Positive Effects Of Exercise Training Research Articles

Antioxidant Supplementation during Exercise Training

High levels of reactive oxygen species (ROS) produced in skeletal muscle during exercise have been associated with muscle damage and impaired muscle function. Supporting endogenous defence systems with additional oral doses of antioxidants has received much attention as a noninvasive strategy to prevent or reduce oxidative stress, decrease muscle damage and improve exercise performance. Over 150 articles have been published on this topic, with almost all of these being small-scale, low-quality studies. The consistent finding is that antioxidant supplementation attenuates exercise-induced oxidative stress. However, any physiological implications of this have yet to be consistently demonstrated, with most studies reporting no effects on exercise-induced muscle damage and performance. Moreover, a growing body of evidence indicates detrimental effects of antioxidant supplementation on the health and performance benefits of exercise training. Indeed, although ROS are associated with harmful biological events, they are also essential to the development and optimal function of every cell. The aim of this review is to present and discuss 23 studies that have shown that antioxidant supplementation interferes with exercise training-induced adaptations. The main findings of these studies are that, in certain situations, loading the cell with high doses of antioxidants leads to a blunting of the positive effects of exercise training and interferes with important ROS-mediated physiological processes, such as vasodilation and insulin signalling. More research is needed to produce evidence-based guidelines regarding the use of antioxidant supplementation during exercise training. We recommend that an adequate intake of vitamins and minerals through a varied and balanced diet remains the best approach to maintain the optimal antioxidant status in exercising individuals.

Impact of Swimming Exercise Training on the Effects of Modulation of Mitochondrial Permeability Transition and NOS-1 Activation in Medullary Cardiovascular Neurons of Rats

Physical inactivity can be considered one of the major risk factors related to cardiovascular diseases. There are reasons to believe that the positive effect of exercise training is, to a large extent, mediated by modulation of the nervous control of the circulation system. In our previous studies, we showed that modulation of mitochondrial permeability transition in medullary cardiovascular neurons significantly contributes to the hemodynamic reactions in both the norm and a number of pathological states. In this study, we examined in acute experiments on urethane-anesthetized rats the hemodynamic effects mediated by either modulation of mitochondrial permeability transition in medullary neurons, or activation of neuronal NO synthase (NOS-1) in these neuronal populations after preliminary moderate exercise training (everyday swimming sessions of increased duration carried out for four weeks). It was shown that, after exercise training had been completed, the effects of injections of an inductor of mitochondrial permeability transition pore (MPTP) opening, phenylarsine oxide (PAO, 0.5 to 1.5 nmol), into populations of cardiovascular neurons in the medullary autonomic nuclei (nucl. tractus solitarius and paramedian and lateral reticular nuclei) were less expressed, as compared with those in control (untrained) animals. The data obtained suggest that exercise training can exert a protective action on functional activity of medullary neurons due to the decreased sensitivity of MPTPs to their opening. Injections of an inhibitor of MPTP opening, melatonin (0.7 to 2.1 nmol), into populations of medullary neurons under study in trained rats induced a decrease in the systemic arterial pressure (SAP), in contrast to untrained animals demonstrating mostly hypertensive responses following injections of melatonin into the above nuclei. Injections of an activator of neuronal NO synthase (NOS-1), L-arginine, into the medullary nuclei of swimming-trained rats resulted in more expressed hemodynamic shifts than in control animals, which suggests an increase in the activity of neuronal NO synthase in medullary neurons of such animals.

Exercise Effects on Risk of Cardiovascular Disease among Iranian Women

Physical inactivity is more prevalent among women than men, varies by ethnic group, and becomes increasingly prevalent with age. The aim of this study was to examine the effects of a 12-week exercise program on the cardiovascular disease risk and fitness of Iranian middle aged women. This was a randomized controlled trial study. Participants in the training group (n=20) performed treadmill running exercise at a high intensity (70-80% of maximum heart rate, 0% grade) for 30 min/day, 3 days/week. On the other hand, participants in the control group (n=20) were asked to maintain their habitual lifestyle and not change their activity or dietary habits. Measurements of body mass index, waist/hip ratio, blood pressure, total cholesterol, and lipoprotein subtractions were taken before program and after 12 weeks. Changes in 10-year risk scores for coronary heart disease were calculated using Framingham risk equation. Significant decreases in systolic and diastolic blood pressure, reduction in 10-year risk of coronary heart disease, and reduction in lipid levels were found within the training group between baseline and 12-week measurements. No changes were found in these parameters within the control group. The study provides evidence for the positive effects of exercise training on the reduction of cardiovascular disease risks among women aged 40-55 years.

