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Dehydration accrued during intense prolonged whole‐body exercise in the heat compromises peripheral blood flow and cardiac output (Q˙). A markedly reduced stroke volume (SV) is a key feature of the dehydration‐induced cardiovascular strain, but whether the lower output of the heart is mediated by peripheral or cardiac factors remains unknown. Therefore, we repeatedly quantified left ventricular (LV) volumes, LV mechanics (LV twist, a marker of systolic muscle function, and LV untwisting rate, an independent marker of LV muscle relaxation), left intra‐ventricular pressure gradients, blood volume and peripheral blood flow during 2 hr of cycling in the heat with and without dehydration (DEH: 4.0 ± 0.2% body mass loss and EUH: euhydration control, respectively) in eight participants (three females and five males). While brachial and carotid blood flow, blood volume, SV, LV end‐diastolic volume (LVEDV), cardiac filling time, systemic vascular conductance and Q˙ were reduced in DEH compared to EUH after 2 hr, LV twist and untwisting rate tended to be higher (p = .09 and .06, respectively) and intra‐ventricular pressure gradients were not different between the two conditions (p = .22). Furthermore, LVEDV in DEH correlated strongly with blood volume (r = .995, p < .01), head and forearms beat volume (r = .98, p < .05), and diastolic LV filling time (r = .98, p < .05). These findings suggest that the decline in SV underpinning the blunted Q˙ with exercise‐induced dehydration is caused by compromised LV filling and venous return, but not intrinsic systolic or diastolic LV function. Dehydration reduces stroke volume and cardiac output during intense prolonged exercise in the heat, but the underlying peripheral and cardiac mechanisms are not fully understood. We show that the reduced stroke volume accounting for the impaired cardiac output is closely associated with diminished left ventricular filling secondary to decreased peripheral blood flow and volume, compromised venous return, and reduced cardiac filling time. These findings highlight the importance of peripheral mechanisms in cardiac performance during exercise.

During exercise stress, heart rate (HR) increases to support cardiac output, which also reduces ventricular filling time. Although echocardiography is widely used to assess cardiac function, studies display conflicting data on the dynamic changes in the healthy trained and untrained heart during rest and acute exercise stress. To address these discrepancies, we tested a new echocardiography exercise protocol on two groups with significant differences in cardiorespiratory fitness. Ten untrained individuals with maximal oxygen uptake of 38 ± 8 ml/kg/min and 10 endurance‐trained athletes matched for body surface area but with higher maximal oxygen uptake (71 ± 5 ml/kg/min) were evaluated at rest, during semi‐recumbent cycling at 25 and 75 W and at a relative workload intensity eliciting a HR of 140 beats/min (HR140). Stroke volume was 36% higher in the trained at rest, and this difference increased during exercise to 42% at 25 W, 46% at 75 W and 63% at HR140 (all P < 0.05). In contrast, no group differences were found in markers of myocardial function (ventricular contraction and relaxation velocities) or other traditional echocardiographic measures of ventricular function at rest or exercise for a given HR. However, while similar at rest, diastolic and systolic function provided limited insight into differences between less fit and highly fit individuals. The new exercise echocardiography protocol improves the ability to uncover differences in dynamic changes in diastolic filling capacity that explain the previously reported higher end‐diastolic compliance in endurance‐trained athletes. What is the central question of this study? Do dynamic changes in cardiac function during acute exercise stress differ between healthy untrained and endurance‐trained individuals, and does exercise echocardiography improve detection of potential differences? What is the main finding and its importance? Endurance‐trained athletes exhibit significantly higher stroke volumes and diastolic filling rates during exercise compared with untrained individuals, despite similar echocardiographic markers when matched for heart rate. Our study shows that conventional echocardiographic measures are insufficient to detect these functional differences. The key finding lies in the ability of the new exercise echocardiography protocol to reveal enhanced diastolic filling capacity in athletes, which explains the higher end‐diastolic compliance observed in endurance‐trained individuals.

