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BACKGROUND: Obesity has become a global health issue, often accompanied by complications including obesity-related muscle atrophy. While exercise has been reported to improve various obesity-related diseases, there is limited research focusing on exercise modes. OBJECTIVE: To compare the effects of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) on obesity-related muscle atrophy in mice under the premise of the same exercise distance, providing a scientific basis for exercise interventions for obesity-related muscle atrophy. METHODS: Seventy-two male C57BL/6 mice were divided into six groups (n=12 per group): standard chow diet, standard chow diet+MICT, standard chow diet+HIIT, high-fat diet, high-fat diet+MICT, and high-fat diet+HIIT. The study evaluated the effects of 8-week treadmill training with different exercise modes on long-term high-fat diet-induced muscle atrophy by detecting muscle mass, muscle index, muscle fiber cross-sectional area, muscle lipid deposition, and the expression of muscle atrophy marker genes Murf-1 and Atrogin-1 in the gastrocnemius muscle of mice exposed to long-term high-fat diet. RESULTS AND CONCLUSION: Compared to the high-fat diet group, both MICT and HIIT improved the decrease in gastrocnemius muscle index (MICT+18.8% vs. HIIT+17.6%, not significant between the two modes), muscle fiber atrophy (MICT+15.5% vs. HIIT+13.7%, not significant between the two modes), and muscle lipid deposition (MICT-19.8% vs. HIIT-17.1%, not significant between the two modes). At the gene level, compared with the high-fat diet group, both MICT and HIIT could significantly down-regulate the expression of Murf-1 (MICT-62.4% vs. HIIT-52.6%, the down-regulation caused by MICT was significantly greater than that by HIIT; P < 0.01) and Atrogin-1 (MICT-43.3% vs. HIIT-29.8%, the down-regulation caused by MICT was significantly greater than that by HIIT; P < 0.01). Based on exercise mode comfort and genetic evidence, MICT mode might be more suitable for exercise interventions in obesity-related muscle atrophy. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exercise has been widely recognized in the prevention and treatment of diabetes. Aerobic exercise has become an important part of the treatment of type 1 diabetes. However, the effect of treadmill exercise on the metabolism and chronic neuroinflammation of type 1 diabetes in different sexes needs further discussion. OBJECTIVE: To study the effects of treadmill exercise on metabolism and chronic neuroinflammation in type 1 diabetes mice of different sexes. METHODS: Forty C57BL/6 mice were divided into male group and female group, with 20 mice in each group. Then, a diabetes model was established by continuous injection of streptozotocin at 80 mg/kg for 3 days. Ten rats from each group were randomly selected to perform 6-week treadmill exercise as the diabetes+exercise group and another 10 rats from each group were selected as the diabetes group. Serum sex hormones, liver tissue oxidative stress, brain tissue inflammatory factors, and liver pathology were detected, and Morris water maze was performed for the observation of behavioral changes in mice. RESULTS AND CONCLUSION: Compared with the diabetes group, the diabetes+exercise group delayed the rise of blood sugar in type 1 diabetes mice (P < 0.05) and showed a significant reduction in serum follicle-stimulating hormone, luteinizing hormone, liver superoxide dismutase, malondialdehyde, brain tumor necrosis factor α, interleukin-6 and interleukin-1β levels (P < 0.01), while serum estradiol, progesterone, estrogen, and liver glutathione peroxidase protein levels were significantly increased (P < 0.01, P < 0.05). Compared with male type 1 diabetes mice, female type 1 diabetes mice had significantly higher estradiol levels and lower luteinizing hormone levels (P < 0.05). Compared with the male diabetes+exercise group, the female diabetes+exercise group had lower liver glutathione peroxidase levels (P < 0.05). Compared with type 1 diabetes mice, the escape latency of exercise training mice was shorter (P < 0.01). In male mice, exercises significantly increased the time and platform crossing times of type 1 diabetes mice in the target quadrant (P < 0.01 or P < 0.05), while in female mice, exercises significantly increased the time of type 1 diabetes mice in the target quadrant (P < 0.05). Correlation analysis results showed that the levels of follicle-stimulating hormone, luteinizing hormone, progesterone, superoxide dismutase, malondialdehyde, tumor necrosis factor α, and interleukin-6 were positively correlated with the level of interleukin-1β (P < 0.05 or P < 0.01), whereas the levels of estradiol and progesterone were negatively correlated with the levels of superoxide dismutase, malondialdehyde, tumor necrosis factor α, interleukin-6 and interleukin-1β (P < 0.05 or P < 0.01). Overall, there are sex differences in the effects of treadmill exercise on metabolic indicators and chronic neuroinflammatory regulation in diabetes mice. Sex hormones are an important variable of treadmill exercise in the metabolic, inflammatory and cognitive responses in diabetes mice. [ABSTRACT FROM AUTHOR]

