Optimizing cardiovascular benefits of exercise: a review of rodent models.
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ABSTRACT:
SUBMITTER: Davis B
PROVIDER: S-EPMC3699221 | biostudies-other | 2013 Mar
REPOSITORIES: biostudies-other
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Project description:Exercise stimulates systemic and tissue-specific adaptations that protect against lifestyle related diseases including obesity and type 2 diabetes. Exercise places high mechanical and energetic demands on contracting skeletal muscle, which require finely-tuned protein post-translational modifications involving signal transduction (e.g. phosphorylation) to elicit appropriate short- and long-term adaptive responses. To uncover the breadth of protein phosphorylation events underlying the adaptive responses to endurance exercise and skeletal muscle contraction, we performed global, unbiased mass spectrometry-based phosphoproteomic analyses of skeletal muscle from two rodent models, in situ muscle contraction in rats and treadmill-based endurance exercise in mice.
2019-07-22 | PXD010452 | Pride
Project description:The extremes of exercise capacity and health are considered a complex interplay between genes and the environment. In general, the study of animal models has proven critical for deep mechanistic exploration that provides guidance for focused and hypothesis-driven discovery in humans. Hypotheses underlying molecular mechanisms of disease and gene/tissue function can be tested in rodents to generate sufficient evidence to resolve and progress our understanding of human biology. Here we provide examples of three alternative uses of rodent models that have been applied successfully to advance knowledge that bridges our understanding of the connection between exercise capacity and health status. First we review the strong association between exercise capacity and all-cause morbidity and mortality in humans through artificial selection on low and high exercise performance in the rat and the consequent generation of the "energy transfer hypothesis." Second we review specific transgenic and knockout mouse models that replicate the human disease condition and performance. This includes human glycogen storage diseases (McArdle and Pompe) and α-actinin-3 deficiency. Together these rodent models provide an overview of the advancements of molecular knowledge required for clinical translation. Continued study of these models in conjunction with human association studies will be critical to resolving the complex gene-environment interplay linking exercise capacity, health, and disease.
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Project description:Exercise is advocated in the management of type 1 diabetes (T1D), but the effects of different forms of exercise training on cardiovascular risk factors in T1D still remain unclear. The aim of this study was to conduct a systematic review and meta-analysis on exercise training for cardiovascular risk factors in T1D. Six electronic databases were systematically searched for randomized or non-randomized controlled studies reporting associations between exercise training and cardiovascular risk factors in T1D. Weighted mean differences (WMD) of each cardiovascular risk factor between exercise groups and control groups were calculated using a random effects model. A total of 24 studies reported the effects of exercise training on cardiovascular risk factors. Exercise training increased maximal aerobic power (3.01 mL·kg-1·min-1, 95% confidence interval, CI, 0.94 to 6.38) and reduced glycated hemoglobin (HbA1c; -0.45%, 95% CI -0.73 to -0.17), daily insulin dosage (-0.88 U·kg-1, 95% CI -1.27 to -0.48), and total cholesterol (-0.38 mmol·L-1, 95% CI -0.71 to -0.04). Exercise training did not lead to consistent changes in body mass index (BMI), blood pressure, triglycerides, high-density lipoprotein cholesterol (HDL-C), or low-density lipoprotein cholesterol (LDL-C). In persons living with T1D, exercise training is associated with a beneficial cardiovascular profile, including improvements in lipid profile, glycemic control (decreased daily insulin dosage and HbA1c), and aerobic fitness.
