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Background There is a lack of international consensus regarding the prescription of high-intensity interval training (HIIT) for people with coronary artery disease (CAD) attending cardiac rehabilitation (CR). Aims To assess the clinical effectiveness and safety of low-volume HIIT compared with moderate-intensity steady-state (MISS) exercise training for people with CAD. Methods and results We conducted a multi-centre RCT, recruiting 382 patients from 6 outpatient CR centres. Participants were randomized to twice-weekly HIIT (n = 187) or MISS (n = 195) for 8 weeks. HIIT consisted of 10 × 1 min intervals of vigorous exercise (>85% maximum capacity) interspersed with 1 min periods of recovery. MISS was 20–40 min of moderate-intensity continuous exercise (60–80% maximum capacity). The primary outcome was the change in cardiorespiratory fitness [peak oxygen uptake (VO2 peak)] at 8 week follow-up. Secondary outcomes included cardiovascular disease risk markers, cardiac structure and function, adverse events, and health-related quality of life. At 8 weeks, VO2 peak improved more with HIIT (2.37 mL.kg−1.min−1; SD, 3.11) compared with MISS (1.32 mL.kg−1.min−1; SD, 2.66). After adjusting for age, sex, and study site, the difference between arms was 1.04 mL.kg−1.min−1 (95% CI, 0.38 to 1.69; P = 0.002). Only one serious adverse event was possibly related to HIIT. Conclusions In stable CAD, low-volume HIIT improved cardiorespiratory fitness more than MISS by a clinically meaningful margin. Low-volume HIIT is a safe, well-tolerated, and clinically effective intervention that produces short-term improvement in cardiorespiratory fitness. It should be considered by all CR programmes as an adjunct or alternative to MISS. Trial registration ClinicalTrials.gov: NCT02784873. https://clinicaltrials.gov/ct2/show/NCT02784873.

Dependent on timing of assessment, anesthetic agents and specifically medetomidine negatively affect cardiac function in great apes. The aim of this study was to determine the influence of tiletamine–zolazepam (TZ) with and without medetomidine on cardiac structure and function in healthy chimpanzees (Pan troglodytes) during a period of relative blood pressure stability. Twenty-four chimpanzees living in an African wildlife sanctuary undergoing routine health assessments were stratified by age, sex, and body mass and randomized to be anesthetized using either TZ (6 mg/kg; n = 13; seven males and six females) or a combination of TZ (2 mg/kg) and medetomidine (TZM; 0.02 mg/kg; n = 11; five males and six females). During health checks, regular heart rate and blood pressure readings were taken and a standardized echocardiogram was performed 20–30 min after induction. Data were compared between the two anesthetic groups using independent-samples t or Mann–Whitney U tests. Although heart rate (mean ± SD; TZ: 76 ± 10 bpm; TZM: 65 ± 14 bpm, P = 0.027), cardiac output (TZ: 3.0 ± 0.7 L/min; TZM: 2.4 ± 0.7 L/min, P = 0.032), and mitral A-wave velocities (TZ: 0.51 ± 0.16 cm/s; TZM: 0.36 ± 0.10 cm/s, P = 0.013) were lower in the TZM group, there were no statistically significant differences in cardiac structure or the remaining functional variables between groups. Furthermore, there were no statistical differences in systolic (TZ 114.6 ± 14.9 mmHg; TZM: 123.0 ± 28.1 mmHg; P = 0.289) or diastolic blood pressure (TZ: 81.8 ± 22.3 mmHg, TZM: 83.8 ± 20.1 mmHg; P = 0.827) between the groups during the echocardiogram. This study has shown that during a period of relative blood pressure stability, during the first 20–30 min after induction there are few differences in measures of cardiac structure and function between protocols using TZ with or without medetomidine in healthy chimpanzees.

OBJECTIVE To comprehensively characterize cardiac structure and function, from infancy to adulthood, in male and female wild-born captive chimpanzees (Pan troglodytes) living in sanctuaries. ANIMALS 290 wild-born captive chimpanzees. PROCEDURES Physical and echocardiographic examinations were performed on anesthetized chimpanzees in 3 sanctuaries in Africa between October 2013 and May 2017. Results were evaluated across age groups and between sexes, and potential differences were assessed with multiple 1-way independent Kruskal-Wallis tests. RESULTS Results indicated that left ventricular diastolic and systolic function declined at a younger age in males than in females. Although differences in right ventricular diastolic function were not identified among age groups, right ventricular systolic function was lower in adult chimpanzees (> 12 years old), compared with subadult (8 to 12 years old) and juvenile (5 to 7 years old) chimpanzees. In addition, male subadult and adult chimpanzees had larger cardiac wall dimensions and chamber volumes than did their female counterparts. CONCLUSIONS AND CLINICAL RELEVANCE Results of the present study provided useful reference intervals for cardiac structure and function in captive chimpanzees categorized on the basis of age and sex; however, further research is warranted to examine isolated and combined impacts of blood pressure, age, body weight, and anesthetic agents on cardiac structure and function in chimpanzees.

Purpose The increased physiological demand of pregnancy results in the profound adaptation of the maternal cardiovascular system, reflected by greater resting cardiac output and left ventricular (LV) deformation. Whether the increased resting demand alters acute cardiac responses to exercise in healthy pregnant women is not well understood. Methods Healthy nonpregnant (n = 18), pregnant (n = 14, 22-26 wk gestation), and postpartum women (n = 13, 12-16 wk postdelivery) underwent assessments of cardiac function and LV mechanics at rest, during a sustained isometric forearm contraction (30% maximum), and during low-intensity (LOW) and moderate-intensity (MOD) dynamic cycling exercise (25% and 50% peak power output). Significant differences (α = 0.05) were determined using ANCOVA and general linear model (resting value included as covariate). Results When accounting for higher resting cardiac output in pregnant women, pregnant women had greater cardiac output during isometric contraction (2.0 ± 0.3 L·min-1·m-1.83; nonpregnant, 1.3 ± 0.2 L·min-1·m-1.83; postpartum, 1.5 ± 0.5 L·min-1·m-1.83; P = 0.02) but similar values during dynamic cycling exercise (pregnant, LOW = 2.8 ± 0.4 L·min-1·m-1.83, MOD = 3.4 ± 0.7 L·min-1·m-1.83; nonpregnant, LOW = 2.4 ± 0.3 L·min-1·m-1.83, MOD = 3.0 ± 0.3 L·min-1·m-1.83; postpartum, LOW = 2.3 ± 0.4 L·min-1·m-1.83, MOD = 3.0 ± 0.5 L·min-1·m-1.83; P = 0.96). Basal circumferential strain was higher in pregnant women at rest, during the sustained isometric forearm contraction (-23.5% ± 1.2%; nonpregnant, -14.6% ± 1.4%; P = 0.001), and during dynamic cycling exercise (LOW = -27.0% ± 4.9%, MOD = -27.4% ± 4.6%; nonpregnant, LOW = -15.8% ± 4.5%, MOD = -15.2% ± 6.7%; P = 0.012); however, other parameters of LV mechanics were not different between groups. Conclusion The results support that the maternal heart can appropriately respond to additional cardiac demand and altered loading experienced during acute isometric and dynamic exercise, although subtle differences in responses to these challenges were observed. In addition, the LV mechanics that underpin global cardiac function are greater in pregnant women during exercise, leading to the speculation that the hormonal milieu of pregnancy influences regional deformation.