It is widely accepted that cardiac output matches the prevailing peripheral demand in healthy humans. However, it remains unknown whether stroke volume and heart rate are regulated interdependently to arrive at a specific cardiac output. The aim of this study was to determine whether the healthy human heart responds specifically according to the peripheral demands of heat stress and exercise. Eleven healthy humans (women/men n = 3/8; age = 26 ± 2 years; body mass = 73 ± 11 kg) underwent leg heat stress and cycling exercise (60 W), with and without blood flow restriction (pressure set at the prevailing mean arterial pressure of the individual). Cardiac output was measured with triplane echocardiography. Additionally, haemodynamics, oxygen consumption, carbon dioxide production and lactate were assessed. Data were analysed using two‐way repeated‐measures ANOVA. Despite stable heat and exercise demands, cardiac output decreased significantly with blood flow restriction in both conditions (Δ−0.87 and −1.03 L min−1, 17% and 11%, respectively, p = 0.01), owing to a decline in end‐diastolic volume (p < 0.0001) and stroke volume (p < 0.0001) not sufficiently compensated for by an increase in heart rate (p = 0.001). Importantly, these responses were accompanied by an increased rate of skin temperature rise (p = 0.04) during heat stress and a significantly greater rise in circulating lactate (p < 0.0001) during exercise. The cardiac output response to local heat stress and submaximal exercise does not appear to be entirely specific to the peripheral thermal and energetic requirements. This finding supports the theory that even the healthy heart does not coordinate stroke volume and heart rate to arrive at a specific target output. What is the central question of this study? Cardiac output supposedly matches an increased peripheral demand in healthy humans. Conversely, the mismatch of supply and demand is a hallmark of cardiovascular diseases, such as hypertension and heart failure. Here, we partly separated the local blood flow supply and demand to examine whether cardiac output responds specifically to the peripheral demand in healthy humans. What is the main finding and its importance? The cardiac output response to local heat stress and submaximal exercise does not appear to be entirely specific to the peripheral thermal and energetic requirements. Interpretation of clinical presentations might need to be altered, because even the healthy heart does not supply a specific cardiac output during heat stress and exercise.

PurposeIn 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.MethodsTwenty-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.ResultsThe 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.ConclusionsAn 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.

While it is well‐established that a period of interval training performed at near maximal effort, such as speed endurance training (SET), enhances intense exercise performance in well‐trained individuals, less is known about its effect on cardiac morphology and function as well as blood volume. To investigate this, we subjected 12 Under‐20 Danish national team ice hockey players (age 18 ± 1 years, mean ± SD) to 4 weeks of SET, consisting of 6–10 × 20 s skating bouts at maximal effort interspersed by 2 min of recovery conducted three times weekly. This was followed by 4 weeks of regular training (follow‐up). We assessed resting cardiac function and dimensions using transthoracic echocardiography and quantified total blood volume with the carbon monoxide rebreathing technique at three time points: before SET, after SET and after the follow‐up period. After SET, stroke volume had increased by 10 (2–18) mL (mean (95% CI)), left atrial end‐diastolic volume by 10 (3–17) mL, and circumferential strain improved by 0.9%‐points (1.7–0.1) (all P < 0.05). At follow‐up, circumferential strain and left atrial end‐diastolic volume were reverted to baseline levels, while stroke volume remained elevated. Blood volume and morphological parameters for the left ventricle, including mass and end‐diastolic volume, did not change during the study. In conclusion, our findings demonstrate that a brief period of SET elicits beneficial central cardiac adaptations in elite ice hockey players independent of changes in blood volume. What is the central question of this study? Can a short 4‐week period of speed endurance training (SET) enhance central cardiovascular function and blood volume in youth elite ice hockey players? What is the main finding and its importance? Only a few weeks of SET enhances several markers of cardiac function in youth elite ice hockey players. These findings emphasize the potential benefits of incorporating SET into the training regimen of elite athletes, contributing valuable insights into optimizing cardiovascular performance in this population.

