Robert Lakin

Effects of moderate-intensity aerobic cycling and swim exercise on post-exertional blood pressure in healthy young untrained and triathlon-trained men and women

Aerobic exercises such as running, walking and cycling are known to elicit a PEH (post-exercise hypotensive) response in both trained and UT (untrained) subjects. However, it is not known whether swim exercise produces a similar effect in normotensive individuals. The complex acute physiological responses to water immersion suggest swimming may affect BP (blood pressure) differently than other forms of aerobic exercises. We tested the hypothesis that an acute bout of swimming would fail to elicit a PEH BP response compared with an equivalent bout of stationary cycling, regardless of training state. We studied 11 UT and ten triathlon-trained young healthy normotensive [SBP/DBP (systolic BP/diastolic BP) <120/80 mmHg)] men and women (age 23±1 years) who underwent 30 min of intensity-matched cycling and swimming sessions to assess changes in BP during a 75-min seated recovery. CO (cardiac output), SV (stroke volume), TPR (total peripheral resistance), HR (heart rate), HRV (HR variability) and core and skin temperature were also assessed. In UT subjects, PEH was similar between cycling (-3.1±1 mmHg) and swimming (-5.8±1 mmHg), with the greater magnitude of PEH following swimming, reflecting a significant fall in SV between modalities (P<0.05). Trained individuals did not exhibit a PEH response following swimming (0.3±1 mmHg), yet had a significant fall in SBP at 50 min post-cycling exercise (-3.7±1 mmHg) (P<0.05). The absence of PEH after swimming in the trained group may reflect a higher cardiac sympathetic outflow [as indicated by the LF (low-frequency) spectral component of HRV) (25 and 50 min) (P<0.05)] and a slower return of vagal tone, consistent with a significant increase in HR between modalities at all time points (P<0.05). These results suggest that training may limit the potential for an effective post-exertional hypotensive response to aerobic swimming.

Characterizing fast pathway in typical and atypical atrioventricular nodal re-entrant tachycardia by atrial-His and His-atrial: more to consider.

We read with interest the paper by Katritsis et al. 1 published in Europace recently. In this study, the authors sought to assess the prevalence, electrophysiological characteristics, and mechanism underlying atypical atrioventricular nodal re-entrant tachycardia (AVNRT), which is not clinically well-defined. It was shown that the atrial-His (AH) interval in atypical ‘fast-slow’ (F-S) AVNRT is longer than His-atrial (HA) interval in typical ‘slow-fast’ (S-F) AVNRT, implying that different fast conduction pathways are utilized in these two types of tachycardia. However, we are holding the following interpretations: …

Letter by Sun et al Regarding Article, "Electrogram Analysis and Pacing Are Complimentary for Recognition of Abnormal Conduction and Far-Field Potentials During Substrate Mapping of Infarct-Related Ventricular Tachycardia".

We read with great interest the article by Baldinger et al1 published in Circulation: Arrhythmia and Electrophysiology recently. The authors showed a correlation between electrogram characteristic with pace capture and S-QRS durations, and a complementary usage of the two was suggested. However, there are some issues that must be addressed before using this combined method in practice. First, 47% of sites without any characteristics for conduction delay on the electrogram showed a prolonged S-QRS duration with pacing. We owe this to the difference between recording ranges …

Getting at the heart of the issue: advanced imaging and stem cell-based therapy offer a novel approach to cardiac resynchronization.

The pump function of the left ventricle (LV) is dependent on synchronous depolarization and contraction to expel blood efficiently. The propagation of the apical-to-basal ventricular contraction pattern is controlled by electrical signalling of the fibre system down the interventricular septum and woven through the free walls of the ventricular myocardium. Dyssynchronous contraction results in mechanical inefficiency, decreased external work, and reduced cardiac output. Myocardial infarction (MI) may cause wall motion abnormalities not only through disturbed electrical conduction, but also through myocardial damage and non-viable tissue. Therapy targeted at preventing adverse remodelling and improving the viability of non-contracting tissue may have the potential for great improvement in ventricular synchronization by addressing mechanical disturbances in the myocardium. Recent advances in stem cell therapy hold promise for regenerative cardiac interventions, as the use of undifferentiated stem cells delivered to the myocardium may be effective in forming functional cardiac tissue and restoring global heart function. While the potential use of such therapies has gained recent attention, the administration of stem cell therapy to ameliorate regional dyssynchrony related to MI has not been examined.