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]

The one of the most commonly used reference system for clinical gait analysis is an optical motion capture system (OMC) using a multi-segment foot model. A time- and cost-efficient alternative could be an inertial measurement unit (IMU)-based systems. However, these are limited to a single segment approach for the foot and ankle. Therefore, the current setup was modified to be based on a 2-segment foot model, allowing for a separate analysis of the hind- and midfoot. The study aimed to evaluate the reliability (inter-rater, intra-rater, and test-retest reliability) of an IMU-based 2-segment foot model. Twelve healthy subjects were recruited to test the inter-rater, intra-rater, and test-retest reliability of the new IMU based 2-segment foot model. Gait analysis was performed on a treadmill at a constant speed of 4 km/h. Kinematic data of the tibia/hindfoot, tibia/forefoot and hindfoot/forefoot over 100 % gait cycle were analyzed. The reliability was tested by using statistical parametric mapping (SPM) and the intraclass correlation coefficient (ICC). The SPM showed no significant difference for inter-, intra-rater, and test-retest reliability, but for a small segment of tibia/forefoot dorsiflexion test-retest reliability (2.1° difference). The single standard deviation measurement error for the sagittal and transverse plane was <5° and worse for the frontal plane. The new 2-segment foot model revealed a high inter-rater, intra-rater, and test-retest reliability. It is suitable for use in adult clinical practice. Still, comparative data to the OMC system using a multi-segment foot model are missing. • Assessing the reliability of an IMU-based 2-segment foot model as an extension of the traditionally used 1-segment models. • Resulting kinematic curves for the foot and ankle were tested for differences using statistical parametric mapping. • The 2-segment foot model showed good inter-, intra- and test-retest reliability with no clinical relevant differences. • Gait analysis with IMUs provide a cost and time effective alternative to optical motion capture. [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]

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]

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]

Objective: To explore the effect of 8-week treadmill exercise on myocardial fibrosis in mice with T2DM and its molecular mechanism. Method: Eight m/m mice were used as the control group, and 32 db/db mice were randomly divided into control group, model group, exercise intervention group, inhibitor alone group and exercise combined with inhibitor intervention group. Fasting blood glucose was monitored weekly. After 8 weeks, triglycerides (TG) and total cholesterol (TC) were measured. Masson staining was used to observe the degree of myocardial fibrosis, and immunofluorescence staining was used to observe the expression of Collagen Ⅰ and α-SMA. Western Blot was used to detect the expression levels of fibrosis, inflammation, pyroptosis and p38MAPK related proteins. Result: The model group showed a significant increase in fasting blood glucose, TG and TC (P<0.0001), Collagen Ⅲ (P<0.05) and TGF- β1 (P<0.01) expression compared with control group. Compared to the model group, Masson staining in the other groups showed a significant improvement in disordered myocardial cell arrangement and a decrease in blue collagen fibers between the interstitial tissue and perivascular tissue；immunofluorescence staining also showed that the expression levels of Collagen I and α-SMA and the expression levels of fibrosis-related proteins were significantly decreased in these groups. The expression levels of inflammation and pyroptosis related proteins in the exercise intervention group were significantly lower than those in the model group. Compared to the model group, the phosphorylation level of p38MAPK in the exercise intervention group and the simple inhibitor group was significantly decreased (P<0.05, P<0.01), but the phosphorylation level was not further decreased after the combined intervention. Compared to the model group, the expression levels of NLRP3 and GSDMD-N in the single inhibitor group were significantly decreased (P<0.05), and the combined intervention further inhibited the expression of Caspase- 1 (P<0.05), Cleaved-Caspase- 1 (P< 0.05), and GSDMD-N (P<0.001). Conclusion: Eight- week treadmill exercise can significantly improve myocardial fibrosis in db/db mice. The mechanism may reduce the phosphorylation of p38MAPK and pyroptosis of cardiomyocytes, thus improving myocardial fibrosis in db/db mice. The combination of treadmill exercise and SB203580 can further reduce pyroptosis. [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]

