Bariatric procedures are on the rise as a surgical treatment for morbid obesity. In reproductive age of women, bariatric surgeries will improve factors related to anovulation and lead to spontaneous fertility. Spontaneous pregnancy can happen within a year after bariatric surgery due to higher level of sex hormone binding globulin and follicular stimulating hormone and reduction in androgens level. Reduction of length of follicular phase of menstrual cycle was reported and contribute to improved ovulatory status.

This study aimed to compare the effects of intensity (I) and duration (D) on the oxidative stress marker (malondialdehyde, MDA) and the responses of the antioxidant enzymes (catalase, CAT; glutathione peroxidase, GPx; superoxide dismutase, SOD) among sedentary adults. In a crossover design, 25 sedentary adults performed nine cycling exercise sessions with a constant load of 50%, 60%, and 70% VO₂peak for 10-, 20-, and 30-min each. Plasma MDA, CAT, GPx, and SOD activity were measured before and immediately after each exercise session. Results show that MDA concentration and SOD activity increased significantly immediately after exercise at all intensities and durations, except SOD decreased significantly at 70% $\dot{\mathrm{V}}$O₂pk for 30 min. CAT activities also increased significantly after exercise at 50% $\dot{\mathrm{V}}$O₂pk for 10 and 20 min but decreased at 60% $\dot{\mathrm{V}}$O₂pk for 30 min and at 70% $\dot{\mathrm{V}}$O₂pk for all durations. GPx activity decreased significantly after 20 and 30 min at all intensity levels. In conclusion, our results show that cycling at 50%, 60%, and 70% $\dot{\mathrm{V}}$O₂pk for 10, 20, and 30 min increased oxidative stress and antioxidant activities, but with different responses. These findings suggest that the starting exercise intensity for sedentary adults should not exceed 70% $\dot{\mathrm{V}}$O₂pk.

Musculoskeletal disorder (MSD) is a major health problem, which can lead to an enormous burden to the institution as well as chronic disability to the individual. Teachers are at risk of developing MSD due to the exposure to various ergonomic risk factors. Teachers of special education, for example, are expected to perform extra duty such as lifting and moving students, feeding food, changing diapers, and helping them in ambulation. Although there is an adequate amount of scientific research on MSD’s prevalence and its risk factors among regular teachers, only few studies have focused on special education teachers. This review aimed to address these gaps by describing the evidence from various papers on the prevalence of MSD among regular and special education teachers and the related risk factors. The papers have been gathered using electronic databases, including PubMed, Science Direct, Google Scholar, and Springer. The prevalence of MSD among regular teachers ranges from 48.7% to 73.7%, while the prevalence ranges from 38.7% to 94% in special education teachers. Risk factors, such as individual (age, duration of teaching, working hours, and work burden), physical (teaching activities, affected body areas), and psychological factors (stress, anxiety, fear), were identified. From the review, it is recommended to implement ergonomically designed workplaces, comprehensive ergonomic training, psychological approaches, and functional training among teachers at risk.

