Purpose: The purpose of this review is to promote awareness of non-exercise activity thermogenesis (NEAT) as a new strategy to increase energy expenditure, and to manage obesity.
Methods: The content of this review is based on a literature search of PubMed and the Google Scholar search engine, using the search terms obesity, energy expenditure, non-exercise activity thermogenesis (NEAT), and sitting disease.
Results: Daily energy expenditure is of great interest because most obese individuals have no exercise activity-related thermogenesis (EAT); thus their physical activity-related energy expenditure (PEE) is comprised almost entirely of NEAT. Consequently, NEAT represents the main variable component of daily total energy expenditure (TEE); this varies considerably, both within among individuals. These somewhat unplanned and unstructured low level physical activities are associated with energy expenditure in excess of the resting metabolic rate (RMR). They may therefore have the potential to stimulate greater energy expenditure over time with a higher rate of adherence.
Conclusion: In conclusion, NEAT is a highly variable component of daily TEE and a low level of NEAT is associated with obesity. NEAT enhances lifestyle, and variations in individual and environmental factors can significantly affect daily energy expenditure. Therefore, well designed longitudinal studies that focus on personal behavioral approaches and re-engineered environments to increase NEAT should be conducted in the future.
Purpose: Elastin is one of the major determinants of arterial distensibility of large blood vessels that forms the principal component of elastic fibers from the media of arteries. However, the association between elastin(ELN) genotype and vascular function is still unclear.
Methods: 120women were recruited from the Saha-gu (Busan, Korea) Community Center. Measurements of body composition and vascular function included carotid intima-media thickness (CIMT), carotid artery luminal diameter (CLD), minimum (diastolic) artery luminal diameter (CLDmin) and maximum (systolic) artery luminal diameter (CLDmax). Genotyping for the ELN (rs 2071307) polymorphism was performed using the TaqMan approach. ELN gene distribution of subjects were in the Hardy-Weinberg equilibrium (p=0.402).
Results: The relative CIMT differed significantly among the ELN genotypes. And not significant differences in CLD and CIMT/CLD ratio, but AA genotype was tended higher than other genotypes (AG and GG). The relative CIMT and CLD min differed significantly between the ELN alleles. And not significant differences in CLD max and CIMT/CLD ratio, but A allele was tended higher than G allele.
Conclusion: These results suggest that ELN gene polymorphism might be used a one of the genetic determinants of vascular disease in both pre- and postmenopausal women.
Purpose: We investigated whether treadmill exercise (TE)-induced neuroprotection was associated with enhanced autophagy and reduced apoptosis in a mouse model of pharmacologically induced Parkinson's disease (PD).
Methods: PD was induced via the administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). C57BL/6 male mice were randomly assigned to the following three groups: control (C57BL, n=10), MPTP with probenecid (MPTP/C, n=10), and MPTP/ C plus exercise (MPTP-TE, n=10). The MPTP-TE mice performed TE training (10 m/min, 60 min/day, 5 days/week) for 8 weeks. The rotarod test was used to assess motor function.
Results: TE restored MPTP/P-induced motor dysfunctionand increased tyrosine hydroxylase levels. Furthermore, TE diminished the levels of α-synuclein (α-syn), a neurotoxin; modulated the levels of autophagy-associated proteins, including microtubule-associated protein 1 light chain 3-II, p62, BECLIN1, BNIP3, and lysosomal-associated membrane protein-2, which enhanced autophagy; inhibited the activation of proapoptotic proteins (caspase-3 and BAX);and upregulated BCL-2, an antiapoptosis protein.
Conclusion: Taken together, these results suggested that the TE-induced neuroprotection against MPTP-induced cell death was associated with enhanced autophagy and neuronal regeneration based on the findings of inhibited proapoptotic events in the brains of the TE-trained animals.
Purpose: This study aimed to clearly evaluate the effects of obesity on cerebral health. Thus, we induced obesity in rats using a long-term high-fat diet (HFD), then investigated its effects on insulin signaling and tau hyperphosphorylation. Additionally, we examined the effects of 8 weeks of treadmill exercise (TE) on insulin signaling and tau hyperphosphorylation.
