Contractile activity is necessary to trigger intermittent hypobaric hypoxia-induced fiber size and vascular adaptations in skeletal muscle

Altitude training has become increasingly popular in recent decades. Its central and peripheral effects are well-described; however, few studies have analysed the effects of intermittent hypobaric hypoxia (IHH) alone on skeletal muscle morphofunctionality. Here, we studied the effects of IHH on different myofibre morphofunctional parameters, investigating whether contractile activity is required to elicit hypoxia-induced adaptations in trained rats. Eighteen male Sprague-Dawley rats were trained one month and then divided into three groups: (1) rats in normobaria (trained normobaric inactive, TNI); (2) rats subjected daily to a 4-hour exposure to hypobaric hypoxia equivalent to 4,000 m (trained hypobaric inactive, THI); and (3) rats subjected daily to a 4-hour exposure to hypobaric hypoxia just before performing light exercise (trained hypobaric active, THA). After two weeks, the tibialis anterior muscle (TA) was excised. Muscle cross-sections were stained for: (1) succinate dehydrogenase to identify oxidative metabolism; (2) myosin-ATPase to identify slow- and fast-twitch fibres; and (3) endothelial-ATPase to stain capillaries. Fibres were classified as slow oxidative (SO), fast oxidative glycolytic (FOG), fast intermediate glycolytic (FIG) or fast glycolytic (FG) and the following parameters were measured: fibre cross-sectional area (FCSA), number of capillaries per fibre (NCF), NCF per 1,000 µm2 of FCSA (CCA), fibre and capillary density (FD and CD), and the ratio between CD and FD (C/F). THI rats did not exhibit significant changes in most of the parameters, while THA animals showed reduced fibre size. Compared to TNI rats, FOG fibres from the lateral/medial fields, as well as FIG and FG fibres from the lateral region, had smaller FCSA in THA rats. Moreover, THA rats had increased NCF in FG fibres from all fields, in medial and posterior FIG fibres and in posterior FOG fibres. All fibre types from the three analysed regions (except the posterior FG fibres) displayed a significantly increased CCA ratio compared to TNI rats. Global capillarisation was also increased in lateral and medial fields. Our results show that IHH alone does not induce alterations in the TA muscle. The inclusion of exercise immediately after the hypoxic exposure is enough to trigger a morphofunctional response that overall improves muscle capillarisation

Exercise alters liver mitochondria phospholipidomic profile and mitochondrial activity in non-alcoholic steatohepatitis

Mitochondrial membrane lipid composition is a critical factor in non-alcoholic steatohepatitis (NASH). Exercise is the most prescribed therapeutic strategy against NASH and a potential modulator of lipidmembrane. Thus, we aimed to analyze whether physical exercise exerted preventive (voluntary physical activity - VPA) and therapeutic (endurance training - ET) effect on NASH-induced mitochondrial membrane changes. Sprague-Dawley rats (n = 36) were divided into standard-diet sedentary (SS, n = 12),standard-diet VPA (SVPA, n = 6), high-fat diet sedentary (HS, n = 12) and high-fat diet VPA (HVPA, n = 6). After 9 weeks of diet-specific feeding, half of SS and HS group were engaged in an ET program for 8 weeks/5 day/week/1 h/day (SET, HET). Liver mitochondria were isolated for oxygen consumption and transmembrane-electric potential (Δψ) assays. Mitochondrial phospholipid classes and fatty acids were quantified through thin layer chromatography and gas chromatography, respectively, while cardiolipin(CL), phosphatidylcholine (PC) phosphatidylethanolamine (PE) and phosphatidylinositol (PI) molecular profile was determined by electrospray mass spectrometry. In parallel with histological signs of NASH,high-fat diet decreased PI, CL and PC/PE ratio, whereas PE and phosphatidic acid content increased insedentary animals (HS vs. SS). Moreover, a decrease in linolelaidic, monounsaturated fatty acids content and an increase in saturated fatty acids (SFAS) were observed. Along with phospholipidomic alterations,HS animals showed a decrease in respiratory control ratio (RCR), Δψ and FCCP-induced uncoupling respiration (HS vs. SS). Both phospholipidomic (PC/PE, SFAS) and mitochondrial respiratory alterations were counteracted by exercise interventions. Exercise used as preventive (VPA) or therapeutic (ET) strategies preserved liver mitochondrial phospholipidomic profile and maintained mitochondrial function in a model of NASH

The effect of high-frequency neuromuscular electrical stimulation training on skeletal muscle properties in mice

