Posts Tagged: exercise

Environmental Determinants of Cardiovascular Disease

Environmental Determinants of Cardiovascular Disease

Aruni Bhatnagar

The effect of sunlight on cardiovascular health. The visible range of sunlight regulates the master clock located in the pacemaker neurons of the suprachiasmatic nucleus, which sets the intrinsic 24-h cycle and synchronizes the light-insensitive peripheral clocks to coordinate cycles of waking, sleeping, and feeding. The UVB radiation converts 7-dehydrocholesterol in the epidermis to pre–vitamin D3, which undergoes thermal isomerization to vitamin D. Vitamin D3 formed in the skin appear in the circulation and is then transported to the liver where it is converted to 25(OH)D3. In kidney, 25(OH) D3 undergoes hydroxylation to form biologically active 1,25(OH)2D. The UVA radiation induces photodegradation of nitrosothiols, such as S-nitrosylglutathione, which leads to the generation of NO, an important regulator of blood pressure. (Illustration credit: Ben Smith.) [Powerpoint File]

The Role of Exercise in Cardiac Aging: From Physiology to Molecular Mechanisms

The Role of Exercise in Cardiac Aging: From Physiology to Molecular Mechanisms

Jason Roh, James Rhee, Vinita Chaudhari, Anthony Rosenzweig

Multiple mechanisms have been proposed for impaired cardiomyocyte function observed in aging, and how exercise partially reverses their effects. (1) Diminished cardiac performance in the pathological hypertrophy of aging is linked to decreased insulin-like growth factor-I (IGF-I)–phosphatidylinositol 3-kinase (PI3K)–AKT and β-adrenergic receptor (β-AR)–cAMP–protein kinase A (PKA) signaling, decreased sarcoplasmic reticulum Ca2+–ATPase2a (SERCA2a) expression and activity and inefficient calcium handling, and mitochondrial dysfunction secondary to excessive reactive oxygen species (ROS). (2) Exercise confers physiological hypertrophy and cardioprotection in the form of enhanced β-adrenergic and IGF-1 signaling, SERCA2a activity and calcium handling, and mitochondrial dynamics, the latter mediated largely through peroxisome proliferator-activated receptor γ coactivator (PGC)-1α. (3) These benefits of exercise potentially mitigate the effects of aging (Illustration Credit: Ben Smith). [Powerpoint File]

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

William R. Hiatt, Ehrin J. Armstrong, Christopher J. Larson, Eric P. Brass

Metabolic and mitochondrial abnormalities in peripheral artery disease. FAD indicates flavin adenine dinucleotide; and NAD, nicotine adenine dinucleotide. Reprinted from Hiatt and Brass [Powerpoint File]

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

William R. Hiatt, Ehrin J. Armstrong, Christopher J. Larson, Eric P. Brass

Hemodynamic alterations in peripheral artery disease. Top, A healthy arterial bed with normal large vessel and microcirculatory flow characteristics. Bottom, A peripheral artery with atherosclerotic occlusive disease. ABI indicates ankle-brachial index. Reprinted from Hiatt and Brass. [Powerpoint File]