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Moderate-intensity aerobic exercise attenuates airway hyperresponsiveness (AHR) in ovalbumin (OVA)-treated mice. Mice were OVA treated and exercised as described in MATERIALS AND METHODS (open squares: sedentary, saline-treated; open circles: exercised, salinetreated; open triangles: sedentary, OVA-treated; solid triangles: exercised, OVA-treated). At the conclusion of the protocol, mice were assessed for changes in AHR via mechanical ventilation with methacholine challenge at increasing concentrations. Results are presented as total lung resistance (cm H 2 O/ml/s; *P , 0.02, as compared with sedentary, OVA-treated mice; n 5 6-8 mice per group).
Source publication
We have reported that moderate-intensity aerobic exercise training attenuates airway inflammation in mice sensitized/challenged with ovalbumin (OVA). The current study determined the effects of repeated bouts of aerobic exercise at a moderate intensity on airway hyperresponsiveness (AHR) in these mice. Mice were sensitized/challenged with OVA or sa...
Contexts in source publication
Context 1
... determine the effect of a moderate-intensity aerobic exercise training on AHR in OVA-treated mice, mice were mechanically ven- tilated and challenged with increasing concentrations of methacholine (0-50 mg/ml); changes in resistance (R) were recorded continuously. Results shown in Figure 1 demonstrate that, at the highest methacho- line dose, OVA-treated, sedentary (SO) mice exhibited a total lung resistance that was approximately 4-fold greater than saline-treated sedentary (S) and exercise (E) controls. In contrast, mice that were OVA-treated and exercised (EO) displayed a 65% reduction in total lung resistance as compared with OVA-treated, sedentary mice (SO); this level of resistance was equivalent to that observed in S and E control groups. ...
Context 2
... contrast, mice that were OVA-treated and exercised (EO) displayed a 65% reduction in total lung resistance as compared with OVA-treated, sedentary mice (SO); this level of resistance was equivalent to that observed in S and E control groups. Significant decreases in overall lung resistance were also observed in OVA-treated and exercised (EO) mice at intermediate methacholine doses (20 mg/ml, 40 mg/ml) as compared with sedentary controls (Figure 1). ...
Context 3
... Improvement of AHR in OVA-Treated Mice Is Dependent upon b 2 -AR b 2 -AR expressed within the airways facilitates bronchodilata- tion (1, 8); therefore, the role of b 2 -AR in exercise-mediated attenuation of AHR in OVA-treated mice was examined. Mice were ventilated and challenged with methacholine at increasing concentrations as described above. ...
Citations
... Several randomized controlled trials in the literature have found that aerobic exercise training is beneficial for functional capacity, airway inflammation, asthma exacerbation, control, healthcare utilization, psychological state, and quality of life [22]. ...
... Thus, under environmental pollution caused by DEP, moderate-intensity aerobic exercise seems to be a protective factor against increases in airway resistance and decreases in lung expansibility that would require a greater pressure and influx of air to maintain active movement. These results appear to corroborate those of previous studies (63,64) and seem to suggest that it is better to be in movement in a TRAP-heavy environment, as opposed to sedentariness; in other words, even under polluted conditions there are still some health benefits to be gained from physical exercise. Our results seem to support those of Tainio et al. (65), who concluded that when traveling to work in polluted cities, it would be better to do so with active aerobic movement than under passive conditions (such as motorized transport). ...