Article published in ESC Heart Failure available open access at https://doi.org/10.1002/ehf2.12293

Background Preclinical studies have reported that a single treadmill session performed 24 h prior to doxorubicin provides cardio-protection. We aimed to characterize the acute change in cardiac function following an initial doxorubicin treatment in humans and determine whether an exercise session performed 24 h prior to treatment changes this response. Methods Breast cancer patients were randomized to either 30 min of vigorous-intensity exercise 24 h prior to the first doxorubicin treatment (n = 13), or no vigorous exercise for 72 h prior to treatment (control, n = 11). Echocardiographically-derived left ventricular volumes, longitudinal strain, twist, E/A ratio, and circulating NT-proBNP, a marker of later cardiotoxicity, were measured before and 24–48 h after the treatment. Results Following treatment in the control group, NT-proBNP, end-diastolic and stroke volumes, cardiac output, E/A ratio, strain, diastolic strain rate, twist, and untwist velocity significantly increased (all p ≤ 0.01). Whereas systemic vascular resistance (p < 0.01) decreased, and ejection fraction (p = 0.02) and systolic strain rate (p < 0.01) increased in the exercise group only. Relative to control, the exercise group had a significantly lower NT-proBNP (p < 0.01) and a 46% risk reduction of exceeding the cut-point used to exclude acute heart failure. Conclusion The first doxorubicin treatment is associated with acutely increased NT-proBNP, echocardiographic parameters of myocardial relaxation, left ventricular volume overload, and changes in longitudinal strain and twist opposite in direction to documented longer-term changes. An exercise session performed 24 h prior to treatment attenuated NT-proBNP release and increased systolic function. Future investigations should verify these findings in a larger cohort and across multiple courses of doxorubicin. Background Preclinical studies have reported that a single treadmill session performed 24 h prior to doxorubicin provides cardio-protection. We aimed to characterize the acute change in cardiac function following an initial doxorubicin treatment in humans and determine whether an exercise session performed 24 h prior to treatment changes this response. Methods Breast cancer patients were randomized to either 30 min of vigorous-intensity exercise 24 h prior to the first doxorubicin treatment (n = 13), or no vigorous exercise for 72 h prior to treatment (control, n = 11). Echocardiographically-derived left ventricular volumes, longitudinal strain, twist, E/A ratio, and circulating NT-proBNP, a marker of later cardiotoxicity, were measured before and 24–48 h after the treatment. Results Following treatment in the control group, NT-proBNP, end-diastolic and stroke volumes, cardiac output, E/A ratio, strain, diastolic strain rate, twist, and untwist velocity significantly increased (all p ≤ 0.01). Whereas systemic vascular resistance (p < 0.01) decreased, and ejection fraction (p = 0.02) and systolic strain rate (p < 0.01) increased in the exercise group only. Relative to control, the exercise group had a significantly lower NT-proBNP (p < 0.01) and a 46% risk reduction of exceeding the cut-point used to exclude acute heart failure. Conclusion The first doxorubicin treatment is associated with acutely increased NT-proBNP, echocardiographic parameters of myocardial relaxation, left ventricular volume overload, and changes in longitudinal strain and twist opposite in direction to documented longer-term changes. An exercise session performed 24 h prior to treatment attenuated NT-proBNP release and increased systolic function. Future investigations should verify these findings in a larger cohort and across multiple courses of doxorubicin.

This article was published in Experimental Physiology on 01 August 2017, available at http://dx.doi.org/10.1113/EP086429

There is growing evidence that dilated cardiomyopathy may be a major cause of death in captive Livingstone's fruit bats (Pteropus livingstonii). Therefore, the primary aim of this prospective, exploratory study was to examine whether a systematic cardiac ultrasound protocol is feasible in this critically endangered species and to report basic measures of cardiac structure and function from a cohort of apparently healthy bats. A secondary aim was to test the effect posture (dorsal recumbency vs. roosting) has upon cardiac function in this species. Transthoracic echocardiograms, including 2D, Doppler, and tissue Doppler measures of cardiac structure and function were completed as part of routine health examinations for bats at a single center (n = 19). Bats were then grouped by age and disease status and the mean and range data reported for each group. In healthy adult bats, with the exception of a reduction in heart rate (P ≤ 0.05), right atrial systolic area (P ≤ 0.05), and right ventricular velocity during atrial contraction, there were no significant changes in cardiac structure or function in response to the roosting position. However, in the bats presenting with dilated cardiomyopathy the current data suggest that left ventricular ejection fraction is improved while roosting. Further work is required to confirm our initial findings, generate diagnostic reference intervals, and explore the causes of dilated cardiomyopathy in this species.

Cardiovascular function generally decreases with age, but whether this decrease differs between men and women is unclear. Our aims were twofold: (1) to investigate age-related sex differences in left ventricular (LV) structure, function and mechanics, and (2) to compare these measures between pre- and postmenopausal women in the middle-aged group.Resting echocardiography was performed in a cross-sectional sample of 82 healthy adults (14 young men, 19 middle-aged men, 15 young women, 34 middle-aged women: 15 premenopausal and 19 postmenopausal). Two-way ANOVAs were used to examine sex × age interactions, and t-tests to compare pre- and postmenopausal women (α 0.1).Normalized LV mass, stroke volume and end-diastolic volume were significantly lower in middle-aged than young men, but this difference was smaller between middle-aged and young women. Peak systolic apical mechanics were significantly greater in middle-aged men than in middle-aged women, but not between young men and women. Postmenopausal women had significantly lower LV relaxation and mechanics (torsion, twisting velocity and apical circumferential strain rates) compared with middle-aged premenopausal women.Our cross-sectional findings suggest that the hearts of men and women may age differently, with men displaying greater differences in LV volumes accompanied by differences in apical mechanics.

