A single 1,500 m freestyle at maximal speed decreases cognitive function in athletes.

Introduction: Physical exercise can improve cognitive function, and the degree of impact on cognitive function is related to exercise modality, intensity, and duration. However, few studies have been conducted on the effects of competitive sports on cognitive function. The 1,500 m freestyle is the longest pool-based swimming event in the Olympic Games. This study explores the effects of 1,500 m freestyle at maximal speed on athletes' cognitive function and analyzes the potential mechanism of cognitive function reduction in freestyle at maximal speed from the perspective of hemoglobin oxygenation difference (Hbdiff). Methods: A total of 13 male university swimmers were required to take part in a 1,500 m freestyle competition, swimming at maximal speed. The relevant indicators, including cognitive function and freestyle at maximal speed, before and after the competition were tested and analyzed. Cognitive function was assessed using the Schulte grid test (SGT), the trail-making test (TMT), and the digit span test (DST). The neurobiological characteristics of cognitive function, such as the prefrontal cortex (PFC), response time (RT), and accuracy rate (ACC), were tested using functional near-infrared spectroscopy (fNIRS). Results: A significant decrease in scores for SGT, TMT, and digit span test-backward (DST-B) (p < 0.01). Oxygenated hemoglobin (Oxy-Hb) concentrations in the right frontopolar area (R-FPA) of brain channels 8 (p < 0.01) and 9 (CH8, 9) (p < 0.05), the right dorsolateral prefrontal cortex (R-DLPFC) CH10 (p < 0.05), and the middle dorsolateral prefrontal cortex (M-DLPFC) CH18 (p < 0.01) were significantly altered, and the right area of the brain was activated. The total Oxy-Hb concentrations in the regions of interest (ROIs) of R-FPA, R-DLFPC, and M-DLFPC were changed significantly (p < 0.01). Discussion: The exhaustive performance of a 1,500 m freestyle event resulted in both physical fatigue and a decline in cognitive function. This decline may be attributed to the activation of specific regions of interest, namely the FPA, DLPFC, and M-DLPFC, within the prefrontal cortex (PFC), as well as alterations in functional connectivity.

Konjac Glucomannan Counteracted the Side Effects of Excessive Exercise on Gut Microbiome, Endurance, and Strength in an Overtraining Mice Model.

Excessive exercise without adequate rest can lead to overtraining syndrome, which manifests a series of side effects, including fatigue, gut dysbiosis, and decremental sports performance. Konjac glucomannan (KGM) is a plant polysaccharide with numerous health-improving effects, but few studies reported its effects on the gut microbiome, endurance, and strength in an overtraining model. This study assessed the effect of KGM on gut microbiome, endurance, and strength in mice with excessive exercise. Three doses of KGM (1.25, 2.50, and 5.00 mg/mL) were administrated in drinking water to mice during 42 days of a treadmill overtraining program. The results showed that excessive exercise induced a significant microbial shift compared with the control group, while a high dose (5.00 mg/mL) of KGM maintained the microbial composition. The proportion of Sutterella in feces was significantly increased in the excessive exercise group, while the moderate dose (2.50 mg/mL) of KGM dramatically increased the relative abundance of Lactobacillus and SCFA production in feces. Additionally, the moderate dose and high dose of KGM counteracted the negative effects of excessive exercise on strength or/and endurance (43.14% and 39.94% increase through a moderate dose of KGM, Bonferroni corrected p < 0.05, compared with the excessive exercise group). Therefore, it suggests that KGM could prevent overtraining and improve sports performance in animal models.

Exercise improves subchondral bone microenvironment through regulating bone-cartilage crosstalk.

Articular cartilage degeneration has been proved to cause a variety of joint diseases, among which osteoarthritis is the most typical. Osteoarthritis is characterized by articular cartilage degeneration and persistent pain, which affects the quality of life of patients as well as brings a heavy burden to society. The occurrence and development of osteoarthritis is related to the disorder of the subchondral bone microenvironment. Appropriate exercise can improve the subchondral bone microenvironment, thus playing an essential role in preventing and treating osteoarthritis. However, the exact mechanism whereby exercise improves the subchondral bone microenvironment remains unclear. There is biomechanical interaction as well as biochemical crosstalk between bone and cartilage. And the crosstalk between bone and cartilage is the key to bone-cartilage homeostasis maintenance. From the perspective of biomechanical and biochemical crosstalk between bone and cartilage, this paper reviews the effects of exercise-mediated bone-cartilage crosstalk on the subchondral bone microenvironment, aiming to provide a theoretical basis for the prevention and treatment of degenerative bone diseases.

[Exercise regulates bone metabolism via microRNAs].

