Mild hyperbaric oxygen inhibits the growth-related decline in skeletal muscle oxidative capacity and prevents hyperglycemia in rats with type 2 diabetes mellitus.

BACKGROUND: Humans and animals with type 2 diabetes mellitus (T2DM) exhibit low skeletal muscle oxidative capacity and impaired glucose metabolism. The aim of the present study was to investigate the effects of exposure to mild hyperbaric oxygen on these changes in obese rats with T2DM. METHODS: Five-week-old non-diabetic Long-Evans Tokushima Otsuka (LETO) and diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats were divided into normobaric (LETO-NB and OLETF-NB) and mild hyperbaric oxygen (LETO-MHO and OLETF-MHO) groups. The LETO-MHO and OLETF-MHO groups received 1266 hPa with 36% oxygen for 3 h daily for 22 weeks. RESULTS: Fasting and non-fasting blood glucose, HbA1c, and triglyceride levels were lower in the OLETF-MHO group than in the OLETF-NB group (P < 0.05). In the soleus muscle, peroxisome proliferator-activated receptor δ/ß (Pparδ/ß), Pparγ, and PPARγ coactivator-1α (Pgc-1α) mRNA levels were lower in the OLETF-NB group than in all other groups (P < 0.05), whereas myogenin (Myog) and myogenic factor 5 (Myf5) mRNA levels were higher in the OLETF-MHO group than in the LETO-NB and OLETF-NB groups (P < 0.05). The soleus muscles in the OLETF-NB group contained only low-oxidative Type I fibers, whereas those in all other groups contained high-oxidative Type IIA and Type IIC fibers in addition to Type I fibers. CONCLUSIONS: Exposure to mild hyperbaric oxygen inhibits the decline in skeletal muscle oxidative capacity and prevents the hyperglycemia associated with T2DM. Pgc-1α, Myog, and Myf5 mRNA levels appear to be closely associated with skeletal muscle oxidative capacity in rats with T2DM.

Amelioration of capillary regression and atrophy of the soleus muscle in hindlimb-unloaded rats by astaxanthin supplementation and intermittent loading.

A chronic decrease in neuromuscular activity (activation and/or loading) results in muscle atrophy and capillary regression that are due, in part, to the overproduction of reactive oxygen species. We have reported that antioxidant treatment with astaxanthin attenuates the overexpression of reactive oxygen species in atrophied muscles that, in turn, ameliorates capillary regression in hindlimb-unloaded rats. Astaxanthin supplementation, however, had little effect on muscle mass and fibre cross-sectional area. In contrast, intermittent loading of the hindlimbs of hindlimb-unloaded rats ameliorates muscle atrophy. Therefore, we hypothesized that the combination of astaxanthin supplementation and intermittent loading would attenuate both muscle atrophy and capillary regression during hindlimb unloading. As expected, 2 weeks of hindlimb unloading resulted in atrophy, a decrease in capillary volume and a shift towards smaller-diameter capillaries in the soleus muscle. Intermittent loading alone (1 h of cage ambulation per day) attenuated atrophy of the soleus, while astaxanthin treatment alone maintained the capillary network to near control levels. The combination of intermittent loading and astaxanthin treatment, however, ameliorated atrophy of the soleus and maintained the capillary volume and luminal diameters and the superoxide dismutase-1 protein levels near control values. These results indicate that intermittent loading combined with astaxanthin supplementation could be an effective therapy for both the muscle atrophy and the capillary regression associated with a chronic decrease in neuromuscular activity.

Effects of hyperbaric oxygen on metabolic capacity of the skeletal muscle in type 2 diabetic rats with obesity.

We investigated whether hyperbaric oxygen enhances the oxidative metabolic capacity of the skeletal muscle and attenuates adipocyte hypertrophy in type 2 diabetic rats with obesity. Five-week-old male Otsuka Long-Evans Tokushima fatty (OLETF) and Long-Evans Tokushima Otsuka (LETO) rats were used as diabetic animals and nondiabetic controls, respectively, and assigned to control and hyperbaric oxygen groups. Animals in the hyperbaric oxygen group were exposed to an atmospheric pressure of 1.25 with an oxygen concentration of 36% for 3 h daily. The glucose level at 27 weeks of age was significantly higher in OLETF rats than in LETO rats, but the elevation was inhibited in OLETF rats exposed to hyperbaric oxygen. The slow-to-fast fiber transition in the skeletal muscle was observed in OLETF rats, but the shift was inhibited in OLETF rats exposed to hyperbaric oxygen. Additionally, the oxidative enzyme activity of muscle fibers was increased by hyperbaric oxygen. The adipocyte size was larger in OLETF rats than in LETO rats, but hypertrophied adipocytes were not observed in OLETF rats exposed to hyperbaric oxygen. Hyperbaric oxygen enhances glucose and lipid metabolism in the skeletal muscle, indicating that hyperbaric oxygen can prevent elevation of glucose and adipocyte hypertrophy in diabetic rats with obesity.

