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Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Physical exercise has been shown to be beneficial for individuals with Alzheimer's disease (AD), although the underlying mechanisms are not fully understood. Methods: Six-month-old Amyloid precursor protein/Presenilin 1 (APP/PS1) transgenic (Tg) mice and wild-type (Wt) mice were randomly assigned to either a sedentary group (Tg-Sed, Wt-Sed) or an exercise group (Tg-Ex, Wt-Ex) undertaking a 12-week, moderate-intensity treadmill running program. Consequently, all mice were tested for memory function and amyloid β (Aβ) levels and phosphorylation of tau and protein kinase B (Akt)/glycogen synthase kinase-3 (GSK3) were examined in tissues of both the cortex and hippocampus. Results: Tg-Sed mice had severely impaired memory, higher levels of Aβ, and increased phosphorylation of tau, GSK3α tyrosine279, and GSK3β tyrosine216, but less phosphorylation of GSK3α serine21, GSK3β serine9, and Akt serine473 in both tissues than Wt-Sed mice in respective tissues. Tg-Ex mice showed significant improvement in memory function along with lower levels of Aβ and less phosphorylation of tau (both tissues), GSK3α tyrosine279 (both tissues), and GSK3β tyrosine216 (hippocampus only), but increased phosphorylation of GSK3α serine21 (both tissues), GSK3β serine9 (hippocampus only), and Akt serine473 (both tissues) compared with Tg-Sed mice in respective tissues. Conclusions: Moderate-intensity aerobic exercise is highly effective in improving memory function in 9-month-old APP/PS1 mice, most likely through differential modulation of GSK3α/β phosphorylation in the cortex and hippocampus. [ABSTRACT FROM AUTHOR]

Purpose: This study investigated whether a running-adapted version of the cycling-based "step–ramp–step" (SRS) protocol would improve prediction of V ˙ O2 in treadmill exercise compared to the traditional prescriptive approach. Methods: Fourteen healthy individuals (6 females; 25 ± 6 years; 66.1 ± 12.7 kg) performed a treadmill-based SRS protocol including a ramp-incremental test to task failure followed by two constant-speed bouts within the moderate-(MODstep—below estimated lactate threshold; θLT), and heavy-intensity domains (HVYstep—between θLT and respiratory compensation point; RCP). Using the uncorrected V ˙ O2-to-speed relationship from the ramp exercise, three constant-speed bouts were performed at 40–50% between: baseline and θLT (CSEMOD); θLT and RCP (CSEHVY); and RCP and peak (CSESEV). For CSEMOD, CSEHVY, and CSESEV measured end-exercise V ˙ O2 was compared to predicted V ˙ O2 based on the: (i) "SRS-corrected" V ˙ O2-to-speed relationship (where MODstep and HVYstep were used to adjust the V ˙ O2 relative to speed); and (ii) linear "uncorrected" data. Results: Average treadmill speeds for CSEMOD and CSEHVY were 7.8 ± 0.8 and 11.0 ± 1.4 km·h−1, respectively, eliciting end-exercise V ˙ O2 of 1979 ± 390 and 2574 ± 540 mL·min−1. End-exercise V ˙ O2 values were not different compared to SRS-predicted V ˙ O2 at CSEMOD (mean difference: 5 ± 166 mL·min−1; p = 0.912) and CSEHVY (20 ± 128 mL·min−1; p = 0.568). The linear "uncorrected" estimates were not different for CSEMOD (− 91 ± 172 mL·min−1; p = 0.068) but lower for CSEHVY (− 195 ± 146 mL·min−1; p < 0.001). For CSESEV (running speed: 13.8 ± 1.7 km·h−1), the end-exercise V ˙ O2 was not different from peak V ˙ O2 achieved during the ramp (3027 ± 682 vs. 2979 ± 655 mL·min−1; p = 0.231). Conclusion: In healthy individuals, the SRS protocol more accurately predicts speeds for a target V ˙ O2 compared to traditional approaches. [ABSTRACT FROM AUTHOR]

Exoskeleton robots have the potential to augment human motor capabilities. however, current control strategies often require task-specific control laws tailored for different scenarios, which limits the applicability of exoskeletons. In this study, we propose a control strategy for exoskeleton robots that is adaptable across various scenarios. We employ adaptive oscillators (AO) with feedback control to rapidly estimate the wearer'smotion phase and subsequently provide torque assistance to the wearer's hip joint based on a TCN-LSTM model. During experiments, we collected surface electromyographic (sEMG) signals from the tibialis anterior, gastrocnemius, and rectus muscles of seven groups of subjects performing treadmill walking and inclined treadmill exercises. We utilized the short-time Fourier transform to extract frequency characteristics of the signals and statistically analyzed the rate of frequency change in each muscle group under different strategies. The results indicate that when wearing the exoskeleton, the overall muscle frequency changes more slowly, suggesting that subjects can maintain activity for a longer duration before fatigue sets in. This control strategy effectively reduces the energetic cost of lower limb work for the wearer and enhances the exoskeleton's versatility in various applications. [ABSTRACT FROM AUTHOR]

This study compared the immediate effects of two common post-exercise cool-down methods to a control condition on subsequent morphologic change in femoral cartilage and vascular response in the posterior tibial artery after running. Sixteen healthy young males (23.6 ± 2.2 years, 172.8 ± 4.9 cm, 72.2 ± 7.1 kg) visited the laboratory during three separate sessions and performed 30-min of treadmill running (7.5 km/h for the initial 5-min, followed 8.5 km/h for 25-min). After running, participants experienced one of three 30-min cool-down protocols: active cool-down, cold application, or control (seated rest with their knee fully extended), in a counterbalanced order. Ultrasonographic assessments of femoral cartilage thickness (intercondylar, lateral, and medial) and posterior tibial artery blood flow were compared. To test condition effects over time, two-way analysis of variances and Tukey tests were used (p < 0.05) with Cohen's d effect sizes (ES). There was no condition by time interaction in femoral cartilage thickness (intercondylar: F30,705 = 0.91, p = 0.61; lateral: F30,705 = 1.24, p = 0.18; medial: F30,705 = 0.49, p = 0.99). Regardless of time (condition effect: F2,705 > 3.24, p < 0.04 for all tests), femoral cartilage in the cold application condition was thicker than the control condition (intercondylar: p = 0.01, ES = 0.16; lateral: p < 0.0001, ES = 0.24; medial: p = 0.04. ES = 0.16). Regardless of condition (time effect: F15,705 > 10.31, p < 0.0001 for all tests), femoral cartilage thickness was decreased after running (intercondylar: p < 0.0001, ES = 1.37; lateral: p < 0.0001, ES = 1.58; medial: p < 0.0001, ES = 0.81) and returned to baseline levels within 40-min (intercondylar: p = 0.09; lateral: p = 0.64; medial: p = 0.26). Blood flow volume was different (condition × time: F30,705 = 2.36, p < 0.0001) that running-induced blood flow volume was maintained for 30-min for the active cool-down condition (p < 0.0001, ES = 1.64), whereas it returned to baseline levels within 10-min for other conditions (cold application: p = 0.67; control: p = 0.62). Neither blood flow nor temperature had a significant impact on the recovery in femoral cartilage after running. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) causes a decline in skeletal muscle function, which can further exacerbate the cognitive dysfunction of patients with AD. It has been widely established that exercise improves AD brain pathology, but the role of skeletal muscle in AD is still poorly understood. In this study, we investigated the effects of treadmill exercise on the exercise ability of APP/PS1 transgenic AD mice and explored potential gene expression changes in their skeletal muscle. The APP/PS1 mice were subjected to a treadmill exercise for 12 weeks, followed by the Morris water maze and the open field test. After behavioral experiments, the changes in morphology, area, collagen fiber deposition, and ultrastructure of the skeletal muscle were determined; the balance of skeletal muscle protein synthesis and decomposition was analyzed; and changes in gene expression were investigated using RNA-Seq. We found that this exercise strategy can promote the learning and memory abilities of AD mice, reduce their anxiety-like behavior, improve their exercise ability, alleviate skeletal muscle atrophy, and optimize the microstructure. It can also enhance skeletal muscle protein synthesis and decomposition and improve several signaling pathways, such as the JAK–STAT, Wnt, and NOD-like receptors while decreasing calcium, cAMP, cGMP–PKG, and other signaling pathways. Six KEGG enrichment signaling pathways were downregulated and five signaling pathways were upregulated in the AD mice compared with wild-type mice, and these pathways were precisely reversed after the treadmill exercise. The expression of transcription factors such as Fosb and Egr1 in the skeletal muscle of AD mice decreased, followed by a decrease in the regulated target genes Socs1, Srrm4, and Il1b, a trend that was reversed following the exercise intervention. After exercise, AD mice exhibited a similar gene expression to that of wild-type mice, indicating enhanced exercise ability. The potential regulatory pathways and related genes identified in this study provide valuable insights for the clinical management and treatment of AD. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Rehabilitation Medicine is the property of China Association of Rehabilitation Medicine, China-Japan Friendship Hospital and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This article describes the development and validation of accurate whole body sweat rate prediction equations for individuals performing indoor cycle ergometer and treadmill exercise, where power output can be measured or derived from simple inputs. For cycle ergometry, 112 trials (67 participants) were used for model development and another 56 trials (42 participants) for model validation. For treadmill exercise, 171 trials (67 participants) were used for model development and another 95 trials (63 participants) for model validation. Trials were conducted over a range of dry-bulb temperature (20°C to 40°C), relative humidity (14% to 60%), and exercise intensity (∼40% to 85% of peak aerobic power) conditions, which were matched between model development and model validation. Whole body sweat rates were measured, and proprietary prediction models were developed (accounting for all relevant biophysical factors) and then validated. For model validation, mean absolute error for predicted sweating rate was 0.01 and 0.02 L·h−1 for cycle and treadmill trials, respectively. The 95% confidence intervals were modest for cycle ergometer (+0.25 and −0.22 L·h−1) and treadmill exercise (+0.33 and −0.29 L·h−1). The accounted for variance between predicted and measured values was 92% and 78% for cycle and treadmill exercise, respectively. Bland–Altman analysis indicated that zero and one predicted value exceeded the a priori acceptable level of agreement (equivalent to ±2% of total body mass in 3 h) for cycle and treadmill exercise, respectively. There were fewer trials with female subjects, but their values did not differ from those expected for males. This is the foremost study to develop and validate whole body sweat rate prediction equations for indoor treadmill and cycle ergometer exercise of moderate to high intensity. These prediction equations are publicly available for use (https://sweatratecalculator.com). NEW & NOTEWORTHY: This study presents the development of new proprietary whole body sweat rate prediction models for people exercising indoors on a cycle ergometer or treadmill using simple input parameters and delivered through a publicly available online calculator: https://sweatratecalculator.com. In an independent validation group, the predictive models for both indoor cycling and treadmill exercise were accurate across moderate to high exercise intensities in temperate to hot conditions. These equations will enable individualized hydration management during physical training and exercise physiology experiments. [ABSTRACT FROM AUTHOR]

