Bioinformatics Analysis Identifies Key Genes in the Effect of Resistance Training on Female Skeletal Muscle Aging.

Resistance training is used to combat skeletal muscle function decline in older adults. Few studies have been designed specific for females, resulting in very limited treatment options for skeletal muscle atrophy in aging women. Here, we analyzed the gene expression profiles of skeletal muscle samples from sedentary young women, sedentary older women, and resistance-trained older women, using microarray data from public database. A total of 45 genes that were differentially expressed during female muscle aging and reversed by resistance training were identified. Functional and pathway enrichment analysis, protein-protein interaction network analysis, and receiver operating characteristic analysis were performed to reveal the key genes and pathways involved in the effects of resistance training on female muscle aging. The collagen genes COL1A1, COL3A1, and COL4A1 were identified important regulators of female muscle aging and resistance training, by modulating multiple signaling pathways, such as PI3 kinase-Akt signaling, focal adhesions, extracellular matrix-receptor interactions, and relaxin signaling. Interestingly, the expression of CDKN1A and TP63 were increased during aging, and further upregulated by resistance training in older women, suggesting they may negatively affect resistance training outcomes. Our findings provide novel insights into the molecular mechanisms of resistance training on female muscle aging and identify potential biomarkers and targets for clinical intervention.

Exercise and vascular function in sedentary lifestyles in humans.

People with sedentary lifestyles engage in minimal or no physical activity. A sedentary lifestyle promotes dysregulation of cellular redox balance, diminishes mitochondrial function, and increases NADPH oxidase activity. These changes collectively increase cellular oxidative stress, which alters endothelial function by oxidizing LDL-C, reducing NO production, and causing eNOS uncoupling. Reduced levels of nitric oxide (NO) leads to vasoconstriction, vascular remodeling, and vascular inflammation. Exercise modulates reactive oxygen species (ROS) to modify NRF2-KEAP signaling, leading to the activation of NRF2 to alleviate oxidative stress. While regular moderate exercise activates NRF2 through ROS production, high-intensity intermittent exercise stimulates NRF2 activation to a greater degree by reducing KEAP levels, which can be more beneficial for sedentary individuals. We review the damaging effects of a sedentary lifestyle on the vascular system and the health benefits of regular and intermittent exercise.

Time-dependent Effects of Moderate- and High-intensity Exercises on Myocardial Transcriptomics.

The heart is a highly adaptable organ that responds to changes in functional requirements due to exposure to internal and external stimuli. Physical exercise has unique stimulatory effects on the myocardium in both healthy individuals and those with health disorders, where the effects are primarily determined by the intensity and recovery time of exercise. We investigated the time-dependent effects of different exercise intensities on myocardial transcriptional expression in rats. Moderate intensity exercise induced more differentially expressed genes in the myocardium than high intensity exercise, while 16 differentially expressed genes were down-regulated by moderate intensity exercise but up-regulated by high intensity exercise at 12 h post- exercise. Both Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis indicated that moderate intensity exercise specifically regulated gene expression related to heart adaptation, energy metabolism, and oxidative stress, while high intensity exercise specifically regulated gene expression related to immunity, inflammation, and apoptosis. Moreover, there was increased expression of Tbx5, Casq1, Igsf1, and Ddah1 at all time points after moderate intensity exercise, while there was increased expression of Card9 at all time points after high intensity exercise. Our study provides a better understanding of the intensity dependent effects of physical exercise of the molecular mechanisms of cardiac adaptation to physical exercise.

Potential harms of supplementation with high doses of antioxidants in athletes.

Vigorous exercise generates large amounts of reactive oxygen species (ROS) as a result of the consumption of large volumes of O2 in athletes, causing some athletes to consume antioxidants in the erroneous belief that this will counteract the damaging effects of ROS. There is currently no convincing evidence to support the benefits of antioxidant supplementation in acute physical exercise and exercise training. On the contrary, exogenous antioxidants prevent some physiological functions of free radicals that are needed for cell signaling, causing higher dosages of antioxidants to hamper or prevent performance-enhancing and health-promoting training adaptation such as mitochondrial biogenesis, skeletal and cardiac muscle hypertrophy, and improved insulin sensitivity. However, there remains the perception that antioxidants can counterbalance oxidative stress and benefit exercise adaptation and performance in athletes. It is likely that the negative effects of high doses of antioxidant supplementation exceed their potential benefits. We discuss some proposed pathways of potential side effects of exogenous antioxidant supplementation in athletes.