Validation of a Wrist-Worn Optical Heart Rate Monitor During Maximal Treadmill Exercise Testing. JEPonline 2024;27(5): 50-56. Heart rate (HR) watches using photoplethysmography (PPG) are a popular, portable, and practical alternative to electrocardiogram (ECG) for HR monitoring. The purpose of this study was to determine validity for a PPM watch for measuring HR during incremental treadmill exercise using ECG as the criterion. Twenty-two subjects (13 men, 9 women; 35.8 ± 6.3 yr) performed a Bruce treadmill protocol exercise test. HR was recorded at rest and each minute with the Mio Alpha PPM and ECG simultaneously. HR was compared between methods using paired-samples t-tests. Validity coefficients were determined using Pearson correlations. HR had a significant correlation between methods overall (r = 0.97). Significant correlations were observed for rest and each stage (r values from 0.67 to 0.96). HR was significantly different between methods for rest (ECG = 66 ± 13 b·min-1, Mio = 68 ± 16 b·min-1), stage 3 (ECG = 144 ± 13 b·min-1, Mio = 143 ± 13 b·min-1), stage 4 (ECG = 168 ± 13 b·min-1, Mio = 164 ± 14 b·min-1), and stage 5 (ECG = 178 ± 12 b·min-1, Mio = 173 ± 18 b·min-1). There was a strong agreement between the HR methods and mean differences did not exceed 3 b·min-1 except for stage 5. Therefore, a PPM watch may provide accurate HR monitoring at most exercise intensities. [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]

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]

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.)

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]

Spinal cord injury necessitates effective rehabilitation strategies, with exercise therapies showing promise in promoting recovery. This study investigated the impact of rehabilitation exercise on functional recovery and morphological changes following thoracic contusive spinal cord injury. After a 7-day recovery period after spinal cord injury, mice were assigned to either a trained group (10 weeks of voluntary running wheel or forced treadmill exercise) or an untrained group. Bi-weekly assessments revealed that the exercise-trained group, particularly the voluntary wheel exercise subgroup, displayed significantly improved locomotor recovery, more plasticity of dopaminergic and serotonin modulation compared with the untrained group. Additionally, exercise interventions led to gait pattern restoration and enhanced transcranial magnetic motor-evoked potentials. Despite consistent injury areas across groups, exercise training promoted terminal innervation of descending axons. In summary, voluntary wheel exercise shows promise for enhancing outcomes after thoracic contusive spinal cord injury, emphasizing the role of exercise modality in promoting recovery and morphological changes in spinal cord injuries. Our findings will influence future strategies for rehabilitation exercises, restoring functional movement after spinal cord injury.

BACKGROUND: Chronic myofascial trigger points can identify differential metabolite changes through non targeted metabolomics techniques, helping to understand and further explore the pathophysiological processes and pathogenesis of chronic myofascial trigger points from the perspective of endogenous small molecule metabolites. OBJECTIVE: To investigate potential biomarkers and related metabolic pathways based on urine metabolomics in the rat model of chronic myofascial trigger points. METHODS: Sixteen Sprague-Dawley rats were randomly divided into a model group and a normal group. The model group was used to establish a chronic myofascial trigger point animal model by combining blunt hitting with centrifugal exercise (treadmill slope: -16°, running speed: 16 m/min, training time: 90 minutes each), once a week for 8 continuous weeks, with 4 weeks off. After 12 weeks of modeling, the metabolic cage method was used to collect urine from rats at 24 hours after modeling. Liquid chromatography-mass spectrometry non-targeted metabolomics technology was used to detect metabolic profiles in the urine samples, screen common differential metabolites, and conduct bioinformatics analysis. RESULTS AND CONCLUSION: Compared with the normal group, there were 32 differential metabolic markers in the model group, of which 21 were upregulated and 11 were downregulated. A total of 14 differential metabolites were identified as potential biomarkers based on the value of variable important in projection greater than 3. The enrichment analysis of the Kyoto Encyclopedia of Genes and Genomes indicated that the formation of chronic myofascial trigger points is closely related to metabolic pathways such as primary bile acid biosynthesis and arachidonic acid metabolism. [ABSTRACT FROM AUTHOR]

