Treadmill exercise enhances ABCA1 expression in rat liver

ATP-binding cassette transporters (ABCs) belong to a large family and include 49 mammalian transmembrane transporters that transfer a variety of substrates across the lipid bilayers in an energy-dependent manner. ABCA1 is a member of this family which plays a crucial role in plasma HDL-C remodeling. The purpose of this study was to investigate liver ABCA1 expression and plasma HDL level in response to treadmill running program in rats. Ten adult Wistar male rats (12-14weeks old, 200-220g) were used for this study. Animals were divided into control (Con, n=5) and Training (TR, n=5) groups. Training group was given exercise on a motor-driven treadmill at 25m/min (0% grade) for 90min/day, 5 days/week for 6 weeks. Rats were sacrificed 24h after the last session of exercise portion of the liver was excised, immediately washed in ice-cold saline, and frozen in liquid nitrogen for extraction of ABCA1 mRNA. Plasma was collected for HDL-C, LDL, TC, TG, and VLDL-C measurements. Liver ABCA1 mRNA expression was significantly (P<0.001) higher in trained rats compared to control rats. Plasma HDL-C, LCAT, pre-beta-HDL concentrations were significantly higher (P<0.01, P<0.001, P<0.028, respectively) in trained rats at the end of treadmill exercise. However, plasma lipids, other lipoproteins and TC/HDL and LDL/HDL ratio were unchanged. In conclusion, a treadmill running-induced elevated plasma HDL-C concentration was accompanied with a higher liver ABCA1 mRNA expression and increased in LCAT and pre-beta-HDL levels.     

跑台运动改善海马线粒体功能提高APP/PS1小鼠学习记忆能力

为研究跑台运动对APP/PS1小鼠海马线粒体融合、分裂作用的影响,将遗传背景为C57BL/6的3月龄APP/PS1小鼠和野生小鼠各42只分别随机分为APP/PS1安静对照组（ADC,n=21）和运动组（ADE,n=21）,野生安静对照组（WTC,n=21）和运动组（WTE,n=21）。ADE、WTE组进行12周跑台运动,同时ADC、WTC组置于安静跑台环境。水迷宫实验检测小鼠的空间学习记忆能力,RT-PCR法检测线粒体功能关键酶的mRNA水平,Western印迹检测海马融合、分裂及线粒体关键酶的蛋白质表达情况,透射电镜观察海马线粒体融合、分裂状态。结果发现,6月龄APP/PS1小鼠学习记忆能力降低（P<0.05）;海马线粒体融合蛋白质Mfn1、Mfn2、Opa1表达降低（P<0.05）,线粒体分裂蛋白质Drp1、Mff表达增高（P<0.05）;线粒体膜结构模糊,嵴不明显,线粒体碎片增多,空泡化线粒体增多;线粒体呼吸关键酶COX IV及ATP合酶表达均下调（P<0.05）。12周跑台运动可逆转APP/PS1小鼠的上述变化,改善海马线粒体结构和功能,提高学习记忆能力。综上提示：12周跑台运动改善APP/PS1小鼠学习记忆能力的机制可能与其对线粒体结构与功能的改善有关。     

Irreversible plasma and muscle protein oxidation and physical exercise

The imbalance between the reactive oxygen (ROS) and nitrogen (RNS) species production and their handling by the antioxidant machinery (low molecular weight antioxidant molecules and antioxidant enzymes), also known as oxidative stress, is a condition caused by physiological and pathological processes. Moreover, oxidative stress may be due to an overproduction of free radicals during physical exercise. Excess of radical species leads to the modification of molecules, such as proteins – the most susceptible to oxidative modification – lipids and DNA. With regard to the oxidation of proteins, carbonylation is an oxidative modification that has been widely described. Several studies have detected changes in the total amount of protein carbonyls following different types of physical exercise, but only few of these identified the specific amino acidic residues targets of such oxidation. In this respect, proteomic approaches allow to identify the proteins susceptible to carbonylation and in many cases, it is also possible to identify the specific protein carbonylation sites. This review focuses on the role of protein oxidation, and specifically carbonyl formation, for plasma and skeletal muscle proteins, following different types of physical exercise performed at different intensities. Furthermore, we focused on the proteomic strategies used to identify the specific protein targets of carbonylation. Overall, our analysis suggests that regular physical activity promotes a protection against protein carbonylation, due to the activation of the antioxidant defence or of the turnover of protein carbonyls. However, we can conclude that from the comprehensive bibliography analysed, there is no clearly defined specific physiological role about this post-translational modification of proteins.     