Neuroinflammation is critical to the pathogenesis and progression of epileptic seizures, and the inflammatory pathway is controlled by an interplay of highly regulated mediators such as cytokines. The combination of treadmill exercise program and curcumin administration has been shown to offer neuroprotection against epileptic seizure but without detailed mechanism of action being elucidated. This study therefore evaluated the responses of pro-inflammatory (tumor necrosis factor alpha [TNFα] and interleukin 6 [IL-6]) and anti-inflammatory (interleukin 10 [IL-10]) cytokines, as well as the transcription factor regulator (nuclear factor kappa B [NFκB]) gene expressions to combinatory therapy of curcumin and treadmill exercise in cortex and hippocampus of pilocarpine-induced epileptic seizure in rats. The rats were grouped into control, pilocarpine-induced, pilocarpine + curcumin, pilocarpine + curcumin + exercise for 14 days thereafter; total ribonucleic acid (RNA) was extracted from the cortex and hippocampus and used for reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) assay for TNFα, IL-6, IL-10, and NFκB. The results revealed that in pilocarpine-induced rats' cortex and hippocampus, the expressions of TNFα, IL-6, and NFκB were significantly upregulated while that of IL-10 was significantly downregulated. However, treatment with either curcumin or curcumin plus exercise significantly ameliorated these impairments in the inflammatory markers 'expression levels. Nevertheless, the combinatory therapy of curcumin and exercise showed significantly higher ameliorative effects in the cortical and hippocampal TNFα and IL-10, as well as cortical NFκB and IL-6. These superior therapeutic properties of the combination of curcumin and treadmill exercise further support the therapeutic potentials of this combinatory regimen in the management of epileptic seizures. Nonetheless, further studies including clinical observations are highly recommended. [ABSTRACT FROM AUTHOR]

Copyright of Retos: Nuevas Perspectivas de Educación Física, Deporte y Recreación is the property of Federacion Espanola de Asociaciones de Docentes de Educacion Fisica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Retos: Nuevas Perspectivas de Educación Física, Deporte y Recreación is the property of Federacion Espanola de Asociaciones de Docentes de Educacion Fisica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Accumulating evidence underscores exercise as a straightforward and cost-effective lifestyle intervention capable of mitigating the risk and slowing the emergence and progression of Alzheimer's disease (AD). However, the intricate cellular and molecular mechanisms mediating these exercise-induced benefits in AD remain elusive. The present study delved into the impact of treadmill exercise on memory retrieval performance, hippocampal synaptic plasticity, synaptic morphology, and the expression and activity of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptors (AMPARs) in 6-month-old APP/PS1 mice. APP/PS1 mice (4-month-old males) were randomly assigned to either a treadmill exercise group or a sedentary group, with C57BL/6J mice (4-month-old males) as the control group (both exercise and sedentary). The exercise regimen spanned 8 weeks. Our findings revealed that 8-week treadmill exercise reversed memory retrieval impairment in step-down fear conditioning in 6-month-old APP/PS1 mice. Additionally, treadmill exercise enhanced basic synaptic strength, short-term potentiation (STP), and long-term potentiation (LTP) of the hippocampus in these mice. Moreover, treadmill exercise correlated with an augmentation in synapse numbers, refinement of synaptic structures, and heightened expression and activity of AMPARs. Our findings suggest that treadmill exercise improves behavioral performance and facilitates synaptic transmission by increasing structural synaptic plasticity and the activity of AMPARs in the hippocampus of 6-month-old APP/PS1 mice, which is involved in pre- and postsynaptic processes. [ABSTRACT FROM AUTHOR]

Background: Adolescence is a critical period filled with life changes. Early implementation of effective health promotion strategies could help alleviate the morbidity and mortality associated with inactivity. This study investigated whether adolescent participation in exercise and sport is associated with device-assessed physical activity (PA) levels in midlife. Methods: A total of 2984 participants (41.2% male) from the 1970 British Cohort Study were included. Participants were surveyed at age 16 years on 5 indicators of exercise and sport participation. Total daily PA and moderate to vigorous PA (MVPA) at age 46 years were measured using a thigh-worn accelerometer, worn for 7 days. Associations between each adolescent exercise or sport indicator and adulthood total daily PA and MVPA were examined using linear regressions, adjusting for sex, wear time, body mass index, smoking, disability, malaise, alcohol consumption, social class, education, and self-rated health. Results: In fully adjusted models, adolescents who reported exercising "much more" than others (8.6 min/d; 95% confidence interval, −0.1 to 17.1), who played sports at the park/playground more than once a week (8.5 [3.0–14.0] min/d), and who exercised on the most recent Saturday (3.8 [0.7–6.9] min/d) had higher adult total PA levels than those who reported the lowest activity levels. There was no evidence of an association between greater sport and exercise participation at age 16 y and MVPA at age 46 y. There was no association between sports at school and either measure of adult PA. Conclusion: Active adolescents, particularly those who engaged in out-of-school exercise, had higher total daily PA levels, but not MVPA levels, in midlife. This highlights the potential of early PA interventions to improve PA levels in adulthood. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The primary pathological change in Parkinson's disease (PD) is the progressive degeneration of dopaminergic neurons in the substantia nigra. Additionally, excessive microglial activation and synaptic loss are also typical features observed in PD samples. Exercise trainings have been proven to improve PD symptoms, delay the disease progression as well as affect excessive microglial synaptic phagocytosis. In this study, we established a mouse model of PD by injecting mouse-derived α-synuclein preformed fibrils (M-α-syn PFFs) into the substantia nigra, and demonstrated that treadmill exercise inhibits microglial activation and synaptic phagocytosis in striatum. Using RNA-Seq and proteomics, we also found that PD involves excessive activation of the complement pathway which is closely related to over-activation of microglia and abnormal synaptic function. More importantly, exercise training can inhibit complement levels and complement-mediated microglial phagocytosis of synapses. It is probably triggered by CD55, as we observed that CD55 in the striatum significantly increased after exercise training and up-regulation of that molecule rescued motor deficits of PD mice, accompanied with reduced microglial synaptic phagocytosis in the striatum. This research elucidated the interplay among microglia, complement, and synapses, and analyzed the effects of exercise training on these factors. Our work also suggested CD55 as a complement-relevant candidate molecule for developing therapeutic strategies of PD. [ABSTRACT FROM AUTHOR]