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Project description:Exercise enhances learning and memory in animals and humans. The role of peripheral factors that may trigger the beneficial effects of running on brain function has been sparsely examined. In particular, it is unknown whether AMP-kinase (AMPK) activation in muscle can predict enhancement of brain plasticity. Here we compare the effects of running and administration of AMPK agonist 5-Aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR, 500 mg/kg), for 3, 7 or 14 days in one-month-old male C57BL/6J mice, on muscle AMPK signaling. At the time-points where we observed equivalent running- and AICAR-induced muscle pAMPK levels (7 and 14 days), cell proliferation, synaptic plasticity and gene expression, as well as markers of oxidative stress and inflammation in the dentate gyrus (DG) of the hippocampus and lateral entorhinal cortex (LEC) were evaluated. At the 7-day time-point, both regimens increased new DG cell number and brain-derived neurotrophic factor (BDNF) protein levels. Furthermore, microarray analysis of DG and LEC tissue showed a remarkable overlap between running and AICAR in the regulation of neuronal, mitochondrial and metabolism related gene classes. Interestingly, while similar outcomes for both treatments were stable over time in muscle, in the brain an inversion occurred at fourteen days. The compound no longer increased DG cell proliferation or neurotrophin levels, and upregulated expression of apoptotic genes and inflammatory cytokine interleukin-1β. Thus, an exercise mimetic that produces changes in muscle consistent with those of exercise does not have the same sustainable positive effects on the brain, indicating that only running consistently benefits brain function.
2015-12-21 | GSE64607 | GEO
Project description:Different literature reviews of gambling disorder (GD) neurobiology have been focused on human studies, others have focused on rodents, and others combined human and rodent studies. The main question of this review was: which are the main neurotransmitters systems and brain structures relevant for GD based on recent rodent studies? This work aims to review the experimental findings regarding the rodent´s neurobiology of GD. A search in the Pub Med database was set (October 2012-October 2017) and 162 references were obtained. After screening, 121 references were excluded, and only 41 references remained from the initial output. More, other 25 references were added to complement (introduction section, neuroanatomical descriptions) the principal part of the work. At the end, a total of 66 references remained for the review. The main conclusions are: 1) according to studies that used noninvasive methods for drug administration, some of the neurotransmitters and receptors involved in behaviors related to GD are: muscarinic, N-methyl-D-aspartate (NMDA), cannabinoid receptor 1 (CB1), cannabinoid receptor 2 (CB2), dopamine 2 receptor (D2), dopamine 3 receptor (D3), and dopamine 4 receptor (D4); 2) moreover, there are other neurotransmitters and receptors involved in GD based on studies that use invasive methods of drug administration (eg, brain microinjection); example of these are: serotonin 1A receptor (5-HT1A), noradrenaline receptors, gamma-aminobutyric acid receptor A (GABAA), and gamma-aminobutyric acid receptor B (GABAB); 3) different brain structures are relevant to behaviors linked to GD, like: amygdala (including basolateral amygdala (BLA)), anterior cingulate cortex (ACC), hippocampus, infralimbic area, insular cortex (anterior and rostral agranular), nucleus accumbens (NAc), olfactory tubercle (island of Calleja), orbitofrontal cortex (OFC), medial prefrontal cortex (mPFC), prefrontal cortex (PFC) - subcortical network, striatum (ventral) and the subthalamic nucleus (STN); and 4) the search for GD treatments should consider this diversity of receptor/neurotransmitter systems and brain areas.
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Project description:Autism is a complex condition with many traits, including differences in auditory sensitivity. Studies in human autism are plagued by the difficulty of controlling for aetiology, whereas studies in individual rodent models cannot represent the full spectrum of human autism. This systematic review compares results in auditory studies across a wide range of established rodent models of autism to mimic the wide range of aetiologies in the human population. A search was conducted in the PubMed and Web of Science databases to find primary research articles in mouse or rat models of autism which investigate central auditory processing. A total of 88 studies were included. These used non-invasive measures of auditory function, such as auditory brainstem response recordings, cortical event-related potentials, electroencephalography, and behavioural tests, which are translatable to human studies. They also included invasive measures, such as electrophysiology and histology, which shed insight on the origins of the phenotypes found in the non-invasive studies. The most consistent results across these studies were increased latency of the N1 peak of event-related potentials, decreased power and coherence of gamma activity in the auditory cortex, and increased auditory startle responses to high sound levels. Invasive studies indicated loss of subcortical inhibitory neurons, hyperactivity in the lateral superior olive and auditory thalamus, and reduced specificity of responses in the auditory cortex. This review compares the auditory phenotypes across rodent models and highlights those that mimic findings in human studies, providing a framework and avenues for future studies to inform understanding of the auditory system in autism.
