The effect of eight weeks combined training with omega-3 supplementation on the levels of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in older women.

BACKGROUND: Elevated levels of ICAM-1 and VCAM-1 are significant risk factors for cardiovascular diseases. Conversely, the regulatory roles of physical activity and omega-3 supplementation in these factors have been reported. The primary aim of the present research was to investigate the impact of an eight-week combined (resistance-endurance) accompanied by omega-3 supplementation on ICAM-1 and VCAM-1 levels in elderly women. METHODS: Forty elderly women, averaging 66.7 ± 4.13 years, were randomly assigned to four groups: placebo, omega-3 supplement, training, and training + omega-3. The combined exercise training program was implemented for eight weeks, three sessions per week. Aerobic training included 20 min of running at 60-70% of the reserve heart rate, while resistance training involved exercises at 70% of 1RM with 10 repetitions per exercise for two sets. The omega-3 and training + omega-3 groups consumed 2000 mg of omega-3 daily. Blood samples were collected 48 h after the last combined exercise training or omega-3 consumption, and the measured variables were analyzed using analysis of covariance test and SPSS-24 software. RESULTS: ICAM-1 and VCAM-1 levels significantly decreased in the training and training + omega-3 groups (p < 0.001). The decrease in ICAM-1 within the training + omega-3 group was also significant compared to the training group (p = 0.024). Additionally, a significant reduction in insulin resistance and body fat percentage was observed in both the training and training + omega-3 groups (p < 0.001). CONCLUSION: The present study's results indicate that omega-3 supplementation can enhance the effectiveness of combined training in regulating cardiovascular risk factors.

Effects of Exercise Training and L-Arginine Loaded Chitosan Nanoparticles on Hippocampus Histopathology, ß-Secretase Enzyme Function, APP, Tau, Iba1and APOE-4 mRNA in Aging Rats.

The objective of this study was to evaluate the combined and independent effects of exercise training and L-Arginine loaded chitosan nanoparticles (LA CNPs) supplementation on hippocampal Tau, App, Iba1, and ApoE gene expression, oxidative stress, ß-secretase enzyme activity, and hippocampus histopathology in aging rats. Thirty-five male Wistar rats were randomly assigned to five groups (n = 7 in each): Young (8 weeks old), Old (20 months old), old + L-arginine supplementation (Old Sup), old + exercise (Old Exe) and old + L-arginine supplementation + exercise (Old Sup + Exe). LA CNPs were administered to the supplement groups through gavage at a dosage of 500 mg/kg/day for 6-weeks. Exercise groups were subjected to a swimming exercise program five days/week for the same duration. Upon the completion of their interventions, the animals underwent behavioral and open-field task tests and were subsequently sacrificed for hippocampus genetic and histopathological evaluation. For histopathological analysis of brain, Cresyl violet staining was used. Congo Red staining was employed to confirm amyloid plaques in the hippocampus. Expressions of Tau, App, Iba1, and ApoE genes were determined by real-time PCR. In contrast to the Old group, Old Exe and Old Sup + Exe groups spent more time in the central space in the open field task (p < 0.05) and have more live cells in the hippocampus. Old rats (Old, Old Sup and Old Exe groups) exhibited a significant Aß peptide accumulation and increases in APP, Tau, Iba1, APOE-4 mRNA and MDA, along with decreases in SOD compared to the young group (p < 0.05). However, LA CNPs supplementation, exercise, and their combination (Old Sup, Old Exe and Old Sup + Exe) significantly reduced MDA, Aß plaque as well as APP, Tau, Iba1, and APOE-4 mRNA compared to the Old group (p < 0.05). Consequently, the administration of LA CNPs supplements and exercise might regulate the risk factors of hippocampus cell and tissue.

Aerobic exercise training reduces deep-frying oil-induced apoptosis of hippocampal tissue by reducing oxidative stress in male rats.

Deep-frying oil (DFO) contains high amounts of free radicals, and consuming foods prepared with this method causes damage to nervous tissue due to oxidative stress (OS). Since moderate-intensity aerobic exercise training (AT) reduces OS, the current search investigated the effects of AT on OS, apoptosis, and neurogenesis markers in the hippocampal tissue of DFO-fed rats. Eighteen Wistar male rats (200-280 gr) were randomly allocated to a control group fed with normal food (Con-ND), a control group receiving DFO (Con-DFO), and a group receiving DFO-aerobic exercise (EX-DFO) (n = 6 in each). DFO was gavaged for four weeks, five days a week, with a dose of 2 ml. AT included running on a treadmill for four weeks and five sessions per week (40 min per session). The expression of genes B-cell lymphoma 2 (BCL-2), Protein X associated with Bcl-2 (BAX), Caspase-3 (Casp-3), and Caspase-9 (Casp-9) was measured by PCR method. The ELISA method was used to calculate levels of Superoxide dismutase (SOD) and Catalase (CAT) activity, malondialdehyde (MDA), and Brain-Derived Neurotrophic Factor (BDNF). Also, the expression of the proteins Cannabinoid receptor type 1(CB1), Cannabinoid receptor type2 (CB2), Glial fibrillary acidic protein (GFAP), Neuronal nuclei (NeuN), and DNA fragmentation was evaluated by Immunohistochemical and TUNEL staining. DFO feeding led to a significant increase in apoptotic markers, such as BAX, Casp-3, and Casp-9 gene expression, and DNA fragmentation (p ≤ 0.05) while decreasing BDNF concentration SOD activity (p ≤ 0.05). AT significantly reduced the BAX, Casp-3, Casp-9, MDA, CB1, GFAP, and DNA fragmentation (p ≤ 0.05). In conclusion, AT can reduce the harmful effects of feeding with DFO on the hippocampal tissue.

