Corrigendum: Characterization of Electrical Activity in Post-myocardial Infarction Scar Tissue in Rat Hearts Using Multiphoton Microscopy.

[This corrects the article DOI: 10.3389/fphys.2018.

Characterization of Electrical Activity in Post-myocardial Infarction Scar Tissue in Rat Hearts Using Multiphoton Microscopy.

The origin of electrical behavior in post-myocardial infarction scar tissue is still under debate. This study aims to examine the extent and nature of the residual electrical activity within a stabilized ventricular infarct scar. An apical infarct was induced in the left ventricle of Wistar rats by coronary artery occlusion.

2-Photon excitation fluorescence microscopy enables deeper high-resolution imaging of voltage and Ca(2+) in intact mice, rat, and rabbit hearts.

We describe a novel two-photon (2P) laser scanning microscopy (2PLSM) protocol that provides ratiometric transmural measurements of membrane voltage (Vm ) via Di-4-ANEPPS in intact mouse, rat and rabbit hearts with subcellular resolution. The same cells were then imaged with Fura-2/AM for intracellular Ca(2+) recordings. Action potentials (APs) were accurately characterized by 2PLSM vs.

Exercise training and losartan improve endothelial function in heart failure rats by different mechanisms.

Objectives: To investigate the mechanisms of losartan- and exercise training-induced improvements on endothelial dysfunction in heart failure.

Design: Sprague-Dawley rats subjected to left coronary artery ligation inducing myocardial infarction and heart failure were randomized to losartan treatment, high-intensity exercise training, or both.

Results: Losartan, but not exercise training, reduced the heart failure-associated elevation in left ventricular end-diastolic pressure (26 ± 2 mmHg vs.

Confocal and multiphoton imaging of intracellular Ca(2+).

This chapter compares the imaging capabilities of a range of systems including multiphoton microscopy in regard to measurements of intracellular Ca(2+) within living cells. In particular, the excitation spectra of popular fluorescent Ca(2+) indicators are shown during 1P and 2P excitation. The strengths and limitations of the current indicators are discussed along with error analysis which highlights the value of matching the Ca(2+) affinity of the dye to a particular aspect of Ca(2+) signaling.

High-intensity aerobic exercise training improves the heart in health and disease.

Regular exercise training confers beneficial effects to the heart as well as to the entire body. This occurs partly because exercise training improves skeletal muscle work capacity and reduces resistance, thus increasing conductance in the peripheral circulation. More directly, exercise training also alters extrinsic modulation of the heart and improves the intrinsic pump capacity of the heart.

Pathological and physiological hypertrophies are regulated by distinct gene programs.

Background: This study aims to investigate changes that occur during progression and establishment of physiological and pathological cardiac hypertrophy, by microarray technology and functional annotations.

Design And Methods: Myocardial infarction leading to heart failure was induced in rats, with animals killed 1, 3, 7, 14, 42, and 92 days after coronary artery ligation. A second group was subjected to daily treadmill exercise and killed 1, 4, 24, and 48 h after a single exercise bout, or after 28 or 56 days of exercise training.

Interval training normalizes cardiomyocyte function, diastolic Ca2+ control, and SR Ca2+ release synchronicity in a mouse model of diabetic cardiomyopathy.

Rationale: In the present study we explored the mechanisms behind excitation-contraction (EC) coupling defects in cardiomyocytes from mice with type-2 diabetes (db/db).

Objective: We determined whether 13 weeks of aerobic interval training could restore cardiomyocyte Ca(2+) cycling and EC coupling.

Methods And Results: Reduced contractility in cardiomyocytes isolated from sedentary db/db was associated with increased diastolic sarcoplasmic reticulum (SR)-Ca(2+) leak, reduced synchrony of Ca(2+) release, reduced transverse (T)-tubule density, and lower peak systolic and diastolic Ca(2+) and caffeine-induced Ca(2+) release.

Gene expression profiling of skeletal muscle in exercise-trained and sedentary rats with inborn high and low VO2max.

The relationship between inborn maximal oxygen uptake (VO(2max)) and skeletal muscle gene expression is unknown. Since low VO(2max) is a strong predictor of cardiovascular mortality, genes related to low VO(2max) might also be involved in cardiovascular disease. To establish the relationship between inborn VO(2max) and gene expression, we performed microarray analysis of the soleus muscle of rats artificially selected for high- and low running capacity (HCR and LCR, respectively).

Unilateral arm strength training improves contralateral peak force and rate of force development.

Neural adaptation following maximal strength training improves the ability to rapidly develop force. Unilateral strength training also leads to contralateral strength improvement, due to cross-over effects. However, adaptations in the rate of force development and peak force in the contralateral untrained arm after one-arm training have not been determined.

Myocardial sarcoplasmic reticulum Ca2+ ATPase function is increased by aerobic interval training.

Objective: Reduced activity of the sarcoplasmic reticulum Ca ATPase-2a (SERCA-2a) contributes to myocardial dysfunction. Exercise training improves myocardial Ca-handling, but SERCA-2a function is uncertain. We assessed SERCA-2a activity after exercise training.

Aerobic capacity-dependent differences in cardiac gene expression.

Aerobic capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn aerobic capacity and cardiac gene expression we examined genome-wide gene expression in hearts of rats artificially selected for high and low running capacity (HCR and LCR, respectively) over 16 generations. The artificial selection of LCR caused accumulation of risk factors of cardiovascular disease similar to the metabolic syndrome seen in human, whereas HCR had markedly better cardiac function.

Activation or inactivation of cardiac Akt/mTOR signaling diverges physiological from pathological hypertrophy.

Cardiomyocyte hypertrophy differs according to the stress exerted on the myocardium. While pressure overload-induced cardiomyocyte hypertrophy is associated with depressed contractile function, physiological hypertrophy after exercise training associates with preserved or increased inotropy. We determined the activation state of myocardial Akt signaling with downstream substrates and fetal gene reactivation in exercise-induced physiological and pressure overload-induced pathological hypertrophies.

Aerobic fitness is associated with cardiomyocyte contractile capacity and endothelial function in exercise training and detraining.

Background: Physical fitness and level of regular exercise are closely related to cardiovascular health. A regimen of regular intensity-controlled treadmill exercise was implemented and withdrawn to identify cellular mechanisms associated with exercise capacity and maximal oxygen uptake (VO2max).

Methods And Results: Time-dependent associations between cardiomyocyte dimensions, contractile capacity, and VO2max were assessed in adult rats after high-level intensity-controlled treadmill running for 2, 4, 8, and 13 weeks and detraining for 2 and 4 weeks.

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy.

Whereas novel pathways of pathological heart enlargement have been unveiled by thoracic aorta constriction in genetically modified mice, the molecular mechanisms of adaptive cardiac hypertrophy remain virtually unexplored and call for an effective and well-characterized model of physiological mechanical loading. Experimental procedures of maximal oxygen consumption (VO(2 max)) and intensity-controlled treadmill running were established in 40 female and 36 male C57BL/6J mice. An inclination-dependent VO(2 max) with 0.