Effects evaluation of different exercises on subclinical left ventricular dysfunction in obese rats by speckle-tracking echocardiography.

OBJECTIVE: To identify subclinical left ventricle dysfunction (LVD) in obese rats by speckle-tracking echocardiography, and to evaluate the effects of 12-week Moderate-Intensity Continuous Training (MICT) or High-Intensity Interval Training (HIIT) on LV geometry, histology and function in obese rats. METHODS: Eighteen male standard or obese Sprague-Dawley rats were randomly divided into the Control group, the MICT group, and the HIIT group. Exercise interventions were conducted for 12 weeks, with equal total load and increased intensity gradient. Using dual-energy X-ray, two-dimensional speckle-tracking echocardiography, pulse Doppler, and HE staining to evalucate body shape, LV morphology, structure, and myocardial mechanics function. RESULTS: (1) Both MICT and HIIT have good weight loss shaping effect. (2) The LV of obese rats underwent pathological remodeling, with decreased longitudinal contractility and synchrony, and increased circumferential contractility and synchrony. (3) Exercise can inhibit LV pathological remodeling, improve myocardial mechanical function. HIIT is superior to MICT. (4) The global longitudinal strain of obese rats in the HIIT group showed a significant correlation with Fat% and Lean%. CONCLUSION: Obesity can induce LV pathological remodeling and subclinical dysfunction. Compared with MICT, 12-week HIIT can effectively inhibit the pathological remodeling of LV and promote the benign development of myocardial mechanical function in obese rats.

Exercise against nonalcoholic fatty liver disease: Possible role and mechanism of lipophagy.

Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease worldwide. NAFLD is prevalent in about 30% of people worldwide. The lack of physical activity is considered as one of the risks for NAFLD, and approximately one-third of NAFLD patients hardly engage in physical activity. It is acknowledged that exercise is one of the optimal non-pharmacological methods for preventing and treating NAFLD. Different forms of exercise such as aerobic exercise, resistance exercise and even simply physical activity in a higher level can be beneficial in reducing liver lipid accumulation and disease progression for NAFLD patients. In NAFLD patients, exercise is helpful in lowering steatosis and enhancing liver function. The mechanisms underlying the prevention and treatment of NAFLD by exercise are various and complex. Current studies on the mechanisms have focused on the pro-lipolytic, anti-inflammatory, and antioxidant and lipophagy. Promotion of lipophagy is regarded as an important mechanism for prevention and improvement of NAFLD by exercise. Recent studies have investigated the above mechanism, yet the potential mechanism has not been completely elucidated. Thus, in this review, we cover the recent advances of exercise-promoted lipophagy in NAFLD treatment and prevention. Furthermore, given the fact that exercise activates SIRT1, we discuss the possible regulatory mechanisms of lipophagy by SIRT1 during exercise. These mechanisms need to be verified by further experimental studies.

Diet and exercise interventions reduce serum asprosin and the corresponding hypothalamic- pituitary-gonad-axis dysfunction in obese men.

Background: Asprosin (ASP) is a recently discovered adipocyte factor that participates in glucose metabolism and inflammatory reactions. Recent findings suggest that it may be involved in the regulation of sex hormone secretion in the hypothalamic-pituitary-gonad (HPG) axis, but no studies have been reported in related populations. The purpose of this study was to evaluate the changes in serum ASP levels in healthy men and obese men, as well as before and after exercise weight loss, and to investigate male hypogonadism, insulin resistance, inflammatory response, and relationships induced by ASP and obesity. Methods: Thirty-eight young male volunteers were recruited and divided into a normal group (n = 20) and an obese group (n = 18) according to their body mass index. Fourteen of the obese men underwent a 14-week exercise and diet intervention (first 8 weeks of aerobic exercise at 60%-70% HRmax for 30-50 min/4 days a week). Beginning at week 9, the intensity was increased to 75% HRmax. Participants in the obese groups maintained a calorie-restricted diet throughout the study period. Results: Serum ASP levels in the obese group were significantly higher than those in the normal group, and serum gonadotropin-releasing hormone (GnRh), luteinizing hormone (LH), and testosterone (T) levels were decreased. After 14 weeks of exercise and diet intervention, serum ASP decreased significantly, the levels of body weight, lean body weight, body fat rate, fasting insulin (FINS), homeostatic model assessment for insulin resistance, TNF-α, IL-6, and IL-1ß decreased significantly, and the serum GnRH, LH, and T levels increased significantly. ASP was positively correlated with body weight, body fat percentage, FINS, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1ß and negatively correlated with relative lean body weight and serum LH and T levels. Conclusion: The serum ASP levels were increased in obese men compared with those of normal weight individuals, resulting in a chronic inflammatory reaction, high serum insulin, and HPG axis injury. Fourteen weeks of exercise and diet intervention effectively alleviated this phenomenon. It has been speculated that ASP might regulate male reproductive function by regulating the inflammatory response and insulin sensitivity.