Research and Evaluation on Wear in Power-Shift Steering Transmission Through Oil Spectral Analysis with RKPCA Method.

The most common methodology used in element concentration measurement and analyzing of wear particles is Atomic emission (AE) spectroscopy. The present paper presents an evaluation method on wear in power-shift steering transmission (PSST). By removing the problematic components which were highly correlated with oil additives, the robust kernel principal component analysis (RKPCA) method and the principal component analysis (PCA) method were accessed to extract the principal components of spectral data for oil samples collected from the life-cycle test of PSST in different stage and to calculate the amount of each principal component and its contribution rate respectively. A comparison between the above mentioned two methods was made to show that RKPCA method has fewer amounts of principal components and higher cumulative contribution rate indicating that RKPCA method acts more effectively in variable dimension reduction due to the outliers and nonlinearity of spectral data. Therefore, the effectiveness of RKPCA method in classification and identification of the wear in friction pairs was demonstrated subsequently. through the correlation analysis between the variable coefficients of RKPCA and metal elements of friction pairs. The demonstration showed that RKPCA functioned precisely in the classification and identification of the wear in friction pairs, and in the evaluation on the wear in PSST. Thereafter, to detect the threshold point where the wear took place, the fuzzy C-means clustering algorithm was introduced to classify the RKPCA eigenvalues, and the results were compared with that of the spectral clustering algorithm. The fuzzy C-means clustering algorithm showed higher sensitivity in detecting the threshold point indicting a more precise evaluation on the wear in PSST. It is clear that the introduction of RKPCA method in wear evaluation, which takes the eigenvalues of spectral data as a critical variable to classify and identify the wear in different friction pairs as well as in the integral PSST configuration, shows better accuracy in wear prediction and will contribute to the reliable determination of life between overhauls and the accurate positioning of worn-out parts. As might be expected, the proposed method can be extended to other cases of wear detection and evaluation in complex mechanical system.

Influence of exercise prescription intervention based on WeChat on glycolipid metabolism and fitness of suboptimal-health teachers.

Exercise is an effective means to promote health, but adherence is low. Due to the advantages of immediacy, economy and effectiveness, the use of WeChat social software has permeated into every aspect in daily life in China. To explore the influence of WeChat-based exercise prescription intervention mode on glycolipid metabolism and fitness of suboptimal-health teachers. 293 suboptimal-health teachers with senior professional titles were randomized to a control group (CG) or an experimental group (e.g.). The CG exercised on its own, while the e.g. adopted the exercise prescription intervention based on WeChat. The intervention period was 6 months. Finally, 264 cases were adhered to and completed, including 132 cases in the CG and 132 cases in the e.g.. The Suboptimal-Health Status Questionnaires-25 scores (SHSQ-25 scores), exercise adherence, subjective feelings, physical fitness, blood glucose and blood lipids were detected before and after intervention and compared between 2 groups. After the intervention, the SHSQ-25 scores in the e.g. was significantly decreased than those in the CG (P < .01). The complete exercise adherence in the e.g. was significantly higher than those in the CG (P < .01). After intervention, the subjective feelings of e.g. were significantly improved compared to CG (P < .05). The body shape, body function and physical quality in the e.g. was higher than those in the CG (P < .05). Total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) decreased significantly in the e.g. but not in the CG (P < .05). Fasting blood glucose (FBG) decreased significantly in the e.g. but not in the CG, with a significant difference between groups (P < .05). The subjects in the e.g. were very satisfied with WeChat management. WeChat-based exercise prescription intervention could improve SHS, exercise adherence, subjective feelings, physical fitness and glycolipid metabolism.

Effect of 11 Weeks of Physical Exercise on Physical Fitness and Executive Functions in Children.

