI (P < 0.04), but early and late filling velocities during diastole were not different between groups (P > 0.05). CONCLUSIONS:Highly trained athletes with cervical SCI exhibit a restrictive pulmonary defect, weakness of the expiratory and diaphragm muscles, atrophy of the heart, and reduced systolic cardiac function.

Syncope is widely reported following prolonged exercise. It is often assumed that the magnitude of exercise-induced hypotension (post-exercise hypotension; PEH), and the hypotensive response to postural change (initial orthostatic hypotension; IOH) are predictors of syncope post-exercise. The aim of this study was to determine the relationship between PEH, IOH, the residual IOH and syncope following prolonged exercise. Blood pressure (BP; Finometer) was measured continuously in 19 athletes (47 ± 20 years; BMI: 23.2 ± 2.2 kg m2; \( \dot{V} \)O2 max: 51.3 ± 10.8 mL kg−1 min−1) whilst supine and during head-up tilt (HUT) to 60° for 15 min (or to syncope), prior to and following 4 h of running at 70–80% maximal heart rate. Syncope developed in 15 of 19 athletes post-exercise [HUT-time completed, Pre: 14:39 (min:s) ± 0:55; Post: 5:59 ± 4:53; P < 0.01]. PEH was apparent (−7 ± 7 mmHg; −8 ± 8%), but was unrelated to HUT-time completed (r 2 = 0.09; P > 0.05). Although the magnitude of IOH was similar to post-exercise [−28 ± 12 vs. −20 ± 14% (pre-exercise); P > 0.05], the BP recovery following IOH was incomplete [−9 ± 9 vs. −1 ± 11 (pre-exercise); P < 0.05]; however, neither showed a relation to HUT-time completed (r 2 = 0.18, r 2 = 0.01; P > 0.05, respectively). Although an inability to maintain BP is a common feature of syncope post-exercise, the magnitude of PEH, IOH and residual IOH do not predict time to syncope. Practically, endurance athletes who present with greater hypotension are not necessarily at a greater risk of syncope than those who present with lesser reductions in BP.

We asked whether abdominal binding improves cardiorespiratory function in individuals with cervical spinal cord injury (SCI). 13 participants with chronic SCI (C5–C7) and 8 able-bodied controls were exposed to varying degrees of elastic abdominal compression (unbound [UB], loose-bound [LB], and tight-bound [TB]) while seated. In SCI, TB increased vital capacity (14%), expiratory flow throughout vital capacity (15%), inspiratory capacity (21%), and maximal expiratory mouth pressure (25%). In contrast, TB reduced residual volume (−34%) and functional residual capacity (−23%). TB increased tidal and twitch transdiaphragmatic pressures (∼45%), primarily by increasing the gastric pressure contributions. TB increased cardiac output (28%), systolic mitral annular velocity (22%), and late-diastolic mitral annular velocity (50%). Selected measures of cardiorespiratory function improved with LB, but the changes were less compared to TB. In able-bodied, changes were inconsistent and always less than in SCI. In conclusion, abdominal-binding improved cardiorespiratory function in low-cervical SCI by optimising operating lung volumes, increasing expiratory flow, enhancing diaphragmatic pressure production, and improving left-ventricular function.

We proposed that experiencing unpleasant emotions during performance represents unsuccessful emotion-regulatory efforts, and that such effort concurrently tax physiological resources. We used data from 2-h cycling trials (N = 28) at a power output equivalent to lactate threshold. Emotions were calculated before and during cycling with ongoing assessments of ventilation, respiratory quotient, heart rate, and oxygen uptake. Emotion data indicated significant changes over time with all participants reporting decreases in vigour and increases in fatigue, with 14 cases of concurrent increases in anger, depression, and tension. After grouping participants into positive and negative emotion groups, a time x unpleasant emotion group ANOVA indicated a significant interaction effect for changes in ventilation (F 6,21 = 3.09, P = .03, Partial Eta2 = .47) over time, with no significant difference in other physiological variables or perceived exertion. Among athletes reporting negative emotions, ventilation increased during the middle section, whereas among athletes reporting positive emotions, ventilation increased shortly before completion. Findings suggest that regulating negative emotion is an effortful process taxing physiological substrates.