While a low degree of energy compensation is typically reported over the 24 h following a session of exercise, the prolonged impact of a bout of exercise on energy intake remains unclear. To overcome the challenge associated with accurately measuring energy intake in a free‐living environment, this study employed the use of a meal replacement beverage to assess the 3 day impact of an exercise session on energy intake. In a randomized, crossover study, 14 participants (8 male, 6 female) completed two trials: (1) EX: 75 min exercise on a motorized treadmill (75% VO2peak); and (2) SED: 75 min sedentary control session. Each condition was followed by 3 days of exclusive ad libitum consumption of a meal replacement beverage. Appetite‐regulating hormones, subjective appetite, energy intake, and energy expenditure were assessed. Exercise transiently suppressed the orexigenic hormone acyl‐ghrelin (p < 0.05) and elevated the appetite‐supressing hepatokine GDF‐15 (p < 0.05). Despite these acute changes, overall perceived appetite was elevated over the 3 day assessment period with exercise (p < 0.05). No increase in energy intake or change in postexercise physical activity patterns were observed. One acute session of moderate to vigorous exercise is unlikely to affect short‐term, three‐day energy balance in healthy individuals. [ABSTRACT FROM AUTHOR]

Exercise training is considered a nonpharmacological therapeutic approach for many diseases. Mild-to-moderate endurance exercise training is suggested to improve the mental and physical state of people with amyotrophic lateral sclerosis (ALS). The aim of the present study was to determine the capacity of symptomatic rNLS8 mice, which develop ALS-reminiscent TAR DNA-binding protein 43 (TDP-43) pathology and motor dysfunction, to perform mild-to-moderate intensity treadmill exercise training and to evaluate the effects of this training on skeletal muscle health and disease progression. Symptomatic rNLS8 mice were able to complete 4 wk of mild-to-moderate treadmill running (30 min at 6–13 m/min, 3 days a week). Exercise training induced an increase in the percentage of type IIA fibers in the tibialis anterior muscle as well as minor adaptations in molecular markers of myogenic, mitochondrial, and neuromuscular junction health in some forelimb and hindlimb muscles. However, this exercise training protocol did not attenuate the loss in motor function or delay disease progression. Alternative exercise regimens need to be investigated to better understand the role exercise training may play in alleviating symptoms of ALS. NEW & NOTEWORTHY: This is the first study to investigate the capacity of symptomatic rNLS8 mice, which develop ALS-reminiscent TDP-43 pathology and motor dysfunction, to perform exercise training. We demonstrate that despite the ALS-reminiscent aggressive disease progression characterizing the rNLS8 mouse model, rNLS8 mice are capable of performing mild-to-moderate endurance treadmill training for at least 3–4 wk. We demonstrate that exercise training induces several minor skeletal muscle adaptations without delaying disease progression in rNLS8 mice. [ABSTRACT FROM AUTHOR]

The aim of this research was to explore the potential of treadmill exercise in preventing brain aging and neurodegenerative diseases caused by oxidative stress, by studying its effects on d-galactose-induced mice and the mechanisms involved. The results showed that C57BL/6 mice induced with d-gal exhibited cognitive impairment and oxidative stress damage, which was ameliorated by treadmill exercise. The Morris water maze also showed that exercise improved cognitive performance in aging mice and alleviated hippocampal and mitochondrial damage. The study also found that treadmill exercise increased the expression of nuclear factor Nrf2, p-GSK3β, HO-1, NQO1, BDNF, and Bcl-2 proteins while decreasing the expression of Bax. Furthermore, there was a substantial increase in the levels of CAT, GSH-PX and SOD in the serum, along with a decrease in MDA levels. The outcomes propose that aerobic exercise has the potential to hinder oxidative stress and cell death in mitochondria through the modulation of the Nrf2/GSK3β signaling pathway, thus improving cognitive impairment observed in the aging model induced by d-galactose. It appears that treadmill exercise could potentially serve as an effective therapeutic approach to mitigating brain aging and neurodegenerative diseases triggered by oxidative stress. [ABSTRACT FROM AUTHOR]

Background: Exercise is recognized for its broad health benefits, influencing various physiological processes, including the behavior of adipose tissue macrophages (ATMs). While existing studies mainly associate ATM activity with obesity and metabolic syndrome, our study explores the impact of aerobic exercise on ATM microRNA expression profiling in a non-obese context, highlighting its general health-promoting mechanisms. Methods: Sixty male C57BL/6 mice were randomly assigned to either a sedentary (S) or an exercise (E) group. The S group remained inactive, while the E group underwent a one-week treadmill adaptation, followed by an 8-week aerobic treadmill exercise protocol (60 min/day, 5 days/week, at 65%-75% VO2max). Posttraining, glucose tolerance and the serum lipid levels were measured in mice subjected to both exercise and non-exercise conditions. ATMs harvested from visceral adipose tissues were analyzed and sorted using flow cytometer. To further investigate the effects of exercise in ATMs at the molecular level, miRNA microarray analysis was performed, followed by bioinformatic analysis. Results: The 8-week regimen of moderate-intensity aerobic exercise ameliorated glucolipid metabolism and fostered a dynamic shift toward an M2 macrophage phenotype in the adipose tissue, independent of obesity. A total of 62 differentially expressed miRNAs were identified in ATMs of mice postexercise. Notably, six miRNAs (miR-212-5p, miR-511-5p, miR-7b-5p, miR-142- 3p, miR-1894-3p, and miR-31-5p) as well as their target gene were consistently altered and associated with macrophage polarization and metabolic regulation. Conclusion: Our findings broaden the understanding of how exercise regulates ATM functions through significant changes in microRNA profiles, emphasizing its potential to enhance health and prevent chronic conditions. This study supports the application of aerobic exercise for its preventive effects on chronic diseases and underscores the importance of microRNA profiling in understanding the immune-modulatory impacts of exercise. [ABSTRACT FROM AUTHOR]

Summary: Background: Horses exercised 'onto the bit' with periods of induced poll flexion can demonstrate a unique array of upper respiratory tract (URT) disorders. Objectives: To describe a previously unreported exercise‐related disorder of the epiglottis associated with poll flexion in harness racehorses. Study design: Retrospective observational study. Methods: Medical records of all harness racehorses that presented for exercising URT endoscopy between 2005 and 2022 were reviewed. These horses were exercised on a high‐speed treadmill using a previously standardised protocol with alternating 1‐min phases of free head carriage (no rein tension on the bit) and poll flexion (driven onto the bit with long reins) until they could no longer maintain the trotting gait. Results: Seven Standardbreds and 11 Norwegian‐Swedish Coldblooded trotters were diagnosed with unilateral or bilateral compression of the epiglottis during exercise in poll flexion. These horses demonstrated progression of this disorder during the phases of induced poll flexion and showed no signs of epiglottic compression during phases exercised with free head carriage. Main limitations: Retrospective nature of study and limited sample size due to low prevalence. Conclusions: Exercise‐related compression of the base of the epiglottis is a URT disorder only evident videoendoscopically when horses are driven onto the bit leading to poll flexion. It is most often seen in association with dynamic laryngeal collapse but can also be witnessed as a solitary disorder. Videoendoscopically, it appears that the compression is initiated by the rostral advancement of the larynx and hyoid apparatus within a progressively narrowing intermandibular space during poll flexion. Visually, this leads to local inward compression of the lateral nasopharyngeal walls and base of the epiglottis. Further studies are ongoing to confirm this hypothesis and to objectively quantify the degree of URT obstruction caused by this conformational narrowing of the epiglottis during poll flexion. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of the present study was to compare the acute effects of different rest period durations after general warm-up (GWU) and dynamic stretching (DS) on endurance running performance. Methods: Eight male runners performed endurance running performance tests after three types of intervention. The interventions were as follows: (1) GWU + 5 min Rest, (2) GWU + DS + 5 min Rest, and (3) GWU + DS + 10 min Rest. The GWU consisted of running exercises on a treadmill at a velocity equivalent to 70% of maximum oxygen uptake (V̇O2max) for 15 min. The DS consisted of performing 10 repetitions as quickly as possible for the five muscle groups of the lower extremities. Endurance running performance was measured by time to exhaustion (TTE) during running on the treadmill at a velocity equivalent to 90% V̇O2max. Results: TTE (884.5 ± 244.9 s) after GWU + DS + 10 min Rest intervention was significantly (p < 0.05) longer than that (719.8 ± 227.9 s) after GWU + 5 min Rest. TTE (734.5 ± 274.2 s) after GWU + DS + 5 min Rest intervention was not significantly different than that of the other two interventions. Conclusion: The results demonstrated that the endurance running performance at the velocity equivalent to 90% V̇O2max was enhanced by GWU + DS + 10 min Rest, but not GWU + DS + 5 min Rest. We recommend that runners rest for approximately 10 min after GWU + DS to enhance endurance running performance. [ABSTRACT FROM AUTHOR]