It has been well documented that exercise can improve bone metabolism, promote bone growth and development, and alleviate bone loss. MicroRNAs (miRNAs) are widely involved in the proliferation and differentiation of bone marrow mesenchymal stem cells, osteoblasts, osteoclasts and other bone tissue cells, and regulation of balance between bone formation and bone resorption by targeting osteogenic factors or bone resorption factors. Thus miRNAs play an important role in the regulation of bone metabolism. Recently, regulation of miRNAs are shown to be one of the ways by which exercise or mechanical stress promotes the positive balance of bone metabolism. Exercise induces changes of miRNAs expression in bone tissue and regulates the expression of related osteogenic factors or bone resorption factors, to further strengthen the osteogenic effect of exercise. This review summarizes relevant studies on the mechanism whereby exercise regulates bone metabolism via miRNAs, providing a theoretical basis for osteoporosis prevention and treatment with exercise.

Effect of Cold Exposure and Exercise on Insulin Sensitivity and Serum Free Fatty Acids in Obese Rats.

PURPOSE: This study aimed to explore the effect of exercise and cold exposure on insulin sensitivity and the level of serum free fatty acids (FFA) in diet-induced obese rats. METHODS: Sixty-four diet-induced obese rats were randomly assigned to eight groups: room temperature-sedentary, room temperature-exercise, acute cold exposure-sedentary, acute cold exposure-exercise, intermittent cold exposure-sedentary, intermittent cold exposure-exercise, sustained cold exposure-sedentary, and sustained cold exposure-exercise. After the interventions, the homeostatic model assessment for insulin resistance (HOMA-IR) values, the level of serum FFA, subcutaneous fat ratio (SFR) and visceral fat ratio, enzyme activities of adipose triglyceride lipase, and lipoprotein lipase (LPL) in inguinal adipose tissue, and protein expression of PGC1-α and p38 MAPK in skeletal muscle were investigated. RESULTS: We found that exercise ( P = 0.0136) and cold exposure ( P < 0.0001) reduced HOMA-IR values independently. Exercise reduced serum FFA ( P = 0.0041), whereas cold exposure did not affect them. Moreover, the HOMA-IR values were positively correlated with the serum FFA levels ( r = 0.32, P = 0.01). SFR or visceral fat ratio was coordinately reduced by the interaction (for SFR, P = 0.0015) or opposing main effects between or of cold exposure and exercise, supporting the reduction of serum FFA. However, cold exposure or exercise increased the activity of adipose triglyceride lipase and LPL independently or interactively (for LPL, P = 0.0143), suggesting an increase in serum FFA. Finally, cold exposure and exercise enhanced protein expression of PGC1-α and p38 MAPK independently or interactively (for p38 MAPK, P = 0.0226), suggesting increased uptake and oxidation of serum FFA in muscle. CONCLUSIONS: These results suggest that the combination of exercise and cold exposure may result in more serum FFA utilization than production and thus lead to reduced serum FFA and increased insulin sensitivity.

Advances in the Study of Exosomes as Drug Delivery Systems for Bone-Related Diseases.

Bone-related diseases are major problems and heavy burdens faced by modern society. Current clinical approaches for the treatment of these pathological conditions often lead to complications and have limited therapeutic efficacy. In this context, the development of nanotherapeutic platforms, such as extracellular vesicles, can improve the relevant therapeutic effects. In particular, exosomes are nano-sized, lipid bilayer extracellular vesicles secreted by many cells in mammals. Due to their innate capacity to transport materials-including proteins, lipids, and genes-among cells, as well as their innate attraction to target cells, they are considered to be a crucial medium for cell communication and are involved in a number of biological processes. Exosomes have been used as drug delivery vehicles in recent bone tissue engineering studies, in order to regulate bone homeostasis. However, the precise workings of the exosome regulatory network in maintaining bone homeostasis and its potential for treating bone injury remain unclear. To provide a fresh perspective for the study of exosomes in drug delivery and bone-related diseases, in this paper, we review recent studies on the roles of exosomes for drug delivery in bone homeostasis and bone-related diseases, as well as the composition and characteristics of exosomes and their regulatory roles in bone homeostasis and bone-related diseases, aiming to provide new ideas for the therapeutic application of exosomes in the treatment of bone-related diseases.

The Effect of Sleep Restriction, With or Without Exercise, on Skeletal Muscle Transcriptomic Profiles in Healthy Young Males.