OBJECT: The aim of our study was to evaluate and compare the effects of physical exercise interventions on physical fitness and executive functions in children. METHODS: Six-year-old children participated in the study and were randomly divided into physical exercise group (PE group, n = 43) and control group (C group, n = 46). The children in the PE group participated in a physical exercise program for 45 min daily, four days a week for 11 weeks. The children in the C group continued with their usual routines. Then, all the children were tested before and after the experiment for body composition (height, weight, BMI), physical fitness (20-m shuttle run test, standing long jump test, grip strength test, 4 × 10 m shuttle run test and sit and reach tests), and executive functions test (animal go/no-go task, working memory span task, simple reaction test and flexible item selection task) before and after the 11-week period. RESULTS: The 11 weeks of physical exercise did not significantly affect the body composition of the children (p > 0.05). The physical fitness and executive functions test results showed that 11 weeks of physical exercise interventions improves physical fitness (cardiopulmonary fitness, muscle strength, speed sensitivity and flexibility quality) and executive functions parameters (inhibitory control, working memory, the reaction time, and cognitive flexibility) in children (p < 0.05, p < 0.01). CONCLUSION: 11 weeks of physical exercise can improve the physical fitness and executive functions of six-year-old children.

Acute aerobic exercise regulation of myocardial calcium homeostasis involves CASQ1, CASQ2, and TRDN.

Exercise maintains cardiac calcium homeostasis and promotes cardiovascular health. This study explored temporal changes of calcium-related myocardial transcriptome changes during the recovery phase following a single bout of moderate-intensity aerobic exercise. Healthy male Sprague-Dawley rats were anesthetized with sodium pentobarbital after moderate-intensity aerobic exercise at four time points (0, 12, 24, and 72 h postexercise). The hearts were removed and RNA-seq and bioinformatics analyses were used to examine temporal transcriptional changes in the myocardium. Casq1, Casq2, and Trdn were identified as key genes in the regulation of calcium homeostasis during myocardial recovery. The highest expression of Casq1, Casq2, and Trdn genes and the proteins they encode occurred 24 h after exercise. An in vitro calcium overload heart model using the Langendorff heart perfusion method was used to examine myocardial calcium buffering capacity. Calcium overload caused the least changes in left ventricular developed pressure, infarct area, Lactate dehydrogenase release, and extent of morphological damage to myocardial cells, with the highest protein expressions of CASQ1, CASQ2, and TRDN at 24 h after acute exercise. This study indicates that maximal myocardial Ca2+ buffering capacity occurs 24 h postexercise in rats. Our study provides insights into exercise-mediated improvements in cardiovascular function and exercise preconditioning.NEW & NOTEWORTHY Acute aerobic exercise upregulates myocardial Casq1, Casq2, and Trdn genes and the proteins they encode in rats. Higher protein levels of CASQ1, CASQ2, and TRDN conferred an improved ability of the myocardium to resist calcium overload. Furthermore, 24 h postexercise is the time point with optimal myocardial calcium buffer capacity.

The role of MOTS-c-mediated antioxidant defense in aerobic exercise alleviating diabetic myocardial injury.

Myocardial remodeling and dysfunction are commonly observed in type 2 diabetes mellitus (T2DM). Aerobic exercise can partly alleviate diabetes-induced myocardial dysfunction through its antioxidant actions. MOTS-c is a potential exercise mimic. This study aimed to investigate the effects of MOTS-c on improving diabetic heart function and its mechanism and to identify whether MOTS-c improved antioxidant defenses due to aerobic exercise. Herein, we established a rat model of T2DM induced by high-fat diet combined with a low-dose streptozotocin injection. Interventions were performed using intraperitoneal injections of MOTS-c (i.p. 0.5 mg/kg/day, 7 days/week) or aerobic exercise training (treadmill, 20 m/min, 60 min/day, 5 days/week) for 8 weeks. Myocardial ultrastructure was assessed using transmission electron microscopy (TEM), myocardial lipid peroxidation levels (MDA), superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) levels were assessed using colorimetric methods, and molecular analyses including MOTS-c, Kelch-like ECH-associated protein 1 (Keap1), Nuclear factor E2-related factor 2 (Nrf2), adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)and phospho-AMPK (p-AMPK) were examined using Western blot. The results showed that MOTS-c, with or without exercise, reduced myocardial ultrastructural damage and improved glucolipid metabolism and cardiac function in T2DM. Furthermore, MOTS-c increased antioxidant markers such as SOD, CAT, and the protein expression of myocardial MOTS-c, Keap1, Nrf2, and p-AMPK. MOTS-c with exercise treatment reduced myocardial MDA and increased p-AMPK significantly comparing to only exercise or MOTS-c alone. Our findings suggest that MOTS-c may be a helpful supplement for overcoming exercise insufficiency and improving myocardial structure and function in diabetes.

