Energy Expenditure Research Articles

Association between Volunteer Activity Participation and Daily Sedentary Time among Adults in Japan: A Cross-sectional Study

Introduction Sedentary behavior, involving low energy expenditure while sitting or reclining, is linked to health risks. Volunteering may help reduce sedentary time through social interaction and physical activity, but this relationship is understudied in non-Western contexts. This study investigated the association between volunteer activity frequency and daily sitting time among adults in Aichi and Kanagawa Prefectures, Japan, regions with higher aging. Methods A cross-sectional study was conducted in two regions of Japan, with a sample of 1,224 adults (585 men and 639 women) from these regions. Data on volunteer activity frequency and daily sitting time were collected using questionnaires. Multiple regression models explored the relationship between volunteer frequency and sitting time, adjusting for confounders. Results The mean daily sitting time was 357.66 ± 240.40 minutes. Participants volunteering four or more times weekly reported significantly shorter sitting times compared to non-participants, with an average difference of 131.96 minutes (95% CI: -253.83 to -10.08) in the multivariable-adjusted model. This association was stronger among males (difference: 180.51 minutes; 95% CI: -353.84 to -7.28) and older adults aged ≥65 years (difference of 142.48 minutes; 95% CI: -272.58 to -12.38). Conclusion Frequent volunteering is associated with shorter sitting times, particularly among males and older adults. However, due to the cross-sectional design, causal inferences cannot be made, and the associations should be interpreted with caution. Compared to Western populations, sitting time was lower, but it still exceeded public health recommendations. Future research should explore the longitudinal effects and identify specific volunteer activities that promote active lifestyles.

Opa1 and MT-Nd6 mutations induce early mitochondrial changes in the retina and prelaminar optic nerve of hereditary optic neuropathy mouse models

Abstract Hereditary optic neuropathies (HON), including dominant optic atrophy and Leber's hereditary optic neuropathy, are genetic disorders characterized by retinal ganglion cell (RGC) degeneration leading to vision loss, mainly associated with mitochondrial dysfunction. In this study, we analyzed mitochondrial distribution and ultrastructure in the retina and longitudinal optic nerve sections of presymptomatic HON mouse models with Opa1 and Nd6 deficiency to identify early mitochondrial changes. Our results show significant mitochondrial fragmentation and increased mitophagy in Opa1+/- mice, indicating early mitochondrial changes prior to neuronal loss. Conversely Nd6P25L mice exhibited mitochondrial hypertrophy, suggesting an adaptive response to compensate for altered energy metabolism. These pre-symptomatic mitochondrial changes were mainly observed in the unmyelinated portion of the RGC axons, where the transmission of the visual information requires high energy expenditure, constituting the specific point of vulnerability in HON. These findings highlight early focal mitochondrial changes prior to neuronal loss in HON and provide insight into presymptomatic therapeutic approaches.

Impact-Driven Penetration of Multi-Strength Fiber Concrete Pyramid-Prismatic Piles

The article focuses on studying the impact-driven penetration of multi-strength fibroconcrete pyramid-prismatic piles. The research object includes multi-strength pyramid-prismatic piles with varying types of reinforcement and different levels of concrete compressive strength. The aim of the study is to experimentally investigate the enhancement of pile impact resistance through the differentiated selection of concrete strength based on the dynamic stresses in the pile shaft caused by impact forces. As a result of the experimental studies on the piles, it was found that the difference in energy costs for driving them does not exceed 3.7–4.1%, proving the insignificant influence of the type of reinforcement and fiber concrete strength on the energy expenditure during driving. At the same time, it was established that the type of reinforcement and the type of fiber significantly affect the strength and impact-resistant properties of the pile shaft, ensuring defect-free driving. For example, the defectiveness (e.g., chips, cracks, potholes, spalling) of the head of the steel fiber concrete (SFC) pile reaches 57.5%, while for the polypropylene fiber concrete (PFC) pile it does not exceed 5.2%, demonstrating the advantages of using polypropylene fiber under impact conditions.