Acute effect of high-intensity interval exercise on vascular endothelial function and possible mechanisms of wall shear stress in young obese males.

Objective: To investigate the mechanisms of wall shear stress (WSS) responsible for the effects of high-intensity interval exercise (HIIE) on vascular endothelial function in young obese males. Methods: A within-subject study design was used. We examined the response of the reactive hyperemia index (RHI) to acute HIIE in young obese males (n = 20, age = 20.38 ± 1.40 years, body mass index [BMI] = 31.22 ± 3.57, body fat percentage [BF (%)] = 31.76 ± 3.57). WSS was manipulated using 100, 80, or 60 mmHg cuff inflation during the HIIE to determine the proper inflation capable of maintaining WSS near baseline levels. One-way repeated measures analysis of variance and LSD post hoc tests were performed to compare changes in WSS and vascular endothelial function at baseline HIIE and following HIIE using different cuff inflations. Results: There were no significant differences in RHI and WSS between the three cuff inflation values (p > 0.05). WSS was significantly higher in obese male individuals after HIIE and HIIE with 100 mmHg cuff inflation (p = 0.018, p = 0.005) than that at baseline, with no significant differences observed comparing HIIE and HIIE with 100 mmHg inflation (p = 0.23). The RHI after HIIE was significantly higher (p = 0.012) than that at baseline, while no significant differences were detected after HIIE at 100 mmHg (p = 0.91). The RHI was significantly lower after HIIE with 100 mmHg than that after HIIE (p = 0.007). WSS (p = 0.004) and RHI (p = 0.017) were significantly higher after HIIE than that at baseline, while no significant differences were observed after HIIE with either 80 or 60 mmHg cuff inflation (baseline vs. HIIE + 80 mmHg: WSS: p = 0.33, RHI: p = 0.38; baseline vs. HIIE + 60 mmHg: WSS: p = 0.58, RHI: p = 0.45). WSS was similar to HIIE, after HIIE with either 80 or 60 mmHg inflation (p = 0.36, p = 0.40). However, RHI was significantly higher for HIIE than for HIIE with both 80 and 60 mmHg inflation (p = 0.011, p = 0.006). Conclusion: HIIE could significantly improve WSS and vascular endothelial function. HIIE intervention with 60 or 80 mmHg inflation might enhance WSS near the baseline level. HIIE-induced acute changes in WSS may provide the primary physiological stimulus for vascular endothelial adaptation to HIIE in young obese males.

The effects of high-intensity interval training and moderate-intensity continuous training on visceral fat and carotid hemodynamics parameters in obese adults.

