Effects of Hyperbaric Oxygen Therapy on Inflammation, Oxidative/Antioxidant Balance, and Muscle Damage after Acute Exercise in Normobaric, Normoxic and Hypobaric, Hypoxic Environments: A Pilot Study.

The purpose of this study was to investigate the effects of hyperbaric oxygen therapy (HBOT) on inflammation, the oxidative/antioxidant balance, and muscle damage after acute exercise in normobaric, normoxic (NN) and hypobaric, hypoxic (HH) environments. Eighteen healthy males were selected and randomly assigned to three groups: exercise in NN conditions (NN group, n = 6), HBOT treatment after exercise in NN conditions (HNN group, n = 6), and HBOT treatment after exercise in HH conditions (HHH group, n = 6). All subjects performed treadmill running for 60 min at 75-80% maximum heart rate (HRmax) exercise intensity under each condition. The HBOT treatments consisted of breathing 100% oxygen at 2.5 atmosphere absolute (ATA) for 60 min. Blood samples were collected before exercise (BE), after exercise (AE), and after HBOT (AH) to examine inflammation (fibrinogen, interleukin-6 [IL-6], and tumor necrosis factor-α (TNF-α)), the oxidative/antioxidant balance (derivatives of reactive oxygen metabolites (d-ROMs) and the biological antioxidant potential (BAP)), and muscle damage (creatine kinase (CK) and lactate dehydrogenase (LDH)). Plasma fibrinogen, serum IL-6, CK, and LDH levels were significantly increased AE compared to BE in all groups (p < 0.05). Plasma fibrinogen levels were significantly decreased AH compared to AE in all groups (p < 0.05), and the HNN group had a significantly lower AH compared to BE (p < 0.05). Serum IL-6 levels were significantly decreased AH compared to AE in the HNN and HHH groups (p < 0.05). Serum CK levels were significantly decreased AH compared to AE in the HHH group (p < 0.05). Serum LDH levels were significantly decreased AH compared to AE in the HNN and HHH groups (p < 0.05), and the NN and HNN groups had significantly higher AH serum LDH levels compared to BE (p < 0.05). These results suggest that acute exercise in both the NN and HH environments could induce temporary inflammatory responses and muscle damage, whereas HBOT treatment may be effective in alleviating exercise-induced inflammatory responses and muscle damage.

Exercise training improves intramuscular triglyceride lipolysis sensitivity in high-fat diet induced obese mice.

BACKGROUND: The purpose of this study was to determine whether regular exercise training enhances intramuscular triglyceride (IMTG) lipolysis sensitivity during consumption of a continued high-fat diet by exploring changes in biochemical factors activated by IMTG lipolysis. METHODS: Male C57BL/6 mice aged 4 weeks were randomly divided into a high-fat diet group (HF) to induce obesity for 6 weeks and a control (CO) group. Thereafter, the HF group was divided into a high-fat diet group (HF) and high-fat diet + training group (HFT). The HFT group was trained on an animal treadmill 40 min/day, 5 days/week for 8 weeks. PKA, Plin5, p-Plin5, CGI-58, ATGL, and HSL were analyzed to investigate IMTG sensitivity by western blotting. RESULTS: PKA, CGI-58, and HSL protein levels in the HF group were significantly lower than those in the CO group (p < 0.05). However, PKA, CGI-58, and HSL protein levels in the HFT group were significantly higher than those in the HF group, and ATGL and p-Plin5 protein levels as well as the p-Plin5/Plin5 ratio in the HFT group were significantly higher than those in the HF group (p < 0.05). In addition, the HF group showed a significantly higher IMTG volume than the CO and HFT groups (p < 0.05). CONCLUSIONS: These results suggest that in an obese mouse model, 8 weeks of treadmill exercise contributes to decreased IMTG volume by activating lipolysis factors, such as PKA, PLIN5, CGI-58, and lipases. Therefore, regular exercise training may play an important role in obesity treatment by increasing IMTG lipolysis sensitivity.

The effects of detraining and training on adipose tissue lipid droplet in obese mice after chronic high-fat diet.