Abstract 4135662: Dietary Inulin Improves Glucose Metabolism and Energy Balance in Obese Mice via Adipocyte Free Fatty Acid Receptor 2 (FFAR2)

Background: Inulin is a non-digestible prebiotic dietary fiber that can promote metabolic health including reduced body weight and improved glucose metabolism via effects on gut microbiota. We hypothesize that inulin prevents obesity-associated cardiometabolic alterations by augmenting the production of short-chain fatty acids (SCFA) from gut microbiota, which activate free fatty acid receptor 2 (FFAR2), a major SCFA receptor, in murine adipose tissue. Methods: 8-week-old male C57BL/6J (wild-type, WT; n=34) and adipocyte FFAR2-knockout (Ad-FFAR2 KO; n=25) mice were fed a high-fat high-sucrose (HFHS) diet for 8 weeks, then randomized into experimental groups to receive either continued HFHS (n=8-13), or HFHS containing inulin (10% w/w chicory root inulin; n=17-21) for a further 5 weeks. Body weight was recorded weekly, food intake, body composition, and indirect calorimetry were assessed before and after the inulin intervention, and intraperitoneal glucose and insulin tolerance tests were performed. Subcutaneous and visceral white adipose tissue (WAT) samples were collected at the study termination. Results: HFHS-fed Ad-FFAR2 KO mice showed higher body weight (7.4%), fat mass, and WAT weight due to increased food intake, with worse glucose tolerance compared to WT mice. In WT mice, inulin significantly reduced body weight gain and body adiposity. These effects were associated with reduced locomotor activity and respiratory quotient (RQ) without effects on energy expenditure and were accompanied by improvements in glucose tolerance. Strikingly, inulin had no effect on body weight or body adiposity in Ad-FFAR2 KO mice but reduced RQ, locomotor activity, and improved glucose tolerance similar to WT mice. Conclusions: Our findings suggest that FFAR2 signaling in adipose tissue is crucial for improving cardiometabolic outcomes in obesity and that gut metabolites responsive to dietary interventions, such as inulin, are potential targets for obesity treatment strategies.

Abstract 4140191: ChREBP Drives Brown Adipocyte Differentiation and Lipid Utilization for Excess Energy Expenditure

Introduction: Although several anti-obesity drugs have become recently available, they reduce patients’ appetite, which might worsen cardiovascular disease (CVD) prognosis by malnutrition/cachexia. Brown adipose tissue (BAT) oxidizes glucose and lipids for thermogenesis, a process that requires excess energy expenditure provided by uncoupling protein 1 (UCP1) + cells. Recently, critical roles of BAT in cardio-protection have been discovered. Taken together, boosting BAT activity can be a novel anti-obesity treatment suitable for CVD patients. In this study, we aimed to establish anti-obesity strategy by manipulation of the glucose-sensing lipid-storage transcription factor, ChREBP, with unexpected function of boosting lipid utilization in BAT. Methods and Results: Through mouse/human single-cell/nucleus RNA sequencing analyses, we identified ChREBP as specifically expressed in highly thermogenic UCP1 + brown adipocytes ( Fig.A ). To investigate the role of ChREBP in BAT formation, we generated human brown adipocyte-like model from induced pluripotent stem cells (iPSC-BAT, Fig.B ). The iPSC-BAT exhibited high UCP1 and ChREBP expression, multi-locular lipid droplets, and vigorous oxygen consumption. Knocking down ChREBP strongly blocked iPSC-BAT differentiation ( Fig.C ) and impaired lipid utilization ( Fig.D ). Consistently, in vitro deletion of ChREBP in mouse BAT progenitors impeded differentiation, lipid droplet accumulation, and oxygen consumption ( Fig.E-F ). In vivo, BAT-specific deletion of all ChREBP isoforms reduced lipid accumulation and BAT characteristics. Conversely, using a new mouse model for Cre-mediated ChREBPβ overexpression, we showed that ChREBPβ overexpression in BAT (Chβ BATOX) increased BAT cellularity and activated lipogenic machineries, with paradoxical decreased lipid content, suggesting excessively activated lipid consumption in BAT ( Fig.G ). More importantly, Chβ BATOX maintained UCP1 expression and reduced fat volume ( Fig.H ) even after strongly inhibiting BAT activity. Conclusion: In summary, ChREBP is essential for BAT development and thermogenic capacity by affecting lipid utilization. Our results suggest that ChREBPβ activation may be a novel anti-obesity avenue for CVD patients.