Objectives: The present study aimed to examine the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on visceral fat and hemodynamic parameters in obese adults. Methods: Fifty-two males were included in this study and divided into three groups: HIIT group (n = 21, age = 20.86 ± 1.62 years, BF (%) = 30.10 ± 5.02), MICT group (n = 22, age = 20.76 ± 1.14 years, BF (%) = 30.19 ± 5.76), and control group (CON) (n = 9, age = 21.38 ± 1.77 years, BF (%) = 30.40 ± 5.10). The HIIT and MICT groups received the exercise intervention three to four times per week for eight weeks (HIIT: exercise intensity 80-95% HRmax, circuit; MICT: exercise intensity 60-70% HRmax, running), and the control (CON) group received health education and guidance without exercise intervention. The body compositions and serum lipid indexes were tested to calculated LAP and VAI. The color doppler ultrasound diagnostic technology was used to test the artery diameter and blood velocity before and after the intervention. Based on the test data, MATLAB software and Womersley theory were used to calculate the hemodynamic parameters of the common carotid artery, including wall shear stress, flow rate, blood pressure, oscillatory shear index, elasticity modulus, dynamic resistance, artery diameter, arterial stiffness, circumferential strain and pulsatility index. Results: We found that lipid accumulation product (LAP) was significantly decreased in both the HIIT group (p < 0.01) and MICT (p < 0.05) group but not in the CON group (p > 0.05). In contrast, visceral adiposity index (VAI) decreased in both the HIIT and MICT groups and increased in the CON group, although the difference among groups was not significant (p > 0.05). After 8 weeks of intervention, the blood velocity and wall shear stress were greater after HIIT and MICT intervention (p < 0.01). Artery diameter, oscillatory shear index, arterial stiffness, and pulsatility index decreased significantly, and circumferential strain increased significantly in the HIIT group (all, p < 0.01, p < 0.05) but not in the MICT group (p > 0.05). Dynamic resistance was significantly decreased in the MICT group. There was no difference in the CON group after the period of intervention (all, p > 0.05). LAP was positively related to artery diameter (r = 0.48, p = 0.011), blood pressure (r = 0.46, p = 0.002), flow rate (r = 0.31, p = 0.04), oscillatory shear index (r = 0.44, p = 0.03), and elasticity modulus (r = 0.33, p = 0.029) but inversely related to circumferential strain (r = -0.36, p = 0.028). The VAI was also positively associated with artery diameter (r = 0.33, p = 0.03), elasticity modulus (r = 0.38, p = 0.009), and arterial stiffness (r = 0.39, p = 0.012). In addition, the VAI was negatively correlated with the circumferential strain (r = -0.33, p = 0.04). Conclusion: The present study demonstrated that both HIIT and MICT exercises for 8 weeks could effectively enhance visceral fat indices and partial hemodynamic parameters. Therefore, HIIT and MICT exert important effects on reducing fat content and improving hemodynamic environment. But HIIT on oscillatory shear index, arterial stiffness, circumferential strain, and pulsatility index was superior to MICT. In addition, there are close correlations between visceral fat and partial hemodynamic parameters of the common carotid artery.

Study on the association between the polymorphism of MCP-1 rs1024611 and the genetic susceptibility of type 2 diabetes with sepsis.

Monocyte chemoattractant protein-1 (MCP-1) rs1024611 (-2518 A > G) polymorphism are associated with inflammatory diseases. In this study, we investigate the relationship between MCP-1 rs1024611 polymorphism and genetic susceptibility of type 2 diabetes mellitus (T2DM) with sepsis. Two hundred eighty-five patients with T2DM are divided into the diabetes with sepsis group (combined group, 113 cases) and the diabetes group (172 cases). Blood samples and corresponding clinical data were collected. MCP-1 rs1024611 polymorphism in blood samples was detected by pyrosequencing. Meanwhile, the expressions of MCP-1, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1ß, and IL-6 in blood samples were detected by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The relationship between different genotypes of MCP-1 rs1024611 polymorphic locus and T2DM with sepsis was analyzed by combining with the clinical data of the patients. The frequencies of rs1024611 AG/GG genotypes and G allele in T2DM with sepsis group were significantly higher than those in T2DM patients without sepsis (P = .004 for AG/GG vs AA genotypes; P = .037 for G allele vs A allele). Subgroup analysis showed that the rs1024611 G allele frequency in the septic shock group was significantly higher than the general sepsis group (P = .02). The expressions of MCP-1 and TNF-α in GG genotypes in T2DM with sepsis group were significantly higher than AA or GA genotypes (P < .05). This study preliminarily showed that the rs1024611 A > G polymorphism within the promoter region of MCP-1 gene can upregulate the expression of MCP-1 gene and proinflammatory cytokine TNF-α, which ultimately contributed to the predisposition and progression of T2DM with sepsis.

