Preconditioning with hydrogen peroxide (H2O2) or ischemia in H2O2-induced cardiac dysfunction

To assess whether allantoin levels in serum and urine are influenced by exhaustive and moderate exercise and whether allantoin is a useful indicator of exercise-induced oxidative stress in humans, we made subjects perform exhaustive and moderate (100% and 40% VO₂max) cycling exercise and examined the levels of allantoin, thiobarbituric acid reactive substances (TBARS) and urate in serum and urine. Immediately after exercise at 100% VO₂max, the serum allantoin/urate ratio was significantly elevated compared with the resting levels while the serum urate levels was significantly elevated 30 min after exercise. The serum TBARS levels did not increase significantly compared with the resting levels. Urinary allantoin excretion significantly increased during 60 min of recovery after exercise, however, urinary urate excretion decreased significantly during the same period. The urinary allantoin/urate ratio also rapidly increased during 60 min of recovery after exercise. Urinary TBARS excretion decreased during the first 60 min of the recovery period and thereafter significantly increased during the latter half of the recovery period. On the contrary, after 40% VO₂max of exercise, no significant changes in the levels of urate, allantoin and TBARS in serum or urine were observed. These findings suggest that allantoin levels in serum and urine may reflect the extent of oxidative stress in vivo and that the allantoin which appeared following exercise may have originated not from urate formed as a result of exercise but from urate that previously existed in the body. Furthermore, these findings support the view that allantoin in serum and urine is a more sensitive and reliable indicator of in vivo oxidative stress than lipid peroxidation products measured as TBARS.     

Increased plasma levels of palmitoleic acid may contribute to beneficial effects of Krill oil on glucose homeostasis in dietary obese mice

Omega-3 polyunsatuarted fatty acids (PUFA) are associated with hypolipidemic and anti-inflammatory effects. However, omega-3 PUFA, usually administered as triacylglycerols or ethyl esters, could also compromise glucose metabolism, especially in obese type 2 diabetics. Phospholipids represent an alternative source of omega-3 PUFA, but their impact on glucose homeostasis is poorly explored. Male C57BL/6N mice were fed for 8 weeks a corn oil-based high-fat diet (cHF) alone or cHF-based diets containing eicosapentaenoic acid and docosahexaenoic acid (~3%; wt/wt), admixed either as a concentrate of re-esterified triacylglycerols (ω3TG) or Krill oil containing mainly phospholipids (ω3PL). Lean controls were fed a low-fat diet. Insulin sensitivity (hyperinsulinemic-euglycemic clamps), parameters of glucose homeostasis, adipose tissue function, and plasma levels of N-acylethanolamines, monoacylglycerols and fatty acids were determined.Feeding cHF induced obesity and worsened (~4.3-fold) insulin sensitivity as determined by clamp. Insulin sensitivity was almost preserved in ω3PL but not ω3TG mice. Compared with cHF mice, endogenous glucose production was reduced to 47%, whereas whole-body and muscle glycogen synthesis increased ~3-fold in ω3PL mice that showed improved adipose tissue function and elevated plasma adiponectin levels. Besides eicosapentaenoic and docosapentaenoic acids, principal component analysis of plasma fatty acids identified palmitoleic acid (C16:1n-7) as the most discriminating analyte whose levels were increased in ω3PL mice and correlated negatively with the degree of cHF-induced glucose intolerance.While palmitoleic acid from Krill oil may help improve glucose homeostasis, our findings provide a general rationale for using omega-3 PUFA-containing phospholipids as nutritional supplements with potent insulin-sensitizing effects.     