This article was published in Journal of Physiology on 11 February 2017 (online ahead of print), available at http://dx.doi.org/10.1113/JP273368

The anatomy of the adult human left ventricle (LV) is the result of its complex interaction with its environment. From the fetal to the neonatal to the adult form, the human LV undergoes an anatomical transformation that finally results in the most complex of the four cardiac chambers. In its adult form, the human LV consists of two muscular helixes that surround the midventricular circumferential layer of muscle fibers. Contraction of these endocardial and epicardial helixes results in a twisting motion that is thought to minimize the transmural stress of the LV muscle. In the healthy myocardium, the LV twist response to stimuli that alter preload, afterload, or contractility has been described and is deemed relatively consistent and predictable. Conversely, the LV twist response in patient populations appears to be a little more variable and less predictable, yet it has revealed important insight into the effect of cardiovascular disease on LV mechanical function. This review discusses important methodological aspects of assessing LV twist and evaluates the LV twist responses to the main physiological and pathophysiological states. It is concluded that correct assessment of LV twist mechanics holds significant potential to advance our understanding of LV function in human health and cardiovascular disease.

This article was published in Journal of Small Animal Practice on 4 August 2016 (online), available at http://dx.doi.org/10.1111/jsap.12536

Left ventricular (LV) twist mechanics differ between men and women during acute physiological stress, which may be partly mediated by sex differences in autonomic control. While men appear to have greater adrenergic control of LV twist, the potential contribution of vagal modulation to sex differences in LV twist remains unknown. Therefore, the present study examined the role of vagal control on sex differences in LV twist during graded lower body negative pressure (LBNP) and supine cycling. On two separate visits, LV mechanics were assessed using two-dimensional speckle-tracking echocardiography in 18 men (22 ± 2 yr) and 17 women (21 ± 4 yr) during −40- and −60-mmHg LBNP and 25% and 50% of peak supine cycling workload with and without glycopyrrolate (vagal blockade). LV twist was not different at baseline but was greater in women during −60 mmHg in both control (women: 16.0 ± 3.4° and men: 12.9 ± 2.3°, P = 0.004) and glycopyrrolate trials (women: 17.7 ± 5.9° and men: 13.9 ± 3.3°, P < 0.001) due to greater apical rotation during control (women: 11.9 ± 3.6° and men: 7.8 ± 1.5°, P < 0.001) and glycopyrrolate (women: 11.6 ± 4.9° and men: 7.1 ± 3.6°, P = 0.009). These sex differences in LV twist consistently coincided with a greater LV sphericity index (i.e., ellipsoid geometry) in women compared with men. In contrast, LV twist did not differ between the sexes during exercise with or without glycopyrrolate. In conclusion, women have augmented LV twist compared with men during large reductions to preload, even during vagal blockade. As such, differences in vagal control do not appear to contribute to sex differences in the LV twist responses to physiological stress, but they may be related to differences in ventricular geometry. NEW & NOTEWORTHY This is the first study to specifically examine the role of vagal autonomic control on sex-related differences in left ventricular (LV) mechanics. Contrary to our hypothesis, vagal control does not appear to primarily determine sex differences in LV mechanical or hemodynamic responses to acute physiological stress. Instead, differences in LV geometry may be a more important contributor to sex differences in LV mechanics.

Background\ud Cardiac rehabilitation (CR) exercise training is beneficial after myocardial infarction (MI). Whilst the peripheral adaptations to training are well defined, little is known regarding the effect on left ventricular (LV) remodelling, particularly LV function. Efficient LV ejection and filling is achieved through deformation and rotation of the myocardium in systole and diastole – LV mechanics. The response of LV mechanics to CR exercise training in MI patients is unknown.\ud \ud Methods\ud In this observational exploratory study, 36 (of 40 enrolled) male, MI patients completed either 10-weeks of twice-weekly gym based cardiovascular exercise at 60–80% VO2peak (n = 18), or a non-exercise control period (n = 18). Cardiopulmonary exercise testing and speckle tracking echocardiography were performed at baseline and 10 weeks.\ud \ud Results\ud Compared to the non-exercise group, VO2peak improved with CR exercise training (Difference: +4.28 [95% CI: 1.34 to 7.23] ml.kg−1.min−1, P = 0.01). Neither conventional LV structural or functional indices, nor LV global longitudinal strain, significantly changed in either group. In contrast, LV twist and twist velocity decreased in the exercise group and increased in the non-exercise group (Difference: −3.95° [95% CI: −7.92 to 0.03°], P = 0.05 and −19.2°.s−1 [95% CI: −35.9 to −2.7°.s−1], P = 0.02, respectively).\ud \ud Conclusion\ud In MI patients who completed CR exercise training, LV twist and twist velocity decreased, whereas these parameters increased in patients who did not exercise. These preliminary data may indicate reverse LV functional remodelling and improved functional reserve. The assessment of LV twist may serve as an indicator of the therapeutic benefit of CR exercise training and should be investigated in larger trials.

Purpose: In rodents, a single exercise bout performed 24 h prior to a single doxorubicin treatment provides cardio-protection. This study investigated whether performing this intervention prior to every doxorubicin treatment for breast cancer reduced subclinical cardiotoxicity and treatment symptoms. Methods: Twenty-four women with early stage breast cancer were randomly assigned to perform a 30-min, vigorous-intensity treadmill bout 24 h prior to each of four doxorubicin-containing chemotherapy treatments or to usual care. Established echocardiographic and circulating biomarkers of subclinical cardiotoxicity, as well as blood pressure and body weight were measured before the first and 7–14 days after the last treatment. The Rotterdam symptom checklist was used to assess patient-reported symptoms. Results: The exercise and usual care groups did not differ in the doxorubicin-related change in longitudinal strain, twist, or cardiac troponin. However, the four total exercise bouts prevented changes in hemodynamics (increased cardiac output, resting heart rate, decreased systemic vascular resistance, p < 0.01) and reduced body weight gain, prevalence of depressed mood, sore muscles, and low back pain after the last treatment (p < 0.05) relative to the usual care group. No adverse events occurred. Conclusions: An exercise bout performed 24 h prior to every doxorubicin treatment did not have an effect on markers of subclinical cardiotoxicity, but had a positive systemic effect on hemodynamics, musculoskeletal symptoms, mood, and body weight in women with breast cancer. A single exercise bout prior to chemotherapy treatments may be a simple clinical modality to reduce symptoms and weight gain among women with breast cancer.

Impaired myocardial systolic contraction and diastolic relaxation have been suggested as possible mechanisms contributing to the decreased stroke volume (SV) observed at high altitude (HA). To determine whether intrinsic myocardial performance is a limiting factor in the generation of SV at HA, we assessed left ventricular (LV) systolic and diastolic mechanics and volumes in 10 healthy participants (aged 32 ± 7; mean ± SD) at rest and during exercise at sea level (SL; 344 m) and after 10 days at 5,050 m. In contrast to SL, LV end-diastolic volume was ∼19% lower at rest ( P = 0.004) and did not increase during exercise despite a greater untwisting velocity. Furthermore, resting SV was lower at HA (∼17%; 60 ± 10 vs. 70 ± 8 ml) despite higher LV twist (43%), apical rotation (115%), and circumferential strain (17%). With exercise at HA, the increase in SV was limited (12 vs. 22 ml at SL), and LV apical rotation failed to augment. For the first time, we have demonstrated that EDV does not increase upon exercise at high altitude despite enhanced in vivo diastolic relaxation. The increase in LV mechanics at rest may represent a mechanism by which SV is defended in the presence of a reduced EDV. However, likely because of the higher LV mechanics at rest, no further increase was observed up to 50% peak power. Consequently, although hypoxia does not suppress systolic function per se, the capacity to increase SV through greater deformation during submaximal exercise at HA is restricted.