Aerobic exercise is an increasing trend worldwide. However, people are increasingly exercising outdoors, alongside roadways where heavy vehicles release diesel exhaust. We analyzed respiratory effects caused by inhaled diesel particulate emitted by vehicles adhering to Brazilian legislation, PROCONVE Phase P7 (equivalent to EURO 5), as well the effects of exposure during moderate-intensity aerobic exercise. Male C57BL/6 mice were divided into 4 groups for a 4-week treadmill protocol: CE (n=8) received intranasal sterile physiological saline and then performed moderate-intensity exercise (control), CS (n=10) received saline and then remained stationary on the treadmill (control), DS (n=9) received intranasal diesel exhaust particles and then remained stationary, and DE (n=10) was exposed to diesel exhaust and then exercised at moderate intensity. Mice were subsequently connected to a mechanical ventilator (SCIREQ{copyright, serif} flexiVent®, Canada) to analyze the following respiratory mechanics parameters: tissue resistance, elastance, inspiratory capacity, static compliance, Newtonian resistance, and pressure-volume loop area. After euthanasia, peripheral pulmonary tissue strips were extracted and subjected to force-length tests to evaluate parenchymal elastic and mechanical properties, using oscillations applied by a computer-controlled force transducer system; parameters obtained were tissue resistance, elastance, and hysteresivity. DS displayed impaired respiratory mechanics for all parameters, in comparison to CS. DE exhibited significantly reduced inspiratory capacity and static compliance, and increased Newtonian resistance when compared to CE. Exposure to diesel exhaust, both during exercise and rest, still exerts harmful pulmonary effects, even at current legislation limits. These results justify further changes in environmental standards, to reduce the health risks caused by traffic-related pollution.
... These data showed that A779 did not completely prevent the increase in animal performance in the physical test, despite these mice having important pulmonary inflammation and airway remodeling. Ang-(1-7)/Mas pathway is an important anti-inflammatory and anti-fibrotic mechanism triggered by exercise to fight allergic pulmonary inflammation, however, other mechanisms induced by training, such as increased levels of hormones and adrenaline, muscle adaptations, factors released by the muscle [46][47][48] can have accounted for the improvement in physical capacity and have prevented the fall in maximal effort time in OVA-TRE-A779. We also observed that CTRL-SED mice showed an increase in 11% in the maximum effector time at the end of the protocol probably due to the natural gain in muscle mass with growth, since protocol was started in animals with 8 weeks old and finished with 12 weeks old. ...
Aims:
Exercise training increases circulating and tissue levels of angiotensin-(1-7) [Ang-(1-7)], which was shown to attenuate inflammation and fibrosis in different diseases. Here, we evaluated whether Ang-(1-7)/Mas receptor is involved in the beneficial effects of aerobic training in a chronic model of asthma.
Material and methods:
BALB/c mice were subjected to a protocol of asthma induced by ovalbumin sensitization (OVA; 4 i.p. injections) and OVA challenge (3 times/week for 4 weeks). Simultaneously to the challenge period, part of the animals was continuously treated with Mas receptor antagonist (A779, 1 μg/h; for 28 days) and trained in a treadmill (TRE; 60% of the maximal capacity, 1 h/day, 5 days/week during 4 weeks). PGC1-α mRNA expression (qRT-PCR), plasma IgE and lung cytokines (ELISA), inflammatory cells infiltration (enzymatic activity assay) and airway remodeling (by histology) were evaluated.
Key findings:
Blocking the Mas receptor with A779 increased IgE and IL-13 levels and prevented the reduction in extracellular matrix deposition in airways in OVA-TRE mice. Mas receptor blockade prevented the reduction of myeloperoxidase activity, as well as, prevented exercise-induced IL-10 increase. These data show that activation of Ang-(1-7)/Mas receptor pathway is involved in the anti-inflammatory and anti-fibrotic effects of aerobic training in an experimental model of chronic asthma.
Significance:
Our results support exercise training as a non-pharmacological tool to defeat lung remodeling induced by chronic pulmonary inflammation. Further, our result also supports development of new therapy based on Ang-(1-7) or Mas agonists as important tool for asthma treatment in those patients that cannot perform aerobic training.
... Hewitt et al., stated that epinephrine known as a hormone able to dilate bronchus. Obese people whom doing aerobic exercise routinely, is thought to have maximum inspiration volume capacity, and maximum airflow to the lung (Hewitt et al., 2010;Bora, Sudhir and Swamy, 2017). ...