Time-restricted feeding mice a high-fat diet induces a unique lipidomic profile

Time-restricted feeding (TRF) can reduce adiposity and lessen the co-morbidities of obesity. Mice consuming obesogenic high-fat (HF) diets develop insulin resistance and hepatic steatosis, but have elevated indices of long-chain polyunsaturated fatty acids (LCPUFA) that may be beneficial. While TRF impacts lipid metabolism, scant data exist regarding the impact of TRF upon lipidomic composition of tissues. We (1) tested the hypothesis that TRF of a HF diet elevates LCPUFA indices while preventing insulin resistance and hepatic steatosis and (2) determined the impact of TRF upon the lipidome in plasma, liver, and adipose tissue. For 12 weeks, male, adult mice were fed a control diet ad libitum, a HF diet ad libitum (HF-AL), or a HF diet with TRF, 12 hours during the dark phase (HF-TRF). HF-TRF prevented insulin resistance and hepatic steatosis resulting from by HF-AL treatment. TRF-blocked plasma increases in LCPUFA induced by HF-AL treatment but elevated concentrations of triacylglycerols and non-esterified saturated fatty acids. Analysis of the hepatic lipidome demonstrated that TRF did not elevate LCPUFA while reducing steatosis. However, TRF created (1) a separate hepatic lipid signature for triacylglycerols, phosphatidylcholine, and phosphatidylethanolamine species and (2) modified gene and protein expression consistent with reduced fatty acid synthesis and restoration of diurnal gene signaling. TRF increased the saturated fatty acid content in visceral adipose tissue. In summary, TRF of a HF diet alters the lipidomic profile of plasma, liver, and adipose tissue, creating a third distinct lipid metabolic state indicative of positive metabolic adaptations following HF intake.     

Individual Responses to Completion of Short-Term and Chronic Interval Training: A Retrospective Study

Alterations in maximal oxygen uptake (VO₂max), heart rate (HR), and fat oxidation occur in response to chronic endurance training. However, many studies report frequent incidence of “non-responders” who do not adapt to continuous moderate exercise. Whether this is the case in response to high intensity interval training (HIT), which elicits similar adaptations as endurance training, is unknown. The aim of this retrospective study was to examine individual responses to two paradigms of interval training. In the first study (study 1), twenty active men and women (age and baseline VO₂max = 24.0±4.6 yr and 42.8±4.8 mL/kg/min) performed 6 d of sprint interval training (SIT) consisting of 4–6 Wingate tests per day, while in a separate study (study 2), 20 sedentary women (age and baseline VO₂max = 23.7±6.2 yr and 30.0±4.9 mL/kg/min) performed 12 wk of high-volume HIT at workloads ranging from 60–90% maximal workload. Individual changes in VO₂max, HR, and fat oxidation were examined in each study, and multiple regression analysis was used to identify predictors of training adaptations to SIT and HIT. Data showed high frequency of increased VO₂max (95%) and attenuated exercise HR (85%) in response to HIT, and low frequency of response for VO₂max (65%) and exercise HR (55%) via SIT. Frequency of improved fat oxidation was similar (60–65%) across regimens. Only one participant across both interventions showed non-response for all variables. Baseline values of VO₂max, exercise HR, respiratory exchange ratio, and body fat were significant predictors of adaptations to interval training. Frequency of positive responses to interval training seems to be greater in response to prolonged, higher volume interval training compared to similar durations of endurance training.     

Muscle fibre conduction velocity and cardiorespiratory response during incremental cycling exercise in young and older individuals with different training status

We investigated the effect of ageing and training on muscle fibre conduction velocity (MFCV) and cardiorespiratory response during incremental cycling exercise. Eight young (YT; 24 ± 5 yrs) and eight older (OT; 64 ± 3 yrs) cyclists, together with eight young (YU; 27 ± 4 yrs) and eight older (OU; 63 ± 2 yrs) untrained individuals underwent to an incremental maximal test on a cycle ergometer. Ventilatory threshold (VT), respiratory compensation point (RCP) and maximal oxygen uptake (VO₂max) were identified and MFCV recorded from the vastus lateralis muscle using surface electromyography with linear arrays electrodes.In YT MFCV increased with the exercise intensity, reaching a peak of 4.99 ± 1.02 [m/s] at VT. Thereafter, and up to VO₂max, MFCV declined. In YU MFCV showed a similar trend although the peak [4.55 ± 0.53 m/s] was observed, at 75% of VO₂max an intensity higher than VT (66% of VO₂max). In both YT and YU MFCV did not decline until RPC, which occurred at 78% VO₂max in YU and at 92% VO₂max (P < 0.01) in YT. Differently from young individuals, MFCV in older subjects did not increase with exercise intensity. Moreover, maximal MFCV in OU was significantly lower [3.53 ± 0.40 m/s;] than that of YT (P < 0.005) and YU (P < 0.05).The present study shows that, especially in young individuals, MFCV reflects cardiorespiratory response during incremental dynamic cyclic exercise and hence can be used to investigate motor unit recruitment strategies.     

Impact of Exercise and Moderate Hypoxia on Glycemic Regulation and Substrate Oxidation Pattern

Objective

We examined metabolic and endocrine responses during rest and exercise in moderate hypoxia over a 7.5 h time courses during daytime.