Methods: Rats were separated into Normal Diet-Control, HFD-Control, and HFD-TE groups. TE loads were gradually increased. A passive avoidance test was used to evaluate cognitive function. Western blots were used to examine the abundance of the insulin receptor,phosphoinositide 3-kinase, protein kinase B, glycogen synthase kinase-3β, and tau proteins in the cerebral cortex; immunohistochemical analyses were used to examine the abundance of hyperphosphorylated tau in the cerebral cortex.
Results: TE in HFD-fed rats resulted in a significant lowering of bodyweight, abdominal visceral fat (AVF), the area under the glucose response curve, and the homeostatic model assessment-insulin resistance index, while it improved working memory. In addition, TE in HFD-fed rats decreased tau hyperphosphorylation and aggregation, while increasing insulin signaling-related protein activity.
Conclusion: After a 20-week HFD, the experimental animals exhibited increased weight, as well as impaired insulin resistance and blood glucose metabolism. HFD rats demonstrated abnormal insulin signaling and tau hyperphosphorylation in the cerebral cortex, as well as memory impairments that suggested reduced cerebral function. However, TE reduced AVF, improved insulin resistance in the peripheral tissues by increasing insulin sensitivity, and alleviated memory impairments by restoring insulin signaling and reducing tau hyperphosphorylation in the cerebral cortex.
Purpose: The purpose of our study was to determine the effectiveness of carbohydrate loading by additional carbohydrate supplements for 7 days after prolonged interval exercise on exercise performance and energy metabolism during submaximal exercise in team-sports athletes.
Methods: Twenty male team-sports athletes (14 soccer and 6 rugby players) volunteered to participate in the study and were equally divided into the experimental group (EXP, n=10) performing additional carbohydrate supplementation for 7 days after prolonged interval exercise until blood glucose level reaches 50 mg/dL or less and the control group (CON, n=10). Then, maximal oxygen consumption (VO2max) and minute ventilation (VE), oxygen consumption (VO2), carbon dioxide excretion (VCO2), respiratory exchange ratio (RER), blood glucose level, and blood lactate level were measured in all team-sports players during submaximal exercise corresponding to 70% VO2max before and after intervention.
Results: There was no significant interaction in all parameters, but team-sports players in the EXP presented more improved VO2max (CON vs EXP = vs 5.3% vs 6.3%), VE (CON vs EXP = vs 3.8% vs 6.6%), VO2 (CON vs EXP = vs 8.5% vs 9.9%), VCO2 (CON vs EXP = vs 2.8% vs 4.0%), blood glucose level (CON vs EXP = vs -12.9% vs -7.6%), and blood lactate level (CON vs EXP = -18.2% vs -25%) compared to those in the CON.
Conclusion: These findings showed that additional carbohydrate supplementation conducted in our study is not effective in exercise performance and energy metabolism during submaximal exercise.
Purpose: Brown adipose tissue (BAT) plays an important role in metabolizing different substances, including androgens. The aim of this study was to determine whether a single bout of aerobic exercise would increase the androgen hormone concentration in mouse BAT and whether its increase was associated with uncoupling protein-1 (UCP-1), protein kinase A (PKA)-related mechanism in BAT.
Methods: Twenty, 9-week-old ICR adult male micewere randomly divided into three groups: Control (n=6, CON), Exercise (n=7, EX), and Exercise + SRD5A1A2 inhibitor (n=7, EXIN). SRD5A1A2 is an enzyme needed when free testosterone is metabolized to dihydrotestosterone (DHT). SRD5A1A2 was administered intraperitoneally in the EXIN group, while the CON and EX groups were treated with the vehicle only. One hour later, exercise was performed at 60-70% V̇O2max for 30minutes. The levels of testosterone and DHT in BAT were determined by ELISA, and UCP-1 mRNA level was examined by RT-PCR. UCP-1 and PKA protein levels were determined by western blotting.
Results: After a single period of exercise, testosterone and DHT concentrations in BAT were significantly higher in EX than those in CON, and lower in EXIN than those in EX. The ratio of phosphorylated PKA to total PKA in BAT was significantly higher in EX than that in CON, and lower in EXIN than that in EX. UCP-1 levels in BAT were not different in the three groups.
Conclusion: Aerobic exercise increased bioactive androgen hormone levels in BAT in association with the increase in phosphorylated PKA levels. In contrast, 30minutes of treadmill exercise did not affect UCP-1 expression.