OBJECTIVE To generate reference intervals for ECG variables in clinically normal chimpanzees (Pan troglodytes). ANIMALS 100 clinically normal (51 young [< 10 years old] and 49 adult [≥ 10 years old]) wild-born chimpanzees. PROCEDURES Electrocardiograms 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 RELEVANCE Cardiac 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.

Objectives\ud The traditional view of differential left ventricular adaptation to training type has been questioned. Right ventricular (RV) data in athletes are emerging but whether training type mediates this is not clear. The primary aim of this study was to evaluate the RV phenotype in endurance- vs. resistance-trained male athletes. Secondary aims included comparison of RV function in all groups using myocardial speckle tracking, and the impact of allometric scaling on RV data interpretation.\ud \ud Methods\ud A prospective cross-sectional design assessed RV structure and function in 19 endurance-trained (ET), 21 resistance-trained (RT) and 21 sedentary control subjects (CT). Standard 2D tissue Doppler imaging and speckle tracking echocardiography assessed RV structure and function. Indexing of RV structural parameters to body surface area (BSA) was undertaken using allometric scaling.\ud \ud Results\ud A higher absolute RV diastolic area was observed in ET (mean ± SD: 27 ± 4 cm2) compared to CT (22 ± 4 cm2; P < 0.05) that was maintained after scaling. Whilst absolute RV longitudinal dimension was greater in ET (88 ± 9 mm) than CT (81 ± 10 mm; P < 0.05), this difference was removed after scaling. Wall thickness was not different between ET and RT and there were no between group differences in global or regional RV function.\ud \ud Conclusion\ud We present some evidence of RV adaptation to chronic ET in male athletes but limited structural characteristics of an athletic heart were observed in RT. Global and regional RV functions were comparable between groups. Allometric scaling altered data interpretation in some variables.

What is the central question of this study? A reduction in left ventricular (LV) filling, and concomitant increase in heart rate, augments LV mechanics to maintain stroke volume (SV); however, the impact of reduced LV filling in isolation on SV and LV mechanics is currently unknown. What is the main finding and its importance? An isolated decrease in LV filling did not provoke a compensatory increase in mechanics to maintain SV; in contrast, LV mechanics and SV were reduced. These data indicate that when LV filling is reduced without changes in heart rate, LV mechanics do not compensate to maintain SV.An acute non-invasive reduction in preload has been shown to augment cardiac mechanics to maintain stroke volume and cardiac output. Such interventions induce concomitant changes in heart rate, whereas blood volume extraction reduces preload without changes in heart rate. Therefore, the purpose of this study was to determine whether a preload reduction in isolation resulted in augmented stroke volume achieved via enhanced cardiac mechanics. Nine healthy volunteers (four female, age 29 ± 11 years) underwent echocardiography for the assessment of left ventricular (LV) volumes and mechanics in a supine position at baseline and end extraction after the controlled removal of 25% of total blood volume (1062 ± 342 ml). Arterial blood pressure was monitored continuously by a pressure transducer attached to an indwelling radial artery catheter. Heart rate and total peripheral resistance were unchanged from baseline to end extraction, but systolic blood pressure was reduced (from 148 to 127 mmHg). From baseline to end extraction there were significant reductions in left ventricular end-diastolic volume (from 89 to 71 ml) and stroke volume (from 56 to 37 ml); however, there was no change in LV twist, basal or apical rotation. In contrast, LV longitudinal strain (from -20 to -17%) and basal circumferential strain (from -22 to -19%) were significantly reduced from baseline to end extraction. In conclusion, a reduction in preload during blood volume extraction does not result in compensatory changes in stroke volume or cardiac mechanics. Our data suggest that LV strain is dependent on LV filling and consequent geometry, whereas LV twist could be mediated by heart rate.

Limited data are available on hemodynamic responses to anesthetic protocols in wild-born chimpanzees (Pan troglodytes). Accordingly, this study characterized the heart rate (HR) and blood pressure responses to four anesthetic protocols in 176 clinically healthy, wild-born chimpanzees undergoing routine health assessments. Animals were anesthetized with medetomidine-ketamine (MK) (n = 101), tiletamine-zolazepam (TZ) (n = 30), tiletamine-zolazepam-medetomidine (TZM) (n = 24), or medetomidine-ketamine (maintained with isoflurane) (MKI) (n = 21). During each procedure, HR, systolic blood pressure (SBP), and diastolic blood pressure (DBP) were regularly recorded. Data were grouped according to anesthetic protocol, and mean HR, SBP, and DBP were calculated. Differences between mean HR, SBP, and DBP for each anesthetic protocol were assessed using the Kruskall-Wallis test and a Dunn multiple comparisons post hoc analysis. To assess the hemodynamic time course response to each anesthetic protocol, group mean data (±95% confidence interval [CI]) were plotted against time postanesthetic induction. Mean HR (beats/min [CI]) was significantly higher in TZ (86 [80-92]) compared to MKI (69 [61-78]) and MK (62 [60-64]) and in TZM (73 [68-78]) compared to MK. The average SBP and DBP values (mm Hg [CI]) were significantly higher in MK (130 [126-134] and 94 [91-97]) compared to TZ (104 [96-112] and 58 [53-93]) and MKI (113 [103-123] and 78 [69-87]) and in TZM (128 [120-135] and 88 [83-93]) compared to TZ. Time course data were markedly different between protocols, with MKI showing the greatest decline over time. Both the anesthetic protocol adopted and the timing of measurement after injection influence hemodynamic recordings in wild-born chimpanzees and need to be considered when monitoring or assessing cardiovascular health.

To improve the current understanding of the impact of resistance exercise on the heart, by examining the acute responses of left ventricular (LV) strain, twist, and untwisting rate ("LV mechanics").LV echocardiographic images were recorded in systole and diastole before, during and immediately after (7-12 s) double-leg press exercise at two intensities (30% and 60% of maximum strength, one-repetition maximum). Speckle tracking analysis generated LV strain, twist, and untwisting rate data. Additionally, beat-by-beat blood pressure was recorded and systemic vascular resistance (SVR) and LV wall stress were calculated.Responses in both exercise trials were statistically similar (P0.05). During effort, stroke volume decreased, whereas SVR and LV wall stress increased (P0.05). Immediately after effort, stroke volume returned to baseline, whereas SVR and wall stress decreased (P0.05). Similarly, acute exercise was accompanied by a significant decrease in systolic parameters of LV muscle mechanics (P0.05). However, diastolic parameters, including LV untwisting rate, were statistically unaltered (P0.05). Immediately after exercise, systolic LV mechanics returned to baseline levels (P0.05) but LV untwisting rate increased significantly (P0.05).A single, acute bout of double-leg press resistance exercise transiently reduces systolic LV mechanics, but increases diastolic mechanics after exercise, suggesting that resistance exercise has a differential impact on systolic and diastolic heart muscle function. The findings may explain why acute resistance exercise has been associated with reduced stroke volume but chronic exercise training may result in increased LV volumes.