Effects of Acupuncture in Ischemic Stroke Rehabilitation: A Randomized Controlled Trial.

Background: Acupuncture is a well-known treatment option for ischemic stroke recovery, but evidence of its effectiveness remains limited. This is a randomized controlled trial to evaluate the effectiveness of acupuncture treatment for ischemic stroke rehabilitation. Methods: Rehabilitation training was provided to the control group. In acupuncture arm 1, these acupoints were derived from the ancient books, including GV20 (baihui), GV26 (shuigou), PC9 (zhongchong), ST6 (jiache), ST4 (dicang), LI15 (jianyu), LI11 (quchi), LI4 (hegu), GB30 (huantiao), GB31 (fengshi), GB34 (yanglingquan), and GB39 (xuanzhong). In acupuncture arm 2, the acupoints used were GV20 (baihui), PC6 (neiguan), LI11 (quchi), LI10 (shousanli), SJ5 (waiguan), LI4 (hegu), GB30 (huantiao), ST36 (zusanli), GB34 (yanglingquan), SP6 (sanyinjiao), ST41 (jiexi), and LR3 (taichong), which were extracted from Acupuncture and Moxibustion Science. After acupuncture, the needles were left in for 30 min and manually manipulated every 10 min. The three groups received treatment once a day, 5 times a week for 2 weeks. The primary outcome was the National Institutes of Health Stroke Scale (NIHSS), and the secondary outcomes were the Barthel Index (BI) and the Modified Ashworth Scale (MAS). Outcomes were measured in patients both before and after treatment. Results: A total of 497 patients with ischemic stroke were randomized into either arm 1 (159 cases), arm 2 (173 cases), or the control group (165 cases). After 2 weeks of treatment, the NIHSS scores for arm 1 were lower than those of the control group (P = 0.017); the BI scores were higher in arm two than that in the control group at T2 (P = 0.016) and follow-up (P = 0.020). Additionally, there was no significant difference between arm one and the control group for either the BI scores or the MAS scores (P > 0.05) and no significant difference between arm two and the control group for the MAS scores or the NIHSS scores (P > 0.05). Conclusion: The clinical efficacy of arm 1 and arm 2 (acupuncture groups) was superior to that of the control group, but there was no difference between the effects of the two acupuncture groups. Clinical Trial Registration: http://www.chictr.org.cn/index.aspx, identifier: ChiCTR-IOR-16008627.

Aerobic exercise improves LPS-induced sepsis via regulating the Warburg effect in mice.

We investigated the impact of aerobic exercise (AE) on multiple organ dysfunction syndrome (MODS), aortic injury, pathoglycemia, and death during sepsis. ICR mice were randomized into four groups: Control (Con), Lipopolysaccharide (LPS), Exercise (Ex), and Exercise + LPS (Ex + LPS) groups. Mice were trained with low-intensity for 4 weeks. LPS and Ex + LPS mice received 5 mg/kg LPS intraperitoneally for induction of sepsis. Histopathological micrographs showed the organ morphology and damage. This study examined the effects of AE on LPS-induced changes in systemic inflammation, pulmonary inflammation, lung permeability, and bronchoalveolar lavage fluid (BALF) cell count, oxidative stress-related indicators in the lung, blood glucose levels, plasma lactate levels, serum insulin levels, plasma high-mobility group box 1 (HMGB1) levels, glucose transporter 1 (Glut1) and HMGB1, silent information regulator 1 (Sirt-1), and nuclear factor erythroid 2-related factor 2 (Nrf-2) mRNA expression levels in lung tissue. AE improved sepsis-associated multiple organ dysfunction syndrome (MODS), aortic injury, hypoglycemia, and death. AE prominently decreased pulmonary inflammation, pulmonary edema, and modulated redox balance during sepsis. AE prominently decreased neutrophil content in organ. AE prominently downregulated CXCL-1, CXCL-8, IL-6, TNF-α, Glu1, and HMGB1 mRNA expression but activated IL-1RN, IL-10, Sirt-1, and Nrf-2 mRNA expression in the lung during sepsis. AE decreased the serum levels of lactate and HMGB1 but increased blood glucose levels and serum insulin levels during sepsis. A 4-week AE improves sepsis-associated MODS, aortic injury, pathoglycemia, and death. AE impairs LPS-induced lactate and HMGB1 release partly because AE increases serum insulin levels and decreases the levels of Glut1. AE is a novel therapeutic strategy for sepsis targeting aerobic glycolysis.

