ABSTRACT
Objective To explore the changes of cardiovascular system of military personnel during highly intensive training.Methods One hundred and seventy officers and soldiers were as research subjects,including 100 individuals in high-intensity group and 70 in control group.The levels of serum cortisol (COR),high sensitivity C-reactive protein (hs-CRP),cardiacspecific Troponin T (cTnT) and human heart fatty acid binding protein (H-FABP) were measured when military training ended.All subjects were tested with fatigue assessment instrument (FAI).The data of blood pressure and electrocardiogram were collected from 40 individuals randomly selected from high-intensity group and 36 from control group before and after training for analyzing the blood pressure,arrhythmia and heart rate variability (HRV).Results The levels of COR (indicator related to stress) and hs-CRP (indicator related to inflammation) were significantly higher in high intensity group than in control group (P＜0.05).Highly intensive training can lead to the emergence of myocardial micro-injury,the levels of cTnT and H-FABP were obviously higher than those in control group (P＜0.01),and the mean blood pressure and the severity of fatigue status were significantly higher than those in control group (P＜0.05).The incidence of severe ventricular arrhythmia was lower in both groups (P=1.000).The average heart rate,total heart beats,total number of atrial premature beat,total number of ventricular premature beat,the incidence of sinus arrhythmia and intermittent second degree type Ⅰ atrioventricular block were significantly higher in high intensity group than in control group (P＜0.05).The HRV of high intensity group was obviously decreased (P＜0.01).Conclusion Highly intensive training may induce the military personnel into the state of acute stress and inflammation,which may lead to myocardial injury,increase severity of fatigue status,accompanied with the rise of blood pressure,low HRV and increased incidence of various arrhythmias.
ABSTRACT
<p><b>OBJECTIVE</b>The roles of cerebrovascular oxidative stress in vascular functional remodeling have been described in hindlimb-unweighting (HU) rats. However, the underlying mechanism remains to be established.</p><p><b>METHODS</b>We investigated the generation of vascular reactive oxygen species (ROS), Nox2/Nox4 protein and mRNA levels, NADPH oxidase activity, and manganese superoxide dismutase (MnSOD) and glutathione peroxidase-1 (GPx-1) mRNA levels in cerebral and mesenteric smooth muscle cells (VSMCs) of HU rats.</p><p><b>RESULTS</b>ROS production increased in cerebral but not in mesenteric VSMCs of HU rats compared with those in control rats. Nox2 and Nox4 protein and mRNA levels were increased significantly but MnSOD/GPx-1 mRNA levels decreased in HU rat cerebral arteries but not in mesenteric arteries. NADPH oxidases were activated significantly more in cerebral but not in mesenteric arteries of HU rats. NADPH oxidase inhibition with apocynin attenuated cerebrovascular ROS production and partially restored Nox2/Nox4 protein and mRNA levels, NADPH oxidase activity, and MnSOD/GPx-1 mRNA levels in cerebral VSMCs of HU rats.</p><p><b>CONCLUSION</b>These results suggest that vascular NADPH oxidases regulate cerebrovascular redox status and participate in vascular oxidative stress injury during simulated microgravit.</p>