An increasing number of end-stage heart failure patients are now implanted with continuous-flow left ventricular assist devices (CF-LVADs). Although this therapeutic approach is associated with improved clinical outcomes, continuous flow physiology reduces arterial pulse pressure and pulsatility to an extent that is unique to this population. Recent data suggest that high blood pressure (BP) contributes to life-threatening complications such as pump thrombosis and stroke of CF-LVAD patients. However, limited understanding of the distinct hemodynamics of these pumps makes measurement and, consequently, medical management of BP quite challenging. Here, we review the evolution of LVAD design, the impact of CF-LVAD flow, and “artificial pulse” technology on hemodynamics and BP measurement, as well as suggest new approaches for the assessment and interpretation of the unique physiology of modern LVADs.

Increased left ventricular (LV) twist and untwisting rate (LV twist mechanics) are essential responses of the heart to exercise. However, previously a large variability in LV twist mechanics during exercise has been observed, which complicates the interpretation of results. This study aimed to determine some of the physiological sources of variability in LV twist mechanics during exercise. Sixteen healthy males (age: 22 ± 4 years, [Formula: see text]O2peak: 45.5 ± 6.9 ml∙kg-1∙min-1, range of individual anaerobic threshold (IAT): 32-69% of [Formula: see text]O2peak) were assessed at rest and during exercise at: i) the same relative exercise intensity, 40%peak, ii) at 2% above IAT, and, iii) at 40%peak with hypoxia (40%peak+HYP). LV volumes were not significantly different between exercise conditions (P > 0.05). However, the mean margin of error of LV twist was significantly lower (F2,47 = 2.08, P < 0.05) during 40%peak compared with IAT (3.0 vs. 4.1 degrees). Despite the same workload and similar LV volumes, hypoxia increased LV twist and untwisting rate (P < 0.05), but the mean margin of error remained similar to that during 40%peak (3.2 degrees, P > 0.05). Overall, LV twist mechanics were linearly related to rate pressure product. During exercise, the intra-individual variability of LV twist mechanics is smaller at the same relative exercise intensity compared with IAT. However, the absolute magnitude (degrees) of LV twist mechanics appears to be associated with the prevailing rate pressure product. Exercise tests that evaluate LV twist mechanics should be standardised by relative exercise intensity and rate pressure product be taken into account when interpreting results.

ObjectiveCardiac output, a fundamental parameter of cardiovascular function, has consistently been shown to increase across healthy pregnancy; however, the time course and magnitude of adaptation remains equivocal within published literature. The aim of the present meta-analyses was to comprehensively describe the pattern of change in cardiac output during healthy pregnancy.MethodA series of meta-analyses of previously published cardiac output data during healthy, singleton pregnancies was completed. PubMed and Scopus databases were searched for studies published between 1996 and 2014. Included studies reported absolute values during a predetermined gestational age (non-pregnant, late first trimester, early and late second trimester, early and late third trimester, early and late postpartum). Cardiac output was measured through echocardiography, impedance cardiography or inert gas rebreathing. Observational data were meta-analysed at each gestational age using a random-effects model. If reported, related haemodynamic variables were evaluated.ResultsIn total, 39 studies were eligible for inclusion, with pooled sample sizes ranging from 259 to 748. Cardiac output increased during pregnancy reaching its peak in the early third trimester, 1.5 L/min (31%) above non-pregnant values. The observed results from this study indicated a non-linear rise to this point. In the early postpartum, cardiac output had returned to non-pregnant values.ConclusionThe present results suggest that cardiac output peaks in the early third trimester, following a non-linear pattern of adaptation; however, this must be confirmed using longitudinal studies. The findings provide new insight into the normal progression of cardiac output during pregnancy.