Effect of exposure to hyperbaric oxygen on diabetes-induced cataracts in mice.

BACKGROUND: The growth-associated increase in the blood glucose level of animals with Type 2 diabetes is inhibited by moderate hyperbaric exposure at 1.25 atmospheres absolute (ata) with 36% oxygen, presumably due to an increase in oxidative metabolism. However, there are no data available regarding the effect of moderate hyperbaric oxygen (HBO) on diabetes-induced cataracts. METHODS: Four-week-old mice with Type 2 diabetes and cataracts were exposed to 1.25 ata with 36% oxygen, 6 h daily, for 12 weeks, followed by normal conditions at 1 ata with 21% oxygen for 16 weeks (cataract + hyperbaric group). Levels of blood glucose and derivatives of reactive oxygen metabolites (dROMs), used as an index of oxidative stress, and the turbidities of the lenses from these mice at 4, 8, 12, 16, and 32 weeks of age were compared with those of control and diabetic (cataract group) mice not exposed to HBO. RESULTS: Non-fasting and fasting blood glucose levels were lower in the cataract + hyperbaric group at 12, 16, and 32 weeks of age than in the age-matched cataract group. The levels of dROMs were lower in the cataract + hyperbaric group at 16 and 32 weeks of age than in the age-matched cataract group. The turbidities of the peripheral and central regions of the lenses were lower in the cataract + hyperbaric group at 12, 16, and 32 weeks of age than in the age-matched cataract group. CONCLUSIONS: Hyperbaric exposure at 1.25 ata with 36% oxygen delays cataract development and progression in mice with Type 2 diabetes.

Hyperbaric oxygen improves ultraviolet B irradiation-induced melanin pigmentation and diminishes senile spot size.

BACKGROUND: The effects of exposure to hyperbaric oxygen on ultraviolet B (UVB) irradiation-induced melanin pigmentations of skins and on senile spot sizes of faces were investigated. METHODS: In the first experiment, male subjects were irradiated with UVB on their upper arms for inducing erythema and the subsequent melanin pigmentation. They were exposed to a hyperbaric environment at 1.25 atmospheres absolute (ATA) with 32% oxygen for 1 h/day, three times per week. In the second experiment, female subjects were exposed to a hyperbaric environment at 1.25 ATA with 32% oxygen for 1 h/day, two times per week. RESULTS: In the first experiment, melanin pigmentations lightened after 4 weeks of exposure to hyperbaric oxygen. In the second experiment, senile spot sizes became small after 12 weeks of exposure to hyperbaric oxygen. CONCLUSION: We concluded that exposure to hyperbaric oxygen used in this study accelerates both the fading in melanin pigmentation and the decrease in senile spot size.

Effects of hyperbaric oxygenation on blood pressure levels of spontaneously hypertensive rats.

Five-week-old normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were subjected to hyperbaric oxygenation with an enhanced atmospheric pressure (950 mmHg) and an increased oxygen concentration (36%) for 6 h per day. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were monitored for 8 weeks of hyperbaric oxygenation period. After 8 weeks of hyperbaric oxygenation, the derivatives of reactive oxygen metabolites (dROMs) and biological antioxidant potentials (BAPs) were measured. After 5 weeks of hyperbaric oxygenation, the hyperbaric group of WKY exhibited lower SBP than the age-matched normobaric group, while there were no differences in the DBP between the normobaric and hyperbaric groups. After 3 and 7 weeks of hyperbaric oxygenation, the hyperbaric group of SHR exhibited lower SBP and DBP than the age-matched normobaric group. The hyperbaric groups of both WKY and SHR exhibited lower dROMs than the respective normobaric groups. There were no differences in BAPs between the normobaric and hyperbaric groups of WKY. In contrast, the hyperbaric group of SHR exhibited higher BAPs than the normobaric group. We conclude that the hyperbaric oxygenation conditions used in this study effectively repress hypertension.