What is the central question of this study? Does the reduction in cardiac output observed during extreme voluntary apnoea, secondary to high lung volume, result in a reduction in cerebral blood flow, perfusion pressure and oxygen delivery in a group of elite free divers? What is the main finding and its importance? High lung volumes reduce cardiac output and ventricular filling during extreme apnoea, but changes in cerebral blood flow are observed only transiently during the early stages of apnoea. This reveals that whilst cardiac output is important in regulating cerebral haemodynamics, the role of mean arterial pressure in restoring cerebral perfusion pressure is of greater significance to the regulation of cerebral blood flow. We investigated the role of lung volume-induced changes in cardiac output (Q̇) on cerebrovascular regulation during prolonged apnoea. Fifteen elite apnoea divers (one female; 185 ± 7 cm, 82 ± 12 kg, 29 ± 7 years old) attended the laboratory on two separate occasions and completed maximal breath-holds at total lung capacity (TLC) and functional residual capacity (FRC) to elicit disparate cardiovascular responses. Mean arterial pressure (MAP), internal jugular venous pressure and arterial blood gases were measured via cannulation. Global cerebral blood flow was quantified by ultrasound and cardiac output was quantified by via photoplethysmography. At FRC, stroke volume and Q̇ did not change from baseline (P 0.05). In contrast, during the TLC trial stroke volume and Q̇ were decreased until 80 and 40% of apnoea, respectively (P 0.05). During the TLC trial, global cerebral blood flow was significantly lower at 20%, but subsequently increased so that cerebral oxygen delivery was comparable to that during the FRC trial. Internal jugular venous pressure was significantly higher throughout the TLC trial in comparison to FRC. The MAP increased progressively in both trials but to a greater extent at TLC, resulting in a comparable cerebral perfusion pressure between trials by the end of apnoea. In summary, although lung volume has a profound effect on Q̇ during prolonged breath-holding, these changes do not translate to the cerebrovasculature owing to the greater sensitivity of cerebral blood flow to arterial blood gases and MAP; regulatory mechanisms that facilitate the maintenance of cerebral oxygen delivery.

New Findings What is the topic of this review? At high altitude, the cardiovascular system must adapt in order to meet the metabolic demand for oxygen. This review summarizes recent findings relating to short-term and life-long cardiac adaptation to high altitude in the context of exercise capacity. What advances does it highlight? Both Sherpa and lowlanders exhibit smaller left ventricular volumes at high altitude; however, myocardial relaxation, as evidenced by diastolic untwist, is reduced only in Sherpa, indicating that short-term hypoxia does not impair diastolic relaxation. Potential remodelling of systolic function, as evidenced by lower left ventricular systolic twist in Sherpa, may facilitate the requisite sea-level mechanical reserve required during exercise, although this remains to be confirmed. Both short-term and life-long high-altitude exposure challenge the cardiovascular system to meet the metabolic demand for O2 in a hypoxic environment. As the demand for O2 delivery increases during exercise, the circulatory component of oxygen transport is placed under additional stress. Acute adaptation and chronic remodelling of cardiac structure and function may occur to facilitate O2 delivery in lowlanders during sojourn to high altitude and in permanent highland residents. However, our understanding of cardiac structural and functional adaption in Sherpa remains confined to a higher maximal heart rate, lower pulmonary vascular resistance and no differences in resting cardiac output. Ventricular form and function are intrinsically linked through the left ventricular (LV) mechanics that facilitate efficient ejection, minimize myofibre stress during contraction and aid diastolic recoil. Recent examination of LV mechanics has allowed detailed insight into fundamental cardiac adaptation in high-altitude Sherpa. In this symposium report, we review recent advances in our understanding of LV function in both lowlanders and Sherpa at rest and discuss the potential consequences for exercise capacity. Collectively, data indicate chronic structural ventricular adaptation, with adult Sherpa having smaller absolute and relative LV size. Consistent with structural remodelling, cardiac mechanics also differ in Sherpa when compared with lowlanders at high altitude. These differences are characterized by a reduction in resting systolic deformation and slower diastolic untwisting, a surrogate of relaxation. These changes may reflect a functional cardiac adaptation that affords Sherpa the same mechanical reserve seen in lowlanders at sea level, which is absent when they ascend to high altitude.

There is contradictory evidence related to the impact of ultra-marathon running on right ventricular (RV) structure and function. Consequently, the aims of this study were to: (1) comprehensively assess RV structure and function before and immediately following a 100-mile ultra-marathon in highly trained runners, (2) determine the nature of RV recovery 6 h post-race, and (3) document 12-lead electrocardiogram (ECG) changes post-exercise. Echocardiography and 12-lead ECG were assessed in 15 competitors in a repeated measures design before and immediately after completion of the 2013 Western States Endurance Race. A subset of nine was reassessed 6 h into recovery. Standard echocardiography was used to determine RV size, function and wall stress. Myocardial speckle tracking (MST) provided peak, time to peak and temporal indices for RV longitudinal strain and strain rates (e and SR). RV size was increased post-race (inflow tract 14 %, outflow tract 11 %, P = 0.004 and 0.002). RV wall stress was elevated by 11 % post-race. Peak RV e was reduced by 10 % (P = 0.007) and significantly delayed post-race (P = 0.008). Most changes in RV function persisted at the 6-h assessment. Post-race there was an increase in the prevalence of right-sided ECG changes. Completion of a 100-mile ultra-marathon resulted in acute changes in RV structure and function that persisted 6 h into recovery and are consistent with sustained exposure to an elevated RV wall stress. These findings were supported by right-sided changes to the 12-lead ECG.

Cardiac disease has been implicated as a leading cause of death in captive great apes. Trans-thoracic echocardiography provides clinically relevant information that may help differentiate between the myriad of different heart diseases and disorders, guide treatment and aid the management of great apes with underlying cardiac pathology. The purpose of this paper is to provide an outline of the procedures and methodologies required to conduct a thorough trans-thoracic echocardiogram of great apes under general anaesthesia. Basic logistical considerations are discussed before a detailed description of the procedures required for the assessment of overall cardiac structure and function. Using a thorough systematic approach, it is our belief that veterinary professionals may be better able to diagnose, treat and manage captive great apes with, or at risk of developing heart disease.