Copyright of Retos: Nuevas Perspectivas de Educación Física, Deporte y Recreación is the property of Federacion Espanola de Asociaciones de Docentes de Educacion Fisica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The effect of acute exercise on circulating concentrations of vitamin D metabolites is unclear. To address this knowledge gap, we examined the effect of a bout of treadmill‐based exercise versus rest on circulating concentrations of 25(OH)D3, 25(OH)D2, 3‐epi‐25(OH)D3, 24,25(OH)2D3, 1,25(OH)2D3, and vitamin D2 and D3 in healthy men and women. Thirty‐three healthy adults (14 females, 41 (15) years, body mass index 26.2 (3.7) kg/m2, V̇O2max${{\dot{V}}_{{{{\mathrm{O}}}_{\mathrm{2}}}{\mathrm{max}}}}$ 36.2 (9.2) ml/kg/min; mean (SD)) completed two laboratory visits involving 60 min of moderate‐intensity treadmill exercise (60% V̇O2max${{\dot{V}}_{{{{\mathrm{O}}}_{\mathrm{2}}}{\mathrm{max}}}}$) versus 60 min of seated rest, both in an overnight fasted‐state, as part of a randomised crossover design. Venous blood samples were drawn at baseline, immediately (0 h), 1 h and 24 h after the exercise or rest‐period. There was a significant time × trial interaction effect for total circulating 25(OH)D (P = 0.0148), 25(OH)D3 (P = 0.0127) and 1,25(OH)2D3 (P = 0.0226). Immediately post‐exercise, 25(OH)D, 25(OH)D3 and 1,25(OH)2D3 concentrations were significantly elevated compared to the control resting condition, and 1,25(OH) 2D3 remained significantly elevated 1 h later. Circulating albumin, vitamin D binding protein, calcium and parathyroid hormone were elevated immediately post‐exercise. Thus, an acute bout of moderate intensity exercise transiently increases concentrations of circulating 25(OH)D and 1,25(OH)2D3 compared to resting conditions. Key points: Observational studies suggest that acute exercise might change circulating concentrations of vitamin D metabolites, but this has not been investigated using randomised crossover studies and using robust analytical procedures.In this study, we used a randomised crossover design to examine the effect of a bout of treadmill‐based exercise (vs. rest) on circulating concentrations of a wide range of vitamin D metabolites in healthy humans.We show that an acute bout of moderate intensity exercise transiently increases concentrations of circulating 25(OH)D and 1,25(OH)2D3 compared to resting conditions.These findings indicate that regular exercise could lead to transient but regular windows of enhanced vitamin D biological action. [ABSTRACT FROM AUTHOR]

Regular exercise improves several functions, including cognition, in patients with stroke. However, the effect of regular exercise on neurogenesis related to cognition remains doubtful. We investigated the most effective exercise intensity for functional recovery after stroke using RNA sequencing following regular treadmill exercise. Photothrombotic cerebral infarction was conducted for 10-week-old male Sprague-Dawley rats (n = 36). A Morris water maze (MWM) test was performed before a regular treadmill exercise program (5 days/week, 4 weeks). Rats were randomly divided into four groups: group A (no exercise); group B (low intensity, maximal velocity 18 m/min); group C (moderate intensity, maximal velocity 24 m/min) and group D (high intensity, maximal velocity 30 m/min). After 4 weeks, another MWM test was performed, and all rats were sacrificed. RNA sequencing was performed with ipsilesional hippocampal tissue. On the day after cerebral infarction, no differences in escape latency and velocity were observed among the groups. At 4 weeks after cerebral infarction, the escape latencies in groups B, C, and D were shorter than in group A. The escape latencies in groups B and C were shorter than in group D. The velocity in groups A, B, and C was faster than in group D. Thirty gene symbols related to neurogenesis were detected (p < 0.05, fold change > 1.0, average normalized read count > four times). In the neurotrophin-signaling pathway, the CHK gene was upregulated, and the NF-κB gene was downregulated in the low-intensity group. The CHK and NF-κB genes were both downregulated in the moderate-intensity group. The Raf and IRAK genes were downregulated in the high-intensity group. Western blot analysis showed that NF-κB expression was lowest in the moderate-intensity group, whereas CHK and Raf were elevated, and IRAK was decreased in the high-intensity group. Moderate-intensity exercise may contribute to neuroplasticity. Variation in the expression of neurotrophins in neurogenesis according to exercise intensity may reveal the mechanism of neuroplasticity. Thus, NF-κB is the key neurotrophin for neurogenesis related to exercise intensity. [ABSTRACT FROM AUTHOR]

The objective of this study was to examine the effect of consuming ketone monoester plus a high dose of carbohydrate from glucose (KE + CHO) on the change in erythropoietin (EPO) concentrations during load carriage exercise compared with carbohydrate (CHO) alone. Using a randomized, crossover design, 12 males consumed KE + CHO (573 mg KE/kg body mass, 110 g glucose) or CHO (110 g glucose) 30 min before 4 miles of self‐paced treadmill exercise (KE + CHO:51 ± 13%, CHO: 52 ± 12% V̇O2peak) wearing a weighted vest (30% body mass; 25 ± 3 kg). Blood samples for analysis were obtained under resting fasted conditions before (Baseline) consuming the KE + CHO or CHO supplement and immediately after exercise (Post). βHB increased (p < 0.05) from Baseline to Post in KE + CHO, with no change in CHO. Glucose and glycerol increased (p < 0.05) from Baseline to Post in CHO, with no effect of time in KE + CHO. Insulin and lactate increased (p < 0.05) from Baseline to Post independent of treatment. EPO increased (p < 0.05) from Baseline to Post in KE + CHO and CHO with no difference between treatments. Although KE + CHO altered βHB, glucose, and glycerol concentrations, results from this study suggest that KE + CHO supplementation before load carriage exercise does not enhance immediate post‐exercise increases in EPO compared with CHO alone. [ABSTRACT FROM AUTHOR]

Objective: The efficacy of drug therapies in managing neuropathic pain is constrained by their limited effectiveness and potential for adverse effects. In contrast, exercise has emerged as a promising alternative for pain relief. In this study, we conducted a systematic evaluation of the therapeutic impact of exercise on neuropathic pain resulting from sciatic nerve injury in rodent models. Methods: The PubMed, Embase, and Web of Science databases were retrieved before April 2024. A series of studies regarding the effect of treadmill, swimming, wheel and other exercises on neuropathic pain induced by sciatic nerve injury in rats and mice were collected. Using predefined inclusion criteria, two researchers independently performed literature screening, data extraction, and methodological quality assessment utilizing SYRCLE's risk of bias tool for animal studies. Statistical analysis was conducted using RevMan 5.3 and STATA 12.0 analysis software. Results: A total of 12 relevant academic sources were included in the analysis of controlled animal studies, with 133 rodents in the exercise group and 135 rodents in the sedentary group. The meta-analysis revealed that exercise was associated with a significant increase in paw withdrawal mechanical threshold [Standard Mean Difference1 (SMD) = 0.84, 95% confidence interval (CI): 0.28-1.40, p = 0.003] and paw withdrawal thermal latency (SMD = 1.54, 95%CI: 0.93-2.15, p < 0.0001) in rats and mice with sciatic nerve injury. Subgroup analyses were conducted to evaluate the impact of exercise duration on heterogeneity. The results showed that postoperative exercise duration =3 weeks could significantly elevate paw withdrawal mechanical threshold (SMD = 1.04, 95% CI: 0.62-1.46, p < 0.00001). Postoperative exercise duration =4 weeks could significantly improve paw withdrawal thermal latency (SMD = 1.93, 95% CI:1.19-2.67, p < 0.00001). Conclusion: Exercise represents an effective method for improving mechanical and thermal hypersensitivity resulting from sciatic nerve injury in rodents. Factors such as pain models, the initiation of exercise, the type of exercise, and the species of rodent do not significantly impact the development of exercise-induced hypoalgesia. However, the duration of postoperative exercise plays a crucial role in the onset of exercise-induced hypoalgesia. [ABSTRACT FROM AUTHOR]