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Project description:BackgroundMarfan syndrome (MF) leads to aortic root dilatation and a predisposition to aortic dissection, mitral valve prolapse, and primary and secondary cardiomyopathy. Overall, regular physical exercise is recommended for a healthy lifestyle, but dynamic sports are strongly discouraged in MF patients. Nonetheless, evidence supporting this recommendation is lacking. Therefore, we studied the role of long-term dynamic exercise of moderate intensity on the MF cardiovascular phenotype.Methods and resultsIn a transgenic mouse model of MF (Fbn1C1039G/+), 4-month-old wild-type and MF mice were subjected to training on a treadmill for 5 months; sedentary littermates served as controls for each group. Aortic and cardiac remodeling was assessed by echocardiography and histology. The 4-month-old MF mice showed aortic root dilatation, elastic lamina rupture, and tunica media fibrosis, as well as cardiac hypertrophy, left ventricular fibrosis, and intramyocardial vessel remodeling. Over the 5-month experimental period, aortic root dilation rate was significantly greater in the sedentary MF group, compared with the wild-type group (?mm, 0.27±0.07 versus 0.13±0.02, respectively). Exercise significantly blunted the aortic root dilation rate in MF mice compared with sedentary MF littermates (?mm, 0.10±0.04 versus 0.27±0.07, respectively). However, these 2 groups were indistinguishable by aortic root stiffness, tunica media fibrosis, and elastic lamina ruptures. In MF mice, exercise also produced cardiac hypertrophy regression without changes in left ventricular fibrosis.ConclusionsOur results in a transgenic mouse model of MF indicate that moderate dynamic exercise mitigates the progression of the MF cardiovascular phenotype.
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Project description:BackgroundPhysical inactivity is an important risk factor for cardiovascular disease. The benefits of exercise in patients with chronic diseases, including cardiovascular diseases, are well established. For patients with sickle cell disease, medical recommendation was to avoid physical exercise for fear of triggering painful crises or increasing the impairment of the cardiopulmonary function. Only recently, studies have shown safety in exercise programs for this population. Despite that, there is no report that assess the effects of physical exercise on cardiac parameters in patients with sickle cell disease.ObjectiveThis study aimed to evaluate the impact of regular physical exercise (a home-based program) on cardiovascular function in patients with sickle cell disease.DesignA quasi-randomized prospective controlled trial.SettingDuring the years 2015 and 2016, we started recruiting among adult patients treated at a Brazilian Center for Patients with Sickle Cell Disease to participate in a study involving a home exercise program. The experimental (exercise) and control groups were submitted to clinical evaluation and cardiovascular tests before and after the intervention. Analysis of variance was applied to compare groups, considering time and group factors.ParticipantsTwenty-seven adult outpatients with a sickle cell disease diagnosis.InterventionsExercise group (N = 14): a regular home-based aerobic exercise program, three to five times per week not exceeding give times per week, for eight weeks; no prescription for the control group (N = 13).Main outcome measuresEchocardiographic and treadmill test parameters.ResultsThe exercise group showed significant improvement in cardiovascular tests, demonstrated by increased distance traveled on a treadmill (p<0.01), increased ejection fraction (p < 0.01) and improvement of diastolic function assessed by mitral tissue Doppler E' wave on echocardiography (p = 0.04). None of the patients presented a sickle cell crisis or worsening of symptoms during the exercise program.ConclusionThe selected home-based exercise program is safe, feasible, and promotes a favorable impact on functional capacity and cardiovascular function in sickle cell disease patients.
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