Aerobic Exercise Alleviates Inflammation, Oxidative Stress, and Apoptosis in Mice with Chronic Obstructive Pulmonary Disease.

BACKGROUND: Chronic inflammation, oxidative stress, and apoptosis play critical roles in chronic obstructive pulmonary disease (COPD) pathogenesis. Here, we attempted to determine whether aerobic exercise (AE) could improve COPD by counteracting the COPD-associated inflammatory response, oxidative stress, and apoptosis in mice. METHODS: Thirty male ICR mice were assigned into one of three groups: control (Con), COPD, and COPD + AE. COPD was simulated by intratracheal injection of lipopolysaccharide (LPS) for 4 weeks. Low-intensity AE was performed for 4 weeks. Bronchoalveolar lavage fluid (BALF) cell counts and the levels of inflammatory cytokine in BALF and serum were detected. Hematoxylin and eosin (HE), Masson trichrome, and Sirius Red staining as well as terminal deoxynucleotidyl transferase dUTP nick end labeling were performed to identify the degree of pulmonary emphysema, bronchial mucus cell hyperplasia, pulmonary fibrosis, and cell apoptosis. Oxidative stress parameters were measured. Furthermore, gene expression levels for the CXCL1, IL-1ß, IL-10, IL-17, matrix metalloproteinase (MMP)9, TGF-ß, TNF-α, and silent information regulator (sirt)1 were detected in mice lung tissues. RESULTS: AE improved LPS-induced emphysema, pulmonary fibrosis, bronchial mucus cell hyperplasia, bronchoconstriction, and cell apoptosis. AE prevented an LPS-induced increase in the total cell, neutrophil, and macrophage counts. AE decreased malondialdehyde (MDA) and myeloperoxidase (MPO) levels but increased glutathione (GSH) and superoxide dismutase (SOD) levels. AE decreased BALF levels of IL-1ß, TNF-α, and TGF-ß but increased BALF IL-10 levels. AE suppressed the gene expression levels of pro-inflammatory factors CXCL1, IL-1ß, IL-17, and TNF-α and profibrotic factors MMP-9 and TGF-ß but activated those of anti-inflammatory factor IL-10 and lung-protective factor sirt1. CONCLUSION: AE is a potential therapeutic approach for COPD. AE improved emphysema, bronchial mucus cell hyperplasia, and pulmonary fibrosis in mice with COPD by alleviating the inflammatory response, oxidative stress injury, and cell apoptosis as well as activating sirt1.

Regular aerobic exercise activates PDGF-BB/PDGFR-ß signaling and modulates the inflammatory-anti-inflammatory balance in diet-induced obese mice.