Simple Summary: The regulation of oxidative stress at rest and in response to a single session of exercise is vital for cardiovascular and metabolic health. However, the lack of regular physical activity and exercise and the presence of obesity are known to negatively impact oxidative stress under both conditions. In the present study, the oxidative stress response in circulation and within exosome-like extracellular vesicles (ELVs) released by contracting skeletal muscle during exercise was examined following maximal intensity treadmill running. As a result, we demonstrate that aerobically untrained individuals with obesity exhibit an altered oxidative stress response to maximal treadmill running compared to aerobically untrained and aerobically trained individuals without obesity. Similarly, body mass index, an index of obesity, but not cardiorespiratory fitness, was associated with an adverse oxidative response at rest and immediately following maximal treadmill running. These findings suggest that obesity, more than improved cardiorespiratory fitness, differentially regulates plasma and circulating ELV indices of oxidative stress prior to and immediately following acute maximal treadmill exercise. The impact of cardiorespiratory fitness (VO2max) and obesity on indices of oxidative stress in plasma and circulating exosome-like extracellular vesicles (ELVs) were examined following acute exercise. Indices of oxidative stress in plasma and isolated plasma ELVs were examined in aerobically trained (NW-Tr; n = 15) and untrained (NW-UTr; n = 18) normal-weight individuals and aerobically untrained individuals with obesity (Ob-Utr; n = 10) prior to and immediately following acute maximal treadmill running. Following exercise, ELV flotillin-1 expression (p = 0.008) and plasma total antioxidant capacity (TAC; p = 0.010) increased more in NW-UTr compared to NW-Tr and Ob-UTr participants, whereas plasma protein carbonyls (PC) decreased more in Ob-UTr compared to NW-Tr and NW-UTr groups. ELV glutathione (GSH) concentrations decreased more in NW-Tr compared to NW-UTr and Ob-UTr participants (p = 0.009), whereas lipid peroxidase (LPO) concentrations increased more in Ob-UTr compared to NW-Tr and NW-UTr participants (p = 0.003). Body mass index (BMI) was associated negatively with plasma TAC and PC (p < 0.05) and positively with ELV LPO concentration responses (p = 0.009). Finally, plasma-to-total (plasma + ELV) GSH ratios decreased in Ob-UTr compared to NW-Tr and NW-UTr participants (p = 0.006), PC ratios increased in NW-Tr and NW-UTr compared to Ob-UTr subjects (p = 0.008), and reactive oxygen/nitrogen species ratios increased in NW-UTr and decreased in Ob-UTr participants (p < 0.001). BMI, independently of VO2max, differentially regulates indices of oxidative stress within plasma and circulating ELVs prior to and immediately following acute maximal treadmill exercise. [ABSTRACT FROM AUTHOR]

Introduction: Knee Osteoarthritis (OA) is a significant cause of disability globally and is rapidly becoming a major health issue. The part of the knee most affected by OA is the patellofemoral joint. This type of arthritis poses challenges for both patients and healthcare providers in managing symptoms and improving the quality of life for those affected. However, there's a lack of data on specific therapies for the patellofemoral joint. Aim: To investigate if a varied frequency treadmill exercises protocol involving retro-walking has a greater impact on musculoskeletal responses, leading to better improvements in individuals with symptomatic Patellofemoral Joint Osteoarthritis (PFOA). Materials and Methods: The present study was an experimental research design i.e., between -subjects experimental design in which 60 participants with patellofemoral arthritis were enrolled based on the inclusion criteria. The study was conducted in the Department of Orthopaedics, SGT Medical College Hospital and Research Institute in Gurugram, Haryana, India for a duration of one year (May 2022- May 2023). Participants were randomly randomised to three distinct exercise program groups with varying intensity levels for retro-walking on a treadmill for six weeks, and all three groups received conventional treatment six days/week for six weeks. All participants were evaluated at three-time intervals of baseline, at the end of the third week, and after intervention (end of the sixth week) for the evaluation of several musculoskeletal parameters affecting patellofemoral arthritis. Statistical analysis was carried out using the IBM Statistical Package for the Social Sciences (SPSS) version 26.0. Comparison for within group differences between various outcome measures at various intervals of time was done using repeated measures of Analysis of Variance (ANOVA) and post-hoc analysis for mean values with Least Significant Difference (LSD) whereas for between group analysis One-way ANOVA and post-hoc Analysis for mean values was done with p-value set at <0.05. Result: Significant statistical and clinical differences were observed in musculoskeletal responses, Q-angle (p-value=0.001) and popliteal angle (p-value=0.001) in the high frequency group (group C) performing the protocol five times a week for six weeks leading to a better quality of life followed by group B and group A, respectively. Conclusion: The main finding of the present study suggested that the dosage for retro-walking on treadmill among patients with patellofemoral arthritis requires at least walking for five times/week for six weeks to get more clinical improvement in Musculoskeletal Disorders (MSD). [ABSTRACT FROM AUTHOR]

OBJECTIVE: Little is known about the extent to which microvascular disease is associated with cardiorespiratory fitness (CRF) among individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS: A total of 4,766 participants with type 2 diabetes underwent maximal exercise testing in the Look AHEAD (Action for Health in Diabetes) study at baseline. Low CRF was defined based on the Aerobics Center Longitudinal Study reference standards. Microvascular disease was defined as having one or more of diabetes-related kidney disease (DKD), retinopathy, and neuropathy. The burden of microvascular disease was defined as the number of microvascular beds affected. RESULTS: Of the 4,766 participants (mean age 58.9 ± 6.7 years, 58.5% women, 66.1% White individuals), 1,761 (37%) had microvascular disease. Participants with microvascular complications in three vascular territories had a lower CFR than those without any microvascular disease (mean adjusted metabolic equivalent of task [MET] 6.58 vs. 7.26, P = 0.001). Participants with any microvascular disease had higher odds of low CRF than those without microvascular disease (adjusted odds ratio [OR] 1.45, 95% CI 1.24–1.71). An increasing burden of microvascular disease was associated with higher odds of low CRF (for microvascular disease in three vascular territories, adjusted OR 2.82, 95% CI 1.36–5.85). Adjusted ORs for low CRF were 1.24 (95% CI 0.99–1.55), 1.34 (95% CI 1.02–1.76), and 1.44 (95% CI 1.20–1.73) for neuropathy, retinopathy, and DKD associations, respectively. CONCLUSIONS: In a large cohort of adults with type 2 diabetes, the presence of microvascular disease and its burden were independently associated with lower CRF. [ABSTRACT FROM AUTHOR]

Postmenopausal osteoporosis is a prevalent metabolic bone disorder characterized by a decrease in bone mineral density and deterioration of bone microstructure. Despite the high prevalence of this disease, no effective treatment for osteoporosis has been developed. Exercise has long been considered a potent anabolic factor that promotes bone mass via upregulation of myokines secreted by skeletal muscle, exerting long‐term osteoprotective effects and few side effects. Irisin was recently identified as a novel myokine that is significantly upregulated by exercise and could increase bone mass. However, the mechanisms underlying exercise‐induced muscle‐bone crosstalk remain unclear. Here, we identified that polyunsaturated fatty acids (arachidonic acid and docosahexaenoic acid) are increased in skeletal muscles following a 10‐week treadmill exercise programme, which then promotes the expression and release of FNDC5/irisin. In osteoblasts, irisin binds directly to Cav1, which recruits and interacts with AMP‐activated protein kinase α (AMPKα) to activate the AMPK pathway. Nrf2 is the downstream target of the AMPK pathway and increases the transcription of HMOX1 and Fpn. HMOX1 is involved in regulating the cell cycle and promotes the proliferation of osteoblasts. Moreover, upregulation of Fpn in osteoblasts enhanced iron removal, thereby suppressing ferroptosis in osteoblasts. Additionally, we confirmed that myotube‐derived exosomes are involved in the transportation of irisin and enter osteoblasts through caveolae‐mediated endocytosis. In conclusion, our findings highlight the crucial role of irisin, present in myotube‐derived exosomes, as a crucial regulator of exercise‐induced protective effects on bone, which provides novel insights into the mechanisms underlying exercise‐dependent treatment of osteoporosis. [ABSTRACT FROM AUTHOR]

