Delayed Impairment of Postural, Physical, and Muscular Functions Following Downhill Compared to Level Walking in Older People

Transient symptoms of muscle damage emanating from unaccustomed eccentric exercise can adversely affect muscle function and potentially increase the risk of falling for several days. Therefore, the aims of the present study were to investigate the shorter- and longer-lasting temporal characteristics of muscle fatigue and damage induced by level (i.e., concentrically biased contractions) or downhill (i.e., eccentrically biased contractions) walking on postural, physical, and muscular functions in older people. Nineteen participants were matched in pairs for sex, age and self-selected walking speed and allocated to a level (n = 10, age = 72.3 ± 2.9 years) or downhill (n = 9, age = 72.1 ± 2.2 years) walking group. Postural sway, muscle torque and power, physical function (5× and 60 s sit-to-stand; STS), and mobility (Timed-Up-and-Go; TUG) were evaluated at baseline (pre-exercise), 1 min, 15 min, 30 min, 24 h, and 48 h after 30 min of level (0% gradient) or downhill (−10% gradient) walking on a treadmill. Following downhill walking, postural sway (+66 to 256%), TUG (+29%), 60 s STS (+29%), five times STS (−25%) and concentric power (−33%) did not change at 1–30 min post exercise, but were significantly different (p 0.05). These findings have established for the first time distinct impairment profiles between concentric and eccentric exercise. Muscle damage emanating from eccentrically biased exercise can lead to muscle weakness, postural instability and impaired physical function persisting for several days, possibly endangering older adult’s safety during activities of daily living by increasing the risk of falls

Endothelial Dysfunction and Heart Failure with Preserved Ejection Fraction—An Updated Review of the Literature

Heart failure (HF) is a clinical syndrome consisting of typical symptoms and signs due to structural and/or functional abnormalities of the heart, resulting in elevated intracardiac pressures and/or inadequate cardiac output. The vascular system plays a crucial role in the development and progression of HF regardless of ejection fraction, with endothelial dysfunction (ED) as one of the principal features of HF. The main ED manifestations (i.e., impaired endothelium-dependent vasodilation, increased oxidative stress, chronic inflammation, leukocyte adhesion, and endothelial cell senescence) affect the systemic and pulmonary haemodynamic and the renal and coronary circulation. The present review is aimed to discuss the contribution of ED to HF pathophysiology—in particular, HF with preserved ejection fraction—ED role in HF patients, and the possible effects of pharmacological and non-pharmacological approaches. For this purpose, relevant data from a literature search (PubMed, Scopus, EMBASE, and Medline) were reviewed. As a result, ED, assessed via venous occlusion plethysmography or flow-mediated dilation, was shown to be independently associated with poor outcomes in HF patients (e.g., mortality, cardiovascular events, and hospitalization due to worsening HF). In addition, SGLT2 inhibitors, endothelin antagonists, endothelial nitric oxide synthase cofactors, antioxidants, and exercise training were shown to positively modulate ED in HF. Despite the need for future research to better clarify the role of the vascular endothelium in HF, ED represents an interesting and promising potential therapeutic target

Endothelial dysfunction and heart failure with preserved ejection fraction—an updated review of the literature

Heart failure (HF) is a clinical syndrome consisting of typical symptoms and signs due to structural and/or functional abnormalities of the heart, resulting in elevated intracardiac pressures and/or inadequate cardiac output. The vascular system plays a crucial role in the development and progression of HF regardless of ejection fraction, with endothelial dysfunction (ED) as one of the principal features of HF. The main ED manifestations (i.e., impaired endothelium-dependent vasodilation, increased oxidative stress, chronic inflammation, leukocyte adhesion, and endothelial cell senescence) affect the systemic and pulmonary haemodynamic and the renal and coronary circulation. The present review is aimed to discuss the contribution of ED to HF pathophysiology—in particular, HF with preserved ejection fraction—ED role in HF patients, and the possible effects of pharmacological and non-pharmacological approaches. For this purpose, relevant data from a literature search (PubMed, Scopus, EMBASE, and Medline) were reviewed. As a result, ED, assessed via venous occlusion plethysmography or flow-mediated dilation, was shown to be independently associated with poor outcomes in HF patients (e.g., mortality, cardiovascular events, and hospitalization due to worsening HF). In addition, SGLT2 inhibitors, endothelin antagonists, endothelial nitric oxide synthase cofactors, antioxidants, and exercise training were shown to positively modulate ED in HF. Despite the need for future research to better clarify the role of the vascular endothelium in HF, ED represents an interesting and promising potential therapeutic target.</p