Archive for October 2016

What are the functional and molecular mechanisms underlying prediabetes? Listen as Consulting Editor Michael Wolin (New York Medical College) interviews lead author Zoltan Giricz (Semmelweis University, Hungary) and content expert Hemal Patel (VA San Diego Healthcare System, University of California, San Diego) about the intriguing new work by Koncsos et al, which used a non-genetic rodent model of prediabetes to assess the deterioration of cardiac function in prediabetes caused by disturbances in multiple cellular processes, including mitochondrial oxidative stress. Why did the authors choose a high-fat diet model rather than a genetic model of prediabetes? Is oxidant stress at the sub-sarcolemmal mitochondria level the trigger point for downstream cardiovascular dysfunction? Listen and learn.

Gábor Koncsos, Zoltan V Varga, Tamas Baranyai, Kerstin Boengler, Susanne Rohrbach, Ling Li, Klaus-Dieter Schluter, Rolf Schreckenberg, Tamás Radovits, Attila Oláh, Csaba Mátyás, Árpád Lux, Mahmoud Al-Khrasani, Tímea Komlódi, Nóra Bukosza, Domokos Máthé, László Deres, Monika Barteková, Tomáš Rajtík, Adriana Adameová, Krisztián Szigeti, Péter Hamar, Zsuzsanna Helyes, László Tretter, Pal Pacher, Béla Merkely, Zoltán Giricz, Rainer Schulz, Péter Ferdinandy Diastolic dysfunction in prediabetic male rats: Role of mitochondrial oxidative stress Am J Physiol Heart Circ Physiol, published October 1, 2016. DOI: 10.1152/ajpheart.00049.2016

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What exactly is happening in the metabolism of the exercising individual? Listen as Associate Editor Gary Lopaschuk (University of Alberta, Canada) interviews lead author Kari Kalliokoski (University of Turku, Finland) and content expert Michael Nelson (University of Texas at Arlington) about the work by Heiskanen et al, which studied energy metabolism in the heart during cardiac hypertrophy that was not pathological, but rather a result of exercise. Kalliokoski and colleagues measured changes in myocardial metabolism for healthy, untrained individuals who participated in either high intensity interval training (HIIT) or moderate intensity continuous aerobic training. Using PET imaging, once with a euglycemic hyperinsulinemic clamp and once in a traditional fasting state, Kalliokoski and co-authors studied the right ventricular response to exercise and its training adaptation. Did the HIIT training group achieve better results with just 3 minutes of exercise, compared to the moderate intensity aerobic group which exercised 40 – 60 minutes? Listen now.

Marja A. Heiskanen, Tuija Leskinen, Ilkka H. A. Heinonen, Eliisa Löyttyniemi, Jari-Joonas Eskelinen, Kirsi Virtanen, Jarna C. Hannukainen, Kari K. Kalliokoski Right ventricular metabolic adaptations to high-intensity interval and moderate-intensity continuous training in healthy middle-aged men Am J Physiol Heart Circ Physiol, published September 1, 2016. DOI: 10.1152/ajpheart.00399.2016

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Elevations in systolic blood pressure during both resistance and cardiovascular exercise, and during regular daily activities, are predictive in the development of cardiovascular disease. Can higher levels of general physical activity reduce the rise in systolic blood pressure that occurs with resistance exercise? Listen as Consulting Editor David Gutterman (Medical College of Wisconsin) interviews lead author Takeshi Otsuki (Ryutsu Keizai University, Japan) and content expert Shane Phillips (University of Illinois-Chicago) about the work by Otsuki and colleagues which combined both observational and interventional human studies involving moderate intensity exercise programs. Is blood pressure during exercise a more sensitive predictor of cardiovascular risk than resting blood pressure? Does brachial arterial stiffness affect blood pressure during exercise? Listen and find out.

Takeshi Otsuki, Takahiro Kotato, Asako Zempo-Miyaki Habitual exercise decreases systolic blood pressure during low-intensity resistance exercise in healthy middle-aged and older individuals Am J Physiol Heart Circ Physiol, published October 1, 2016. DOI: 10.1152/ajpheart.00379.2016

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Is there one microRNA playing a primary role in the complex pathogenesis of right ventricular failure caused by pulmonary hypertension? Listen as Associate Editor Fabio Recchia (Temple University Lewis Katz School of Medicine, and Scuola Superiore Sant'Anna, Pisa, Italy) interviews lead author Sachin Gupte (New York Medical College) and content expert Paras Mishra (University of Nebraska Medical Center) about the work by Joshi et al, which used microarray analysis to focus on MiR140 as a potential therapeutic target in a Sugen5416/hypoxia/normoxia model of pulmonary arterial hypertension (PAH). Is MiR31 also a major player in the pathogenesis of this disease? What is the translational relevance of the work by Gupte and colleagues on afterload-induced right ventricular failure? Listen to find out.

Sachindra Raj Joshi, Vidhi Dhagia, Salina Gairhe, John G. Edwards, Ivan F. McMurtry, Sachin A Gupte MicroRNA-140 is elevated and mitofusin-1 is downregulated in the right ventricle of the Sugen5416/Hypoxia/Normoxia model of pulmonary arterial hypertension Am J Physiol Heart Circ Physiol, published July 15, 2016. DOI: 10.1152/ajpheart.00264.2016

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