L-aspartate ameliorates diet-induced obesity by increasing adipocyte energy expenditure.

Obesity always leads to profound perturbation of metabolome. Metabolome studies enrich the knowledge on associations between endogenous metabolites and obesity, potentially providing innovative strategies for the development of novel anti-obesity pharmacotherapy. This study aims to identify an endogenous metabolite that regulates energy expenditure and to explore its application for obesity treatment. C57BL/6 mice were fed with a high-fat and high-cholesterol (HFC) diet, comprising 60% fat and 1.2% cholesterol, for 12 weeks to induce obesity. Significant metabolites were identified in the livers of both health and obese mice through comparative hepatic metabolomics analysis. Correlation between serum or adipose L-aspartate level and body weight in obese mice, as well as human body mass index (BMI), was evaluated. In addition, saline or 200 mg/kg L-aspartate was orally administrated to HFC diet mice and HFC diet-induced obese mice for 6-7 weeks. Body weight, adipose tissue weight, glucose tolerance and liver damage were assessed to evaluate the effect on obesity prevention and treatment. Comprehensive lab animal monitoring system (CLAMS) and seahorse assay were employed to investigate the regulatory effect of L-aspartate on energy metabolism in vivo and in vitro, respectively. 3T3-L1 preadipocytes and murine white adipose tissue (WAT) were utilized to examine the impact of L-aspartate on adipocyte adipogenesis and lipogenesis and cellular signalling pathway in vitro and in vivo. L-aspartate, an approved drug for liver injury and chronic fatigue, was identified as an endogenous inducer of energy expenditure. Serum or adipose L-aspartate levels were found to be negatively correlated with the severity of obesity in both humans and mice. Administration of L-aspartate to HFC diet mice led to a significant reduction in body weight, with decreases of 14.5% in HFC diet mice and 8.5% in HFC diet-induced obese mice, respectively. In addition, the treatment improved related metabolic syndrome (Figure 2 and Figure S3). These therapeutics were associated with enhancements in whole-body energy expenditure and suppression of adipocyte adipogenesis along with activation of Adenosine 5'-monophosphate-activated protein kinase (AMPK) signalling pathway. L-aspartate may serve as a novel endogenous inducer of energy expenditure and suppressor of adipogenesis and lipogenesis along with activation of AMPK, thereby offering a promising therapeutic strategy for obesity prevention and treatment.

The impact of leadership on employees’ innovation behavior: evidence from China’s energy listed companies

This paper provides an in-depth analysis of how management efficiency affects sustainable development in China’s top 10 private energy companies from 2005 to 2021, using the CUP-FM technique. The study finds a notable correlation: a 1% improvement in management efficiency results in a 0.21% reduction in energy expenditure. This highlights the significance of efficient management practices, such as streamlined processes, better resource allocation, and advanced technology use, in optimizing energy consumption and promoting sustainability. Conversely, a 1% increase in the number of employees leads to a 0.49% increase in energy expenditure due to increased operational activities and resource needs. The research also explores the impact of other variables, including earnings per share (EPS), tax payments, and technology spending, on energy expenditure among listed energy companies in China. To foster innovation among employees through improved management efficiency, the paper suggests practical policies such as enhancing sustainable literacy, providing green loans, implementing standardized reporting, and encouraging collaboration and knowledge sharing among energy companies.