The athlete's heart (AH) remains a popular topic of study. Controversy related to training-specific cardiac adaptation in male athletes, and continuing developments in imaging technology and scaling prompted this systematic review and meta-analysis.To provide new insight in relation to: 1) cardiac adaptation to divergent training patterns in male athletes, 2) a developing research database using cardiac magnetic resonance (CMR) in athletes; 3) functional data derived from tissue-Doppler analysis as well as right ventricular (RV) and left atrial (LA) measurements in athletes; and 4) an awareness of the impact of body size on cardiac dimensions.Systematic review and meta-analysis of prospective trials. Data extraction performed by two researchers.Pub Med, Medline, Scopus and ISI Web of knowledge scholarly data base.Prospective studies were included if they were echocardiographic or CMR trials of elite young male athletes, with clear indication of type of sports and passed a quality criteria checklist.All left ventricular (LV) structural parameters were higher in athletes than in controls. Only LV end-diastolic diameter and volume were higher in endurance athletes than in resistance athletes: 54.8 mm (95% CI 54.1 to 55.6) vs 52.4 mm (95% CI 51.2 to 53.6); p0.001 and 171 ml (95% CI 157 to 185) vs 131 ml (95% CI 120 to 142); p0.001, respectively. RV end-diastolic volume, mass and LA diameter were higher in endurance athletes than controls. LV end-diastolic volume was larger when CMR was used rather than echocardiography: 178 ml (95% CI Q7 162 to 194) vs 135 ml (95% CI 128 to 142); p0.001. Meta-analysis regression models demonstrated positive and significant associations between body surface area (BSA) and LV mass, RV mass and LA diameter.Morphological features of the male AH were noted in both athlete groups. A training-specific pattern of concentric hypertrophy was not discerned in resistance athletes. Both imaging mode and BSA can have a significant impact on the interpretation of AH data.

To establish reference intervals for echocardiographic measures of longitudinal left ventricular function in adult English Springer spaniel (ESS) dogs.This study involved 42 healthy adult ESS.Animals were prospectively recruited from a general practice population in the United Kingdom. Dogs were examined twice, at least 12 months apart, to exclude dogs with progressive cardiac disease. Mitral annular plane systolic excursion, tissue Doppler imaging mitral annular velocities and two-dimensional speckle-tracking echocardiographic left ventricular longitudinal strain and strain rate were measured. Intraoperator and intraobserver variability were examined and reference intervals were calculated. The potential effects of body weight, age and heart rate on these variables were examined.Intraoperator and intraobserver variability was10% for all parameters except tissue Doppler imaging E' (the peak velocity of early diastolic mitral annular motion as determined by pulsed wave Doppler) and two-dimensional speckle-tracking echocardiographic variables, which were all20%. Thirty-nine dogs were used to create reference intervals. Significant (but mostly weak) effects of age, heart rate and body weight on were detected. Reference intervals were similar to previously published values in different breeds.Breed specific reference intervals for measures of longitudinal left ventricular function in the ESS are presented.

Introduction: Current international guidelines for cardiac rehabilitation (CR) advocate moderate-intensity exercise training (MISS, moderate-intensity steady state). This recommendation predates significant advances in medical therapy for coronary heart disease (CHD) and may not be the most appropriate strategy for the ‘modern’ patient with CHD. High-intensity interval training (HIIT) appears to be a safe and effective alternative, resulting in greater improvements in peak oxygen uptake (VO2 peak). To date, HIIT trials have predominantly been proof-of-concept studies in the laboratory setting and conducted outside the UK. The purpose of this multicentre randomised controlled trial is to compare the effects of HIIT and MISS training in patients with CHD attending UK CR programmes. \ud \ud Methods and analysis: This pragmatic study will randomly allocate 510 patients with CHD to 8 weeks of twice weekly HIIT or MISS training at 3 centres in the UK. HIIT will consist of 10 high-intensity (85–90% peak power output (PPO)) and 10 low-intensity (20–25% PPO) intervals, each lasting 1 min. MISS training will follow usual care recommendations, adhering to currently accepted UK guidelines (ie, >20 min continuous exercise at 40–70% heart rate reserve). Outcome measures will be assessed at baseline, 8 weeks and 12 months. The primary outcome for the trial will be change in VO2 peak as determined by maximal cardiopulmonary exercise testing. Secondary measures will assess physiological, psychosocial and economic outcomes. \ud \ud Ethics and dissemination: The study protocol V.1.0, dated 1 February 2016, was approved by the NHS Health Research Authority, East Midlands— Leicester South Research Ethics Committee (16/EM/ 0079). Recruitment will start in August 2016 and will be completed in June 2018. Results will be published in peer-reviewed journals, presented at national and international scientific meetings and are expected to inform future national guidelines for exercise training in UK CR. Trial registration number: NCT02784873; pre-results.

Compared to males, females have smaller left ventricular (LV) dimensions and volumes, higher ejection fractions (EF), and higher LV longitudinal and circumferential strain. LV twist mechanics determine ventricular function and are preload-dependent. Therefore, the sex differences in LV structure and myocardial function may result in different mechanics when preload is altered. This study investigated sex differences in LV mechanics during acute challenges to preload. With the use of conventional and speckle-tracking echocardiography, LV structure and function were assessed in 20 males (24 ± 6.2 yr) and 20 females (23 ± 3.1 yr) at baseline and during progressive levels of lower body negative pressure (LBNP). Fourteen participants (8 males, 6 females) were also assessed following a rapid infusion of saline. LV end-diastolic volume, end-systolic volume, stroke volume (SV), and EF were reduced in both groups during LBNP ( P < 0.001). While males had greater absolute volumes ( P < 0.001), there were no sex differences in allometrically scaled volumes at any stage. Sex differences were not detected at baseline in basal rotation, apical rotation, or twist. Apical rotation and twist increased in both groups ( P < 0.001) with LBNP. At −60 mmHg, females had greater apical rotation ( P = 0.009), twist ( P = 0.008), and torsion ( P = 0.002) and faster untwisting velocity ( P = 0.02) than males. There were no differences in mechanics following saline infusion. Females have larger LV twist and a faster untwisting velocity than males during large reductions to preload, supporting that females have a greater reliance on LV twist mechanics to maintain SV during severe reductions to preload.