Methods

Eight sedentary, overweight men (28.6±0.8 kg/m²) completed four experimental trials: a rest trial in normoxia (FiO₂ = 20.9%, NOR-Rest), an exercise trial in normoxia (NOR-Ex), a rest trial in hypoxia (FiO₂ = 15.0%, HYP-Rest), and an exercise trial in hypoxia (HYP-Ex). Experimental trials were performed from 8:00 to 15:30 in an environmental chamber. Blood and respiratory gas samples were collected over 7.5 h. In the exercise trials, subjects performed 30 min of pedaling exercise at 60% of VO₂max at 8:00, 10:30, and 13:00, and rested during the remaining period in each environment. Standard meals were provided at 8:30, 11:00, and 13:30.

Results

The areas under the curves for blood glucose and serum insulin concentrations over 7.5 h did not differ among the four trials. At baseline, %carbohydrate contribution was significantly higher in the hypoxic trials than in the normoxic trials (P<0.05). Although exercise promoted carbohydrate oxidation in the NOR-Ex and HYP-Ex trials, %carbohydrate contribution during each exercise and post-exercise period were significantly higher in the HYP-Ex trial than in the NOR-Ex trial (P<0.05).

Conclusion

Three sessions of 30 min exercise (60% of VO₂max) in moderate hypoxia over 7.5 h did not attenuate postprandial glucose and insulin responses in young, overweight men. However, carbohydrate oxidation was significantly enhanced when the exercise was conducted in moderate hypoxia.     

CHANGE IN BLOOD GELSOLIN CONCENTRATION IN RESPONSE TO PHYSICAL EXERCISE

Plasma gelsolin (pGSN) produced by muscle is an abundant protein of extracellular fluids capable of severing actin filaments and eliminating actin from the circulation. Additionally, pGSN modulates the cellular effects of some bioactive lipids. In this study we test the hypothesis that hormonal and metabolic adaptations to exercise are associated with changes in gelsolin concentration in blood. Plasma samples were collected from twenty healthy males recruited from untrained (UT, n=10) and endurance trained (ET, n=10) groups that performed 30-60 minutes of exercise on a cycloergometer at a workload corresponding to 70% of VO₂max. Gelsolin concentration was determined by quantitative Western blot analysis with an anti-human gelsolin antibody. The gelsolin concentration in UT and ET subjects before starting exercise ranged from 104 to 330 and 163 to 337 µg · ml^-1 respectively. After 30 minutes of exercise we observed a significant decrease of plasma gelsolin in the UT group (p<0.05) while the gelsolin concentration in the ET group rose on average from 244 to 271 µg · ml^-1. However, this increase did not reach statistical significance. Endurance training might increase the ability of muscle tissue to express plasma gelsolin as part of an adaptive mechanism.     

Elevated tissue omega-3 fatty acid status prevents age-related glucose intolerance in fat-1 transgenic mice

The objective of this study was to investigate the impact of elevated tissue omega-3 (n-3) polyunsaturated fatty acids (PUFA) status on age-related glucose intolerance utilizing the fat-1 transgenic mouse model, which can endogenously synthesize n-3 PUFA from omega-6 (n-6) PUFA. Fat-1 and wild-type mice, maintained on the same dietary regime of a 10% corn oil diet, were tested at two different ages (2 months old and 8 months old) for various glucose homeostasis parameters and related gene expression. The older wild-type mice exhibited significantly increased levels of blood insulin, fasting blood glucose, liver triglycerides, and glucose intolerance, compared to the younger mice, indicating an age-related impairment of glucose homeostasis. In contrast, these age-related changes in glucose metabolism were largely prevented in the older fat-1 mice. Compared to the older wild-type mice, the older fat-1 mice also displayed a lower capacity for gluconeogenesis, as measured by pyruvate tolerance testing (PTT) and hepatic gene expression of phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6 phosphatase (G6Pase). Furthermore, the older fat-1 mice showed a significant decrease in body weight, epididymal fat mass, inflammatory activity (NFκ-B and p-IκB expression), and hepatic lipogenesis (acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) expression), as well as increased peroxisomal activity (70-kDa peroxisomal membrane protein (PMP70) and acyl-CoA oxidase1 (ACOX1) expression). Altogether, the older fat-1 mice exhibit improved glucose homeostasis in comparison to the older wild-type mice. These findings support the beneficial effects of elevated tissue n-3 fatty acid status in the prevention and treatment of age-related chronic metabolic diseases.     