Enhancing efficiency and economic viability in Rectisol system with cryogenic liquid expander

AbstractCryogenic liquid expanders have emerged as a potential energy‐saving alternative to Joule–Thomson (JT) valves in cryogenic processes. The potential impact of incorporating a liquid expander into the Rectisol process has not been quantitatively evaluated. This study seeks to assess the effectiveness of replacing the JT valve with a liquid expander in the Rectisol process through the development of thermodynamic models for each component and conducting simulations using the ASPEN software. Additional analyses, including energy, CO2 footprint, exergy, and economic evaluations, are performed for the Rectisol system. Utilizing an expander has been shown to lower energy usage by 2.52% and boost CO2 capture by 5.55%, resulting in a 7.65% decrease in energy expenditure per unit CO2 and a 1.29% rise in total exergy efficiency. Lower expander outlet temperatures and the green power output generated by the expander are the main reasons for these benefits, and the CO2 footprint analysis explains how they work. The application of an expander in the Rectisol process is an economical and low‐risk solution; the payback period is 0.32 years, and the lifetime profit is 53 folds of the investment.

The effect of vo2max on muscle oxygen saturation (SMO2) in University Badminton Athletes

Muscle oxygen saturation (SmO2) is an additional physiological parameter that helps identify the transition from aerobic to anaerobic workload. Additionally, it can be used to predict performance by calculating Vo2 and energy expenditure. Muscle oxygen saturation (SmO2) is a measure of oxygen saturation in muscle tissue that can be used to evaluate metabolic zones, training intensity, and athlete performance. An athlete's muscle oxygen saturation (SMO2) is a measure of how well their muscles use oxygen, which is important for evaluating performance and creating training programs. This research is a week-long experimental study with a one-shot case study design, research intends to look at the effect of Vo2Max on muscle oxygen saturation (SMO2) in university badminton athletes. The subjects of this research are student athletes who actively practice badminton. There were 6 respondents who were willing to be research subjects and had met the specified criteria, namely actively exercising three times a week and being in good health. Then the author took data on athletes who had the highest and lowest Vo2Max to analyze SMO2 optimization, which was the focus of this research. The results of the analysis show that there is a significant influence between Vo2max and SMO2 optimization; this can be seen by the difference through the t test with a sig (2-tailed) value of 0.000 < 0.05. Another finding is that athletes with higher Vo2max show better SMO2 recovery results. better than athletes with low Vo2max; in this study, athletes with higher Vo2max showed a 37% increase in SMO2 over two minutes, while athletes with lower Vo2max showed a 21% increase. This is an interesting finding for coaches and athletes regarding the importance of Vo2 max capacity in optimizing SMO2.

Weight loss and metabolic effects of an ALDH1A1-specific inhibitor, FSI-TN42, in a diet induced mouse model of obesity.

Retinoic acid (RA) participates in weight regulation and energy metabolism. Mice lacking ALDH1A1, one of the major enzymes responsible for RA biosynthesis, are resistant to diet-induced obesity. Previously, we identified FSI-TN42 (N42) as an ALDH1A1-specific inhibitor and reported its pharmacokinetics and pharmacodynamics as well as its efficacy in weight suppression. In the first study, C57BL/6 J male mice were fed a high fat diet for 8 weeks to induce obesity. Mice were then divided into three groups and fed (1) moderate fat diet (MFD), (2) MFD + WIN 18,446 (1 g/kg diet), or (3) MFD + N42 (1 g/kg diet) for 8 weeks. A control group of mice were fed a low-fat diet for the entire period. Mice were weighed weekly and fasting glucose was determined every 4 weeks. Tissues were examined for potential toxicity using histopathology and complete blood counts. In the second study, we examined influences of N42 on energy balance and/or appetite by determining food intake, activity and energy expenditure in mice with obesity treated with MFD or MFD + N42. Lastly, we tested fertility with a mating study. N42 significantly accelerated weight loss compared to MFD alone in mice with obesity by reducing fat mass without decreasing lean mass. N42 did not alter food intake or activity levels. While mice treated with N42 lost significantly more weight, they maintained a similar level of energy expenditure compared to mice fed MFD only. Mice fed N42 preferentially used fat postprandially, especially under thermoneutral or mild cold challenge. N42 did not affect male fertility. N42 promotes weight loss when used with MFD in mice with diet-induced obesity without causing significant organ toxicity or male infertility. Future studies will determine if N42 can be used to promote further weight loss if combined with current weight loss drugs.