The aim of this study was to analyze the effects of high-frequency neuromuscular electrical stimulation training (NMES) on the structure, function and oxidative capacity of the skeletal muscle using a mice model (C57BL/6J strain, n=8). The left tibialis anterior muscle in mice was electro-stimulated (ST) whereas the right muscle was maintained as an internal control (CT). The ST limb was submitted to eight surface (100 Hz) NMES sessions in two weeks, with a minimum gap of 24 h between sessions. NMES training increased muscle mass (42.0±3.3 vs. 36.1±5.4 mg, p<0.05, effect size [ES] r=0.55), the mean fiber cross-sectional area (FCSA) (3318±333 vs. 2577±405 μ2, p<0.001, ES=0.71), maximal force (224.7±13.8 vs. 184.5±30.9 mN, p<0.01, ES=0.64), and the rate of force development (1.63±0.14 vs. 1.34±0.20 mN/ms, p<0.05, ES=0.64), with no effects on the muscle oxidative profile. These results demonstrate that surface NMES induced muscle hypertrophy and instigated an improvement in the contractile properties of the TA muscle in mice. Therefore, this animal model appears to be suitable for the study of hypertrophic processes as it enables better control of the stimulus properties (intensity, duration, frequency, etc.) than other traditionally used animal models and does not require negative reinforcements or surgical procedures

Vitamin D insufficiency is associated with metabolic risk factors in women with polycystic ovary syndrome

Seven healthy young men were submitted twice to a hypoxia tolerance test at a simulated altitude (3000m). Their first acute exposure was in a hypobaric chamber; and the second, in a hypoxic tent. Cardiorespiratory parameters and heart rate variability measurements were obtained under each hypoxic condition. A significant decrease of 6% to 8% compared to normal oxygen conditions was observed in arterial oxygen saturation (SpO2) in both hypoxic conditions at rest; whereas exercise led to decreases of 10% in SpO2 despite an increase of 27% in respiratory minute volume. The low frequency (LF) and high frequency (HF) components of heart rate variability significantly changed from normoxia (LF: 37.1, HF: 62.9, LF/HF: 1.27) to hypobaric hypoxia (HH) (LF: 49.1, HF: 50.6, LF/HF: 1.96). However, these changes were not observed under normobaric hypoxia. Thus, heart rate variability behaved differently in the two hypoxic conditions, supporting the hypothesis that normobaric hypoxia and hypobaric

Contractile Activity Is Necessary to Trigger Intermittent Hypobaric Hypoxia-Induced Fiber Size and Vascular Adaptations in Skeletal Muscle

Altitude training has become increasingly popular in recent decades. Its central and peripheral effects are well-described; however, few studies have analyzed the effects of intermittent hypobaric hypoxia (IHH) alone on skeletal muscle morphofunctionality. Here, we studied the effects of IHH on different myofiber morphofunctional parameters, investigating whether contractile activity is required to elicit hypoxia-induced adaptations in trained rats. Eighteen male Sprague-Dawley rats were trained 1 month and then divided into three groups: (1) rats in normobaria (trained normobaric inactive, TNI); (2) rats subjected daily to a 4-h exposure to hypobaric hypoxia equivalent to 4,000 m (trained hypobaric inactive, THI); and (3) rats subjected daily to a 4-h exposure to hypobaric hypoxia just before performing light exercise (trained hypobaric active, THA). After 2 weeks, the tibialis anterior muscle (TA) was excised. Muscle cross-sections were stained for: (1) succinate dehydrogenase to identify oxidative metabolism; (2) myosin-ATPase to identify slow- and fast-twitch fibers; and (3) endothelial-ATPase to stain capillaries. Fibers were classified as slow oxidative (SO), fast oxidative glycolytic (FOG), fast intermediate glycolytic (FIG) or fast glycolytic (FG) and the following parameters were measured: fiber cross-sectional area (FCSA), number of capillaries per fiber (NCF), NCF per 1,000 μm2 of FCSA (CCA), fiber and capillary density (FD and CD), and the ratio between CD and FD (C/F). THI rats did not exhibit significant changes in most of the parameters, while THA animals showed reduced fiber size. Compared to TNI rats, FOG fibers from the lateral/medial fields, as well as FIG and FG fibers from the lateral region, had smaller FCSA in THA rats. Moreover, THA rats had increased NCF in FG fibers from all fields, in medial and posterior FIG fibers and in posterior FOG fibers. All fiber types from the three analyzed regions (except the posterior FG fibers) displayed a significantly increased CCA ratio compared to TNI rats. Global capillarisation was also increased in lateral and medial fields. Our results show that IHH alone does not induce alterations in the TA muscle. The inclusion of exercise immediately after the tested hypoxic conditions is enough to trigger a morphofunctional response that improves muscle capillarisation

Exercise alters liver mitochondria phospholipidomic profile and mitochondrial activity in non-alcoholic steatohepatitis