The purpose of this study was to examine ventricular structure and function in Sherpa adolescents to determine whether age-specific differences in oxygen saturation (SpO2) and pulmonary artery systolic pressure (PASP) influence cardiac adaptation to chronic hypoxia early in life. Two-dimensional, Doppler, and speckle-tracking echocardiography were performed on adolescent (9–16 yr) highland Sherpa (HLS; 3,840 m; n = 26) and compared with age-matched lowland Sherpa (LLS; 1,400 m; n = 10) and lowland Caucasian controls (LLC; sea level; n = 30). The HLS were subdivided into pre- and postadolescence; SpO2 was also recorded. Only HLS exhibited a smaller relative left ventricular (LV) end-diastolic volume; however, both HLS and LLS demonstrated a lower peak LV untwisting velocity compared with LLC (92 ± 26 and 100 ± 45 vs. 130 ± 43°/s, P < 0.05). Although SpO2 was similar between groups, PASP was higher in post- vs. preadolescent HLS (30 ± 5 vs. 25 ± 5 mmHg, P < 0.05), which negatively correlated with right ventricular strain rate ( r = 0.50, P < 0.01). Much like their adult counterparts, HLS and LLS adolescents exhibit slower LV diastolic relaxation, despite residing at different altitudes. These findings suggest fundamental differences exist in the diastolic function of Sherpa that are present at an early age and may be retained after migration to lower altitudes. The higher PASP in postadolescent Sherpa is in contrast to previous reports of lowland children at high altitude and, unlike that in lowlanders, was not explained by differences in SpO2; thus different regulatory mechanisms seem to exist between these two distinct populations.

The impact of endurance exercise training on the heart has received significant research and clinical attention for well over a century. Despite this, many issues remain controversial and clinical interpretation can be complex of biomarkers of cardiomyocyte insult. This review assesses the current state of knowledge related to two areas of research where problems with clinical decision making may arise: (1) the impact of chronic endurance exercise training on cardiac structure, function and electrical activity to the point where the athletic heart phenotype may be similar to the expression of some cardiac pathologies (a diagnostic dilemma referred to as the 'grey-zone') and (2) the impact of acute bouts of prolonged exercise on cardiac function and the presentation of biomarkers and cardiomyocyte insult in the circulatory system. The combination of acute endurance exercise stress on the heart and prolonged periods of training are considered together in the final section.

Individuals with high aerobic fitness have lower systolic left ventricular strain, rotation and twist (‘left ventricular (LV) mechanics’) at rest, suggesting a beneficial reduction in LV myofibre stress and more efficient systolic function. However, the mechanisms responsible for this functional adaptation are not known and the influence of aerobic fitness on LV mechanics during dynamic exercise has never been studied. We assessed LV mechanics, LV wall thickness and dimensions, central augmentation index (AIx), aortic pulse wave velocity (aPWV), blood pressure and heart rate in 28 males (age: 21±2 years SD) with a consistent physical activity level (no change>6 months). Individuals were examined at rest and during exercise (40% peak exercise capacity) and separated post hoc into a moderate and high aerobic fitness group (˙V(O2peak): 49 ± 5 and 63 ± 7ml kg−1 min−1, respectively, P 0.05).However, for the same AIx, the high ˙V(O2peak) group had significantly lower LV apical rotation (P =0.002) and LV twist (P =0.003) while basal rotation and strain indices did not differ between groups (P >0.05).We conclude that young males with high aerobic fitness have lower LVapical rotation at rest and during submaximal exercise that can occur without changes in gross LV structure, arterial haemodynamics or heart rate. The findings suggest a previously unknown type of physiological adaptation of the left ventricle that may have important implications for exercise training in older individuals and patient populations in which exercise training has previously failed to show clear benefits for LV function.

Introduction It is well established that endurance exercise results in cardiac adaptation including eccentric hypertrophy of the left ventricle which can complicate the differential diagnosis of the athletic heart from some cardiac pathologies that may pre-dispose to sudden cardiac death. The impact of physiological conditioning on RV structure and function, and a similar diagnostic challenge with arrhythmogenic right ventricular cardiomyopathy (ARVC), has received less attention. A recent guideline paper from the American Society of Echocardiography (ASE) has provided a range for normal RV dimensions and functional deformation. These guidelines suggest the RV inflow (RVI) should be 36 mm or 21 mm/m 2 is a major criterion for the diagnosis of ARVC and furthermore longitudinal RV deformation has been shown to be impaired in these patients. In view of this, the aims of this study are twofold: To provide a range of absolute values for RV dimensions in 102 endurance athletes as well as providing a range of data indexed for body surface area (BSA). To provide normal athlete data for indices of RV strain (ɛ) and strain rate (SR). Methods and Results One hundred and two (102) endurance athletes (86 males and 16 females) with a broad age range (mean ± SD age (range)=36 ± 11 (21–71) years) volunteered and were consecutively enrolled in the study. All subjects were either endurance runners or cyclists and were scanned at peak condition. Echocardiography provided measurements of RVI, RV length, RVOT and RV diastolic area (RVDarea). A 2D strain technique was utilised to provide indices of RVɛ and systolic and diastolic SR. The values for RVI ranged from 30 to 55 mm with 57% of the population having values greater than the normal range. Proximal RVOT ranged from 26 to 49 mm with 40% of the population above the normal range. 28% of the population had RVOT values greater than the proposed “major criteria” for ARVC. RV length ranged from 70 to 110 mm and RVDarea from 13 to 38 cm 2 with values falling above ASE cut-offs in 69% and 59% of the population, respectively. When indexed (ratio scaling) for BSA proximal RVOT ranged from 13 to 25 mm/m 2 with 6% of the population meeting the major criteria for ARVC. Peak RVɛ ranged from −18 to −41% and peak RV SRS′ from −0.75 to −2.65 l/s, consistent with normal ranges proposed by the ASE. RV diastolic deformation indices displayed marked individual variability with a dominant SRE′ (mean ± SD=2.0±0.61 l/s) and smaller SRA′ (1.25±0.56 l/s). Conclusion RV dimensions in endurance athletes are higher than those proposed as “normal” and likewise may be consistent with the criteria for ARVC. Despite this enlargement, RV function in endurance athletes is preserved and therefore the role of RV strain imaging may provide additional diagnostic value in differentiating physiological from pathological adaptation.

The purpose of this study was to determine whether the reduction in stroke volume (SV), previously shown to occur with dehydration and increases in internal body temperatures during prolonged exercise, is caused by a reduction in left ventricular (LV) function, as indicated by LV volumes, strain, and twist (“LV mechanics”). Eight healthy men [age: 20 ± 2, maximal oxygen uptake (VO2max): 58 ± 7 ml·kg−1·min−1] completed two, 1-h bouts of cycling in the heat (35°C, 50% peak power) without fluid replacement, resulting in 2% and 3.5% dehydration, respectively. Conventional and two-dimensional speckle-tracking echocardiography was used to determine LV volumes, strain, and twist at rest and during one-legged knee-extensor exercise at baseline, both levels of dehydration, and following rehydration. Progressive dehydration caused a significant reduction in end-diastolic volume (EDV) and SV at rest and during one-legged knee-extensor exercise (rest: Δ − 33 ± 14 and Δ − 21 ± 14 ml, respectively; exercise: Δ − 30 ± 10 and Δ − 22 ± 9 ml, respectively, during 3.5% dehydration). In contrast to the marked decline in EDV and SV, systolic and diastolic LV mechanics were either maintained or even enhanced with dehydration at rest and during knee-extensor exercise. We conclude that dehydration-induced reductions in SV at rest and during exercise are the result of reduced LV filling, as reflected by the decline in EDV. The concomitant maintenance of LV mechanics suggests that the decrease in LV filling, and consequently ejection, is likely caused by the reduction in blood volume and/or diminished filling time rather than impaired LV function.