Purpose: This study aimed to examine the independent effect of electrical pulse stimulation(EPS) and nitric oxide(NO) on muscle contraction and their synergistic or combined effect on contraction phenomenon using C2C12 mouse skeletal muscle cells.
Methods: Some differentiated C2C12 myotube cells were untreated (control). Other cells did not receive EPS and did receive 0.5, 1.0, or 2.0 mM of the NO donor, S-nitroso-N-acetyl-penicillamine (SNAP; -E/S0.5, -E/S1.0, and -E/S2.0, respectively). For the EPS treatments (0.3 V/mm, 1.0 Hz, and 4.0 ms), differentiated C2C12 myotube cells received only EPS or both EPS and the SNAPtreatments at the same concentrations (+E/-S, +E/S0.5, +E/S1.0, and +E/S2.0, respectively). All samples were then cultured for 4 days.
Results: Differentiated C2C12 cellswere stimulated by the EPS, NO, and EPS+NO treatments. The cell length of the +E/S2.0 Group after the 4-day culture (84.2±13.2㎛) was the shortest of all the groups. The expressions of AMPK, JNK, Akt, eNOS, GLUT4, and PGC1α proteins were noticeably dominant. The results indicated synergistic effect on muscle contraction of simultaneously applied EPS and SNAP.
Conclusion: Motor skills were significantly improved when exercise was accompanied by the intake of NO precursor and/or NO, compared to that upon their independent application or treatment.
Purpose: Prader-Willi syndrome (PWS) is a genetic disorder characterized by excessive appetite with progressive obesity and growth hormone (GH) deficiency. Excessive eating causes progressive obesity with increased risk of morbidities and mortality. Although GH treatment has beneficial effects on patients with PWS, adverse events have occurred during GH treatment. Exercise potentially has a positive effect on obesity management. The purpose of this research was to examine the effects of 24-week complex exercise program on changes in body composition, blood lipid profiles, and growth factor hormone levels in a patient with PWS.
Methods: The case study participant was a 23-year-old man with PWS who also had type II diabetes mellitus because of extreme obesity. Complex exercises, including strength and aerobic exercises, were conducted 5 times one week for 60 minutes per session, over 24 weeks. Blood sampling was conducted five times: before and at 8, 16, 20, and 24 weeks after commencement of the exercise program.
Results: Weight, fat mass, triglycerides/high-density lipoprotein (TG/HDL) ratio, mean blood glucose, and GH decreased after training. Blood insulin and insulin-like growth factor (IGF-1) levels increased after training. At 15 and 20 weeks, insulin injection was discontinued. Insulin levels increased and average blood glucose decreased to normal levels; IGF-1 increased continuously during the 24-week exercise program.
Conclusion: Conclusion] Twenty-four weeks of complex exercises had a positive effect on obesity and diabetes in the patient with PWS. Therefore, long-period complex exercises might be an effective intervention for improvement of metabolic factors in PWS patients.
Purpose: The purpose of this study was to evaluate the reliability, reproducibility, and validity of the 6-minute walk test and step test as substitutes for ergometer exercise in patients with type 2 diabetes mellitus.
Methods: The study included 54 women aged 50-70 years who had type 2 diabetes mellitus. All the patients performed a cycle ergometer-graded exercise test for cardiorespiratory fitness (V̇O2max), followed by 6-minute walk and step tests.
Results: The mean distance covered during the 6-minute walk test was 538 ± 54 m, and the mean recovery heart rate after the step test was 93 ± 11 beats/min. A significant correlation was found between the distances covered during the cardiorespiratory fitness test (V̇O2max) and those covered the 6-minute walk test (r = 0.542, p < 0.01) and step test (r = -0.490, p < 0.01) in the patients with type 2 diabetes mellitus. Regression equations for the prediction of V̇O2max were constructed from the distance covered, heart rate, age, weight, height, fasting blood glucose level, 2-hour postprandial glucose level, and glycated hemoglobin level during the 6-minute walk test and step test.
Conclusion: The 6-minute walk and step tests are simple to perform and reliable for the evaluation of cardiorespiratory fitness in patients with type 2 diabetes mellitus.
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