坐式八段锦联合运动康复治疗对急性冠脉综合征PCI术后患者运动耐力、血清心肌损伤标志物和生活质量的影响

摘要 目的：探讨坐式八段锦联合运动康复治疗对急性冠脉综合征（ACS）经皮冠状动脉介入治疗术（PCI）后患者运动耐力、血清心肌损伤标志物和生活质量的影响。方法：根据随机数字表法,将我院2020年4月~2021年5月期间收治的ACS行PCI术的患者（n=120）分为对照组（运动康复治疗,n=60）和研究组（坐式八段锦联合运动康复治疗,n=60）。对比两组心功能指标[左心室舒张末期内径（LVEDD）、左心室射血分数（LVEF）、氨基末端B型脑利钠肽前体（NT-proBNP）、左心室舒张末期容积（LVEDV）]、心肌损伤标志物[肌酸激酶同工酶（CK-MB）、心肌肌钙蛋白I（cTnI）]、运动耐力指标[无氧阈（AT）、最大摄氧量（VO_2max ）、运动持续时间（ED）]和生活质量[西雅图心绞痛量表（SAQ）评分：躯体活动受限程度（PL）、心绞痛稳定情况（AS）、疾病认知程度（DS）、心绞痛发作状况（AF）和治疗满意程度（TS）],并纪录两组不良心血管事件发生情况。结果：研究组的心血管不良事件发生率低于对照组（P<0.05）。研究组治疗3个月后LVEF高于对照组,LVEDD、LVEDV、NT-proBNP低于对照组（P<0.05）。研究组治疗3个月后CK-MB、cTnI低于对照组（P<0.05）。研究组治疗3个月后AT、VO_2max 、ED高于对照组（P<0.05）。研究组治疗3个月后PL、AS、DS、AF、TS评分高于对照组（P<0.05）。结论：坐式八段锦联合运动康复治疗可促进ACS患者PCI术后心功能改善,减轻心肌损伤,进而提高运动耐力和生活质量。     

Cold-induced vasodilatation of finger and maximal oxygen consumption of young female athletes born in Hokkaido

To determine whether there is a direct correlation between endurance capacity and cold tolerance, maximal oxygen consumption (VO₂max), and cold-induced vasodilatation (CIVD), we measured these factors in 14 young female athletes born in Hokkaido, Japan's northernmost island. We determined the VO₂max by a standard incremental test on a cycle ergometer and measured the oxygen consumption (VO₂) by means of the Douglas-bag method. We determined the CIVD reaction by measuring the skin temperature of the left middle finger during immersion in cold water at 0°C for 20 min. The athletes showed significant positive correlations between VO₂max, expressed as l/min, and CIVD as well as other peripheral cold tolerance indexes (resistance index against frostbite and CIVD index). The body weight VO₂max (VO₂max/kg body weight) failed to correlate significantly with either the CIVD or with other cold tolerance indexes. These results suggest that CIVD in females may depend on factors other than those determined in this study, in addition to the functional spread of the vascular beds in peripheral tissues, including striated muscle; it is known that the size and the vascular bed in this tissue are affected by exercise training and that this results in the elevation of VO₂max and VO₂max/kg body weight.     

Effects of one bout of endurance exercise on the expression of myogenin in human quadriceps muscle

The objective of this study was to investigate the cellular localisation of MyoD and myogenin in human skeletal muscle fibres as well as the possible alterations in the expression of MyoD and myogenin in response to a single bout of endurance exercise at 40% and 75% of maximum oxygen uptake (VO₂ max). Twenty-five biopsies (5 per subject) from the vastus lateralis muscle were obtained before exercise, from the exercising leg at 40% and 75% of VO₂ max and from the resting leg following these exercise bouts. The tyramide signal amplification-direct and the Vectastain ABC methods using specific monoclonal antibodies were used to determine the exact location of myogenin and MyoD, to identify muscle satellite cells and to determine myosin heavy chain (MyHC) composition. At rest, myonuclei did not express MyoD or myogenin. Following a single bout of exercise at 40% and 75% of VO₂ max, an accumulation of myogenin in myonuclei and not in satellite cells was observed in biopsies from the exercised leg but not in biopsies before exercise and from the resting leg. The number of myogenin-positive myonuclei varied among individuals indicating differences in the response to a single exercise bout. In conclusion, this immunohistochemical study showed that a rapid rearrangement of myogenin expression occurs in exercised human skeletal muscles in response to a single bout of exercise.     