Introduction: Excessive fat accumulation in the obese child causes complex problems in the respiratory system. Respiratory system function can be improved by exercise. One exercise model that is suitable for children is Senam Sehat Anak Indonesia (SSAI). The quality of the respiratory function system is measured using Peak Expiratory Flow Rate (PEFR).
Objective: to validate the PEFR’s differences in obese children before and after performing SSAI.
Methods: This research using one group pre-posttest experimental design with total sample of 20 obese children using purposive sampling method. The research instrument uses weight scale, height scale, and peak flow meter. SSAI was given to all subjects twice a week for six weeks. Paired T Test statistical analysis was used to examine the PEFR’s differences before and after performing SSAI, considered significant if p
... The study of Ueno and coworkers also comes at a time when it has been demonstrated that exercise protects against the development of several features of asthma, as well as reverses established features of asthma, in classical murine models of allergic airway inflammation (10)(11)(12)(13)(14)(15)(16). This has been shown in various strains, both sexes, and different ages of mice using different allergens and different exercise forms, including running and swimming, as well as for highly variable training regimens in terms of duration, frequency, and exercise intensity and in terms of timing and length of the period over which they were performed (10)(11)(12)(13)(14)(15)(16). ...
... The study of Ueno and coworkers also comes at a time when it has been demonstrated that exercise protects against the development of several features of asthma, as well as reverses established features of asthma, in classical murine models of allergic airway inflammation (10)(11)(12)(13)(14)(15)(16). This has been shown in various strains, both sexes, and different ages of mice using different allergens and different exercise forms, including running and swimming, as well as for highly variable training regimens in terms of duration, frequency, and exercise intensity and in terms of timing and length of the period over which they were performed (10)(11)(12)(13)(14)(15)(16). These animal studies are also consistent with human studies showing the salutary effects of physical exercise on asthma symptoms, quality of life, exercise capacity, lung function, and AHR (17,18). ...
... A recent report showed that when aerobic exercise was added to an ovalbumin model of asthma, airway hypersensitivity and airway inflammation improved, and the expression of LT pathways such as 5lipoxygenase, LTC 4 S, and Cys-LT receptors decreased (28). There are several reports that aerobic exercise improves AHR or eosinophilic airway inflammation (29)(30)(31), but it is interesting to report that its effect is manifested by controlling LT production in the airway epithelium (28). The discrepancies between these results and our data presumably reflect differences in exercise intensity and duration, or exercise load in noninflammatory models; however, further analyses will be necessary to explore this issue. ...
Rationale:
It is well known that the prevalence of asthma is higher in athletes, such as Olympic athletes than in the general population.
Objective:
In this study, we analyzed the mechanism of exercise-induced bronchoconstriction by using animal models of athlete asthma.
Methods:
Mice were made to exercise on a treadmill for a total duration of 1 week, 3 weeks, or 5 weeks. We analyzed airway hyperresponsiveness (AHR), bronchoalveolar lavage fluid (BALF), lung homogenates, and tissue histology at each duration. For mice that were treated, i.e., the treatment model, treatments were administered from the 4th to 5th week. We also collected the induced sputum from human athletes with asthma and their supernatant were analyzed.
Results:
AHR to methacholine was enhanced with repeated exercise stimulation, although cell composition in BALF did not change. Exercise-induced hypertrophy of airway smooth muscle and subepithelial collagen deposition. Cysteinyl-leukotrienes (cys-LTs) was significantly increased with exercise duration. Montelukast treatment significantly reduced AHR and airway remodeling. The expressions of phospholipase A2 group IV (PLA2G4) and leukotriene C4 synthase in the airway epithelium were upregulated in the exercise model, and the inhibition of PLA2 ameliorated AHR and airway remodeling with associated lower levels of cys-LTs. The levels of cys-LTs in the sputum of athletes were not different between athletes with and without sputum eosinophilia.
