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This study investigated the chronic and acute influence of resistance exercise on blood pressure in women with metabolic syndrome before and after climacteric. Twenty sedentary women, nine non-menopausal (RNM) and 11 menopausal (RM), performed training for 12 weeks. Meanwhile, 23 controls, 11 not menopausal (CNM) and 12 menopausal (CM), remained sedentary. Blood pressure was measured before and after the training period in conditions of rest and after a session of exercise. Training promoted variations in blood pressure at rest from 116±13 to 118±10 mmHg (p=0.73) and from 128±12 mmHg to 120±11mmHg (p=0.12) in RNM and RM, respectively. CNM and CM varied from 115±11 to 116±12 mmHg (p=0.9) and from 115±14 mmHg to 116±13 mmHg (p=0.74). Blood pressure values in one acute session did not differ between groups (p>0.05). Resistance training did not improve blood pressure in women with metabolic syndrome, regardless of climacteric.

Phase angle, obtained by bioelectrical impedance, is an indicator of cellular integrity and has been proposed as a prognostic parameter in patients who are critically ill. This systematic review aimed to evaluate the association between phase angle and adverse clinical outcomes in hospitalized patients with coronavirus disease–2019 (COVID‐19). An extensive literature search was performed in the MEDLINE/PubMed, Embase, and Web of Science databases, with interest in observational studies evaluating the association between phase angle and adverse clinical outcomes in individuals aged ≥18 years hospitalized with COVID‐19. Studies were independently selected by two reviewers, according to eligibility criteria. Subsequently, data were extracted and presented in a qualitative synthesis. The evaluation of the quality of the studies was performed according to the Newcastle‐Ottawa scale. The full methodology was published in PROSPERO (ID CRD42022306177). A total of 392 articles were identified, resulting in seven selected studies, of which six were prospective cohorts and one was retrospective. In the quality assessment, six studies obtained scores equal to or greater than seven, indicating a low risk of bias. A total of 750 participants composed the samples of the selected studies. Five studies reported an independent association between phase angle and adverse clinical outcomes during hospitalization for COVID‐19, with emphasis on prolonged hospitalization and mechanical ventilation and higher mortality in patients with a lower phase angle. Thus, phase angle measurement can be useful in the early identification of risks in patients hospitalized with COVID‐19, for the purpose of adequacy of clinical management.

Asthma is a heterogeneous disease of the airways characterized by chronic inflammation associated with bronchial and smooth muscle hyperresponsiveness. Currently, different murine models for the study of asthma show poor bronchial hyperresponsiveness due to a scarcity of smooth muscle and large airways, resulting in a failure to reproduce smooth muscle hyperreactivity. Thus, we aimed to standardize a guinea pig model of chronic allergic lung inflammation mimicking airway smooth muscle hyperreactivity observed in asthmatics (Asth). Animals were randomly divided into a control group (Ctrl), which received saline (0.9% NaCl), and the Asth group, subjected to in vivo sensitization with ovalbumin (OVA) nebulization. Morphological analysis was performed by hematoxylin-eosin staining. Bronchial hyperresponsiveness was evaluated by nebulization time in the fifth, sixth, and seventh inhalations (NT5-7) and tracheal isometric contractions were assessed by force transducer. Total antioxidant capacity was measured by the 2,2-diphenyl-1-picrylhydrazyl (DPPH) method and protein expression by Western blot. Histologically, the Asth group developed peribronchial cellular infiltrate, epithelial hyperplasia and smooth muscle thickening. After the fourth nebulization, the Asth group developed bronchial hyperreactivity. The trachea from the Asth group contracted after in vitro stimulation with OVA, differing from the Ctrl group, which showed no response. Additionally, airway smooth muscle hyperreactivity to carbachol and histamine was observed in the Asth group only in intact epithelium preparations, but not to KCl, and this effect was associated with an augmented production of reactive oxygen species. Moreover, lung inflammation impaired the relaxant potency of isoproterenol only in intact epithelium preparations, without interfering with nifedipine, and it was found to be produced by transforming growth factor-β negative modulation of β adrenergic receptors and, furthermore, big-conductance Ca 2+ -sensitive K + channels. These effects were also associated with increased levels of phosphatidylinositol 3-kinases but not extracellular signal-regulated kinases 1/2 or phosphorylation, and augmented α-actin content as well, explaining the increased smooth muscle mass. Furthermore, pulmonary antioxidant capacity was impaired in the Asth group. Therefore, we developed a standardized and easy-to-use, reproducible guinea pig model of lung inflammation that mimics airway smooth muscle hypercontractility, facilitating the investigation of the mechanisms of bronchial hyperresponsiveness in asthma and new therapeutic alternatives.

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