Shared genetic architecture links energy metabolism, behavior and starvation resistance along a power-endurance axis

Abstract Shared developmental, physiological, and molecular mechanisms can generate strong genetic covariances across suites of traits, constraining genetic variability, and evolvability to certain axes in multivariate trait space (“variational modules” or “syndromes”). Such trait suites will not only respond jointly to selection; they will also covary across populations that diverged from one another by genetic drift. We report evidence for such a genetically correlated trait suite that links traits related to energy metabolism along a “power-endurance” axis in Drosophila melanogaster. The “power” pole of the axis is characterized by high potential for energy generation and expenditure—high expression of glycolysis and TCA cycle genes, high abundance of mitochondria, and high spontaneous locomotor activity. The opposite “endurance” pole is characterized by high triglyceride (fat) reserves, locomotor endurance, and starvation resistance (and low values of traits associated with the “power” pole). This trait suite also aligns with the first principal component of metabolome; the “power” direction is characterized by low levels of trehalose (blood sugar) and high levels of some amino acids and their derivatives, including creatine, a compound known to facilitate energy production in muscles. Our evidence comes from six replicate “Selected” populations adapted to a nutrient-poor larval diet regime during 250 generations of experimental evolution and six “Control” populations evolved in parallel on a standard diet regime. We found that, within each of these experimental evolutionary regimes, the above traits strongly covaried along this “power-endurance” axis across replicate populations which diversified by drift, indicating a shared genetic architecture. The two evolutionary regimes also drove divergence along this axis, with Selected populations on average displaced towards the “power” direction compared to Controls. Aspects of this “power-endurance” axis resemble the “pace of life” syndrome and the “thrifty phenotype”; it may have evolved as part of a coordinated organismal response to nutritional conditions.

Nutrition among nursing home residents: results from the NutriCare study.

Older adults living in nursing homes (NHs) are considered a vulnerable population in terms of nutrition. The aim of the present study was to explore the usual intake of energy, macronutrients, and specific food groups, along with offers in the NH menus on a nationally representative sample of Slovenian NH residents and compare dietary patterns with the established recommendations. The study was conducted as part of a cross-sectional NutriCare study on 317 residents (65-101 years) from 20 Slovenian NHs in 9 health regions. Relatively independent residents were selected using quota sampling by sex and age. Data collection involved interviews and anthropometric measurements. Usual dietary intake was assessed by a multiple-source method from two 24-h dietary recalls and food frequency questionnaires. Adherence of dietary intake to the recommendations and dietary composition of NH menus were assessed. The Mini Nutritional Assessment (MNA) was used to explore nutritional status. Notable variability in energy and macronutrient intakes was observed with some participants showing intakes below and others above the recommended values. A high prevalence of BMI > 30 kg/m2 was observed in 39% of participants, indicating potential discrepancies between total energy intake and expenditure. The usual intake of fat was 36% of total energy intake (TEI). The intake of foods of animal origin exceeded dietary guidelines. Intake of carbohydrates (46% TEI in men and 47% TEI in women) as well as dietary fibre (20 g/day for both sexes) was below recommendations. A scarce intake of fruits, vegetables, and cereals was observed. In total, 40% of men and 35% of women had usual daily protein intakes lower than 1 g/kg of body weight. The protein content of breakfast and dinner could be improved. NH residents consumed little food from outside NH. The usual nutrient and food group intakes of residents reflected the NH menu offers. The study results on the usual intake of energy, macronutrients, specific food groups, and offers in the NH menus indicate the potential for optimisation. According to the World Health Organisation, the prevalence of BMI > 30 kg/m2 is notable and warrants attention. Careful meal planning and regular monitoring of the nutritional status of NH residents should be considered.