BACKGROUND: Stem cell transplantation is a novel therapy for myocardial infarction, but the extremely hostile microenvironment in the infarct area results in low survival rate of stem cells and little long-term effect. Exercise preconditioning is a way to induce endogenous protective effects through exercise, which can be used as a new strategy for prevention and treatment of cardiac rehabilitation. OBJECTIVE: To evaluate whether exercise preconditioning potentiates the cardioprotective effects of adipose-derived stem cell transplantation following myocardial infarction in rats and to explore the mechanism of angiogenesis. METHODS: Six-week-old male SD rats were randomly divided into control group, modeling group, stem cell group, and stem cell plus exercise group. Acute myocardial infarction model was made by coronary artery occlusion, and sham operation was performed in control group. The stem cell plus exercise group underwent aerobic exercise for 8 weeks before modeling, and adipose-derived stem cell transplantation was performed 30 minutes after modeling. The stem cell group performed only adipose-derived stem cell transplantation. One and seven days after stem cell transplantation, the expression levels of myocardial total Akt (t-Akt), phosphorylated Akt (p-Akt), vascular endothelial growth factor (VEGF), total endothelial nitric oxide synthase (t-eNOS), and phosphorylated endothelial nitric oxide synthase (p-eNOS) protein were measured by western blotting, and the ratios of p-Akt/t-Akt and p-eNOS/t-eNOS were calculated. At 4 weeks after stem cell transplantation, the heart structure and function as well as myocardial blood flow were detected by color Doppler ultrasound diagnostic system. Myocardial infarction area was measured by TTC staining. Myocardial interstitial collagen deposition was examined by Masson staining. Myocardial capillary density was detected by immunofluorescence staining, and myocardial apoptosis was measured by TUNEL staining. RESULTS AND CONCLUSION: Four weeks after stem cell transplantation: Compared with control group, left ventricular shortening fraction, left ventricular ejection fraction, myocardial capillary density, and myocardial blood flow decreased (P < 0.05), myocardial infarction area, collagen volume fraction, and apoptosis increased (P < 0.05) in the modeling group. Compared with the modeling group, the above indexes (except for left ventricular fractional shortening and left ventricular ejection fraction) in the stem cell group improved (P < 0.05). Compared with the stem cell group, the above parameters were further improved in the stem cell plus exercise group (P < 0.05). One day after stem cell transplantation: Compared with the control group, the protein expression of t-Akt, p-Akt, VEGF, t-eNOS, p-eNOS and the ratio of p-Akt/t-Akt and p-eNOS/t-eNOS had no significant changes in the modeling group (P > 0.05). Compared with the modeling group, there were no significant changes in the above indexes in the stem cell group (P > 0.05), and p-Akt protein expression and the ratio of p-Akt/t-Akt were up-regulated in the stem cell plus exercise group (P < 0.05). Seven days after stem cell transplantation: Compared with the control group, the protein expression of p-Akt, VEGF, p-eNOS and the ratio of p-Akt/t-Akt and p-eNOS/t-eNOS were decreased in the modeling group (P < 0.05). Compared with the modeling group, there were no significant changes in all parameters in the stem cell group (P > 0.05), and the protein expression of p-Akt, VEGF p-eNOS and the ratio of p-Akt/t-Akt and p-eNOS/t-eNOS were increased in the stem cell plus exercise group (P < 0.05). These findings confirm that exercise preconditioning can potentiate the therapeutic effect of adipose-derived stem cells on cardiac remodeling in rats with myocardial infarction, and its mechanism is associated with the promotion of myocardial angiogenesis and blood perfusion. [ABSTRACT FROM AUTHOR]

