An acute exercise at low to moderate intensity attenuated postprandial lipemia and insulin responses.

Objective: The purpose of this study was to investigate the effects of different exercise intensities on postprandial lipemia (PHTG) and insulin resistance in healthy individuals.

Methods: Participants were 10 adult males with normal fasting triglyceride (TG) concentrations (age = 34 ± 2.8 y, body mass = 72.

Bilateral transfer of motor performance as a function of motor imagery training: a systematic review and meta-analysis.

Objective: The objective of this review was to evaluate the efficacy of mental imagery training (MIT) in promoting bilateral transfer (BT) of motor performance for healthy subjects.

Data Sources: We searched 6 online-databases (Jul-Dec 2022) using terms: "mental practice," "motor imagery training," "motor imagery practice," "mental training," "movement imagery," "cognitive training," "bilateral transfer," "interlimb transfer," "cross education," "motor learning," "strength," "force" and "motor performance."

Study Selection And Data Extraction: We selected randomized-controlled studies that examined the effect of MIT on BT.

Strength training attenuates post-infarct cardiac dysfunction and remodeling.

Post-myocardial infarction (MI) exercise has been employed to improve cardiac function. However, most studies have focused on endurance training (Et). Although Et has been reported to preserve cardiac function, evidence suggests that Et increases left ventricle (LV) interior dimensions as a result of albumin-induced plasma expansion.

Post-myocardial infarction exercise training beneficially regulates thyroid hormone receptor isoforms.

Thyroid hormone receptors (TRs) play a critical role in the expression of genes that are major determinants of myocardial contractility, including α-myosin heavy chain (α-MHC) and β-MHC. After myocardial infarction (MI), changes in myocardial TRs consistently correlate with changes in thyroid hormone (TH) target gene transcription, and this is thought to play a key role in the progression to end-stage heart failure. Interestingly, post-MI exercise training has been shown to beneficially alter TH-target gene transcription and preserve cardiac function without changing serum TH.

Cardiac remodeling and physical training post myocardial infarction.

After myocardial infarction (MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction. There is growing clinical consensus that exercise training may beneficially alter the course of post-MI myocardial remodeling and improve cardiac function. This review summarizes the present state of knowledge regarding the effect of post-MI exercise training on infarcted hearts.

Exercise training induced myosin heavy chain isoform alteration in the infarcted heart.

The myosin heavy chain isoform MHC-α has 3-fold higher ATPase activity than MHC-β. After myocardial infarction (MI), MHC-α expression is profoundly downregulated and MHC-β expression is reciprocally upregulated. This shift, which is attributed to low thyroid hormone (TH), contributes to myocardial systolic dysfunction.

Exercise training combined with angiotensin II receptor blockade reduces oxidative stress after myocardial infarction in rats.

An increase in oxidative stress and decrease in antioxidant enzymes have been suggested to be involved in the pathophysiology of myocardial infarction (MI). In this study in rats, treadmill exercise training and losartan treatment began 1 week post-myocardial infarction (MI) and lasted 8 weeks. We evaluated the changes in the mRNA and protein expressions for the enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase after exercise and losartan treatment post-MI.

Proteomic analysis reveals late exercise effects on cardiac remodeling following myocardial infarction.

Exercise has been shown to improve function of the left ventricle (LV) following myocardial infarction (MI). The mechanisms to explain this benefit have not been fully delineated, but may involve improved mechanics resulting in unloading effects and increased endothelial nitric oxide synthase levels [1,2]. Accordingly, the goal of this study was to determine how the LV infarct proteome is altered by a post-MI exercise regimen.

Effects of exercise and L-arginine on ventricular remodeling and oxidative stress.

Objective: Our aim was to characterize the changes in messenger RNA (mRNA) abundance, protein, and activity levels of the enzymatic antioxidants, superoxide dismutase (SOD), glutathione peroxidase, and catalase by exercise training combined with L-arginine after myocardial infarction (MI).

Methods: L-Arginine (1 g x kg(-1) x d(-1)) and N(G)-nitro-L-arginine methyl ester (L-NAME; 10 mg x kg(-1) x d(-1)) were administered in drinking water for 8 wk. Sprague-Dawley rats were randomized to the following groups: sham-operated control (Sham); MI sedentary (Sed); MI exercise (Ex); MI sedentary + L-arginine (Sed + LA); MI exercise + L-arginine (Ex + LA); MI sedentary + L-NAME (Sed + L-NAME); and MI exercise + L-NAME (Ex + L-NAME).

Predicting postprandial lipemia in healthy adults and in at-risk individuals with components of the cardiometabolic syndrome.