MOTS-c and aerobic exercise induce cardiac physiological adaptation via NRG1/ErbB4/CEBPß modification in rats.

AIMS: To determine the effects of the mitochondrial open reading frame of the 12S ribosomal RNA type-c (MOTS-c) and aerobic exercise on cardiac structure and function and explore the role of neuregulin-1 (NRG1)- ErbB2 receptor tyrosine kinase 4(ErbB4)- CCAAT-enhancer binding protein ß (C/EBPß) in cardiac physiological adaptation induced by MOTS-c and aerobic training. MAIN METHODS: We used Hematoxylin-Eosin staining(HE)and Transmission Electron Microscope (TEM) to observe the cardiac myocardial structure, carotid artery catheterization to test cardiac function, and real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting to describe the changes of NRG1, ErbB4, C/EBPß, and Gata in cardiac physiological adaptation. KEY FINDINGS: MOTS-c and aerobic training significantly increased heart weight and heart weight index (HWI) (all p < 0.05). Aerobic exercise and MOTS-c treatment thickened myocardial fibers, with a tendency of hypertrophy. Heart rate (HR) (p < 0.001, p = 0.010, p = 0.011), the isovolumic diastolic time constant (Tau) (p < 0.001, p < 0.001, p < 0.001) in exercised (E), MOST-c treated (M) and their combination (ME) decreased significantly, while the dP/dtmax (p < 0.001, p < 0.001, p = 0.039) and dP/dtmin (p < 0.001, p < 0.001, p = 0.001) in groups E, M and ME were significantly higher than those in group C, but EDP (p = 0.903, p = 0.708, p = 0.744) remained unchanged. Moreover, C/EBPß gene levels were significantly decreased in the differential gene expression between groups C and M transcriptomics sequencing. The levels of ErbB4 mRNA (p < 0.001, p < 0.001, p < 0.001) and Gata4 mRNA (p < 0.001, p < 0.001, p = 0.001) in groups E, M and ME increased significantly, while C/EBPß mRNA expression decreased significantly (p < 0.001, p = 0.002, p = 0.001), which was consistent with the results of transcriptome sequencing. NRG1 mRNA in group E was significantly higher than that in group C (p = 0.003), but there was no significant difference between groups M and ME (p = 0.804, p = 0.320). The protein expression of NRG1 (p = 0.026, p < 0.001, p < 0.001), ErbB4 (p < 0.001, p < 0.001, p < 0.001) and Gata4 (p = 0.014, p < 0.001, p = 0.006) in groups E, M and ME increased significantly, while C/EBPß decreased significantly (p < 0.001, p = 0.001, p = 0.002). SIGNIFICANCE: Our findings suggest that MOTS-c and aerobic exercise had similar effects, improving myocardial morphology and structure and enhancing cardiac function through activation of the NRG1-ErbB4-C/EBPß pathway.

MOTS-c and Exercise Restore Cardiac Function by Activating of NRG1-ErbB Signaling in Diabetic Rats.

Pathologic cardiac remodeling and dysfunction are the most common complications of type 2 diabetes. Physical exercise is important in inhibiting myocardial pathologic remodeling and restoring cardiac function in diabetes. The mitochondrial-derived peptide MOTS-c has exercise-like effects by improving insulin resistance, combatting hyperglycemia, and reducing lipid accumulation. We investigated the effects and transcriptomic profiling of MOTS-c and aerobic exercise on cardiac properties in a rat model of type 2 diabetes which was induced by feeding a high fat high sugar diet combined with an injection of a low dose of streptozotocin. Both aerobic exercise and MOTS-c treatment reduced abnormalities in cardiac structure and function. Transcriptomic function enrichment analysis revealed that MOTS-c had exercise-like effects on inflammation, myocardial apoptosis, angiogenesis and endothelial cell proliferation and migration, and showed that the NRG1-ErbB4 pathway might be an important component in both MOTS-c and exercise induced attenuation of cardiac dysfunction in diabetes. Moreover, our findings suggest that MOTS-c activates NRG1-ErbB4 signaling and mimics exercise-induced cardio-protection in diabetes.