BACKGROUND: It is well known that exercise promotes lipolysis by stimulating the lipid droplet (LD) signaling pathway. However, few studies have been conducted to examine the effect of detraining with high fat diet (HFD) and training effects after long-term HFD. Here, we investigated the effect of detraining and training on adipose tissue LD pathway in diet-induced obese mice after continuous HFD. METHODS: Seventy male C57BL/6 mice were randomly assigned into a Normal diet + Sedentary group (ND, n = 10) or a High-fat diet + Sedentary group (HF, n = 50); in the HF group, obesity was induced by a 45% fat chow for six weeks. For the subsequent eight weeks, the HF group was randomly subdivided into an HF (n = 30) or an HF + training group (HFT, n = 20), and the HFT group was subjected to treadmill training while on an HFD. Following this eight-week period, the HFT group stopped exercising (HFT-DT group, n = 10), and the mice in the HF group were randomly subdivided into an HF (n = 10) or an HF + training group (HF-T, n = 10). After training and detraining, abdominal visceral fat was obtained and analyzed by histological staining and western blot. RESULTS: Treadmill exercise decreased body weight and fat mass (P <0.05), and increased the levels of PKA, perilipin1, CGI-58, ATGL, and HSL (P <0.05) after eight weeks of training. Following eight weeks of detraining, the levels of PKA and HSL were decreased (P <0.05); however, exercise after chronic HFD increased the levels of PKA, perilipin1, CGI-58, ATGL, and HSL (P <0.05), and decreased body weight and fat mass (P <0.05). CONCLUSIONS: Regardless of dietary restrictions, exercise is an effective treatment for obesity, owing to the regulation of LD signaling proteins. Moreover, the effects of regular exercise after chronic HFD were similar to those of exercise in the absence of HFD. Therefore, although obesity is induced by chronic HFD, exercise without dietary change is sufficiently effective for obesity treatment regardless of the preceding HFD period.

Exercise and dietary change ameliorate high fat diet induced obesity and insulin resistance via mTOR signaling pathway.

PURPOSE: The purpose of this study was to investigate the effect of exercise and dietary change on obesity and insulin resistance and mTOR signaling protein levels in skeletal muscles of obese rats. METHODS: Sixty male Sprague-Dawley rats were divided into CO (Normal diet) and HF (High Fat diet) groups in order to induce obesity for 15 weeks. The rats were then subdivided into CO, COT (CO + Training), HF, HFT (HF + Training), HFND (Dietary change), and HFNDT (HFND + Training) groups (10 rats / group). The training groups underwent moderate-intensity treadmill exercise for 8 weeks, after which soleus muscles were excised and analyzed. Data was statistically analyzed by independent t-test and One-way ANOVA tests with a 0.05 significance level. RESULTS: Fasting blood glucose, plasma insulin, and HOMA-IR in the HF group were significantly higher, as compared with other groups (p <.05). Protein levels of insulin receptor subunit-1 (IRS-1), IRS-2, and p-Akt were significantly higher in the HFT, HFND, and HFNDT groups, as compared with HF group. In addition, the protein levels of the mammalian target of rapamycin complex 1 (mTORC1) and ribosomal S6 protein kinase 1 were significantly decreased by exercise and dietary change (p <.05). However, mTORC2 and phosphoinositide 3-kinase were significantly increased (p <.05). CONCLUSION: In summary, despite the negative impact of continuous high fat intake, regular exercise and dietary change showed a positive effect on insulin resistance and mTOR signaling protein levels.

Effects of treadmill exercise on skeletal muscle†mTOR signaling pathway in high-fat diet-induced obese mice.

[Purpose] The aim of this study was to investigate the effects of regular treadmill exercise on skeletal muscle Rictor-Akt and mTOR-Raptor-S6K1 signaling pathway in high-fat diet-induced obese mice. [Subjects and Methods] Four- week-old C57BL/6 mice were adopted and classified into normal diet group (ND, n = 10), normal diet and training group (NDT, n = 10), high-fat diet group (HF, n = 10), and high-fat diet and training group (HFT, n = 10). The exercise program consisted of a treadmill exercise provided at low intensity for 1-4 weeks, and moderate intensity for 5-8 weeks. [Results] The Western blot method was used to measure the expression of mTOR, Raptor, S6K1, Rictor, and Akt proteins in the soleus muscle. mTOR levels were significantly higher in the HF group than in the ND and NDT groups. Raptor/mTORC1 and S6K1 levels were significantly higher in the HF group than in all the other groups. Akt levels were significantly lower in the HF group than in the NDT group. The risk of obesity may be associated with the overactivation of the mTOR-Raptor-S6K1 signaling pathway and a decrease in Akt levels. [Conclusion] This study also indicates that performing aerobic exercise may be associated with the downregulation of the mTOR-Raptor-S6K1 pathway.