RESUMEN
(1) Background: Years of research have identified ischemic preconditioning (IPC) as a crucial endogenous protective mechanism against myocardial ischemia-reperfusion injury, enhancing the myocardial cell's tolerance to subsequent ischemic damage. High-intensity interval training (HIIT) is promoted by athletes because it reduces exercise duration and improves metabolic response and cardiopulmonary function. Our objective was to evaluate and compare whether HIIT and IPC could reduce myocardial ischemia and reperfusion injury in rats. (2) Methods: Male Sprague-Dawley rats were divided into four groups: sham surgery, coronary artery occlusion (CAO), high-intensity interval training (HIIT), and ischemic preconditioning (IPC). The CAO, HIIT, and IPC groups experienced 40 min of coronary artery occlusion followed by 3 h of reperfusion to induce myocardial ischemia-reperfusion injury. Subsequently, the rats were sacrificed, and blood samples along with cardiac tissues were examined. The HIIT group received 4 weeks of training before surgery, and the IPC group underwent preconditioning before the ischemia-reperfusion procedure. (3) Results: The HIIT and IPC interventions significantly reduced the extent of the myocardial infarction size and the levels of serum troponin I and lactate dehydrogenase. Through these two interventions, serum pro-inflammatory cytokines, including TNF-α, IL-1ß, and IL-6, were significantly decreased, while the anti-inflammatory cytokine IL-10 was increased. Furthermore, the expression of pro-apoptotic proteins PTEN, caspase-3, TNF-α, and Bax in the myocardium was reduced, and the expression of anti-apoptotic B-cell lymphoma 2 (Bcl-2) was increased, ultimately reducing cellular apoptosis in the myocardium. In conclusion, both HIIT and IPC demonstrated effective strategies with potential for mitigating myocardial ischemia-reperfusion injury for the heart.
RESUMEN
Introduction: Lactobacillus plantarum PS128 (PS128) could be considered an antioxidant supplement to reduce muscle fatigue and improve exercise capacity recovery after vigorous exercise. Purpose: The purpose of this study is to investigate the effect of PS128 on muscle fatigue and electromyography (EMG) activity after a half-marathon (HM). Methods: The experimental design used a repeated-measures design with a double-blind approach. The participants either took two capsules of PS128 for 4 weeks as the PS128 group (PSG, n = 8) or took two capsules of a placebo for 4 weeks as the placebo group (PLG, n = 8) to ensure counterbalancing. The time points of the maximal voluntary isometric contraction (MVIC) and EMG activity test were set before probiotics were taken (baseline), 48 h before HM (Pre), and immediately at 0 h, 3 h, 24 h, 48 h, 72 h, and 96 h after HM. Results: EMG activity included median power frequency (MDF), integrated EMG (iEMG), and neuromuscular efficiency (peak torque/iEMG). The MVICs of knee extensors, analyzed by using an isokinetic dynamometer, showed a decrease from the Pre to 0 h (p = 0.0001), 3 h (p < 0.0001), 24 h (p < 0.0001), 48 h (p < 0.0001), 72 h (p = 0.0002), and 96 h (p = 0.0408) time points in the PLG. Sidak's multiple comparisons tests showed that the PLG was significantly lower than the PSG at 0 h (p = 0.0173), 3 h (p < 0.0001), 24 h (p < 0.0001), 48 h (p < 0.0001), 72 h (p < 0.0001), and 96 h (p = 0.0004) time points. The MDF of vastus medialis oblique (VMO) in the PLG was significantly decreased 24 h after HM and significantly lower than that in the PSG at all times points after HM. The iEMG of VMO in the PLG was significantly decreased 48 h after HM and significantly lower than that in the PSG at 0 h, 3 h, 24 h, 48 h, and 72 h after HM. Conclusion: The PS128 supplementation may prevent the decrease in MDF, iEMG, and peak torque after vigorous exercise. Recreational runners may consider implementing a probiotic supplementation regimen as a potential strategy to mitigate muscle fatigue following HM.
RESUMEN
Allergenic serine proteases are important in the pathogenesis of asthma. One of these, Pen c 13, is the immunodominant allergen produced by Penicillium citrinum. Many serine proteases induce cytokine expression, but whether Pen c 13 does so in human respiratory epithelial cells is not known. In this study, we investigated whether Pen c 13 caused IL-8 release and activated protease-activated receptors (PARs) in airway epithelial cells. In airway-derived A549 cells and normal human airway epithelial cells, Pen c 13 induced IL-8 release in a dose-dependent manner. Pen c 13 also increased IL-8 release in a time-dependent manner in A549 cells. Pen c 13 cleaved PAR-1 and PAR-2 at their activation sites. Treatment with Pen c 13 induced intracellular Ca(2+) mobilization and desensitized the cells to the action of other proteases and PAR-1 and PAR-2 agonists. Moreover, Pen c 13-mediated IL-8 release was significantly decreased in Ca(2+)-free medium and was abolished by the protease inhibitors, PMSF and 4-(2-aminoethyl) benzenesulfonyl fluoride. Blocking Abs against the cleavage sites of PAR-1 and PAR-2, but not of PAR-4, inhibited Pen c 13-induced IL-8 production, as did inhibition of phospholipase C. Pen c 13 induced IL-8 expression via activation of ERK 1/2, and not of p38 and JNK. In addition, treatment of A549 cells or normal human airway epithelial cells with Pen c 13 increased phosphorylation of ERK 1/2 by a Ca(2+)-dependent pathway. These finding show that Pen c 13 induces IL-8 release in airway epithelial cells and that this is dependent on PAR-1 and PAR-2 activation and intracellular calcium.