MOTS-c repairs myocardial damage by inhibiting the CCN1/ERK1/2/EGR1 pathway in diabetic rats.

Cardiac structure remodeling and dysfunction are common complications of diabetes, often leading to serious cardiovascular events. MOTS-c, a mitochondria-derived peptide, regulates metabolic homeostasis by accelerating glucose uptake and improving insulin sensitivity. Plasma levels of MOTS-c are decreased in patients with diabetes. MOTS-c can improve vascular endothelial function, making it a novel therapeutic target for the cardiovascular complications of diabetes. We investigated the effects of MOTS-c on cardiac structure and function and analyzed transcriptomic characteristics in diabetic rats. Our results indicate that treatment with MOTS-c for 8-week repaired myocardial mitochondrial damage and preserved cardiac systolic and diastolic function. Transcriptomic analysis revealed that MOTS-c altered 47 disease causing genes. Functional enrichment analysis indicated MOTS-c attenuated diabetic heart disease involved apoptosis, immunoregulation, angiogenesis and fatty acid metabolism. Moreover, MOTS-c reduced myocardial apoptosis by downregulating CCN1 genes and thereby inhibiting the activation of ERK1/2 and the expression of its downstream EGR1 gene. Our findings identify potential therapeutic targets for the treatment of T2D and diabetic cardiomyopathy.

Predicting individual muscle fatigue tolerance by resting-state EEG brain network.

Objective.Exercise-induced muscle fatigue is a complex physiological phenomenon involving the central and peripheral nervous systems, and fatigue tolerance varies across individuals. Various studies have emphasized the close relationships between muscle fatigue and the brain. However, the relationships between the resting-state electroencephalogram (rsEEG) brain network and individual muscle fatigue tolerance remain unexplored.Approach.Eighteen elite water polo athletes took part in our experiment. Five-minute before- and after-fatigue-exercise rsEEG and fatiguing task (i.e. elbow flexion and extension) electromyography (EMG) data were recorded. Based on the graph theory, we constructed the before- and after-task rsEEG coherence network and compared the network differences between them. Then, the correlation between the before-fatigue rsEEG network properties and the EMG fatigue indexes when a subject cannot keep on exercising anymore was profiled. Finally, a prediction model based on the before-fatigue rsEEG network properties was established to predict fatigue tolerance.Main results. Results of this study revealed the significant differences between the before- and after-exercise rsEEG brain network and found significant high correlations between before-exercise rsEEG network properties in the beta band and individual muscle fatigue tolerance. Finally, an efficient support vector regression (SVR) model based on the before-exercise rsEEG network properties in the beta band was constructed and achieved the accurate prediction of individual fatigue tolerance. Similar results were also revealed on another 30 subject swimmer data set further demonstrating the reliability of predicting fatigue tolerance based on the rsEEG network.Significance.Our study investigates the relationship between the rsEEG brain network and individual muscle fatigue tolerance and provides a potential objective physiological biomarker for tolerance prediction and the regulation of muscle fatigue.

Harnessing the cardiovascular benefits of exercise: Are Nrf2 activators useful?

The ability of physical activity to ameliorate cardiovascular disease and improve cardiovascular health is well accepted, but many aspects of the molecular mechanisms underlying these benefits are incompletely understood. Exercise increases the levels of reactive oxygen species (ROS) through various mechanisms. This triggers the activation of Nrf2, a redox-sensitive transcription factor activated by increases in oxidative stress. Activation of Nrf2 mitigates oxidative stress by increasing the nuclear transcription of many antioxidant genes while also mediating additional beneficial effects through the cytoprotective nature of Nrf2 signaling. Understanding the transcriptional patterns of Nrf2 caused by exercise can help in the design of pharmacological mimicry of the process in patients who are unable to exercise for various reasons.

Performance Improvement of PVDF-HFP-Based Gel Polymer Electrolyte with the Dopant of Octavinyl-Polyhedral Oligomeric Silsesquioxane.