Mitochondrial membrane lipid composition is a critical factor in non-alcoholic steatohepatitis (NASH). Exercise is the most prescribed therapeutic strategy against NASH and a potential modulator of lipid membrane. Thus, we aimed to analyze whether physical exercise exerted preventive (voluntary physical activity – VPA) and therapeutic (endurance training – ET) effect on NASH-induced mitochondrial membrane changes. Sprague-Dawley rats (n = 36) were divided into standard-diet sedentary (SS, n = 12), standard-diet VPA (SVPA, n = 6), high-fat diet sedentary (HS, n = 12) and high-fat diet VPA (HVPA, n = 6). After 9 weeks of diet-specific feeding, half of SS and HS group were engaged in an ET program for 8 weeks/5 day/week/1 h/day (SET, HET). Liver mitochondria were isolated for oxygen consumption and transmembrane-electric potential (ΔΨ) assays. Mitochondrial phospholipid classes and fatty acids were quantified through thin layer chromatography and gas chromatography, respectively, while cardiolipin (CL), phosphatidylcholine (PC) phosphatidylethanolamine (PE) and phosphatidylinositol (PI) molecular profile was determined by electrospray mass spectrometry. In parallel with histological signs of NASH, high-fat diet decreased PI, CL and PC/PE ratio, whereas PE and phosphatidic acid content increased in sedentary animals (HS vs. SS). Moreover, a decrease in linolelaidic, monounsaturated fatty acids content and an increase in saturated fatty acids (SFAS) were observed. Along with phospholipidomic alterations, HS animals showed a decrease in respiratory control ratio (RCR), ΔΨ and FCCP-induced uncoupling respiration (HS vs. SS). Both phospholipidomic (PC/PE, SFAS) and mitochondrial respiratory alterations were counteracted by exercise interventions. Exercise used as preventive (VPA) or therapeutic (ET) strategies preserved liver mitochondrial phospholipidomic profile and maintained mitochondrial function in a model of NASH

Exercise alters liver mitochondria phospholipidomic profile and mitochondrial activity in non-alcoholic steatohepatitis

Mitochondrial membrane lipid composition is a critical factor in non-alcoholic steatohepatitis (NASH). Exercise is the most prescribed therapeutic strategy against NASH and a potential modulator of lipidmembrane. Thus, we aimed to analyze whether physical exercise exerted preventive (voluntary physical activity - VPA) and therapeutic (endurance training - ET) effect on NASH-induced mitochondrial membrane changes. Sprague-Dawley rats (n = 36) were divided into standard-diet sedentary (SS, n = 12),standard-diet VPA (SVPA, n = 6), high-fat diet sedentary (HS, n = 12) and high-fat diet VPA (HVPA, n = 6). After 9 weeks of diet-specific feeding, half of SS and HS group were engaged in an ET program for 8 weeks/5 day/week/1 h/day (SET, HET). Liver mitochondria were isolated for oxygen consumption and transmembrane-electric potential (Δψ) assays. Mitochondrial phospholipid classes and fatty acids were quantified through thin layer chromatography and gas chromatography, respectively, while cardiolipin(CL), phosphatidylcholine (PC) phosphatidylethanolamine (PE) and phosphatidylinositol (PI) molecular profile was determined by electrospray mass spectrometry. In parallel with histological signs of NASH,high-fat diet decreased PI, CL and PC/PE ratio, whereas PE and phosphatidic acid content increased insedentary animals (HS vs. SS). Moreover, a decrease in linolelaidic, monounsaturated fatty acids content and an increase in saturated fatty acids (SFAS) were observed. Along with phospholipidomic alterations,HS animals showed a decrease in respiratory control ratio (RCR), Δψ and FCCP-induced uncoupling respiration (HS vs. SS). Both phospholipidomic (PC/PE, SFAS) and mitochondrial respiratory alterations were counteracted by exercise interventions. Exercise used as preventive (VPA) or therapeutic (ET) strategies preserved liver mitochondrial phospholipidomic profile and maintained mitochondrial function in a model of NASH

Circadian and Sex Differences After Acute High-Altitude Exposure: Are Early Acclimation Responses Improved by Blue Light?

Artículo de publicación ISIObjective.-The possible effects of blue light during acute hypoxia and the circadian rhythm on several physiological and cognitive parameters were studied. Methods.-Fifty-seven volunteers were randomly assigned to 2 groups: nocturnal (2200-0230 hours) or diurnal (0900-1330 hours) and exposed to acute hypoxia (4000 m simulated altitude) in a hypobaric chamber. The participants were illuminated by blue LEDs or common artificial light on 2 different days. During each session, arterial oxygen saturation (Spo(2)), blood pressure, heart rate variability, and cognitive parameters were measured at sea level, after reaching the simulated altitude of 4000 m, and after 3 hours at this altitude. Results.-The circadian rhythm caused significant differences in blood pressure and heart rate variability. A 4% to 9% decrease in waking nocturnal Spo(2) under acute hypoxia was observed. Acute hypoxia also induced a significant reduction (4%-8%) in systolic pressure, slightly more marked (up to 13%) under blue lighting. Women had significantly increased systolic (4%) and diastolic (12%) pressures under acute hypoxia at night compared with daytime pressure; this was not observed in men. Some tendencies toward better cognitive performance (d2 attention test) were seen under blue illumination, although when considered together with physiological parameters and reaction time, there was no conclusive favorable effect of blue light on cognitive fatigue suppression after 3 hours of acute hypobaric hypoxia. Conclusions.-It remains to be seen whether longer exposure to blue light under hypobaric hypoxic conditions would induce favorable effects against fatigue.Spanish Agencia Espanola de Cooperacion Internacional y Desarrollo (AECID) A/025717/09 A/030280/10 Chilean FONDECYT 110016