Abstract Alzheimer's disease (AD) is a neurological condition that is connected with a decline in a person's memory as well as their cognitive ability. One of the key topics of AD research has been the exploration of metabolic causes. We investigated the effects of treadmill exercise and intranasal insulin on learning and memory impairment and the expression of IGF1, BDNF, and GLUT4 in hypothalamus. The animals were put into 9 groups at random. In this study, we examined the impact of insulin on spatial memory in male Wistar rats and analyzed the effects of a 4-week pretreatment of moderate treadmill exercise and insulin on the mechanisms of improved hypothalamic glucose metabolism through changes in gene and protein expression of IGF1, BDNF, and GLUT4. We discovered that rat given Aβ25–35 had impaired spatial learning and memory, which was accompanied by higher levels of Aβ plaque burden in the hippocampus and lower levels of IGF1, BDNF, and GLUT4 mRNA and protein expression in the hypothalamus. Additionally, the administration of exercise training and intranasal insulin results in the enhancement of spatial learning and memory impairments, the reduction of plaque burden in the hippocampus, and the enhancement of the expression of IGF1, BDNF, and GLUT4 in the hypothalamus of rats that were treated with Aβ25–35. Our results show that the improvement of learning and spatial memory due to the improvement of metabolism and upregulation of the IGF1, BDNF, and GLUT4 pathways can be affected by pretreatment exercise and intranasal insulin.

Background The response of heart rate to changes in exercise intensity is comprised of several dynamic modes with differing magnitudes and temporal characteristics. Investigations of empirical identification of dynamic models of heart rate showed that second-order models gave substantially and significantly better model fidelity compared to the first order case. In the present work, we aimed to reanalyse data from previous studies to more closely consider the effect of including a zero and a pure delay in the model. Methods This is a retrospective analysis of 22 treadmill (TM) and 54 cycle ergometer (CE) data sets from a total of 38 healthy participants. A linear, time-invariant plant model structure with up to two poles, a zero and a dead time is considered. Empirical estimation of the free parameters was performed using least-squares optimisation. The primary outcome measure is model fit, which is a normalised root-mean-square model error. Results A model comprising parallel connection of two first-order transfer functions, one with a dead time and one without, was found to give the highest fit (56.7 % for TM, 54.3 % for CE), whereby the non-delayed component appeared to merely capture initial transients in the data and the part with dead time likely represented the true dynamic response of heart rate to the excitation. In comparison, a simple first-order model without dead time gave substantially lower fit than the parallel model (50.2 % for TM, 47.9 % for CE). Conclusions This preliminary analysis points to a linear first-order system with dead time as being an appropriate model for heart rate response to exercise using treadmill and cycle ergometer modalities. In order to avoid biased estimates, it is vitally important that, prior to parameter estimation and validation, careful attention is paid to data preprocessing in order to eliminate transients and trends.

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]

• Moderate-intensity exercise did not prevent significant body weight gain in mice. • Female mice experienced enhanced dopamine signaling with aerobic exercise. • Male high-fat fed mice did not show enhanced endpoints with aerobic exercise. Obesity continues to rise in prevalence and financial burden despite strong evidence linking it to an increased risk of developing several chronic diseases. Dopamine response and receptor density are shown to decrease under conditions of obesity. However, it is unclear if this could be a potential mechanism for treatment without drugs that have a potential for abuse. Therefore, the aim of this study was to investigate whether moderate-intensity exercise could reduce body weight gain and the associated decreases in dopamine signaling observed with high-fat diet-induced adiposity. We hypothesized that exercise would attenuate body weight gain and diet-induced inflammation in high-fat (HF)-fed mice, resulting in dopamine signaling (release and reuptake rate) comparable to sedentary, low-fat (LF)-fed counterparts. This hypothesis was tested using a mouse model of diet-induced obesity (DIO) and fast-scan cyclic voltammetry to measure evoked dopamine release and reuptake rates. Although the exercise protocol employed in this study was not sufficient to prevent significant body weight gain, there was an enhancement of dopamine signaling observed in female mice fed a HF diet that underwent treadmill running. Additionally, aerobic treadmill exercise enhanced the sensitivity to amphetamine (AMPH) in this same group of exercised, HF-fed females. The estrous cycle might influence the ability of exercise to enhance dopamine signaling in females, an effect not observed in male groups. Further research into females by estrous cycle phase, in addition to determining the optimal intensity and duration of aerobic exercise, are logical next steps. [ABSTRACT FROM AUTHOR]