Gel polymer electrolytes have the advantages of both a solid electrolyte and a liquid electrolyte. As a transitional product before which a solid electrolyte can be comprehensively used, gel polymer electrolytes are of great research value. They can reduce the risk of spontaneous combustion and explosion caused by leakage during the use of conventional liquid electrolytes. Poly(vinylidene-fluoride-co-hexafluoropropylene) (PVDF-HFP), a material with excellent performance, has been widely utilized in the preparation of gel polymer electrolytes. Here, PVDF-HFP-based gel polymer membranes with polyvinyl pyrrolidone (PVP) pores were prepared using a phase inversion method, and Octavinyl-polyhedral oligomeric silsesquioxane (OVAPOSS) was doped to improve its temperature resistance as well as its ionic conductivity, to enhance its safety and electrochemical performance. The final prepared polymer membrane had a porosity of 85.06% and still had a certain mechanical strength at 160 °C without any shrinkage. The gel polymer electrolyte prepared with this polymer membrane had an ionic conductivity of 1.62 × 10-3 S·cm-1 at 30 °C, as well as an electrochemical window of about 5.5 V. The LiCoO2-Li button half-cell prepared therefrom had a specific capacity of 141 mAh·g-1 at a rate of 1C. The coulombic efficiency remained above 99% within 100 cycles and the capacity retention rate reached 99.5%, which reveals an excellent cycling stability.

The mitochondrial signaling peptide MOTS-c improves myocardial performance during exercise training in rats.

Cardiac remodeling is a physiological adaptation to aerobic exercise and which is characterized by increases in ventricular volume and the number of cardiomyocytes. The mitochondrial derived peptide MOTS-c functions as an important regulator in physical capacity and performance. Exercise elevates levels of endogenous MOTS-c in circulation and in myocardium, while MOTS-c can significantly enhance exercise capacity. However, the effects of aerobic exercise combined with MOTS-c on cardiac structure and function are unclear. We used pressure-volume conductance catheter technique to examine cardiac function in exercised rats with and without treatment with MOTS-c. Surprisingly, MOTS-c improved myocardial mechanical efficiency, enhanced cardiac systolic function, and had a tendency to improve the diastolic function. The findings suggest that using exercise supplements could be used to modulate the cardiovascular benefits of athletic training.

Exercise modulates heat shock protein 27 activity in diabetic cardiomyopathy.

AIMS: Heat shock protein 27 regulates homeostasis of skeletal and cardiac muscle proteins in various stressful states including diabetes and exercise. Aerobic exercise can inhibit or ameliorate cardiac structural abnormality and dysfunction in diabetic cardiomyopathy. The aim of this study was to evaluate the role of HSP27 in aerobic exercise improving cardiac diastolic dysfunction in type 2 diabetic rats. METHODS: Forty male Sprague-Dawley rats were randomly divided into the following groups: control, control + aerobic exercise, diabetic, and diabetic + aerobic exercise. Diabetes was induced by feeding with a high-fat high-sugar diet for 7-weeks followed by a single intraperitoneal injection of streptozotocin (30 mg/kg) in male rats. Moderate aerobic exercise training was performed on a treadmill for 8 weeks after induction of diabetes. KEY FINDINGS: Aerobic exercise increased left ventricular end-diastolic internal diameter, left ventricular end-diastolic volume, myocardial HSP27 protein expression, HSP27-S82 phosphorylation levels, pHSP27-titin binding and improved cardiac muscle fibre alignment in diabetic rats. SIGNIFICANCE: Our study indicates that moderate aerobic exercise increases HSP27 activation, improves cardiomyocyte fibre alignment and restores cardiac diastolic function.

Changes in Titin and Collagen Modulate Effects of Aerobic and Resistance Exercise on Diabetic Cardiac Function.

Diastolic dysfunction is a common complication that occurs early in diabetes mellitus. Titin and collagen are two important regulators of myocardial passive tension, which contributes to diabetic myocardial diastolic dysfunction. Exercise therapy significantly improves the impaired diabetic cardiac function, but its benefits appear to depend on the type of exercise used. We investigated the effect of aerobic and resistance exercise on cardiac diastolic function in diabetic rats induced by high-fat diet combined with low-dose streptozotocin injection. Interestingly, although resistance training had a more pronounced effect on blood glucose control than did aerobic training in type 2 diabetic rats, improvements in cardiac diastolic parameters benefited more from aerobic training. Moreover, aerobic exercise did significantly increase the expression levels of titin and decrease collagen I, TGFß1 expression level. In summary, out data suggest that aerobic exercise may improve diabetic cardiac function through changes in titin-dependent myocardial stiffness rather than collagen-dependent interstitial fibrosis.