Limited knowledge exists regarding the chronic effect of muscular exercise on muscle function in a murine model of severe Duchenne muscular dystrophy (DMD). Here we determined the effects of 1 month of voluntary wheel running (WR), 1 month of enforced treadmill running (TR) and 1 month of mechanical overloading resulting from the removal of the synergic muscles (OVL) in mice lacking both dystrophin and desmin (DKO). Additionally, we examined the effect of activin receptor administration (AR). DKO mice, displaying severe muscle weakness, atrophy and greater susceptibility to contraction‐induced functional loss, were exercised or treated with AR at 1 month of age and in situ force production of lower leg muscle was measured at the age of 2 months. We found that TR and OVL increased absolute maximal force and the rate of force development of the plantaris muscle in DKO mice. In contrast, those of the tibialis anterior (TA) muscle remained unaffected by TR and WR. Furthermore, the effects of TR and OVL on plantaris muscle function in DKO mice closely resembled those in mdx mice, a less severe murine DMD model. AR also improved absolute maximal force and the rate of force development of the TA muscle in DKO mice. In conclusion, exercise training improved plantaris muscle weakness in severely affected dystrophic mice. Consequently, these preclinical results may contribute to fostering further investigations aimed at assessing the potential benefits of exercise for DMD patients, particularly resistance training involving a low number of intense muscle contractions. Key points: Very little is known about the effects of exercise training in a murine model of severe Duchenne muscular dystrophy (DMD). One reason is that it is feared that chronic muscular exercise, particularly that involving intense muscle contractions, could exacerbate the disease.In DKO mice lacking both dystrophin and desmin, characterized by severe lower leg muscle weakness, atrophy and fragility in comparison to the less severe DMD mdx model, we found that enforced treadmill running improved absolute maximal force of the plantaris muscle, while that of tibialis anterior muscle remained unaffected by both enforced treadmill and voluntary wheel running.Furthermore, mechanical overloading, a non‐physiological model of chronic resistance exercise, reversed plantaris muscle weakness.Consequently, our findings may have the potential to alleviate concerns and pave the way for exploring the prescription of endurance and resistance training as a viable therapeutic approach for the treatment of dystrophic patients. Additionally, such interventions may serve in mitigating the pathophysiological mechanisms induced by physical inactivity. [ABSTRACT FROM AUTHOR]

Rational: Patients experience post-stroke cognitive impairment during aging. To date, no specific treatment solution has been reported for this disorder. Objective: The purpose of this study was to evaluate the effects of exercise training and coenzyme Q10 supplementation on middle cerebral artery occlusion (MCAO) induced behavioral impairment, long-term potentiation inhibition and cerebral infarction size in aging rats. Methods: Fifty aging male rats underwent MCAO surgery and were randomly distributed in to the following groups: 1-Sham, 2- control, 3- Coenzyme Q10, 4- Exercise training and 5- Exercise training with Q10 supplementation (Ex + Q10). Aerobic training groups were allowed to run on a treadmill for 12 weeks. Q10 (50 mg/kg) was administered intragastrically by gavage. Morris water maze, shuttle box and elevated plus maze tests were used to evaluate cognitive function. The population spike (PS) amplitude and slope of excitatory postsynaptic potentials (EPSP) in the dentate gyrus area were recorded as a result of perforant pathway electrical stimulation. Results: Our study showed that Q10 and aerobic training alone ameliorate spatial memory in the acquisition phase, but have no effect on spatial memory in the retention phase. Q10 and exercise training synergistically promoted spatial memory in the retention phase. Q10 and exercise training separately and simultaneously mitigated cerebral ischemia-induced passive avoidance memory impairment in acquisition and retention phases. The EPSP did not differ between the groups, but exercise training and Q10 ameliorate the PS amplitude in hippocampal responses to perforant path stimulation. Exercising and Q10 simultaneously reduced the cerebral infarction volume. Conclusion: Collectively, the findings of the present study imply that 12 weeks of aerobic training and Q10 supplementation alone can simultaneously reverse cerebral ischemia induced neurobehavioral deficits via amelioration of synaptic plasticity and a reduction in cerebral infarction volume in senescent rats. [ABSTRACT FROM AUTHOR]

Our nervous system has the remarkable ability to adapt our gait to accommodate changes in our body or surroundings. However, our adapted walking patterns often generalize only partially (or not at all) between different contexts. Here, we sought to understand how the nervous system generalizes adapted gait patterns from one context to another. Through a series of split-belt treadmill walking experiments, we evaluated different mechanistic hypotheses to explain the partial generalization of adapted gait patterns from split-belt treadmill to overground walking. In support of the credit assignment hypothesis, our experiments revealed the central finding that adaptation involves recalibration of two distinct forward models. Recalibration of the first model generalizes to overground walking, suggesting that the model represents the general movement dynamics of our body. On the other hand, recalibration of the second model does not generalize to overground walking, suggesting the model represents dynamics specific to treadmill walking. These findings reveal that there is a predefined portion of forward model recalibration that generalizes across context, leading to overall partial generalization of walking adaptation. [ABSTRACT FROM AUTHOR]

To evaluate the effectiveness of photobiomodulation (PBM) in conjunction with an aerobic exercise program (AEP) on the level of pain and quality of life of women with fibromyalgia (FM). Methods: A double-blinded randomized controlled trial in which 51 participants with FM were allocated into 4 groups: control group (CG) (n = 12); active PBM group (APG) (n = 12); AEP and placebo PBM group (EPPG) (n = 13); AEP and active PBM group (EAPG) (n = 14). AEP was performed on an ergometric bicycle; and a PBM (with an increase dosage regime) [20 J, 32 J and 40 J] was applied using a cluster device. Both interventions were performed twice a week for 12 weeks. A mixed generalized model analysis was performed, evaluating the time (initial and final) and group (EAPG, EPPG, APG and CG) interaction. All analyses were based on intent-to-treat for a significance level of p ≤ 0.05. Results: The intra-group analysis demonstrated that all treated groups presented a significant improvement in the level of pain and quality of life comparing the initial and final evaluation (p < 0.05). Values for SF-36 and 6-minute walk test increased significant in intragroup analysis for EPPG comparing the initial and final evaluation. No intergroup differences were observed. Conclusions: Both exercised and PBM irradiated volunteers present improvements in the variables analyzed. However, further studies should be performed, with other PBM parameters to determine the best regime of irradiation to optimize the positive effects of physical exercises in FM patients. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Using treadmill training, this study replicated human exercise conditions and triggered exercise-induced fatigue in mice to examine the potential of Pediococcus pentosaceus YF01 in delaying this fatigue by regulating oxidative stress and its impact on the exercise capacity and gut microbiota of mice. The exercise capacity of mice was tested by conducting exhaustion tests, determining histopathological changes in mouse tissues, detecting the levels of serum biochemical markers, and evaluating the mRNA expression levels of relevant genes. YF01 prolonged the exhaustion time of mice, increased the serum levels of oxidative stress-related markers T-AOC, CAT, and GSH, as well as GLU and LA levels in the mice. YF01 decreased the levels of hepatic-related markers AST and ALT, as well as exercise-related markers LDH, BUN, UA, and CRE in the mice. YF01 upregulated the mRNA expression of MyHc I, SIRT1, and PGC in muscle tissues, as well as SOD1, SOD2, and CAT in both liver and muscle tissues. YF01 also downregulated the mRNA expression of MyHc IIa, MyHc IIb, and MyHc IIx in muscle tissues. Furthermore, YF01 increased the abundance of beneficial bacteria such as Lactobacillus and Lachnospiraceae in the gut microbiota of mice. In conclusion, P. pentosaceus YF01 may affect the exercise capacity of mice by modulating oxidative stress levels, thereby offering novel ideas for developing of sports science and human health. [ABSTRACT FROM AUTHOR]