To determine whether a single-point triglyceride (TG) concentration could estimate the 8-hour postprandial lipemic (PPL) response, men and women performed baseline PPL (n=188) and postexercise PPL (n=92) trials. Correlations were generated between TG concentrations at baseline and at various time points after a high-fat meal vs 8-hour area under the TG curve (TG-AUC) and peak TG level. Stepwise multiple regression and bootstrap simulations using TG level and additional predictor variables of sex, age, percentage of body fat, training status, and maximal oxygen consumption indicated that the 4-hour TG concentrations accounted for >90% of the variance in TG-AUC and peak TG responses during the PPL trials.

Exercise training combined with angiotensin II receptor blockade limits post-infarct ventricular remodelling in rats.

Aims: Our aim was to test the hypothesis that angiotensin II receptor blockade combined with exercise training after myocardial infarction (MI) could attenuate post-MI left ventricular remodelling and preserve cardiac function.

Methods And Results: Sprague-Dawley rats underwent ligation of the left descending coronary artery, resulting in MI, or a sham operation. Losartan treatment and exercise training were initiated 1 week after infarction and continued for 8 weeks, either as a single intervention or combined.

Effect of post-myocardial infarction exercise training on the renin-angiotensin-aldosterone system and cardiac function.

After a myocardial infarction (MI), the injured heart undergoes intensive remodeling characterized by activation of the circulating renin-angiotensin-aldosterone system (RAAS), left ventricular (LV) dilation, and contractile dysfunction. Exercise training may attenuate activation of the RAAS and improve myocardial remodeling. In this study, we investigated whether starting exercise training early or late after MI would have different effect on circulating RAAS and LV dilation and function.

Effects of exercise training on cardiac function and myocardial remodeling in post myocardial infarction rats.

To test the hypothesis that early exercise training after myocardial infarction (MI) could preserve cardiac function, alleviate left ventricular (LV) remodeling and induce a protective effect on morphology, male Sprague-Dawley rats underwent coronary ligation or sham operation, and were assigned to 3 groups: Sham, sedentary MI (SedMI), and exercise MI (ExMI). We measured the changes in collagen volume fraction, matrix metalloproteinase (MMP) 1, tissue inhibitor matrix metalloproteinase 1 (TIMP-1), angiotensin II receptor type 1 (AT1), and angiotensin converting enzyme (ACE) at gene and protein levels after 8 weeks of exercise training. Cardiac functions were determined by echocardiographic and hemodynamic measurements.

Effect of exercise duration on postprandial hypertriglyceridemia in men with metabolic syndrome.

We examined the effect of exercise on postprandial hypertriglyceridemia (PHTG) and insulin resistance in individuals with metabolic syndrome. Subjects were 10 hypertriglyceridemic men with insulin resistance [age = 35.0 +/- 1.

Effect of exercise on postprandial lipemia in men with hypertriglyceridemia.

We examined the effect of exercise on postprandial lipemia (PPL) and insulin resistance in individuals with metabolic syndrome. Subjects were 10 hypertriglyceridemia (HTG) males with insulin resistance [age = 40.1 +/- 2.

Effect of exercise timing on postprandial lipemia in hypertriglyceridemic men.

We investigated the effect of exercise timing on attenuation of postprandial hyper-triglyceridemia (PHTG) in individuals with hypertriglyceridemia (HTG). Subjects were 10 males (TG = 290.1 +/- 28.

Activation of nuclear factor-kappaB and its proinflammatory mediator cascade in the infarcted rat heart.

Nuclear transcription factor (NF)-kappaB regulates inflammatory and immune responses by increasing the expression of specific inflammatory genes in various tissues. Whether the infarcted heart includes the activation of NF-kappaB and a proinflammatory mediator cascade that it regulates has not been fully explored. Herein, we monitored the temporal and spatial activation of NF-kappaB, together with expression of tumor necrosis factor (TNF)-alpha, vascular cell adhesion molecule-1 (VCAM-1), and transforming growth factor (TGF)-beta(1), in the infarcted rat heart at and remote to MI from day 3 to day 28 following left coronary artery ligation.

Molecular and cellular events at the site of myocardial infarction: from the perspective of rebuilding myocardial tissue.

The potential for bone marrow-derived progenitor cells (BMDPC) to regenerate myocardial tissue following infarction depends on homing, migration, nourishment, and spatially appropriate growth of BMDPC. Requisite to these objectives is the expression of adhesion molecules (ICAM-1) and chemoattractant cytokines (MCP-1), matrix metalloproteinase (MMP) activity, a neovasculature, and fibrillar collagen scaffolding. We found that enhanced ICAM-l and MCP-1, as well as MMP activity on day 3 and 7 postMI, are present to facilitate the homing, chemotaxis, and migration of circulating cells into the infarct site.

Changes in LPLa and reverse cholesterol transport variables during 24-h postexercise period.

We investigated the time course of exercise-induced lipoprotein lipase activity (LPLa) and reverse cholesterol transport (RCT) during the 24-h postexercise period. Subjects were 10 sedentary normolipidemic males [NTG; fasting triglyceride (TG) = 89.1 +/- 8.