Background: Post-stroke depression (PSD) is a common complication, occurring in approximately one-third of these patients. The neurological symptoms of PSD affect patients' daily life and subsequent recovery. Analyzing the pathogenesis of post-stroke depression from a psychological perspective, it was found that PSD patients often feel despair and anxiety, and it is crucial to explore nonpharmacological ways to improve post-stroke depressive symptoms. A combination of exercise and rich environmental stimulation (RES) has been found effective in improving post-stroke depressive symptoms. Therefore, this study aimed to explore the effects of exercise and rich environmental stimulation on PSD in rats and their potential underlying mechanisms and to provide a theoretical basis for managing PSD. Methods: The PSD rat model was constructed, and the depression-like behaviors of rats in each group were evaluated using the open field test (OFT), sucrose preference test (SPT), and forced swimming test (FST). Moreover, changes in the morphological behavior of rat hippocampus were observed using hematoxylin-eosin (HE) staining and Nissl staining. The expression levels of 5-hydroxytryptamine (5-HT) and norepinephrine (NE) in hippocampus tissues were assessed using enzyme linked immunosorbent assay (ELISA), and the levels of tryptophan-related proteins were determined employing western blot analysis. Additionally, a kynurenine-3-monooxygenase (KMO) inhibitor was administered to the combined stimulation group, and the levels of tryptophan (TRP), 5-HT, kynurenine (KYN), 3-hydroxy-kynurenine (3-HK), and quinolinic acid (QA) were evaluated using liquid chromatography mass spectrometry/mass spectrometry (LC-MS/MS). Results: Treadmill exercise combined with rich environmental stimulation significantly reduced the immobility time in the FST (p < 0.01), increased the exploratory behavior in the OFT (p < 0.05), and increased the sucrose water consumption in the SPT (p < 0.01), indicating that the depression-like behavior was improved. Treadmill exercise combined with rich environmental stimulation also improved the shape of the damaged hippocampus and increased the number of neurons in the hippocampus. Additionally, treadmill exercise combined with rich environmental stimulation significantly increased the levels of 5-HT and NE in hippocampus tissues (p < 0.01) and decreased KMO protein level (p < 0.01). In the KMO inhibitor group, the neural function was efficiently restored, the levels of 3-HK, QA, and KMO in the hippocampus were substantially reduced (p < 0.01), and the expression level of 5-HT was increased (p < 0.01). Conclusions: Exercise stimulation combined with enriched environmental stimuli alleviates post-stroke depression in rats, and the underlying mechanisms may be related to TRP/KYN/3-HK/QA excitotoxicity pathways and increased 5-hydroxytryptamine levels. [ABSTRACT FROM AUTHOR]

This study was designed to evaluate the effect of using maximal cadence criteria cut points established during overground and treadmill walking, on intensity outputs measured during community ambulation. The second aim was to establish the relationship between cardiovascular fitness (predicted VO 2 max capacity) and community ambulation intensity performance, in typically developing individuals. What is the effect on intensity measures when using cadence cut point criteria derived from overground and treadmill walking and does predicted VO 2 max correlate with exercise related community activity in a typically developing population? A group of 37 typically developing participants between 8 and 27 years of age, underwent a graded submaximal VO 2 testing protocol followed by a typical week of community ambulation, recorded with a step activity monitor. Maximum cadence criteria established during overground and treadmill walking were applied and the data were compared. The weekly step activity variables included: total steps, total ambulatory time, intensity, duration, and volume. Predicted VO 2 Max was calculated, and correlations calculated to step activity outputs. Results showed significant differences (p<0.001) between cadence cut point criteria across all intensity measures except in the amount of time spent in the 30–60 % intensity category (p=0.182). Predicted VO 2 max did not significantly correlate with step activity outputs related to exercise (moderate+ intensity and long duration ambulatory bouts; p>0.277). This study illustrates the importance of close consideration in applying recommended cut off criteria when assessing intensity outputs from step activity data. Cadence from both overground and treadmill walking were collected in a controlled lab setting, but the influence of the treadmill mechanical and forced cadence criteria must be considered when selecting intensity cut points. • Step intensity is affected when using treadmill and overground max cadence criteria. • Maximum cadence determined in a lab setting may not correlate to community walking. • Exercise related community ambulation data do not correlate to predicted VO 2 max. [ABSTRACT FROM AUTHOR]