Reducing the Dietary Omega-6:Omega-3 Utilizing α-Linolenic Acid; Not a Sufficient Therapy for Attenuating High-Fat-Diet-Induced Obesity Development Nor Related Detrimental Metabolic and Adipose Tissue Inflammatory Outcomes

Aims

To examine the effect of manipulating the omega-6:omega-3 (1∶1, 5∶1, 10∶1, and 20∶1) utilizing only α-linolenic and linoleic acid within a clinically-relevant high-fat diet (HFD) composed of up to seven sources of fat and designed to be similar to the standard American diet (MUFA∶PUFA of 2∶1, 12% and 40% of calories from saturated and total fat, respectively) on body composition, macrophage polarization, inflammation, and metabolic dysfunction in mice.

Methods

Diets were administered for 20 weeks. Body composition and metabolism (HOMA index and lipid profile) were examined monthly. GC-MS was utilized to determine the eicosapentaenoic acid (EPA):arachidonic acid (AA) and the docosahexaenoic acid (DHA):AA in AT phospholipids. Adipose tissue (AT) mRNA expression of chemokines (MCP-1, Fetuin-A, CXCL14), marker genes for M1 and M2 macrophages (CD11c and CD206, respectively) and inflammatory markers (TNF-α, IL-6, IL-1β, TLR-2, TLR-4, IL-10, GPR120) were measured along with activation of NFκB, JNK, and STAT-3. Macrophage infiltration into AT was examined using F4/80 immunohistochemistry.

Results

Any therapeutic benefit produced by reducing the omega-6:omega-3 was evident only when comparing the 1∶1 to 20∶1 HFD; the 1∶1 HFD resulted in a lower TC:HDL-C and decreased AT CXCL14 gene expression and AT macrophage infiltration, which was linked to a higher EPA:AA and DHA:AA in AT phospholipids. However, despite these effects, and independent of the omega-6:omega-3, all HFDs, in general, led to similar levels of adiposity, insulin resistance, and AT inflammation.

Conclusion

Reducing the omega-6:omega-3 using α-linolenic acid is not an effective therapy for attenuating obesity and type II diabetes mellitus development.     

Exercise training intensity/volume affects plasma and tissue adiponectin concentrations in the male rat

The objective of the study was to determine the effects of exercise training intensity/volume on plasma total and high molecular weight (HMW) adiponectin and tissue total adiponectin concentrations. Thirty-two, eight week-old male Wistar rats (185 ± 5 g) were randomly assigned to one of four groups: high intensity (HI: 34 m/min ∼%80-%85 VO₂max), moderate intensity (MI: 28 m/min ∼%70-%75 VO₂max), low intensity (LI: 20m/min ∼ %50-%55 VO₂max), and sedentary control (SED). Experimental groups completed a 12-week exercise program of treadmill running at 0° slope, 1 h/day, 5 days/week. Since frequency and duration of exercise were identical among training groups, the volume of training was highest in the HI group followed by the MI and LI groups. Compared with SED animals, fasting plasma total and HMW adiponectin and adipose tissue total adiponectin concentrations were significantly higher in the HI and MI groups, but total adiponectin concentrations in liver and soleus muscle were not significantly lower than the SED rats. There were significantly lower plasma total testosterone levels in the HI group vs. SED group. Plasma total and HMW adiponectin were negatively correlated with HOMA-IR and insulin whereas total adiponectin was inversely related to TNF-α and HMW adiponectin was negatively correlated with total testosterone. Thus, data suggest there is a dose effect for exercise training intensity and accompanying volume for the adaptation of adipose tissue and circulating total and HMW adiponectin concentrations, whereas the changes of adiponectin concentrations in skeletal muscle and liver tissue may depend on the body's energy balance in the recovery period.     