Are Improvements in Physical Fitness after an Exercise Program Related to the Symptomatology in Patients with Fibromyalgia

Problem statement: Physical exercise is considered one of the main strategies in management of Fibromyalgia (FM); While many studies have shown relevant improvements in the patients’ physical condition and psychological status, the efficacy of these treatments have not yet been completely determined and whether or not these improvements are related with symptom severity is still debated. The aim of this study was to evaluate the positive effect of exercise training on physical fitness and second to determine whether any change in aerobic capacity, strengthening or flexibility after exercise training is associated with improvements in symptoms severity of patients with FM. Approach: Thirty women with FM were randomized to either combined exercise group (CE, n = 15) which performed twice-weekly sessions of combined aerobic and resistance exercises, or usual care control group (CG, n = 15). Participants had to complete a Visual Analogue Scale (VAS) for stiffness, sleep disturbances, pain, anxiety and depression. Physical fitness (aerobic capacity, handgrip strength and flexibility) was also assessed at baseline and immediately after 12-week intervention. Results: Aerobic capacity and Range Of Motion (ROM) in both shoulders and in the right hip were significantly greater than controls. Inter-group differences were significant in anxiety and depression. Linear regressions of physical fitness variables and symptomatology showed positive correlations. Conclusions: Physical fitness seems to be related with the improvements in symptom´ severity and due to regular physical activity has demonstrated to be beneficial for individuals with FM it should be included in treatment plans for this patients group.

A Longitudinal, Integrated, Clinical, Histological and mRNA Profiling Study of Resistance Exercise in Myositis

Polymyositis and dermatomyositis are orphan, chronic skeletal muscle disorders characterized by weakness, infiltrations by mononuclear inflammatory cells, and fibrosis. Until recently, patients were advised to refrain from physical activity because of fears of exacerbation of muscle inflammation. However, recent studies have shown that moderate exercise training in combination with immunosuppressive drugs can improve muscle performance. Despite the positive effects of exercise training, the molecular mechanisms underlying the exercise-associated clinical improvements remain poorly understood. The present study was designed to define, at the molecular level, the effects of resistance exercise training on muscle performance and disease progression in myositis patients. We evaluated changes in muscle strength, histology and genome-wide mRNA profiles to determine the beneficial effects of exercise and determine the possible molecular changes associated with improved muscle performance. A total of 8 myositis patients underwent a 7-wk resistance exercise training program that resulted in improved muscle strength and increased maximal oxygen uptake (VO(2max)). Training also resulted in marked reductions in gene expression, reflecting reductions in proinflammatory and profibrotic gene networks, changes that were also accompanied by a reduction in tissue fibrosis. Consistent with the exercise-associated increase in VO(2max), a subset of transcripts was associated with a shift toward oxidative metabolism. The changes in gene expression reported in the present study are in agreement with the performance improvements induced by exercise and suggest that resistance exercise training can induce a reduction in inflammation and fibrosis in skeletal muscle.

The Anti-Inflammatory Actions of Exercise Training.

The list of diseases with a known inflammatory etiology is growing. Cardiovascular disease, osteoporosis, diabetes, geriatric cachexia, and Alzheimer's disease have all been shown to be linked to or exacerbated by aberrantly regulated inflammatory processes. Nevertheless, there is mounting evidence that those who are physically active, or who become physically active, have a reduction in biomarkers associated with chronic inflammation. There was strong early consensus that exercise-induced reductions in inflammation were explained by body mass index or body fatness, but recent studies provide support for the contention that exercise has body fat-independent anti-inflammatory effects. With few exceptions, the anti-inflammatory effects of exercise appear to occur regardless of age or the presence of chronic diseases. What remains unclear are the mechanisms by which exercise training induces these anti-inflammatory effects, but there are several intriguing possibilities, including release of endogenous products, such as heat shock proteins; selective reduction of visceral adipose tissue mass or reducing infiltration of adipocytes by macrophages; shift in immune cell phenotype; cross-tolerizing effects; or exercise-induced shifts in accessory proteins of toll-like receptor signaling. However, future research endeavors are likely to uncover additional potential mechanisms, and it could be some time before functional mechanisms are made clear. In summary, the potential anti-inflammatory influences of exercise training may provide a low-cost, readily available, and effective treatment for low-grade systemic inflammation and could contribute significantly to the positive effects of exercise training on chronic disease.

Substrate oxidation, obesity and exercise training.