Exercise training represents a successful and powerful strategy to prevent future cardiovascular disease. Paradoxically, performance of exercise is also associated with an increased risk of acute cardiac events. Accordingly, patients may present to hospital with cardiac symptoms following a bout of unaccustomed physical effort (e.g. exercise). Current guidelines for the identification of an acute myocardial infarction (AMI) importantly depend on the presence of cardiac troponin as a highly sensitive marker of cardiac damage. However, a number of studies have reported elevated cardiac troponin levels in asymptomatic, healthy subjects after endurance exercise (such as a marathon, prolonged cycling or prolonged walking). These observations indicate that elevated cardiac troponin levels can be the result of cardiac ischemia, and subsequent necrosis, but also may be related to strenuous exercise. In this paper, we present three different clinical cases of post-exercise elevations in cardiac troponins, each with a distinct clinical presentation. These case studies emphasize that a detailed assessment of all symptoms and a thorough patient-history are prerequisite for accurate interpretation of a positive cardiac troponin test following exercise.

During incremental exercise, stroke volume (SV) plateaus at 40–50% of maximal exercise capacity. In healthy individuals, left ventricular (LV) twist and untwisting (“LV twist mechanics”) contribute to the generation of SV at rest, but whether the plateau in SV during incremental exercise is related to a blunting in LV twist mechanics remains unknown. To test this hypothesis, nine healthy young males performed continuous and discontinuous incremental supine cycling exercise up to 90% peak power in a randomized order. During both exercise protocols, end-diastolic volume (EDV), end-systolic volume (ESV), and SV reached a plateau at submaximal exercise intensities while heart rate increased continuously. Similar to LV volumes, two-dimensional speckle tracking-derived LV twist and untwisting velocity increased gradually from rest (all P < 0.001) and then leveled off at submaximal intensities. During continuous exercise, LV twist mechanics were linearly related to ESV, SV, heart rate, and cardiac output (all P < 0.01) while the relationship with EDV was exponential. In diastole, the increase in apical untwisting was significantly larger than that of basal untwisting ( P < 0.01), emphasizing the importance of dynamic apical function. In conclusion, during incremental exercise, the plateau in LV twist mechanics and their close relationship with SV and cardiac output indicate a mechanical limitation in maximizing LV output during high exercise intensities. However, LV twist mechanics do not appear to be the sole factor limiting LV output, since EDV reaches its maximum before the plateau in LV twist mechanics, suggesting additional limitations in diastolic filling to the heart.

Service of Biochemistry, Miguel Servet UniversityHospital, Zaragoza, SpainCorresponding author: E. Serrano-Osta´riz, Section of Physical Education and Sports, University of Zaragoza, C/DomingoMiral, s/n-50009 Zaragoza, Spain. Tel: 1349 767 610 00, Fax: 1349 767 617 20, E-mail: enrise@unizar.esAccepted for publication 17 August 2009Numerous studies have observed cardiac biomarker releasewithprolongedexercise.Despitethis,weareunsureastotheconstituent aspects of any given exercise bout that maybe important in promoting cardiac biomarker release.This study examined the influence of exercise durationand intensity on the appearance of cardiac biomarkers.Twenty-one subjects ran for 45, 90 and 180min at 85%and 95% of their individual anaerobic threshold on sixdifferent days randomized. Cardiac troponin I (cTnI) andN-terminal pro-brain natiuretic peptide (NT-proBNP)were assayed from blood samples collected before,30min and 3h post-exercise. NT-proBNP was elevatedafter all exercise trials (range before: 21–32; rangepost: 38–67ng/L). Peak post-exercise concentrationsof NT-proBNP were associated with exercise duration(P50.049), but not exercise intensity (P50.451). cTnIwas elevated after all exercise trials (range before: 0.007–0.011; range post: 0.008–0.021lg/L). Peak post-exerciseconcentrations of cTnI were associated with exercise dura-tion (P50.003) and intensity (P50.037). Data suggestthat while both cTnI and NT-proBNP increased after allexercise trials, the mediating effect of duration influencedboth NT-proBNP and cTnI while intensity influenced onlycTnI.

The purpose of this study was to examine the combined cardiorespiratory and cerebrovascular responses to head-up tilt (HUT) in young and older trained and untrained humans following moderate-duration exercise. Middle cerebral artery blood flow velocity (MCAv; transcranial Doppler ultrasound), blood pressure (BP; Finometer), and stroke volume (SV) were measured continuously whilst supine and during 60° HUT for 15 min or to pre-syncope in 41 participants [nine young trained; eleven young untrained; twelve older trained; nine older untrained] prior to and following 30 min of treadmill exercise at 70–80% maximal HR. Orthostatic tolerance was not reduced following exercise [Mean (all groups) 14:45 ± 1:19, vs. 14:47 ± 0:43 min:s (before exercise); P = 0.73], and did not differ with age or fitness. Mean MCAv was elevated [~ 5 ± 11%] whilst supine after exercise in the older participants but reduced [~−4 ± 12%] in the young [P = 0.03]. The postural reductions in MCAv [~−22% vs. –17%; P = 0.02], MAP [~−8% vs. −3%; P = 0.04] and SV [~−28% vs. −23%; P = 0.03] were increased after exercise (vs. pre-exercise). Orthostatic tolerance was not reduced following 30 min of exercise, and did not differ with age or fitness, despite more pronounced post-exercise reductions in MCAv, MAP and SV with postural change.

This article was published in Experimental Physiology on 23 November 2010 (online), available at http://dx.doi.org/10.1113/expphysiol.2010.055137

Aim: Alterations in the carotid baroreflex (CBR) control of arterial pressure may explain the reduction in arterial pressure and left ventricular (LV) function after prolonged exercise. We examined the CBR control of heart rate (HR) and mean arterial pressure (MAP), in addition to changes in LV function, pre- to post-exercise. Methods: Seven males (age, mean ± SEM; 29 ± 4 years) completed 4 h of ergometer rowing at a workload of 10–15% below the lactate threshold. The CBR control of HR and MAP was assessed via the rapid neck-suction/pressure protocol. LV systolic function was measured by echocardiography, where ejection fraction (EF), the ratio of systolic blood pressure to end systolic volume (SBP/ESV) and stroke volume (SV) were estimated. Results: Following exercise MAP was reduced (12 ± 3%) and HR was elevated (35 ± 5%; P

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 0.05). 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, 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.