Effect of saturated, omega-3 and omega-6 polyunsaturated fatty acids on myocardial infarction

Dietary fatty acids have cholesterol lowering, antiatherogenic, and antiarrhythmic properties that decrease the risk of myocardial infarction (MI). This study was designed to study the effects of various oils rich in either polyunsaturated (omega-3 or omega-6) fatty acids (PUFA) or saturated fatty acids (SFA) on the severity of experimentally induced MI. Male albino Sprague-Dawley rats (100-150 g; n = 20) were fed diets enriched with fish oil (omega-3 PUFA), peanut oil (omega-6 PUFA), or coconut oil (SFA) for 60 days. Experimental MI was induced with isoproterenol. Mortality rates; serum enzymes aspartate amino transferase; alanine amino transferase; creatine phosphokinase (CPK); lipid profiles in serum, myocardium, and aorta; peroxide levels in heart and aorta; activities of catalase and superoxide dismutase; and levels of glutathione were measured. The results demonstrated that mortality rate, CPK levels, myocardial lipid peroxides, and glutathione levels were decreased in the omega-3 PUFA treated group. Maximum increase in parameters indicative of myocardial damage was seen in the coconut oil group. These findings suggest that dietary omega-3 PUFA offers maximum protection in experimentally induced MI in comparison to omega-6 PUFA and SFA enriched diets. SFA was found to have the least protective effect.     

Metformin inhibits mitochondrial adaptations to aerobic exercise training in older adults

Metformin and exercise independently improve insulin sensitivity and decrease the risk of diabetes. Metformin was also recently proposed as a potential therapy to slow aging. However, recent evidence indicates that adding metformin to exercise antagonizes the exercise‐induced improvement in insulin sensitivity and cardiorespiratory fitness. The purpose of this study was to test the hypothesis that metformin diminishes the improvement in insulin sensitivity and cardiorespiratory fitness after aerobic exercise training (AET) by inhibiting skeletal muscle mitochondrial respiration and protein synthesis in older adults (62 ± 1 years). In a double‐blinded fashion, participants were randomized to placebo (n = 26) or metformin (n = 27) treatment during 12 weeks of AET. Independent of treatment, AET decreased fat mass, HbA1c, fasting plasma insulin, 24‐hr ambulant mean glucose, and glycemic variability. However, metformin attenuated the increase in whole‐body insulin sensitivity and VO₂max after AET. In the metformin group, there was no overall change in whole‐body insulin sensitivity after AET due to positive and negative responders. Metformin also abrogated the exercise‐mediated increase in skeletal muscle mitochondrial respiration. The change in whole‐body insulin sensitivity was correlated to the change in mitochondrial respiration. Mitochondrial protein synthesis rates assessed during AET were not different between treatments. The influence of metformin on AET‐induced improvements in physiological function was highly variable and associated with the effect of metformin on the mitochondria. These data suggest that prior to prescribing metformin to slow aging, additional studies are needed to understand the mechanisms that elicit positive and negative responses to metformin with and without exercise.     

Effects of combined exercise on cardiovascular risk factors and serum BDNF level in mid-aged women

[Purpose]

The purposes of this study is first to examine a positive effect of long term combined exercise including aerobic and resistance exercise on increasing level of serum BDNF, and investigate how aerobic exercise is related to improving BDNF circulation and resistance exercise improves fat oxidation in mid-aged women.

[Methods]

Initially, 30 mid-aged women, according to their exercise preference, was randomly assigned as a non-exercise group (n=7, control group; CG) and exercise group (n=23). Then, 23 exercise participants were divided by aerobic exercise group (n=15, AEG) and combination of aerobic and resistance exercise group (n=8, CEG). Prior to the experiment, all participants’maximal oxygen uptake (VO₂max), body composition, and blood factors were measured. Changes (Δ delta value) in body composition, fitness level, and serum BDNF level of the different groups were tested through one way ANOVA.

[Results]

For AEG and CG after 24 weeks, VO₂max and high-density lipoprotein cholesterol (HDL-C) were significantly increased. During this period, CEG had significant increase in muscular strength and decrease in triglyceride (TG) total cholesterol (TC)/HDL-C (p=0.013). Continuously, serum BDNF concentration of both AEG and CEG was significantly increased (F=6.328, p=0.001) compared to CG. There, however, was no significant between-group difference.

[Conclusion]

Although there was no difference in serum BDNF level between AEG and CEG, we confirmed that CEG may have a possibility of positive changes in increase of serum BDNF level in mid-aged women.     