Regular physical exercise is of the utmost importance in the treatment of obesity because exercise is one of the factors determining long-term weight maintenance in weight reduction programmes and because exercise has been associated with a reduced risk for developing type 2 diabetes mellitus and cardiovascular disease. Obesity is associated with an impaired utilization of fat as a fuel during post-absorptive conditions, during beta-adrenergic stimulation and possibly during exercise, although the latter data are controversial. One of the underlying mechanisms for the positive effect of exercise training in obesity may be related to its effects on fat utilization because exercise training has been shown to increase basal fat oxidation and exercise fat oxidation in lean volunteers. Data on the effect of aerobic exercise training on exercise fat oxidation are controversial, whereas the available data indicate that exercise training may not be able to increase resting fat oxidation or 24-hour fat oxidation in obese subjects. Because disturbed muscle fat oxidation may be a primary event in the aetiology of obesity it is of the utmost importance to obtain more information on how and whether exercise training may be able to compensate for these impairments.

Rehabilitation bei neuromuskulären Erkrankungen: Stellenwert der medizinischen Trainingstherapie

Neuromuscular diseases are a heterogeneous population of disorders including the different kinds of muscular dystrophies, myopathies, motor neuron diseases and neuropathies. The leading symptom is the mostly progressive muscle weakness due to myopathy or denervation of muscles. Despite progress of molecular diagnosis and improved therapeutic approaches for the majority of neuromuscular diseases there exists no causal treatment. Symptomatic drug therapy is often not sufficient. There is general agreement on the importance of rehabilitative therapy in neuromuscular disease but the scientific basis for the different methods of rehabilitation is poor, resulting in different opinions on suitable therapy. Especially the benefit or potential damage of active therapy in neuromuscular disease was discussed controversially in the past because of case reports of overwork weakness due to unsupervised exercise training. Persons with neuromuscular disease usually have a sedentary lifestyle resulting in an additional disuse weakness. Secondary deconditioning could be a reversible component of disability in neuromuscular disease. Exercise training improves muscle strength or endurance in healthy people. The response to exercise training may include an element of reversing the effects of disuse as well as altering the natural history of neuromuscular disease itself. However, in neuromuscular disease the different effects of strength or endurance training on each type of disease are not known. Research is lacking in determining whether persons with neuromuscular diseases respond to exercise training in a similar beneficial manner. The effects of exercise training are influenced by the kind, progression and stage of disease and by the type, frequency, intensity and duration of exercise training. Patients must have enough residual muscle strength to be able to respond to an exercise training. The comparative value of strength training versus endurance training in neuromuscular diseases has not been evaluated nor do we know the optimal amount of exercise to maintain or improve muscle function. There are only few studies indicating positive effects of exercise training in slowly progressive neuromuscular diseases, the long-term effects of training are not known. Most studies concerned Duchenne muscular dystrophy, patients with postpoliomyelitis sequelae or a variety of neuromuscular disease. These studies have substantial methodological shortcomings, such as too few patients, a large variety of disorders, a combination of exercise training and other therapeutic interventions and in most studies the lack of a separate nonexercising control group having the same disorder. Only few studies have evaluated changes in functionality. To evaluate the effects of training measurements of functionality and quality of life are necessary and not only measurement of muscle strength or aerobic capacity. The benefit of exercise training may vary between different neuromuscular diseases because of differences in pathophysiology. Research on groups with a variety of neuromuscular disorders is not an appropriate way to evaluate the effects of exercise training. Overwork weakness has not been demonstrated in controlled trials of exercise when training is properly supervised. Because of the lack of controlled studies until today a final assessment is not possible.

Exercise training reduces skeletal muscle membrane arachidonate in the obese (fa/fa) Zucker rat.

Compared with the lean (Fa/-) genotype, obese (fa/fa) Zucker rats have a relative deficiency of muscle phospholipid arachidonate, and skeletal muscle arachidonate in humans is positively correlated with insulin sensitivity. To assess the hypothesis that the positive effects of exercise training on insulin sensitivity are mediated by increased muscle arachidonate, we randomized 20 lean and 20 obese weanling male Zucker rats to sedentary or treadmill exercise groups. After 9 wk, fasting serum, three skeletal muscles (white gastrocnemius, soleus, and extensor digitorum longus), and heart were obtained. Fasting insulin was halved by exercise training in the obese rat. In white gastrocnemius and extensor digitorum longus (fast-twitch muscles), but not in soleus (a slow-twitch muscle) or heart, phospholipid arachidonate was lower in obese than in lean rats (P < 0.001). In all muscles, exercise in the obese rats reduced arachidonate (P < 0.03, by ANOVA contrast). We conclude that improved insulin sensitivity with exercise in the obese genotype is not mediated by increased muscle arachidonate and that reduced muscle arachidonate in obese Zucker rats is unique to fast-twitch muscles.