CHANGES IN HEART RATE AND ITS REGULATION BY THE AUTONOMIC NERVOUS SYSTEM DO NOT DIFFER BETWEEN FORCED AND VOLUNTARY EXERCISE IN MICE

Most exercise studies in mice have relied on forced training which can introduce psychological stress. Consequently, the utility of mouse models for understanding exercise-mediated effects in humans, particularly autonomic nervous system (ANS) remodeling, have been challenged. We compared the effects of voluntary free-wheel running vs. non-voluntary swimming on heart function in mice with a focus on the regulation of heart rate (HR) by the ANS. Under conditions where the total excess O2 consumption associated with exercise was comparable, the two exercise models led to similar improvements in ventricular function as well as comparable reductions in HR and its control by parasympathetic nervous activity (PNA) and sympathetic nervous activity (SNA), compared to sedentary mice. Both exercise models also increased HR variability (HRV) by similar amounts, independent of HR reductions. In all mice, HRV depended primarily on PNA, with SNA weakly affecting HRV at low frequencies. The differences in both HR and HRV between exercised vs. sedentary mice were eliminated by autonomic blockade, consistent with the similar intrinsic beating rates observed in atria isolated from exercised vs. sedentary mice. In conclusion, both forced and voluntary exercise induce comparable ventricular physiological remodeling as well as HR reductions and HR-independent enhancements of HRV which were both primarily dependent on increased PNA. New and noteworthy –No previous mouse studies have compared the effects of forced and voluntary exercise on the heart function and its modulation by the autonomic nervous system (ANS). –Both voluntary free-wheel running and forced swimming induced similar improvements in ventricular contractile function, reductions in heart rate (HR) and enhancements of HR variability (HRV). –HR regulation in exercised mice was linked to increased parasympathetic nerve activity and reduced sympathetic nerve activity. – HRV was independent of HR and depended primarily on PNA in both exercised and sedentary mice. – Complete cardiac autonomic blockade eliminated differences in both HR and HRV between exercised and sedentary mice.

Kept in the loop: longitudinal strain-volume relationships for the assessment of left ventricular mechanical performance

In health, the aortic valve facilitates unidirectional forward flow from the left ventricle (LV) to the systemic circulation. This article is protected by copyright. All rights reserved

Interpretation of discrete potential in idiopathic outflow tract ventricular arrhythmia: more consideration.

We read with interest the article by Liu et al. 1 published recently in EP-Europace . In this article, the authors showed that discrete potentials (DPs) appeared to be a prerequisite for idiopathic outflow tract premature ventricular contractions (PVCs) and ventricular tachyarrhythmias (VTs), with DPs-guided mapping predictive of ablation success. A comparison of DPs with more well-established predictors of substrate mapping and ablation success, including local activation time, pace mapping, and unipolar mapping, is needed. However, the additional information …

Hook, line and sinker: adult zebrafish offer a valid model to study mammalian cardiac contractile mechanics.

On a beat-to-beat basis, cardiac contractile function is driven by a multifaceted and dynamic process that is regulated by both intrinsic (e.g. mechanical loading) and extrinsic (e.g. neuro-hormonal) factors (de Tombe et al. 2010). Specifically, the level of contractile activation of adult mammalian cardiomyocytes is modulated by the magnitude of the Ca2+ transient, the dynamic activation–relaxation kinetic response of the sarcomere to activator Ca2+ and the responsiveness of the myofilament to Ca2+, the last of which is dependent on sarcomere length and is a primary mediator of the Frank–Starling response. While transgenic mouse models have provided important insight into the molecular mechanisms underlying cardiac contractile function in health and disease, they are associated with high cost and relatively long generation times. Recently, the zebrafish has emerged as a promising model for the study of cardiac structure–function relationships, due to short generation times, ease of genetic manipulation and low cost. While multiple studies have characterized zebrafish cardiac electrophysiology, Ca2+ dynamics and myofilament mechanical function, it remains unclear whether the cardiac contractile structure–function relationship of adult zebrafish is comparable to that of the mammalian system.

Reacting to too much excitement: ROS overproduction elicits arrhythmogenic Ca2+ waves in the heart

The cardiac cycle is tightly regulated by a number of proteins that function to transfer the electrical stimulus to the contracting chambers of the heart. Movement of calcium ions (Ca2+) within the cell is central to the excitation–contraction coupling, and a key component in the modulation of the strength of each cycle. Increasing demand for greater cardiac output – through changes in myocardial loading or from exogenous stressors (e.g. exercise) – activates the sympathetic nervous system to initiate compensatory mechanisms to augment inotropic function. This occurs through cardiomyocyte β-adrenoreceptor activation. While this response ensures adequate cardiac output, there is evidence that chronic activation of β-adrenoreceptors can initiate maladaptive responses within contractile cells.