OBJECTIVE: Regular aerobic exercise induces cardioprotection by counteracting the obesity-associated inflammatory response, dyslipidemia. PDGF-BB/PDGFR-ß signaling is established as a crucial mechanism of endothelial cell-cardiomyocyte communication and cardioprotection, but its physiological roles in response to obesity and regular aerobic exercise are unknown. METHODS: Thirty C57BL/6 mice were divided into three groups: a normal diet group, a high-fat diet group, and a high-fat diet plus aerobic exercise group. Glucose metabolic parameters, inflammation-related indicators, and blood lipids indicators were detected. In addition, gene expression levels of the inflammatory factors, PDGF-BB, PDGFR-ß, PI3K, Akt, eNOS, and P53 in cardiac tissue were quantified. Morphological analysis was also used to quantify the magnitude of inflammation. RESULTS: High-fat diet (HFD) feeding resulted in adiposity, dyslipidemia, and low levels of cardioprotective factors such as APN and eNOS (P < 0.05), which were improved significantly by 8 weeks of aerobic exercise (P < 0.05). HFD feeding increased the gene expression levels of proinflammatory cytokines and decreased the gene expression levels of anti-inflammatory cytokines in cardiac tissue (P < 0.05), which was reversed by regular aerobic exercise (P < 0.05). In addition, HFD feeding suppressed the levels of the cardioprotective factors PDGF-BB and eNOS through PDGF-BB/PDGFR-ß/PI3K/Akt/eNOS signaling in cardiac tissue, while regular aerobic exercise activated PDGF-BB/PDGFR-ß/PI3K/Akt/eNOS signaling. CONCLUSION: Regular aerobic exercise improved adiposity, dyslipidemia induced by HFD feeding. Regular aerobic exercise exerted a prominent role in modulating the inflammatory-anti-inflammatory balance and activating the levels of the cardioprotective factors eNOS and PDGF-BB through PDGF-BB/PDGFR-ß signaling.

The impact of acute exercise on implicit cognitive reappraisal in association with left dorsolateral prefronta activation: A fNIRS study.

Despite findings showing that acute exercise may help enhance emotion regulation, the neurophysiological mechanisms of these effects remain poorly understood. In this study, we examined whether acute exercise influences cognitive emotion regulation, and, in particular, an implicit cognitive reappraisal. Twenty sedentary young women were randomly assigned to either a control group (n = 10) or an exercise group (n = 10). Participants underwent an implicit cognitive reappraisal task twice, before and after the 30-min acute exercise or control, alongside functional near-infrared spectroscopy recordings (NIRS). The left dorsolateral prefrontal cortex (dlPFC) and left orbital frontal cortex (OFC) were activated during implicit cognitive reappraisal at baseline, but only the left dlPFC activation was linked with behavioral performance. Acute exercise enhanced the activation of these regions, reflective of the partial neural bases of implicit cognitive reappraisal, in the left dlPFC and left OFC, but did not alter the behavioral performance. Results also showed that acute exercise moderated the positive effect of left dlPFC activation on implicit cognitive reappraisal performance; specifically, this effect was stronger in the exercise group. In conclusion, the enhanced activation of the left dlPFC by acute exercise and the increased link between behavioral performance and its neural indices may point to acute exercise as a promoter of implicit cognitive reappraisal.

Leptin and inflammatory factors play a synergistic role in the regulation of reproduction in male mice through hypothalamic kisspeptin-mediated energy balance.

BACKGROUND: Energy balance is closely related to reproductive function, wherein hypothalamic kisspeptin mediates regulation of the energy balance. However, the central mechanism of kisspeptin in the regulation of male reproductive function under different energy balance states is unclear. Here, high-fat diet (HFD) and exercise were used to change the energy balance to explore the role of leptin and inflammation in the regulation of kisspeptin and the hypothalamic-pituitary-testis (HPT) axis. METHODS: Four-week-old male C57BL/6 J mice were randomly assigned to a normal control group (n = 16) or an HFD (n = 49) group. After 10 weeks of HFD feeding, obese mice were randomly divided into obesity control (n = 16), obesity moderate-load exercise (n = 16), or obesity high-load exercise (n = 17) groups. The obesity moderate-load exercise and obesity high-load exercise groups performed exercise (swimming) for 120 min/day and 120 min × 2 times/day (6 h interval), 5 days/week for 8 weeks, respectively. RESULTS: Compared to the mice in the normal group, in obese mice, the mRNA and protein expression of the leptin receptor, kiss, interleukin-10 (IL-10), and gonadotropin-releasing hormone (GnRH) decreased in the hypothalamus; serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone levels and sperm quality decreased; and serum leptin, estradiol, and tumor necrosis factor-α (TNF-α) levels and sperm apoptosis increased. Moderate- and high-load exercise effectively reduced body fat and serum leptin levels but had the opposite effects on the hypothalamus and serum IL-10 and TNF-α levels. Moderate-load exercise had anti-inflammatory effects accompanied by increased mRNA and protein expression of kiss and GnRH in the hypothalamus and increased serum FSH, LH, and testosterone levels and improved sperm quality. High-load exercise also promoted inflammation, with no significant effect on the mRNA and protein expression of kiss and GnRH in the hypothalamus, serum sex hormone level, or sperm quality. Moderate-load exercise improved leptin resistance and inflammation and reduced the inhibition of kisspeptin and the HPT axis in obese mice. The inflammatory response induced by high-load exercise may counteract the positive effect of improving leptin resistance on kisspeptin and HPT. CONCLUSION: During changes in energy balance, leptin and inflammation jointly regulate kisspeptin expression on the HPT axis.