Impairments in unilateral ankle propulsion may result from restriction by an external device or pathology such as lower limb amputation. Models of gait suggest this reduction may lead to increased collisional force on the contralateral side, potentially increasing force through the knee and increasing the risk of knee pain or osteoarthritis. How do restrictions in unilateral ankle propulsive force affect contralateral knee joint loading in otherwise healthy individuals? 18 individuals without impairment walked on a treadmill at 1.5 m/s for two conditions: one free of restrictions, and one where a randomized limb's ankle propulsive force was restricted using an off-the-shelf ankle-foot orthosis (AFO). Ankle propulsive power, lower extremity joint work, and ground reaction force variables were calculated for the final 3 gait cycles of each condition. Tibiofemoral joint contact force (TJCF) for the limb contralateral to the AFO was calculated through a standard OpenSim workflow utilizing the gait2392 model. Intra-limb pair-wise comparisons were made between conditions. Compared to walking unrestricted, the limb wearing the AFO demonstrated a significant reduction in peak ankle propulsive power and positive ankle work by approximately 50 % each (p<0.01). With ankle restriction, the ipsilateral knee significantly increased positive work (p<0.01). The overall propulsion produced by that limb did not change between conditions, demonstrated by a lack of change in anterior ground reaction force impulse (p=0.11). The knee of the limb contralateral to the AFO did not display differences in any TJCF variable between conditions (all p>0.07). These results suggest a unilateral deficit in ankle propulsion will not increase contralateral knee joint forces in individuals who are able to use other joints of the limb to compensate for the loss of ankle function. However, further research should investigate this relationship in those who display pathologies that may prevent more proximal compensations. • Unilateral ankle propulsion may be restricted by an external device or pathology. • Reduced ankle propulsion theoretically linked to increased contralateral knee loads. • Healthy individuals compensate proximally for lack of ankle propulsion. • Proximal compensations may prevent contralateral knee load increase. • Relationship may differ for those with pathology preventing proximal compensation. [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]

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]

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]

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]

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]

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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]

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]

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]

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]

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]

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]

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]

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]

In this study, we developed an exercise training protocol for assessing both blood pressure dynamics and mRNA expression levels of purine receptors in various vascular tissues during physical activity. The objective is to assess the impact of exercise training on blood pressure regulation in spontaneously hypertensive rats (SHR) and purine receptors in vascular tissues.Wistar Kyoto (WKY) and SHR rats were randomly allocated into sedentary (Sed) and exercise training (ExT) groups. Rats in the Sed groups were allowed unrestricted movement, whereas those in the ExT groups underwent a 16-week regimen of low- to moderate-intensity treadmill exercise. Throughout the intervention period, blood pressure measurements and body weight recordings were conducted. Additionally, mRNA expressions of purine receptors P2X1, P2Y1, and P2Y2 in renal artery (RA), internal carotid artery (Int), thoracic aorta (Aor), and caudal artery (Cau) tissues were assessed.In the Sed group, body weight of SHR rats was observed to be lower compared to the three other groups. Over the course of the exercise regimen, blood pressure in the ExT group of SHR rats reduced gradually, converging towards levels similar to those observed in WKY rats by the conclusion of the exercise period. Regarding mRNA expression patterns of P2X1 receptors across the four blood vessels, WKY and SHR rats demonstrated similar sequences, consistently displaying the highest expression levels in the Cau. Conversely, mRNA expressions of P2Y1 and P2Y2 receptors exhibited distinct sequences across the four blood vessels in both WKY and SHR rats. Notably, compared to the Sed group of WKY rats, mRNA expression of P2X1 receptor in the Int of SHR rats revealed an increase, while expressions in the Aor of WKY rats and the Cau of SHR rats decreased following exercise. Expression of P2Y1 receptor mRNA decreased across all four types of blood vessels in SHR rats. Post-exercise, P2Y1 receptor mRNA expression increased in the Aor, decreased in the Cau of WKY rats, and increased in the Int and renal artery (RA) of SHR rats. Conversely, expressions of P2Y2 receptor mRNA decreased in the Int and Aor of SHR rats. Except for the Aor of WKY rats, expressions of P2Y2 receptor mRNA increased in the other arteries of both rat types following exercise.Differences in the distribution of purine receptor subtypes among distinct arterial segments in both WKY and SHR rats were observed. Exercise training was found to enhance mRNA expression levels of P2Y receptors in these rat models. This finding implies that exercise training might reduce hypertension in SHR rats by bolstering the purinergic relaxation response. [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]

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]