TMIC-40. TARGETING GLIOMA TUMOR MICROENVIRONMENT BY SPECIFIC NEUTRALIZATION OF EXTRACELLULAR NICOTINAMIDE PHOSPHORIBOSYLTRANSFERASE (ENAMPT) USING ALT-100, A NOVEL HUMANIZED MONOCLONAL ANTIBODY

Abstract BACKGROUND Intracellular nicotinamide phosphoribosyltransferase (iNAMPT is the rate-limiting enzyme of NAD salvage pathway and is preferentially used by glioma cells for regulating energy metabolism and homeostasis. When secreted, extracellular NAMPT (eNAMPT) exerts cytokine-like functions and is associated with poor prognosis in cancer patients. We have previously reported an essential role of iNAMPT for glioma cell proliferation and survival. Here, we examined whether eNAMPT influences glioma biology and tumor microenvironment by neutralizing eNAMPT using ALT-100, a novel humanized monoclonal antibody. METHODS Native levels of eNAMPT in blood samples of patients with primary/recurrent gliomas were determined using ELISA under an IRB approved protocol. Next, the effects of ALT-100 on glioma microenvironment were determined by treating viable human glioma tissue slices with ALT-100 and assessing downstream effects on RNA and protein using RNASeq, reverse phase protein array and spatial transcriptomics. Lastly, the in vivo effect of ALT-100-mediated eNAMPT neutralization on survival was determined in a mouse intracranial glioma model. RESULTS Measurable levels of eNAMPT were noted in all patient samples with a range of (3.7-71.2 ng/ml). Preliminary results showed a correlation of eNAMPT levels with grade of tumor. Human organotypic glioma slice cultures treated with ALT-100, showed a profound alteration of gene and protein expression particularly related to key energy metabolism and proliferation pathways and the PD-1/PD-L1 axis. Additionally, results of spatial profiling of ALT-100 treated human organotypic glioma slices will be presented. Survival and response data from ALT-100 treatment in ongoing in vivo experiment will also be reported. CONCLUSIONS This is the first report of ALT-100-mediated eNAMPT neutralization in gliomas and demonstrates profound effects on the tumor and its microenvironment. Given that ALT-100 is in phase 2 trials (NCT05938036) against ARDS, data from our studies can potentially accelerate translating ALT-100-mediated eNAMPT neutralization to treat gliomas.

Theoretical knowledge enhanced genetic algorithm for mine ventilation system optimization considering main fan adjustment

Mining safety heavily depends on ventilation, which constitutes a significant portion of the energy costs in operations. Optimizing mine ventilation systems (MVSO) is crucial for minimizing this energy expenditure. However, current algorithms encounter challenges when applied to large-scale mines, primarily due to the complexity of variables and limited attention to optimizing main fans. This study introduces a theoretical knowledge enhanced genetic algorithm for MVSO, incorporating main fan adjustments. The algorithm models changes in the main fan’s operational status and integrates ventilation network equivalent simplification (VNES) and the minimum spanning tree (MST) to reduce the number of variables in the mine ventilation network. Additionally, leveraging mine ventilation sensitivity theory (MVST) enhances the quality of the initial algorithmic population. A simple case and two engineering cases collectively validated that the algorithm consistently provides effective and reliable optimization solutions for mine ventilation systems across varying scales. Specifically, the algorithm reduced energy consumption from 326.94 to 186.99 kW, 433.14 to 239.48 kW, and 520.53 to 324.90 kW across three different scales of mine ventilation systems. Comparative analysis with four other algorithms shows that, although this algorithm has a longer runtime due to the need to identify the minimum spanning tree during iterations, its ability to reduce problem dimensionality and improve population quality results in more stable and superior convergence performance, especially for large-scale mine ventilation systems.Graphical abstract

A Longer Biliopancreatic Limb and Shorter Common Channel Enhance Weight Loss But May Have Harmful Effects in Mouse Models of Roux-en-Y Gastric Bypass.