Hyperbaric oxygen exposure improves blood glucose level and muscle oxidative capacity in rats with type 2 diabetes.

BACKGROUND: The effects of exposure to hyperbaric oxygen on blood glucose level and muscle oxidative capacity in rats with type 2 diabetes were investigated. METHODS: Five-week-old male Goto-Kakizaki rats were divided into four groups: normobaric (NN; exposed to 21% oxygen at 760 mm Hg for 8 weeks), hyperbaric to normobaric (HN; exposed to 36% oxygen at 950 mm Hg for 4 weeks, followed by 21% oxygen at 760 mm Hg for 4 weeks), normobaric to hyperbaric (NH; exposed to 21% oxygen at 760 mm Hg for 4 weeks, followed by 36% oxygen at 950 mm Hg for 4 weeks), and hyperbaric (HH; exposed to 36% oxygen at 950 mm Hg for 8 weeks). RESULTS: Blood glucose levels were lower in the HN, NH, and HH groups than in the NN group. Up-regulated mRNA expression levels of peroxisome proliferator-activated receptor-gamma co-activator-1alpha were observed in the soleus muscles of the HN, NH, and HH groups and in the plantaris muscles of the HN and HH groups. The soleus muscles of the NN group contained only type I fibers, whereas those of the HN, NH, and HH groups contained type I, type IIA, and type IIC fibers. An increased percentage of type I fibers and a decreased percentage of type IIB fibers were observed in the plantaris muscles of the NH, HN, and HH groups. CONCLUSIONS: Exposure to hyperbaric oxygen reduces high blood glucose levels and improves oxidative capacities in the skeletal muscles of rats with diabetes, and these effects are maintained under normobaric conditions even after exposure to hyperbaric oxygen.

Thermal preconditioning prevents fiber type transformation of the unloading induced-atrophied muscle in rats.

Muscle atrophy is accompanied by a slow-to-fast transformation of the slow muscle, e.g., the soleus muscle, which is characterized by a decrease in the expression of the slow myosin heavy chain (MyHC) isoform. Heat stress before hindlimb unloading, i.e., thermal preconditioning, has been shown to reduce the rate of disuse-induced muscle atrophy. The present study examined whether thermal preconditioning could prevent a slow-to-fast transformation of the MyHC isoform through the induction of heat-shock protein (HSP) 72. Thermally preconditioned rats (Heat + HU) were individually placed in an environmentally controlled heat chamber for 1 h before hindlimb unloading for 2 weeks (HU). Although the mean fiber cross-sectional areas of the soleus muscle decreased in the HU and Heat + HU group, the loss of myofibrillar protein was attenuated in the Heat + HU group. Furthermore, a slow-to-fast transformation of MyHC isoform was inhibited in the Heat + HU group with the overexpression of HSP72. These results indicate that thermal preconditioning before hindlimb unloading attenuates the decrease of the slow MyHC isoform in the soleus muscle. Therefore, thermal preconditioning provides a new approach to prevent disuse-induced fiber type transformation of skeletal muscle.

Bone density of the femur and fiber cross-sectional area and oxidative enzyme activity of the tibialis anterior muscle in type II collagen-induced arthritic mice.

Femur bone densities and tibialis anterior muscle properties of type II collagen-induced arthritic mice were determined. Furthermore, voluntary running activities of arthritic mice were compared with those of controls. Arthritis was induced by an intradermal injection of type II collagen in the adjuvant. Body and muscle weights were lower in arthritic mice than in controls. Cortical and trabecular bone densities and muscle fiber cross-sectional areas were decreased by arthritis. After classifying the arthritic severity into slight, intermediate, and severe levels based on the degree of knuckle swelling, cortical and trabecular bone densities, fiber cross-sectional areas, and fiber succinate dehydrogenase activities were lowest when arthritis was most severe. Furthermore, arthritic mice, especially those with intermediate and severe levels, showed lower voluntary running activities. These findings indicate that lower bone density and muscle atrophy of type II collagen-induced arthritic mice are related to arthritic severity and decreased motor activity.