The Effect of Acute Intense Exercise on Activity of Antioxidant Enzymes in Smokers and Non-Smokers

Kaempferol has been shown to protect cells against cerebral ischemia/reperfusion injury through inhibition of apoptosis. In the present study, we sought to investigate whether ferroptosis is involved in the oxygen-glucose deprivation/reperfusion (OGD/R)-induced neuronal injury and the effects of kaempferol on ferroptosis in OGD/R-treated neurons. Western blot, immunofluorescence, and transmission electron microscopy were used to analyze ferroptosis, whereas cell death was detected using lactate dehydrogenase (LDH) release. We found that OGD/R attenuated SLC7A11 and glutathione peroxidase 4 (GPX4) levels as well as decreased endogenous antioxidants including nicotinamide adenine dinucleotide phosphate (NADPH), glutathione (GSH), and superoxide dismutase (SOD) in neurons. Notably, OGD/R enhanced the accumulation of lipid peroxidation, leading to the induction of ferroptosis in neurons. However, kaempferol activated nuclear factor-E2-related factor 2 (Nrf2)/SLC7A11/GPX4 signaling, augmented antioxidant capacity, and suppressed the accumulation of lipid peroxidation in OGD/R-treated neurons. Furthermore, kaempferol significantly reversed OGD/R-induced ferroptosis. Nevertheless, inhibition of Nrf2 by ML385 blocked the protective effects of kaempferol on antioxidant capacity, lipid peroxidation, and ferroptosis in OGD/R-treated neurons. These results suggest that ferroptosis may be a significant cause of cell death associated with OGD/R. Kaempferol provides protection from OGD/R-induced ferroptosis partly by activating Nrf2/SLC7A11/GPX4 signaling pathway.

Background: Paralympic Powerlifting (PP) training tends to promote fatigue and oxidative stress. Objective: To analyze the effects of ibuprofen use on performance and oxidative stress in post-training PP athletes. Methodology: Ten national level PP athletes (age: 27.13 ± 5.57) were analyzed for oxidative stress in post-training. The study was carried out in three weeks, (1) familiarization and (2 and 3) evaluated the recovery with the use of a placebo (PLA) and ibuprofen (IBU), 800 mg. The Peak Torque (PT), Torque Development Rate (TDR), Fatigue Index (FI), reactive substances to thiobarbituric acid (TBARS) and sulfhydryl groups (SH) were evaluated. The training consisted of five sets of five repetitions (80–90%) 1-Repetition Maximum (1-RM) in the bench press. Results: The IBU showed a higher PT (24 and 48 h, p = 0.04, ɳ2 p = 0.39), a lower FI (24 h, p = 0.01, ɳ2p = 0.74) and an increased lymphocyte count (p < 0.001; ɳ2p = 4.36). There was no change in oxidative stress. Conclusions: The use of IBU provided improvements in strength and did not protect against oxidative stress.

The novel Coronavirus Disease 2019 (COVID-19) crisis is now present in more than 200 countries. It started in December 2019 and has, so far, led to more than 149, 470,968 cases, 3,152,121 deaths, and 127,133,013 survivors recovered by 28 April 2021. COVID-19 has a high morbidity, and mortality of 2%, on average, whereas most people are treated after a period of time. Some people who recover from COVID-19 are left with 20 to 30% decreased lung function. In this context, exercise focused on skeletal muscle with minimal lung involvement could potentially play an important role. Regular exercise protects against diseases associated with chronic low-grade systemic inflammation. This long-term effect of exercise may be ascribed to the anti-inflammatory response elicited by an acute bout of exercise, which is partly mediated by muscle-derived myokines. The isometric training system seems to have this feature, because this system is involved with the skeletal muscle as the target tissue. However, no studies have examined the effect of exercise on the treatment and recovery of COVID-19, and, more importantly, “muscle–lung cross-talk” as a mechanism for COVID-19 treatment. It is suggested that this theoretical construct be examined by researchers.