RYGB consists of the Roux limb (RL), the biliopancreatic limb (BPL), and the common channel (CC). There is no consensus on the optimal limb lengths. Using a mouse model of RYGB, 30 diet-induced obese mice were divided into two groups with varying BPL and CC lengths: a standard BPL with a long CC (RYGB S) and a long BPL with a short CC (RYGB L). Additionally, 9 age-matched, lean control mice (LC) were also included in this study. RYGB S had limb lengths of RL = 17%, BPL = 24%, and CC = 59%. RYGB L had limb lengths of RL = 17%, BPL = 32%, and CC = 51%. RYGB S and RYGB L had 67% and 40% survival, respectively. Mortality in RYGB L included more instances where the cause of death was not apparent. RYGB L demonstrated greater weight loss, lower energy expenditure, and lower heart mass as compared to RYGB S. Both RYGB groups had lower epidydimal fat mass, spleen mass, and bone mineral density compared to LC. RYGB L had a lower heart mass than RYGB S and LC. While the relative abundance of Eubacterium was lower in RYGB L than in RYGB S, no other gut microbiota differences were observed. A longer BPL with a shorter CC induces greater weight loss but may lead to adverse effects, including lower heart mass, reduced bone density, and deaths with unclear causes.

Lipid metabolism and food ingredients from the perspective of thermogenic adipocytes.

The high heat-producing capacity of brown and beige adipocytes, collectively known as thermogenic adipocytes, contributes to whole-body energy expenditure and is an attractive target for the management of obesity. It has been revealed that the functions of thermogenic adipocytes are important for the regulation of whole-body carbohydrate and lipid metabolism, and the activation of thermogenic adipocytes seems to have beneficial effects for the management of obesity-related metabolic disorders, such as dyslipidemia. Recent studies have showed that specific food ingredients have the potential to activate thermogenic adipocytes via various mechanisms. Some of these are effective not only in rodents, but also in humans, and effective prevention of obesity using these food ingredients is expected. In this review, we introduce the recent findings on the regulatory mechanisms of lipid metabolism by thermogenic adipocytes and food ingredients, demonstrating the potential to activate thermogenic adipocytes and their underlying mechanisms.

Focusing on Sedentary Behavior in Comprehensive Cardiac Rehabilitation.

In recent years, the adverse effects of prolonged sedentary behavior in daily life, so-called 'sitting too much', on health have been pointed out. Sedentary behavior is defined as 'all waking behavior in which the energy expenditure in a sitting, semi-recumbent, or recumbent position is 1.5 metabolic equivalents or less'. Even if a person engages in the level of physical activity recommended in the guidelines, sitting for too long at other times may increase the risk of developing various diseases and death. For patients with cardiovascular disease, a comprehensive cardiac rehabilitation program that systematically includes not only medical treatment but also exercise therapy, patient education, and disease management is extremely important. Also, differences in sedentary behavior during the acute and recovery phases are known to affect physical function and activities of daily living at the time of hospital discharge. Here, we discuss cardiac rehabilitation that addresses sedentary behavior and review the previous related research.