Neuropathic pain is a type of chronic pain caused by an injury or somatosensory nervous system disease. Drugs and exercise could effectively relieve neuropathic pain, but no treatment can completely stop neuropathic pain. The integration of exercise into neuropathic pain management has attracted considerable interest in recent years, and treadmill training is the most used among exercise therapies. Neuropathic pain can be effectively treated if its mechanism is clarified. In recent years, the association between neuroinflammation and neuropathic pain has been explored. Neuroinflammation can trigger proinflammatory cytokines, activate microglia, inhibit descending pain modulatory systems, and promote the overexpression of brain-derived neurotrophic factor, which lead to the generation of neuropathic pain and hypersensitivity. Treadmill exercise can alleviate neuropathic pain mainly by regulating neuroinflammation, including inhibiting the activity of pro-inflammatory factors and over activation of microglia in the dorsal horn, regulating the expression of mu opioid receptor expression in the rostral ventromedial medulla and levels of γ-aminobutyric acid to activate the descending pain modulatory system and the overexpression of brain-derived neurotrophic factor. This article reviews and summarizes research on the effect of treadmill exercise on neuropathic pain and its role in the regulation of neuroinflammation to explore its benefits for neuropathic pain treatment. [ABSTRACT FROM AUTHOR]

The myocardium is a highly oxidative tissue in which mitochondria are essential to supply the energy required to maintain pump function. When pathological hypertrophy develops, energy consumption augments and jeopardizes mitochondrial capacity. We explored the cardiac consequences of chronic swimming training, focusing on the mitochondrial network, in spontaneously hypertensive rats (SHR). Male adult SHR were randomized to sedentary or trained (T: 8-week swimming protocol). Blood pressure and echocardiograms were recorded, and hearts were removed at the end of the training period to perform molecular, imaging, or isolated mitochondria studies. Swimming improved cardiac midventricular shortening and decreased the pathological hypertrophic marker atrial natriuretic peptide. Oxidative stress was reduced, and even more interesting, mitochondrial spatial distribution, dynamics, function, and ATP were significantly improved in the myocardium of T rats. In the signaling pathway triggered by training, we detected an increase in the phosphorylation level of both AKT and glycogen synthase kinase-3 β, key downstream targets of insulin-like growth factor 1 signaling that are crucially involved in mitochondria biogenesis and integrity. Aerobic exercise training emerges as an effective approach to improve pathological cardiac hypertrophy and bioenergetics in hypertension-induced cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

Exertional breathlessness is a cardinal symptom of cardiorespiratory disease. How does breathlessness abnormality, graded using normative reference equations during cardiopulmonary exercise testing (CPET), relate to self-reported and physiologic responses in people with chronic airflow limitation (CAL)? An analysis was done of people aged ≥ 40 years with CAL undergoing CPET in the Canadian Cohort Obstructive Lung Disease study. Breathlessness intensity ratings (Borg CR10 scale [0-10 category-ratio scale for breathlessness intensity rating]) were evaluated in relation to power output, rate of oxygen uptake, and minute ventilation at peak exercise, using normative reference equations as follows: (1) probability of breathlessness normality (probability of having an equal or greater Borg CR10 rating among healthy people; lower probability reflecting more severe breathlessness) and (2) presence of abnormal breathlessness (rating above the upper limit of normal). Associations with relevant participant-reported and physiologic outcomes were evaluated. We included 330 participants (44% women): mean ± SD age, 64 ± 10 years (range, 40–89 years); FEV 1 /FVC, 57.3% ± 8.2%; FEV 1 , 75.6% ± 17.9% predicted. Abnormally low exercise capacity (peak rate of oxygen uptake < lower limit of normal) was present in 26%. Relative to peak power output, rate of oxygen uptake, and minute ventilation, abnormally high breathlessness was present in 26%, 25%, and 18% of participants. For all equations, abnormally high exertional breathlessness was associated with worse lung function, exercise capacity, self-reported symptom burden, physical activity, and health-related quality of life; and greater physiologic abnormalities during CPET. Abnormal breathlessness graded using CPET normative reference equations was associated with worse clinical, physiological, and functional outcomes in people with CAL, supporting construct validity of abnormal exertional breathlessness. [ABSTRACT FROM AUTHOR]

Insulin insensitivity decreases exogenous glucose oxidation and metabolic clearance rate (MCR) during aerobic exercise in unacclimatized lowlanders at high altitude (HA). Whether use of an oral insulin sensitizer before acute HA exposure enhances exogenous glucose oxidation is unclear. This study investigated the impact of pioglitazone (PIO) on exogenous glucose oxidation and glucose turnover compared with placebo (PLA) during aerobic exercise at HA. With the use of a randomized crossover design, native lowlanders (n = 7 males, means ± SD, age: 23 ± 6 yr, body mass: 84 ± 11 kg) consumed 145 g (1.8 g/min) of glucose while performing 80 min of steady-state (1.43 ± 0.16 V̇ o 2 L/min) treadmill exercise at HA (460 mmHg; P I O 2 96.6 mmHg) following short-term (5 days) use of PIO (15 mg oral dose per day) or PLA (microcrystalline cellulose pill). Substrate oxidation and glucose turnover were determined using indirect calorimetry and stable isotopes ([13C]glucose and 6,6-[2H2]glucose). Exogenous glucose oxidation was not different between PIO (0.31 ± 0.03 g/min) and PLA (0.32 ± 0.09 g/min). Total carbohydrate oxidation (PIO: 1.65 ± 0.22 g/min, PLA: 1.68 ± 0.32 g/min) or fat oxidation (PIO: 0.10 ± 0.0.08 g/min, PLA: 0.09 ± 0.07 g/min) was not different between treatments. There was no treatment effect on glucose rate of appearance (PIO: 2.46 ± 0.27, PLA: 2.43 ± 0.27 mg/kg/min), disappearance (PIO: 2.19 ± 0.17, PLA: 2.20 ± 0.22 mg/kg/min), or MCR (PIO: 1.63 ± 0.37, PLA: 1.73 ± 0.40 mL/kg/min). Results from this study indicate that PIO is not an effective intervention to enhance exogenous glucose oxidation or MCR during acute HA exposure. Lack of effect with PIO suggests that the etiology of glucose metabolism dysregulation during acute HA exposure may not result from insulin resistance in peripheral tissues. NEW & NOTEWORTHY: Short-term (5 days) use of the oral insulin sensitizer pioglitazone does not alter circulating glucose or insulin responses to enhance exogenous glucose oxidation during steady-state aerobic exercise in young healthy men under simulated acute (8 h) high-altitude (460 mmHg) conditions. These results indicate that dysregulations in glucose metabolism in native lowlanders sojourning at high altitude may not be due to insulin resistance at peripheral tissue. [ABSTRACT FROM AUTHOR]

The London Volcanic Ash Advisory Centre (VAAC) provides forecasts on the expected presence of volcanic ash in the atmosphere to mitigate the risk to aviation. It is fundamentally important that operational capability is regularly tested through exercises, to guarantee an effective response to an event. We have developed exercises which practise the pull-through of scientific advice into the London VAAC, the forecast evaluation process, and the decision-making procedures and discussions needed for generating the best possible forecasts under real-time conditions. London VAAC dispersion model forecasts are evaluated against observations. To test this capability in an exercise, we must create observation data for a hypothetical event. We have developed new methodologies for generating and using simulated satellite and lidar retrievals. These simulated observations enable us to practise our ability to interpret, compare, and evaluate model output and observation data under real-time conditions. Forecast evaluation can benefit from an understanding of how different choices of model setup (input parameters), model physics, and driving meteorological data impact the predicted extent and concentration of ash. Through our exercises, we have practised comparing output from model simulations generated using different models, model setups, and meteorological data, supplied by different institutions. Our exercises also practise the communication and interaction between Met Office (UK) scientists supporting the London VAAC and external experts, enabling knowledge exchange and discussions on the interpretation of model output and observations, as we strive to deliver the best response capability for the aviation industry and stakeholders. In this paper, we outline our exercise methodology, including the use of simulated satellite and lidar observations, and the development of the strategy to compare output generated from different modelling systems. We outline the lessons learnt, including the benefits and challenges of conducting exercises which practise our ability to provide scientific advice for an operational response at the London VAAC. [ABSTRACT FROM AUTHOR]

In the current research, the nanofibrous neural channels were produced by electrospinning of PCL/Gelatin solution loaded with Calendula officinalis extract. The produced scaffolds properties were studied using various in vitro characterization methods. Then, the conduits' healing potential was investigated in a rat model of PNS injury. In vitro results showed that scaffolds were not toxic and quenched DPPH free radicals. In addition, the extract-loaded conduits exhibited significant anti-inflammatory activity. In vivo study showed that the regular treadmill exercise significantly improved the healing efficacy of the Calendula officinalis-delivering conduits by upregulating BDNF and GFAP proteins. [ABSTRACT FROM AUTHOR]