Aerobic Exercise Improves Pulmonary Fibrosis by Improving Insulin Resistance and Inflammation in Obese Mice.

BACKGROUND: Previous studies have demonstrated that obesity is associated with pulmonary fibrosis. We attempted to identify whether regular aerobic exercise (AE) can protect against high-fat diet (HFD)-associated pulmonary fibrosis. METHODS: Forty-eight C57BL/6 mice were randomly assigned to four groups: chow group (Ch), chow plus exercise group (CE), obesity group (Ob), and obesity plus exercise group (OE). The mice were fed either an HFD or a chow diet for 16 weeks, and low-intensity aerobic exercise (AE) was performed in the last 8 weeks. We measured the degree of pulmonary fibrosis; pulmonary inflammation; oxidative stress parameters; insulin resistance-related indicators; the number of inflammatory cells in bronchoalveolar lavage fluid (BALF); the mRNA expression levels of IL-10, IL-1ß, TGF-ß, TNF-α, CXCL-1, IL-17, MMP-9, MPO, NE, and sirt-1; and the BALF levels of CXCL-1, IL-17, TGF-ß, IL-10, IL-1ß, and TNF-α in lung tissue. RESULTS: AE in obese mice protected against obesity-associated pulmonary fibrosis, chronic inflammation, pro-oxidative/antioxidative imbalance, and insulin resistance. AE ameliorated the HFD-induced inflammatory response and neutrophil infiltration in the lung. AE downregulated BALF levels of CXCL-1, IL-1ß, TNF-α IL-17, and TGF-ß but upregulated BALF levels of IL-10. AE decreased IL-1ß, TGF-ß, TNF-α, CXCL-1, IL-17, MMP-9, MPO, and NE mRNA expression levels but upregulated IL-10 and sirt-1 mRNA expression levels in the lung. CONCLUSIONS: AE protects against HFD-induced pulmonary fibrosis by improving obesity-associated insulin resistance, chronic low-grade inflammation, and pro-oxidative/antioxidative imbalance. AE improved HFD-induced pulmonary fibrosis by suppressing IL-17, TGF-ß, NE, and MMP-9 expression and activating IL-10 and sirt-1 expression.

Effect of Different Exercise Loads on Testicular Oxidative Stress and Reproductive Function in Obese Male Mice.

This study is aimed at investigating the effect of different exercise loads on the reproductive function of obese male mice and the underlying mechanisms. Male mice with high-fat diet-induced obesity were divided into obesity control (OC), obesity moderate-load exercise (OME), and obesity high-load exercise (OHE) groups. The OME and OHE groups were subjected to swimming exercise 5 days per week over a duration of 8 weeks, with the exercise load progressively increased to 2 h per day in the OME group and 2 h twice per day in the OHE group. In the OC group mice without exercise regimen, we observed a decrease in mRNA expression of antioxidant enzymes, increase in free radical products, upregulation of mRNA and protein expression of nuclear factor-κB and proinflammatory cytokines, inhibition of mRNA and protein expression of testosterone synthases, decrease in the serum testosterone level and sperm quality, and increase in sperm apoptosis. Although both moderate-load exercise and high-load exercise reduced body fat, only moderate-load exercise effectively alleviated obesity-induced oxidative stress, downregulated the expression of nuclear factor-κB and proinflammatory cytokines, and reversed the decrease in mRNA and protein expression of testosterone synthases, serum testosterone level, and sperm quality. These changes were not observed in the OHE group mice. Obesity-induced testicular oxidative stress and inflammatory response decreased testosterone synthesis and sperm quality. Moderate-load exercise alleviated the negative effect of obesity on male reproductive function by decreasing testicular oxidative stress and inflammatory responses. Although high-load exercise effectively reduced body fat, its effects on alleviating oxidative stress and improving male reproductive function were limited.