Evaluating bioenergetic pathway contributions from single to multiple sprints

This study aims to investigate the changes in bioenergetic pathway contributions during repeated sprint exercises with an increasing number of repetitions. Twelve male amateur soccer players executed a single 20 m sprint and three repeated-sprint protocols (5 × 20 m, 10 × 20 m, 15 × 20 m with 15-second rest intervals), analyzing oxidative, glycolytic, and ATP-PCr energy pathways using the PCr-LA-O2 method. Findings revealed a significant decline in energy expenditure and performance outputs as the number of sprint repetitions increased. While the oxidative and ATP-PCr pathways’ energy contributions significantly rose with more sprints, the glycolytic pathway’s contribution notably increased only up to the 10 × 20 m protocol, then stabilized. Although the ATP-PCr pathway’s energy contribution decreased slightly from sprints 1–5 to 11–15, it remained significantly higher than the oxidative and glycolytic pathways throughout. Initially, glycolytic contribution surpassed oxidative in sprints 1–5, equaled it in sprints 6–10, and fell below in sprints 11–15. Glycolytic activity, a major energy source initially (about 36%), diminished substantially with more sprints (below 7% in the 15th sprint). This indicates that the decrease in non-mitochondrial pathway energy, particularly glycolytic, outstrips the aerobic system’s increased tolerance. These findings offer physiological insights into the relationship between performance decrement and bioenergetic metabolism in repeated sprints.

A Systematic Review of the Long-term Efficacy of Physical Activity Interventions in Reducing Risk Factors for Obesity in Adults

Background: Regular physical activity (PA) provides numerous health advantages, including lowering mortality rates and preventing obesity. Despite well-established guidelines advising 150-300 minutes of moderate-intensity or 75-150 minutes of vigorous-intensity aerobic PA weekly, sedentary lifestyles remain prevalent, especially in industrialised nations. This systematic review examines the long-term effectiveness (12-24 months) of PA interventions aimed at reducing obesity risk among adults, with a particular focus on identifying strategies that promote sustained adherence. Methods: A comprehensive literature search was performed using multiple databases, including Cochrane Library, PubMed, and Embase, focusing on studies published between January 2004 and January 2024. The inclusion criteria focused on randomised controlled trials and similar designs targeting healthy adults, with interventions promoting sustained PA. Primary outcomes assessed were long-term PA adherence, reductions in obesity rates, and improvements in physical and metabolic health. Results: Twenty-one studies met the inclusion criteria, covering a range of intervention strategies. Most interventions featured structured PA programmes, often with personalised components and ongoing support. Several high-quality studies demonstrated long-term PA adherence, increased weekly energy expenditure, and improvements in fitness. However, adherence rates varied, with participants meeting recommended PA levels ranging from 4.6% to 81%. The meta-analysis showed a small to moderate positive effect of PA interventions on outcomes like PA levels and weight loss, with an effect size of 0.37 (CI: 0.25-0.50). Discussion: The results highlight the need for tailored, culturally sensitive interventions, particularly for vulnerable populations. Long-term PA adherence is stronger in older adults than middle-aged ones, but the sustainability of these effects remains unclear, warranting further research

Proteo-metabolomic insights for early dual physical and cognitive impairments: A search for biomarkers of healthy aging based on muscle-brain crosstalk.

We employed an untargeted proteo-metabolomic approach to profile circulating biomarkers in plasma samples from the I-Lan Longitudinal Aging Study, aiming to identify biomarkers and pathways associated with physio-cognitive decline syndrome (PCDS). In 115 propensity score-matched PCDS case-control pairs, pathway analyses implicated dysregulation of fatty acid metabolism and inflammation in PCDS pathogenesis. Sex-specific associations were observed, with disruptions in central carbon metabolism (elevated PKM, MDH1, and GAPDH; decreased MINPP1) and tyrosine metabolism (decreased MIF, DBH; increased thyroxine) characterizing in men. In contrast, perturbations in glutathione and phenylalanine metabolism, including increased ANPEP, GSTP1, and decreased pyroglutamic acid, were identified in women. Results suggest that dysregulated energy and redox homeostasis likely contribute to PCDS development. Notably, ANPEP, PKM, and MIF emerged as potential biomarkers, elucidating the muscle-brain crosstalk framework. Our findings provide insights into potential molecular mechanisms underlying PCDS and the muscle-brain crosstalk, marking progress toward elucidating biomarkers in the journey of healthy aging.