Both estrogen deprivation and diabetes mellitus are known as risk factors for neuronal damage. Using an animal model of ovariectomized and/or streptozotocin (STZ)-induced diabetes mellitus, we examined expression of apoptosis-related proteins, neuronal damage, and astrocyte activation in prefrontal cortex of rats with/without treadmill exercise. Adult female Wistar rats were divided into control, ovariectomized (Ovx, bilateral ovariectomy), diabetic (Dia, STZ 60 mg/kg; i.p.), and ovariectomized diabetic (Ovx + Dia) groups. Next, animals in each group were randomly subdivided into non-exercise and exercise subgroups. Animals in the exercise groups underwent moderate treadmill running for 4 weeks (5 days/week). Thereafter, expression of Bax, Bcl-2, and caspase-3, as apoptosis-related proteins, number of neurons, and number of glial fibrillary acidic protein (GFAP)-positive cells in prefrontal cortex were measured using immunoblotting, cresyl violet staining, and immunohistochemistry, respectively. In both Dia and Ovx + Dia groups, Bax and caspase-3 protein levels and number of GFAP-positive cells were higher than those in the control group, while Bcl-2 protein level and number of neurons compared were lower than the control group. Beneficial effects of exercise to prevent apoptosis-mediated neuronal damage and astrocyte activation were also observed in the Dia group. Based on our results, physical exercise could be beneficial to attenuate diabetes-induced neuronal damage in the prefrontal cortex via inhibition of apoptosis. [ABSTRACT FROM AUTHOR]

Background and Objectives: In adults, 150 to 300 min a week of moderate-intensity physical activity is the recommended daily level to maintain or improve fitness. In subjects with chronic obstructive pulmonary disease (COPD), reductions in daily physical activity (DPA) amounts are related to clinically significant outcomes. In this study, we ascertain whether or not COPD patients, when clustered into active (DPA ≥ 30 min a day, 5 days a week) and inactive (DPA < 30 min a day, 5 days a week), may differ in exercise capacity, as assessed by a cardiopulmonary exercise test (CPET). Materials and Methods: A large sample of clinically stable COPD patients was retrospectively recruited and then underwent spirometry and an incremental ramp protocol 5–15 watts/min CPET. DPA was assessed by a questionnaire. Results: A total of 83 (female 25%, age range 41–85 y) active and 131 (female 31%, age range 49–83 y) inactive participants were enrolled. They were similar in age, sex distribution, body mass index (BMI) and in spirometry. The two groups were significantly different in dyspnea on exertion, as assessed by the modified Medical Research Council (mMRC), and in cardio-metabolic parameters, but not in ventilatory ones, as confirmed by the CPET. Conclusions: COPD patients experiencing physical activity of at least 30 min a day, 5 days a week, showed a greater exercise capacity and an improved cardiovascular response to exercise, when compared to inactive ones. Active and inactive participants did not differ in terms of airflow obstruction severity as well as in dynamic hyperinflation and ventilatory inefficiency during exercise. This study further suggests the benefits of regular physical activity in COPD. [ABSTRACT FROM AUTHOR]

Introduction: Perturbation-based balance training (PBT) is promising for fall prevention in older adults, mimicking real-life fall situations at a person's stability thresholds to improve reactive balance. Hence, it can be associated with anxiety, but knowledge about the acceptability of PBT is scarce. Method: This is a secondary analysis of a randomized controlled trial comparing the effects of two different PBT paradigms that aims to evaluate and compare the acceptability of those training paradigms in fall-prone older adults. Participants (74.9 ± 5.7 years) who completed the training (6 weeks, 3x/week) on either a perturbation treadmill (PBTtreadmill: n = 22) or unstable surfaces in the presence of perturbations (PBTstability: n = 27) were surveyed on the acceptability of PBT using a 21-item questionnaire addressing seven domains (perceived effectiveness, tailoring, demand, safety, burden, devices, affective attitude), based on the theoretical framework of acceptability and context-specific factors. Relative scores (% of absolute maximum) for single items and domains were calculated. Results: Median domain scores of perceived effectiveness, tailoring, safety, devices, and affective attitude were all ≥70% for both paradigms. The highest scores were obtained for tailoring (both paradigms = 100% [interquartile range 80–100%]). Domain scores of demand and burden were in the medium range (40–45%) for both paradigms. No significant differences between paradigms were found for any domain score. Two single items of safety differed significantly, with PBTtreadmill perceived as needing less support (p = 0.015) and leading less often to balance loss (p = 0.026) than PBTstability. Conclusion: PBT conducted on a perturbation treadmill or unstable surfaces is well accepted in this fall-prone older sample, even though it is conducted at individual stability thresholds. Tailoring may play a key role in achieving high levels of perceived effectiveness, appropriate levels of demand and burden, and a high sense of safety. PBT delivered on treadmills might be more appropriate for more anxious persons. [ABSTRACT FROM AUTHOR]

To investigate the impact of multisensory fusion training (MSFT) combined with 7, 8-dihydroxyflavone (DHF) on the behavioral characteristics, protein expression, microbiome, and serum metabolome using the AD model in mice induced with amyloid-β (Aβ). Methods: We assessed cognitive ability, anxiety-like and depression-like behaviors in Aβ mice using behavioral measures. Western blotting was employed to detect the expression of relevant proteins. The 16S rRNA gene sequencing and metabolomics were used to analyze changes in the intestinal microbial composition and serum metabolic profile, respectively, of Aβ mice. Results: The behavioral outcomes indicated that a 4-week intervention combining DHF and MSFT yielded remarkable improvements in cognitive function and reduced anxiety and depression-like behaviors in Aβ mice. In the hippocampus of Aβ mice, the combined intervention increased the levels of BDNF, VGF, PSD-95, Nrf2, p-GSK3β and p-CREB proteins. Analyses of sequence and metabolomic data revealed that Bacteroides and Ruminococcaceae were remarkably more abundant following the combined intervention, influencing the expression of specific metabolites directly linked to the maintenance of neuronal and neurobehavioral functions. These metabolites play a crucial role in vital processes, such as amino acid metabolism, lipid metabolism, and neurotransmitter metabolism in mice. Conclusion: Our study highlighted that MSFT combined with DHF improves cognitive impairment, anxiety, and depression-like behavior in Aβ mice through multiple mechanisms, and further validated the correlation between the gut microbiome and serum metabolome. These findings open up a promising avenue for future investigations into potential treatment strategies for AD. [ABSTRACT FROM AUTHOR]

We investigated the role played by ATP-sensitive purinergic 2 (P2) receptors in evoking the pressor response to treadmill exercise in male and female rats with and without femoral arteries that were ligated for -72 h to induce simulated peripheral artery disease (PAD). We hypothesized that PPADS (P2 receptor antagonist, 10 mg iv) would reduce the pressor response to 4 min of treadmill exercise (15 m·min-1, 1-incline) and steady-state exercise plasma norepinephrine (NE) values in male and female rats, and that the magnitude of effect of PPADS would be greater in rats with simulated PAD ("ligated") than in sham-operated rats. In males, PPADS significantly reduced the difference between steady-state exercise and baseline mean arterial pressure (DMAP) response to treadmill exercise in sham (n = 8; pre-PPADS: 12 ± 2, post-PPADS: 1 ± 5 mmHg; P = 0.037) and ligated (n = 4; pre-PPADS: 20 ± 2, post-PPADS: 11 ± 3 mmHg; P = 0.028) rats with a similar magnitude of effect observed between groups (P = 0.720). In females, PPADS had no effect on the DMAP response to treadmill exercise in sham (n = 6; pre-PPADS: 9 ± 2, post-PPADS: 7 ± 2 mmHg; P = 0.448) or ligated (n = 6; pre-PPADS: 15 ± 2, post-PPADS: 16 ± 3 mmHg; P = 0.684) rats. When NE values were grouped by sex independent of ligation/sham status, PPADS significantly reduced plasma NE in male (P = 0.016) and female (P = 0.027) rats. The data indicate that P2 receptors contribute to the sympathetic response to exercise in both male and female rats but that the sympathoexcitatory role for P2 receptors translates into an obligatory role in the blood pressure response to exercise in male but not in female rats. NEW & NOTEWORTHY Here, we demonstrate that purinergic 2 (P2) receptors contribute significantly to the blood pressure response to treadmill exercise in male rats both with and without simulated PAD induced by femoral artery ligation. We found no role for P2 receptors in the blood pressure response to treadmill exercise in female rats, thus revealing clear sex differences in P2 receptor-mediated blood pressure control during exercise. [ABSTRACT FROM AUTHOR]