Effects of swimming exercise combined with silymarin and vitamin C supplementation on hepatic inflammation, oxidative stress, and histopathology in elderly rats with high-fat diet-induced liver damage.

OBJECTIVES: The aim of this study was to demonstrate that swimming exercise combined with silymarin and vitamin C supplementation improves hepatic inflammation, oxidative stress, and liver histopathology in elderly rats with high-fat diet-induced liver damage. METHODS: Forty elderly male Wistar rats were randomly assigned to five groups (n = 8 in each): a normal diet (control), a high-fat diet (HFD), HFD + silymarin and vitamin C supplementation (HFD+Sup), HFD + swimming exercise (HFD+Exe), and HFD+Sup+Exe group (HFD+Sup+Exe). The non-alcoholic fatty liver model was induced for 6 wk in the HFD groups. After 6 wk of consuming an HFD, a daily supplemental gavage was administered to rats as an intervention along with HFD in the supplement groups for 8 wk. Moreover, rats in the exercise groups were subjected to swimming exercise training 5 d/wk for the same period. RESULTS: The combination of swimming training and supplementation caused significant decreases in liver inflammatory biomarkers tumor necrosis factor-α and interleukin-1ß while increasing total antioxidant capacity and peroxisome proliferator-activated receptor α (P < 0.05). CONCLUSION: In elderly rats with liver injury caused by an HFD, the combination of exercise and silymarin with vitamin C supplementation effectively reduced oxidative stress, liver inflammation, fat accumulation, and regulated liver enzymes.

Swimming and L-arginine loaded chitosan nanoparticles ameliorates aging-induced neuron atrophy, autophagy marker LC3, GABA and BDNF-TrkB pathway in the spinal cord of rats.

Aging is associated with muscle atrophy, and erosion and destruction of neuronal pathways in the spinal cord. The study aim was to assess the effect of swimming training (Sw) and L-arginine loaded chitosan nanoparticles (LA-CNPs) on the sensory and motor neuron population, autophagy marker LC3, total oxidant status/total antioxidant capacity, behavioural test, GABA and BDNF-TrkB pathway in the spinal cord of aging rats. The rats were randomized to five groups: young (8-weeks) control (n = 7), old control (n = 7), old Sw (n = 7), old LA-CNPs (n = 7) and old Sw + LA-CNPs (n = 7). Groups under LA-CNPs supplementation received 500 mg/kg/day. Sw groups performed a swimming exercise programme 5 days per week for 6 weeks. Upon the completion of the interventions the rats were euthanized and the spinal cord was fixed and frozen for histological assessment, IHC, and gene expression analysis. The old group had more atrophy in the spinal cord with higher changes in LC3 as an indicator of autophagy in the spinal cord compared to the young group (p < 0.0001). The old Sw + LA-CNPs group increased (improved) spinal cord GABA (p = 0.0187), BDNF (p = 0.0003), TrkB (p < 0.0001) gene expression, decreased autophagy marker LC3 protein (p < 0.0001), nerve atrophy and jumping/licking latency (p < 0.0001), improved sciatic functional index score and total oxidant status/total antioxidant capacity compared to the old group (p < 0.0001). In conclusion, swimming and LA-CNPs seems to ameliorate aging-induced neuron atrophy, autophagy marker LC3, oxidant-antioxidant status, functional restoration, GABA and BDNF-TrkB pathway in the spinal cord of aging rats. Our study provides experimental evidence for a possible positive role of swimming and L-arginine loaded chitosan nanoparticles to decrease complications of aging.

Swimming exercise and nano-l-arginine supplementation improve oxidative capacity and some autophagy-related genes in the soleus muscle of aging rats.