BACKGROUND: Exercise is an effective method for preventing and treating osteoporosis, but it is unclear whether its effect on postmenopausal osteoporosis is related to changes in bone autophagy levels. OBJECTIVE: To observe the effects of exercise via cellular autophagy on the morphology and mechanical properties of bone tissue in ovariectomized rats, and to explore the mechanism of exercise on bone mass in ovariectomized rats from the perspective of autophagy. METHODS: A rat model of postmenopausal osteoporosis was established, and a 24-week moderate-intensity exercise was used for intervention. After the experiment, serum estradiol levels were measured by ELISA, and bone mineral density and bone microstructure of the cortical and trabecular bone were detected by micro-CT. The biomechanical indicators of the tibia were tested by a three-point bending test. Autophagosomes were observed by transmission electron microscopy. The expression of LC3 and ATG7 proteins was analyzed by western blot. RESULTS AND CONCLUSION: The serum estradiol level in the ovariectomized group was significantly lower than that of the sham-operation group and ovariectomized+exercise group (P < 0.01). The body mass of rats in each group increased, and the order was the ovariectomized group > the ovariectomized+exercise group > the sham-operation group > the sham-operation+exercise group. The bone mineral density and bone mass of rats in all groups significantly increased (P < 0.01), but the increase in the ovariectomized group was significantly lower than that of the other groups, and the increase in the ovariectomized+exercise group was significantly higher than that of the ovariectomized group. Compared with the sham-operation group, the bone mineral density of the tibial cancellous bone in the sham-operation+exercise group was significantly increased (P < 0.01), while the bone mineral density in the ovariectomized and ovariectomized+exercise groups was significantly decreased (P < 0.01). Compared with the ovariectomized+exercise group, the ovariectomized group showed significantly lower bone volume fraction, number of trabeculae, and bone mineral density of cancellous bone (P < 0.05), extremely significantly lower trabecular thickness (P < 0.01), and significantly higher mean trabecular pattern factor, trabecular separation, and structural model index (P < 0.01). Compared with the ovariectomized group, the LC3-II/LC3-I ratio and the relative expression of ATG7 protein significantly increased in the ovariectomized+exercise group (P < 0.05). Compared with the sham-operation and ovariectomized groups, the number of autophagosomes increased in the sham-operation+exercise and ovariectomized+exercise groups, respectively. To conclude, moderate-intensity treadmill exercise can improve the bone microstructure and biomechanical properties of the tibial cancellous bone and increase bone mass in ovariectomized rats by increasing serum estradiol levels and bone autophagy levels. [ABSTRACT FROM AUTHOR]

Exploring the independent effect of mechanical discharge in response to weight loss (WL) seems necessary but remains highly challenging from a methodological point. Anti-gravity treadmills could be relevant to simulate a mechanical WL by body weight support (BWS), but their reliability remains unclear to properly explore exercise energy metabolism, especially at low degrees of alleviations. The study aimed to evaluate the accuracy and reproducibility of an anti-gravity treadmill to generate BWS, and the reproducibility of cardiometabolic responses to an exercise performed at low degrees of BWS on this device. Observed BWS of 18 normal-weight males was obtained twice at seven degrees of target BWS (i.e., 0, 3, 6, 9, 12, 15, 18%) using a digital scale inside the anti-gravity treadmill, and was compared to the expected BWS. Then, 15 of them performed 5-min bout of low-intensity walking exercise at these degrees of BWS in a randomized order, separated by 4-min rest. The exercise was identically repeated on three occasions separated by a minimum of 3 days. Energy metabolism and heart rate (HR) were measured throughout the exercise by indirect calorimetry and a HR monitor, respectively. The observed BWS were significantly different from the expected BWS (p< 0.001), and there was a high inter- and intra-individual variability in BWS generated by the anti-gravity treadmill. Results showed an overall good reliability of VO2 (intraclass correlation coefficients (ICC) values ranging from 0.67 to 0.85) and HR (ICC > 0.8) in response to exercise. An effect of the degree of BWS was observed for VO2 (p< 0.001), illustrating reduced values at 15% and 18% of BWS compared to 0, 3, and 6%. Such device might not be adapted to simulate low degrees of WL in normal-weight males, particularly when it comes to the exploration of energy metabolism. [ABSTRACT FROM AUTHOR]

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]