T2DM is known to cause disturbances in glucose homeostasis and negative changes in the heart muscle, while aging and diabetes are recognized risk factors for CVD. Given this, our study aims to investigate a method for controlling and managing CVDs induced by T2DM in elderly populations. To achieve this, we categorized 40 rats into 5 groups, including HAD (n = 8), HA (n = 8), AD (n = 8), AHT (n = 8), and ADT (n = 8). The exercise protocol consisted of eight weeks of HIIT (three sessions per week) performed at 90–95% of maximal speed. Following cardiac tissue extraction, we assessed the levels of IGF-1, PI3K, and AKT proteins using Western blot technique, and analyzed the histopathological variations of the heart tissue using H&E, Sudan Black, and Masson’s trichrome tissue staining. The histological findings from our study demonstrated that T2DM had a significant impact on the development of pathological hypertrophy and fibrosis in the heart tissue of elderly individuals. However, HIIT not only effectively controlled pathological hypertrophy and fibrosis, but also induced physiological hypertrophy in the AHT and ADT groups compared to the HA and AD groups. Results from Sudan Black staining indicated that there was an increase in lipid droplet accumulation in the cytoplasm of cardiomyocytes and their nuclei in the HA and AD groups, while the accumulation of lipid droplets decreased significantly in the AHT and ADT groups. In both the AHT group and the ADT group, a single HIIT session led to a reduction in collagen fiber accumulation and fibrotic frameworks. Our research also revealed that diabetes caused a significant elevation in the levels of IGF-1, PI3K, and AKT proteins, but after eight weeks of HIIT, the levels of these proteins decreased significantly in the training groups. Overall, our findings suggest that HIIT may be a suitable non-pharmacological approach for improving histological and physiological changes in elderly individuals with T2DM. However, we recommend further research to examine the impact of HIIT training on both healthy and diseased elderly populations.

Background: Type 2 diabetes is one of the most common metabolic diseases in recent years and has become an important risk factor for cardiovascular disorders. The first goal is to reduce type 2 diabetes, and in the case of cardiovascular disease, the second goal is to reduce and manage that disorder.Materials and methods: The rats were divided into 4 groups: Healthy Control (n=8), Diabetes Control (n=8), Diabetes Training (n=8), and Healthy Training (n=8). The protocol consisted of 8 weeks of High-intensity interval (5 sessions per week), where the training started with 80% of the peak speed in the first week, and 10% was added to this speed every week. To measure the level of B-catenin, c-MYC, GSK3B, and Bcl-2 proteins using the western blot method, cardiac pathological changes were measured using hematoxylin and eosin staining, Masson’s trichrome and PAS staining and apoptosis using the TUNEL method.Findings: Histological results showed that diabetes causes significant pathological hypertrophy, fibrosis, and severe apoptosis in heart tissue. HIIT training significantly reduced pathological hypertrophy and fibrosis in heart tissue, and the rate of cardiomyocyte apoptosis was greatly reduced. This research showed that diabetes disorder increases the levels of B-catenin and c-Myc proteins and causes a decrease in the expression of GSK3B and Bcl-2 proteins. After eight weeks of HIIT training, the levels of B-catenin and c-Myc proteins decreased significantly, and the levels of GSK3B and Bcl-2 proteins increased.Conclusion: This study showed that HIIT could be a suitable strategy to reduce cardiomyopathy in type 2 diabetic rats. However, it is suggested that in future studies, researchers should perform different intensities and exercises to promote exercise goals in type 2 diabetic cardiomyopathy.

Myocardial remodelling is a molecular, cellular, and interstitial adaptation of the heart in response to altered environmental demands. The heart undergoes reversible physiological remodelling in response to changes in mechanical loading or irreversible pathological remodelling induced by neurohumoral factors and chronic stress, leading to heart failure. Adenosine triphosphate (ATP) is one of the potent mediators in cardiovascular signalling that act on the ligand-gated (P2X) and G-protein-coupled (P2Y) purinoceptors via the autocrine or paracrine manners. These activations mediate numerous intracellular communications by modulating the production of other messengers, including calcium, growth factors, cytokines, and nitric oxide. ATP is known to play a pleiotropic role in cardiovascular pathophysiology, making it a reliable biomarker for cardiac protection. This review outlines the sources of ATP released under physiological and pathological stress and its cell-specific mechanism of action. We further highlight a series of cardiovascular cell-to-cell communications of extracellular ATP signalling cascades in cardiac remodelling, which can be seen in hypertension, ischemia/reperfusion injury, fibrosis, hypertrophy, and atrophy. Finally, we summarize current pharmacological intervention using the ATP network as a target for cardiac protection. A better understanding of ATP communication in myocardial remodelling could be worthwhile for future drug development and repurposing and the management of cardiovascular diseases.