The present research aims to evaluate the effect of swimming exercise and chitosan-coated l-arginine on mitochondrial oxidation, BCL2 Interacting Protein 3 (Bnip3), NIP-like protein × (Nix), B-cell lymphoma-extra-large (Bcl-xL) and autophagy-related protein light chain 3(LC3) expression in soleus muscle of aging rats. In this experimental research, 25 male Wistar rats were assigned into five groups randomly: young, old, old + Nano l-arginine (Nano L-a), old + exercise (Ex), and old + Nano l-arginine (Nano L-a) + exercise (Ex) (n = 5 in each). They performed a swimming exercise program five days a week for six weeks. To determine the relative strength for rats before and after performing these interventions, the 1repetition maximum (1RM) test was done as a pre and post-test. The exercise program started with 20 min and after four sessions, gradually increased to 60 min and this time was maintained until the completion of the training period. l-arginine coated with chitosan nanoparticles was given to the rats in the l-arginine-supplemented group via gavage at a dosage of 500 mg/kg/day, five days a week, for six weeks. Additionally, the rats in all groups were fed a normal diet (2.87 kcal/g and 15 % energy from fat). Upon the completion of the protocol implementation, the rats were sacrificed and the soleus muscle was fixed and frozen to determine hematoxylin and eosin (H&E) staining, immunohistochemistry (IHC), gene expression analysis, levels of reactive oxygen species (ROS), and total antioxidant capacity (TAC). The results from the present research indicated that swimming exercise and Nano l-arginine improve the strength and histology of muscle tissue in old rats (p < 0.05). Aging significantly increased the expression of Nix and Bnip3 (p < 0.05) and reduced the Bcl-xL gene expression (p < 0.05). The expression of LC3 protein also increased with aging (p < 0.05). Therapeutic interventions, such as combined treatment (old + Nano L-a + Ex) for old animals, reduced the amount of this protein in soleus muscle (p < 0.05). The ROS values also showed a significant reduction only in the old + Nano L-a + Ex group compared to the old group. Moreover, TAC values show a significant decrease in the old and old + Ex groups in comparison to the young group. The use of arginine supplement, especially in nano form, along with swimming exercise seems to reduce the oxidative damage to the elderly muscle tissue, which has a positive effect on the structure and function of the soleus muscle. Since these interventions only had a significant effect on LC3 protein, further studies with more diverse measurement methods for autophagy are suggested.

Resistance exercise promotes functional test via sciatic nerve regeneration, and muscle atrophy improvement through GAP-43 regulation in animal model of traumatic nerve injuries.

Resistance training improves muscle strength through a combination of neural plasticity and muscle hypertrophy. This study aimed to evaluate the effects of resistance exercise on sciatic nerve regeneration and histology, growth-associated protein 43 (GAP-43) expressions, and soleus muscle atrophy following traumatic nerve injuries in Wistar rats. In the present study, 40 male Wistar rats were randomly assigned into four groups: healthy control (HC) as a sham group was exposed to the surgical procedures without any sciatic nerve compression, lesioned control (LC), resistance training (RT,non-lesioned), and lesioned rats + RT (LRT) (n = 10 in each). The RT group performed a resistance-training program 5 days/week for 4 weeks. Sciatic functional index (SFI) score, beam score and Basso, Beattie, and Bresnahan (BBB) score decreased and the hot plate time increased significantly in the LC| group compared to the HC (p < 0.05) group. However, the LRT| group showed a significant increase in the SFI score (p = 0.001) and a significant decrease in hot plate time (p = 0.0232) compared to the LC group. The LC group also showed neurological morphological damage and muscle atrophy and a decrease in GAP-43 in nerve tissue. In comparison to the LC group, a significant increase in sciatic nerve caliber, diameter, number of muscle fibers, and the expression of GAP-43| (p < 0.05) was observed in the LRT group. Doing resistance training even for four weeks seems to affect sciatic nerve lesions and injuries. It can also repair and regenerate nerve tissue by upregulating GAP-43 expression|, improving motor behavioral tests, and controlling muscle atrophy.

Swimming exercise with L-arginine coated nanoparticles supplementation upregulated HAND2 and TBX5 expression in the cardiomyocytes of aging male rats.

We investigated possible cardioprotective mechanisms of L-arginine coated nanoparticles (L-ACN) combined with swimming exercise (SE) in aging male rats considering heart and neural crest derivatives-expressed protein 2 (HAND2) and t-box transcription factor 5 (TBX5). Thirty-five male Wistar rats were randomly assigned into five groups: young, old, old + L-ACN, old + SE, and old + L-ACN + SE (n = 7 in each). L-arginine coated with chitosan nanoparticles was given to L-ACN groups via gavage at 500 mg/kg/day. SE groups performed a swimming exercise program 5 days per week for 6 weeks. The exercise program started with 20 min, gradually increasing to 60 min after four sessions, which was then constant until the completion of the training period. After the protocol completion, the rats were sacrificed, and the heart was fixed and frozen to carry out histological, immunohistochemistry (IHC), and gene expression analyses. The expression of HAND2 protein, HAND2 mRNA, and TBX5 mRNA of the heart tissue was significantly higher in the young group than in all older groups (P < 0.05). The old + L-ACN, old + SE, and old + L-ACN + SE groups showed a significant increase in these factors compared to the old group (P < 0.05). Nano-L-arginine supplement, along with swimming exercises, seems to have cardioprotective potential and improve cardiac function in old age by strengthening cardiomyocyte signaling, especially HAND2 and TBX5. However, more research is required, particularly on human samples.