Dipeptidyl peptidase-4 (DPP-4) inhibitors are a class of oral anti-diabetic drugs, implicated in pleiotropic secondary cardioprotective effects. The aim of the study was to unveil the unknown and possible cardioprotective targets that can be exerted by sitagliptin (Sitg) against ischemia-reperfusion (I/R) injury. Male wistar rats received 2 weeks’ Sitg oral treatment of different doses (25, 50, 100, and 150 mg/kg/day), or saline as a Control. Hearts were then isolated and subjected to two different I/R injury protocols: 10 min perfusion, 45 min regional ischemia, and 120 min reperfusion for infarct size (IS) measurement, or: 10 min perfusion, 45 min regional ischemia and 10 min reperfusion for biochemical analysis: nitric oxide synthases (NOSs) and DPP-4 activity, glucagon-like peptide-1 (GLP-1), Calcium, transient receptor potential vanilloid (TRPV)-1 and calcitonin gene-related peptide (CGRP) levels, transient receptor potential canonical (TRPC)-1 and e-NOS protein expression. NOS inhibitor (l-NAME) and TRPV-1 inhibitor (Capsazepine) were utilized to confirm the implication of both signaling mechanisms in DPP-4 inhibition-induced at the level of IS. Findings show that Sitg (50 mg) resulted in significant decrease in IS and DPP-4 activity, and significant increase in GLP-1, NOS activity, e-NOS expression, TRPV-1 level and TRPC-1 expression, compared to controls. Results of CGRP are in line with TRPV-1, as a downstream regulatory effect. NOS system and transient receptor potential (TRP) channels can contribute to DPP-4 inhibition-mediated cardioprotection against I/R injury using Sitagliptin.

Obesity has been associated with a multitude of metabolic disorders, often clustering with risk factors of cardiovascular disease and type 2 diabetes mellitus, hypertension, dyslipidaemia. Overall, obesity is a worldwide, growing health concern. However, a subgroup of obese individuals with a low burden of metabolic abnormalities have been identified and described as metabolically healthy obese (MHO). Whether the MHO phenotype is protective against obesity-related metabolic disorders in the long-term is presently unclear, and current research examining the potential transition has yielded inconsistent results. In this current narrative review, we aim to provide insights on the role of physical activity (PA) and cardiorespiratory fitness (CRF) in MHO. Lifestyle factors such as PA and CRF may influence the MHO phenotype. Limited studies have characterised energy expenditure and CRF in MHO and metabolically unhealthy obese. However, higher levels of PA, less sedentary behaviour and higher CRF have been observed in MHO individuals. Considering the multiple benefits of PA, it is high time to advocate this lifestyle change beyond its influence on energy balance in a weight loss programme to improve cardiovascular and metabolic risk factors irrespective of body weight and fat mass changes. Improved CRF via increased PA, especially exercise participation, while avoiding weight gain is not only a realistic goal, but should be the primary intervention for MHO populations to prevent the transition to an abnormal metabolic state.

The objective of the study was to determine the effects of tobacco use on selected markers of health and lung function in professional athletes. A total of 108 male professional athletes participated in the study from ten ball game teams in the same sport league in Qatar (age=26.4±5.1 yrs, height=190.6±11.9 cm, and weight=91.5±16.4 kg). The athletes have been playing professionally for about 6.3 years on average. In addition to demographic and tobacco use status, the following clinical variables were measured: resting blood pressure, heart rate, FVC,FEV1 sec, and PEF. The prevalence of tobacco use among the athletes was 27.7%. The FVC, FVC%, andFEV1% were significantly lower among the smokers compared to the nonsmokers (p=0.003, 0.044, and 0.001, resp.). There were no significant differences between cigarettes smokers and nonsmokers in BP, HR,FEV1,FEV1/FVC, PEF, and PEF%. Similarly, those who smoked shisha had lowerFEV1% values as compared to those who did not smoke shisha(p=0.001). The decrease ofFEV1and FVC among smokers compared to nonsmokers is similar to what has been reported in the literature about other populations.

The aim of this study was to investigate the impact of sleep deficiency (SD) on oxidative stress, hs-CRP and cortisol levels and to examine the effects of different intensities of aerobic exercise on these parameters under SD conditions. Thirty-two healthy male university students participated in the study and underwent both normal sleep (NS, 8 h of sleep per night for 3 consecutive days) and SD (4 h of sleep per night for 3 consecutive days). After the SD period, the participants performed treatment for 30 min according to their assigned group [sleep supplement after SD (SSD), low-intensity aerobic exercise after SD (LES), moderate-intensity aerobic exercise after SD (MES), high-intensity aerobic exercise after SD (HES)]. Sleep-related factors were measured at NS and SD, while oxidative stress, hs-CRP and cortisol levels were measured at NS, SD and immediately after treatment by group (AT). The results showed that actual total sleep time (ATST) was significantly reduced during SD compared to NS (p < 0.001), while the visual analogue scale (VAS) and Epworth sleepiness scale (ESS) were significantly increased during SD compared to NS (p < 0.001). The difference in reactive oxygen metabolites (d-ROMs) and cortisol levels showed a significant interaction effect (p < 0.01, p < 0.001, respectively), with LES showing a decrease in d-ROMs and cortisol levels compared to SD (p < 0.05). Similarly, SSD showed a decrease in cortisol levels compared to SD (p < 0.05), while HES led to a significant increase in d-ROMs and cortisol levels compared to SD (p < 0.05). Biological antioxidant potential (BAP) and hs-CRP did not show any significant effect (p > 0.05). These results suggest that LES is the most effective exercise intensity for mitigating the negative effects of SD.