Conclusion:
These data suggested that AHR and airway remodeling was caused by repeated and strenuous exercise. Cys-LTs from the airway epithelium but not inflammatory cells may play an important role in this mouse model.
... In an analysis of relative changes in available non-controlled, controlled and randomized controlled trials in children, adolescent and adult patients with asthma, exercise training in the form of land-based exercise or swimming was shown to improve BHR by 53% and EIB by 9% compared with control conditions; also, improvements in BHR explained part of the observed improvement in quality of life and exercise capacity [87]. Animal studies suggest that aerobic exercise training attenuates BHR via a mechanism that involves β2-adrenergic receptors [92]. ...
Asthma is the commonest respiratory disease and one of unceasingly increasing prevalence and burden. As such, asthma has attracted a major share or scientific interest and clinical attention. With the various clinical and pathophysiological aspects of asthma having been extensively investigated, the important association between asthma and physical activity remains underappreciated and insufficiently explored. Asthma impacts adversely on physical activity. Likewise, poor physical activity may lead to worse asthma outcomes. This concise clinical review presents the current recommendations for physical activity, discusses the available evidence on physical activity in asthma, and examines the causes of low physical activity in adult asthmatic patients. It also reviews the effect of daily physical activity and exercise training on the pathology and clinical outcomes of asthma. Finally, it summarizes the evidence on interventions targeting physical activity in asthma.
... Proper aerobic exercise habits can reduce the likelihood of developing exercise-induced asthma by reducing ventilation during mild and moderate exercise, and it may reduce awareness of breathlessness via strengthening respiratory muscles (Chandratilleke et al., 2012). Exercise also enhances the levels of circulating catecholamines, such as epinephrine (Hewitt et al., 2010), which has been implicated in bronchodilatation (Gilbert et al., 1988). Aerobic exercise improves cardiovascular fitness and the quality of life of asthmatic patients by increasing their physical strength, neuromuscular coordination, and selfconfidence (Chandratilleke et al., 2012). ...
... Previous studies demonstrated that a single bout of moderateintensity aerobic exercise decreased airway inflammation via inhibition of NF-κB phosphorylation, but not AHR or airway remodeling in OVA-challenged mice (Hewitt et al., 2009). While, repeated bouts of moderate-intensity aerobic exercise decreased AHR, airway smooth muscle thickness and increased levels of circulating epinephrine through a mechanism that involves β2adrenergic receptors (Hewitt et al., 2010). Long-term treadmill aerobic exercise inhibited DEP-induced lung inflammation, oxidative, and nitrosative stress in mice . ...
Oxidative stress and inflammation are key pathways responsible for the pathogenesis of asthma. Aquatic exercise (AE) has been proven to elicit a variety of biological activities such as anti-oxidant and anti-inflammatory effects. However, although proper forms of AE provide beneficial health effects, incorrect forms and types of AE are potentially injurious to health. Several studies have investigated AE, but the relationship between types of AE and asthma has not been fully elucidated. This study evaluated the effects of two types of AE according to resistance on ovalbumin (OVA)-induced allergic airway inflammation in mice. BALB/c mice were subjected to OVA sensitization and challenge, and then to different types of AE including, walking and swimming, in a pool filled with water to a height of 2.5 and 13 cm for 30 min, respectively. AE reduced OVA-induced eosinophilic inflammation, airway hyperresponsiveness, and serum immunoglobulin E level. AE significantly inhibited increases in interleukin (IL)-4, IL-5, IL-13, histamine, leukotriene D4, and tryptase levels in bronchoalveolar lavage fluid (BALF). AE also effectively suppressed mucus formation, lung fibrosis, and hypertrophy of airway smooth muscle within the lung tissues. This exercise markedly reduced the levels of malondialdehyde while increased glutathione and superoxide dismutase (SOD) activity in lung tissues. Furthermore, AE significantly decreased tumor necrosis factor-α, IL-6 levels, and prostaglandin E2 production in BALF. The inhibitory effects of swimming on the levels of biomarkers related to oxidative stress and inflammation were greater than that of walking. These effects may have occurred through upregulation of NF-E2-related factor 2/heme oxygenase-1 signaling and suppression of mitogen-activated protein kinase/nuclear factor-κB pathway. Cumulative results from this study suggest that AE might be beneficial in mitigating the levels of biomarkers related to oxidative stress and inflammation. Thus, this therapy represents a crucial non-pharmacological intervention for treatments of allergic airway inflammation.