Effect of hyperoxia on the immune status of oxygen divers and endurance athletes

Physical activity, particularly that, exerted by endurance athletes, impacts the immune status of the human body. Prolonged duration and high-intensity endurance training lead to increased production of reactive oxygen species (ROS) and thereby to oxidative stress. Military combat swimmers (O₂-divers) are regularly exposed to hyperbaric hyperoxia (HBO) in addition to intensive endurance training intervals. They are, therefore, exposed to extreme levels of oxidative stress. Several studies support that the intensity of oxidative stress essentially determines the effect on immune status. The aim of this study was to comparatively characterise peripheral blood mononuclear cells (PBMCs) of O₂-divers (military combat swimmers), endurance athletes (amateur triathletes), and healthy control volunteers with respect to DNA fragmentation, immune status and signs of inflammation. Furthermore, it was investigated how PBMCs from these groups responded acutely to exposure to HBO. We showed that DNA fragmentation was comparable in PBMCs of all three groups under basal conditions directly after HBO exposure. However, significantly higher DNA fragmentation was observed in O₂-divers 18?hours after HBO, possibly indicating a slower recovery. O₂-divers also exhibited a proinflammatory immune status exemplified by an elevated number of CD4⁺CD25⁺ T cells, elevated expression of proinflammatory cytokine IL-12, and diminished expression of anti-inflammatory TGF-β1 compared to controls. Supported by a decreased basal gene expression and prolonged upregulation of anti-oxidative HO-1, these data suggest that higher oxidative stress levels, as present under intermitted hyperbaric hyperoxia, e.g. through oxygen diving, promote a higher inflammatory immune status than oxidative stress through endurance training alone.     

Exercise-induced mitophagy in skeletal muscle occurs in the absence of stabilization of Pink1 on mitochondria

Maintenance of mitochondrial quality is essential for skeletal muscle function and overall health. Exercise training elicits profound adaptations to mitochondria to improve mitochondrial quality in skeletal muscle. We have recently demonstrated that acute exercise promotes removal of damaged/dysfunctional mitochondria via mitophagy in skeletal muscle during recovery through the Ampk-Ulk1 signaling cascade. In this Extra View, we explore whether Pink1 is stabilized on mitochondria following exercise as the signal for mitophagy. We observed no discernable presence of Pink1 in isolated mitochondria from skeletal muscle at any time point following acute exercise, in contrast to clear evidence of stabilization of Pink1 on mitochondria in HeLa cells following treatment with the uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP). Taken together, we conclude that Pink1 is not involved in exercise-induced mitophagy in skeletal muscle.     

Early moderate exercise benefits myocardial infarction healing via improvement of inflammation and ventricular remodelling in rats