How Does Exercise Improve Implicit Emotion Regulation Ability: Preliminary Evidence of Mind-Body Exercise Intervention Combined With Aerobic Jogging and Mindfulness-Based Yoga.

Purpose: The primary aim of the present study is to examine the effect of 8-week mind-body exercise intervention combining aerobic jogging and mindfulness-based yoga on implicit emotion regulation ability. The secondary aim is to explore the specific potential pathways by which the mind-body exercise intervention fosters implicit emotion regulation. This may help us to understand how the key components of exercise intervention contribute to emotional benefits. Methods: Sixty participants were randomly allocated to one of two parallel groups: (1) the intervention group (n = 29) and (2) the waitlist control group (n = 31). Participants were asked to fill out scales measuring mindfulness and instructed to complete an emotion regulation task to assess implicit emotion regulation ability as well as the PWC 170 Test to evaluate aerobic fitness before and after the intervention. Results: The results of the two-way repeated ANOVA revealed that 8 weeks of intervention improved implicit emotion regulation, mindfulness, and aerobic fitness levels. Path analysis showed that only improved aerobic fitness mediated the intervention effect on implicit emotion regulation ability, controlling for change in negative affect. Notably, the relationship between the effects on implicit emotion regulation ability and aerobic fitness was moderated by improved mindfulness. Conclusion: Eight weeks of mind-body exercise intervention improves implicit emotion regulation ability. The aerobic fitness may be an essential pathway which mediates the efficacy on implicit emotion regulation ability. Furthermore, different components, such as aerobic fitness and mindfulness, may interactively contribute to such emotional benefits.

Effects of obesity and exercise on testicular leptin signal transduction and testosterone biosynthesis in male mice.

To explore the role of the testicular leptin and JAK-STAT[leptin (LEP)-JAK-STAT] pathway in testosterone biosynthesis during juvenile stages and exercise for weight loss, male C57BL/6J mice were randomly divided into normal-diet and high-fat diet groups. After 10 wk, mice in the high-fat diet-fed group were further divided randomly into obese control, obese moderate-volume exercise, and obese high-volume exercise groups. Mice in the obese moderate-volume exercise group were provided with 2 h/day, 6 days/wk swimming exercise for 8 wk, and mice in the obese high-volume exercise group underwent twice the amount of daily exercise intervention as the obese moderate-volume exercise group. The results showed that a high-fat diet causes obesity, leptin resistance, inhibition of the testicular LEP-JAK-STAT pathway, decreased mRNA and protein expression of steroidogenic factor-1, steroidogenic acute regulatory protein, and the P-450 side-chain cleavage enzyme, a decrease in the serum testosterone-to-estradiol ratio, and declines in sperm quality parameters. Both moderate and high-volume exercise were able to reduce body fat and increase the mRNA and protein expression of LEP-JAK-STAT, but only moderate exercise significantly increased the mRNA and protein expression of steroidogenic factor-1, steroidogenic acute regulatory protein, and P-450 side-chain cleavage enzyme and significantly reversed the serum testosterone-to-estradiol ratio and sperm quality parameters. These findings suggest that by impairing the testicular LEP-JAK-STAT pathway, early-stage obesity inhibits the biosynthesis of testosterone and sexual development and reduces male reproductive potential. Long-term moderate and high-volume exercise can effectively reduce body fat and improve obesity-induced abnormalities in testicular leptin signal transduction, whereas only moderate-volume exercise can reverse the negative impacts of obesity on male reproductive function.