... Thirdly, animal models have suggested that exercise training reduces airway responsiveness 18 and inflammation in mice 19 . In a Brazilian RCT 10 , a 12-week aerobic training program reduced both BHR and serum proinflammatory cytokines interleukin-6 (IL-6) and monocyte chemoattractant-1 (MCP-1), as well as reduced sputum eosonophils and fractional exhaled nitric oxide (FeNO) in asthma patients with more inflammation. ...
We conducted a randomized controlled trial to test the hypothesis that a 24-week exercise intervention improves asthma control in adults. Adults with mild or moderate asthma were randomly assigned to either the exercise intervention group (IG) or the reference group (RG). Participants in IG received an individualized exercising program, including aerobic exercise at least three times a week for ≥30 minutes, muscle training, and stretching. The primary outcome was asthma control, measured by Asthma Control Test (ACT), asthma-related symptoms, and peak expiratory flow (PEF) variability. We estimated the risk (i.e. probability) of improvement in asthma control and the risk difference (RD) between IG and RG. Of 131 subjects (67 IG/64 RG) entered, 105 subjects (51/54) completed the trial (80%), and 89 (44/45) were analysed (68%). The ACT became better among 26 (62%) participants in IG and among 17 (39%) participants in RG. The effect of intervention on improving asthma control was 23% (RD = 0.23, 95% CI 0.027–0.438; P = 0.0320). The intervention also reduced shortness of breath by 30.1% (RD = 0.301, 95% CI 0.109–0.492; P = 0.003). The change in PEF variability was similar in both groups. Regular exercise improves asthma control measured by the ACT, while has little effect on PEF variability.
... In the present study, skeletal muscle weight and glucose metabolism were increased by exercise, and miso consumption potentiated these effects. The exercise regimen implemented in this study was of moderate intensity, at 50% to 75% of maximal oxygen consumption [41,42], equivalent to gentle running by humans. At this exercise intensity, both carbohydrates and lipids are used as energy sources [43], and the routine was, therefore, effective for suppression of visceral fat accumulation. ...
We investigated whether the difference in miso consumption between the Japanese diets of 1975 and 2010 has influenced the observed increase in diet-induced obesity. To recreate the 2010 and 1975 Japanese high-fat diets with the corresponding proportions of miso, freeze-dried miso was added to high-fat mouse feed at 1.6% and 2.6%, respectively. When 5-week-old male Institute of Cancer Research (ICR) mice were provided each of these diets ad libitum for 8 weeks, it was found that the white adipose tissue weight and adipocyte area were lower in mice receiving the 1975 diet than in those receiving the 2010 diet. Therefore, high miso consumption is one reason why the 1975 Japanese diet tended to not lead to obesity. Next, the combined effects of treadmill exercise and miso consumption were investigated. The mice were divided into three groups, which were provided either a high-fat diet (group C), a high-fat diet with exercise (group C + E), or a miso-supplemented high-fat diet with exercise (group M + E) for 8 weeks. In this experiment, the white adipose tissue weight and adipocyte area in group M + E were lower than in group C. When the mRNA expression of lipid metabolism-associated genes in adipose tissue was measured, we found that expression of Hsl (lipase, hormone sensitive), which is involved in lipolysis, and Pparγ (peroxisome proliferator activated receptor gamma), which regulates adipocyte differentiation upstream of Hsl, was increased in group M + E. These results clearly demonstrated that lipid accumulation in the adipose tissues is suppressed by miso consumption in combination with exercise.