Radio Telemetry of the Electrocardiogram,Fitness Tests,and Oxygen Uptake of Water-Polo Players

During competitive water polo, heart rate in six subjects was monitored by cupped plastic and silver electrodes glued to the skin. Minimum rates during the game averaged 156 beats/min.; maximum rates averaged 186 beats/min. Mean maximum rate with bicycle exercise was 188 beats/min. Maximum oxygen (VO₂ max.) with bicycle exercise of 14 water-polo players was 53.3 ml./kg. Physical working capacity (PWC 170) was 1310 kilopond metres per square metre (k.p.m./sq.m.). PWC 170 correlated well with VO₂ max. in this small group (r = 0.77).Oxygen uptake was measured at three speeds of swimming and four levels of work on a bicycle ergometer. VO₂ max. of swimming was 88% of that obtained on bicycle exercise. The slope of the oxygen uptake vs. pulse rate curves was less for the swimming than for cycling, so that for a given oxygen uptake below the maximal, pulse rate was less in the swimmers. At near-maximal swimming, respiratory quotient was 0.95 compared with 1.27 for cycling, suggesting that the swimmers were underbreathing.     

A Protective Lipidomic Biosignature Associated with a Balanced Omega-6/Omega-3 Ratio in fat-1 Transgenic Mice

A balanced omega-6/omega-3 polyunsaturated fatty acid (PUFA) ratio has been linked to health benefits and the prevention of many chronic diseases. Current dietary intervention studies with different sources of omega-3 fatty acids (omega-3) lack appropriate control diets and carry many other confounding factors derived from genetic and environmental variability. In our study, we used the fat-1 transgenic mouse model as a proxy for long-term omega-3 supplementation to determine, in a well-controlled manner, the molecular phenotype associated with a balanced omega-6/omega-3 ratio. The fat-1 mouse can convert omega-6 to omega-3 PUFAs, which protect against a wide variety of diseases including chronic inflammatory diseases and cancer. Both wild-type (WT) and fat-1 mice were subjected to an identical diet containing 10% corn oil, which has a high omega-6 content similar to that of the Western diet, for a six-month duration. We used a multi-platform lipidomic approach to compare the plasma lipidome between fat-1 and WT mice. In fat-1 mice, an unbiased profiling showed a significant increase in the levels of unesterified eicosapentaenoic acid (EPA), EPA-containing cholesteryl ester, and omega-3 lysophosphospholipids. The increase in omega-3 lipids is accompanied by a significant reduction in omega-6 unesterified docosapentaenoic acid (omega-6 DPA) and DPA-containing cholesteryl ester as well as omega-6 phospholipids and triacylglycerides. Targeted lipidomics profiling highlighted a remarkable increase in EPA-derived diols and epoxides formed via the cytochrome P450 (CYP450) pathway in the plasma of fat-1 mice compared with WT mice. Integration of the results of untargeted and targeted analyses has identified a lipidomic biosignature that may underlie the healthful phenotype associated with a balanced omega-6/omega-3 ratio, and can potentially be used as a circulating biomarker for monitoring the health status and the efficacy of omega-3 intervention in humans.     

Calorie restriction in overweight males ameliorates obesity-related metabolic alterations and cellular adaptations through anti-aging effects,possibly including AMPK and SIRT1 activation

Background

Calorie restriction (CR) is accepted as an experimental anti-aging paradigm. Several important signal transduction pathways including AMPK and SIRT1 are implicated in the regulation of physiological processes of CR. However, the mechanisms responsible for adaptations remain unclear in humans.

Scope of review

Four overweight male participants were enrolled and treated with 25% CR of their baseline energy requirements for 7 weeks. Characteristics, including body weight (BW), body mass index (BMI), %fat, visceral fat area (VFA), mean blood pressure (MBP) and VO₂ max, as well as metabolic parameters, such as insulin, lipid profiles and inflammatory makers and the expression of phosphorylated AMPK and SIRT1 in peripheral blood mononuclear cells (PBMNCs), were determined at baseline and then after 7 weeks. In addition, we assessed the effects of the serum collected from the participants on AMPK and SIRT1 activation and mitochondrial biogenesis in cultured human skeletal muscle cells.

Major conclusions

After CR, BW, BMI, %fat, VFA and MBP all significantly decreased, while VO₂ max increased, compared to those at baseline. The levels of fasting insulin, free fatty acid, and inflammatory makers, such as interleukin-6 and visfatin, were significantly reduced, whereas the expression of phosphorylated AMPK and SIRT1 was significantly increased in PBMNCs collected after CR, compared to those at baseline. The skeletal muscle cells that were cultured in serum collected after CR showed an increase in AMPK and SIRT1 activity as well as mitochondrial biogenesis.

General significance

CR is beneficial for obesity-related metabolic alterations and induces cellular adaptations against aging, possibly through AMPK and SIRT1 activation via circulating factors.