Thus far, the cellular and molecular mechanisms related to early (especially within 24 hours after acute myocardial infarct (MI)) exercise‐mediated beneficial effects on MI have not yet been thoroughly established. In the present study, we demonstrated that acute MI rats that underwent early moderate exercise training beginning one day after MI showed no increase in mortality and displayed significant improvements in MI healing and ventricular remodelling, including an improvement in cardiac function, a decrease in infarct size, cardiomyocyte apoptosis, cardiac fibrosis and cardiomyocyte hypertrophy, and an increase in myocardial angiogenesis, left ventricular wall thickness and the number of cardiac telocytes in the border zone. Integrated miRNA‐mRNA profiling analysis performed by the ingenuity pathway analysis system revealed that the inhibition of the TGFB1 regulatory network, activation of leucocytes and migration of leucocytes into the infarct zone comprise the molecular mechanism underlying early moderate exercise‐mediated improvements in cardiac fibrosis and the pathological inflammatory response. The findings of the present study demonstrate that early moderate exercise training beginning one day after MI is safe and leads to significantly enhanced MI healing and ventricular remodelling. Understanding the mechanism behind the positive effects of this early training protocol will help us to further tailor suitable cardiac rehabilitation programmes for humans.     

Exercise Alleviates Obesity-Induced Metabolic Dysfunction via Enhancing FGF21 Sensitivity in Adipose Tissues

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The effects of eccentric exercise on motor performance in young and older women

The purpose of the present study was to determine if old individuals show a greater exercise-induced decrement in motor performance and slower recovery compared to young individuals. Ten college-age women (23.6 years) and ten older women (67.4 years) performed an exercise consisting of 24 eccentric actions of the forearm flexors. In young subjects, eccentric exercise is known to produce repairable muscle damage. Before the exercise and for 5 days after, isometric strength, soreness, reaction time, and movement time were measured. For both groups, strength was reduced and soreness developed in the days following the exercise, generally indicating that muscle damage had occurred. The older subjects showed a slower strength recovery such that by 5 days after exercise they had not returned to their initial level of strength. There was no significant difference in soreness development between groups. Reaction time and movement time were not adversely affected by the exercise. Thus, the older subjects demonstrated a slower strength recovery after damage-inducing exercise, and, with regard to response speed, the older subjects could compensate for the impaired muscle function as well as the younger subjects.     

Pulmonary function in normal subjects following exercise at cold ambient temperatures

We measured pulmonary function in 12 healthy volunteers before and at 5-min intervals for 30 min following treadmill exercise of 30 min duration performed under control (20 degrees C) and cold (-11 degrees C) ambient temperatures. Post-run changes in forced vital capacity (FVC), residual volume (RV) and peak expiratory flow rate were similar between the two temperature conditions. FVC decreased slightly but significantly 5 min post-run (-0.25 +/- 0.20 l and -0.21 +/- 0.20 l, for control and cold conditions respectively) and returned to baseline by 30 min. RV increased significantly post-exercise (+0.07 +/- 0.09 l and +0.14 +/- 0.1 l, control and cold respectively) and remained elevated for 30 min. Forced expired volume in 1 s was not significantly different following either run. Post-exercise, maximum mid-expiratory flow rate and flows at 50% and 25% of vital capacity were not significantly different between warm and cold conditions. These data suggest that changes in lung volumes following exercise under cold ambient conditions are similar to changes seen following warm exercise of similar duration. In non-asthmatics, moderate exertion under cold ambient conditions does not appear to cause clinically significant decreases in expiratory flow rates as compared to similar exertion under warm conditions.     

Air breathing minimizes post-exercise lactate load in the tropical Pacific tarpon, Megalops cyprinoides Broussonet 1782 but oxygen debt is repaid by aquatic breathing

Swimming in a flume at reduced water pO₂ resulted in muscle and blood lactate levels in Pacific tarpon Megalops cyprinoides that were significantly higher when fish did not have access to air. Blood glucose and haematological variables were unchanged throughout the regimes of exercise at two swimming speeds and hypoxia. Strenuous exercise with bouts of burst swimming, however, resulted in both high blood lactate and glucose, and perturbed haematological status with elevated haemoglobin and reduced mean cell-haemoglobin concentration. Post-exercise recovery was achieved through aquatic breathing rather than by air breathing. The air-breathing organ in Pacific tarpon therefore prolonged aerobic activity, but gill breathing was used to repay oxygen debt.