Background: Inadequate sleep is associated with many detrimental health effects, including increased risk of developing insulin resistance and type 2 diabetes. These effects have been associated with changes to the skeletal muscle transcriptome, although this has not been characterised in response to a period of sleep restriction. Exercise induces a beneficial transcriptional response within skeletal muscle that may counteract some of the negative effects associated with sleep restriction. We hypothesised that sleep restriction would down-regulate transcriptional pathways associated with glucose metabolism, but that performing exercise would mitigate these effects. Methods: 20 healthy young males were allocated to one of three experimental groups: a Normal Sleep (NS) group (8 h time in bed per night (TIB), for five nights (11 pm - 7 am)), a Sleep Restriction (SR) group (4 h TIB, for five nights (3 am - 7 am)), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB, for five nights (3 am - 7 am) and three high-intensity interval exercise (HIIE) sessions (performed at 10 am)). RNA sequencing was performed on muscle samples collected pre- and post-intervention. Our data was then compared to skeletal muscle transcriptomic data previously reported following sleep deprivation (24 h without sleep). Results: Gene set enrichment analysis (GSEA) indicated there was an increased enrichment of inflammatory and immune response related pathways in the SR group post-intervention. However, in the SR+EX group the direction of enrichment in these same pathways occurred in the opposite directions. Despite this, there were no significant changes at the individual gene level from pre- to post-intervention. A set of genes previously shown to be decreased with sleep deprivation was also decreased in the SR group, but increased in the SR+EX group. Conclusion: The alterations to inflammatory and immune related pathways in skeletal muscle, following five nights of sleep restriction, provide insight regarding the transcriptional changes that underpin the detrimental effects associated with sleep loss. Performing three sessions of HIIE during sleep restriction attenuated some of these transcriptional changes. Overall, the transcriptional alterations observed with a moderate period of sleep restriction were less evident than previously reported changes following a period of sleep deprivation.

Intermittent Hypoxia Exposure Helps to Restore the Reduced Hemoglobin Concentration During Intense Exercise Training in Trained Swimmers.

In prolonged intense exercise training, the training load of athletes may be reduced once their hemoglobin concentrations ([Hb]s) are decreased dramatically. We previously reported that intermittent hypoxia exposure (IHE) could be used to alleviate the decrease of [Hb] and help to maintain the training load in rats. To further explore the feasibility of applying IHE intervention to athletes during prolonged intense exercise training, 6 trained swimmers were recruited to conduct a 4-week IHE intervention at the intervals after their [Hb] dropped for 10% or more during their training season. IHE intervention lasted 1 h and took place once a day and five times a week. Hematological and hormonal parameters, including [Hb], red blood cells (RBC), hematocrit (Hct), reticulocytes, serum erythropoietin (EPO), testosterone (T) and cortisol (C) were examined. After the IHE intervention was launched, [Hb], RBC and Hct of the subjects were increased progressively with their maximum levels (P < 0.01) showing at the third or fourth week, respectively. An increase in reticulocyte count (P < 0.01) suggests that IHE intervention promotes erythropoiesis to increase [Hb]. Besides, serum level of EPO, the hormone known to stimulate erythropoiesis, was overall higher than that before the IHE intervention, although it was statistically insignificant. Furthermore, the serum level of T, another hormone known to stimulate erythropoiesis, was increased progressively with the maximum level showing at the fourth week. Collectively, this study further confirms that IHE intervention may be used as a new strategy to prevent intense exercise training-induced reductions in [Hb].

Intermittent Hypoxia Exposure Can Prevent Reductions in Hemoglobin Concentration After Intense Exercise Training in Rats.

Intense exercise training can induce low concentrations of hemoglobin, which may be followed by maladaptation. Therefore, it is important for athletes to prevent low concentrations of hemoglobin during intense exercise training. In this study, we explored whether different protocols of intermittent hypoxic exposure (IHE, normobaric hypoxia, 14.5% O2) could prevent the exercise training-induced reduction in hemoglobin concentration in rats. Six-week-old male Sprague-Dawley rats were subjected to progressive intense treadmill exercise training over three weeks followed by three weeks of training with IHE after exercise. IHE lasted either 1 h, 2 h, or 1 h + 1 h (separated by a 3-h interval) after the exercise sessions. Hematological parameters, including hemoglobin concentration [(Hb)], red blood cells (RBCs), and hematocrit (Hct), and both renal and serum erythropoietin (EPO) were examined. We found that intense exercise training significantly reduced [Hb], RBCs, Hct, food intake and body weight (P < 0.01). Analysis of reticulocyte hemoglobin content (CHr) and reticulocyte counts in the serum of the rats suggested that this reduction was not due to iron deficiency or other cofounding factors. The addition of IHE after the intense exercise training sessions significantly alleviated the reduction in [Hb], RBCs, and Hct (P < 0.05) without an obvious impact on either food intake or body weight (P > 0.05). Increase in reticulocyte count in the rats from the IHE groups (P < 0.05 or P < 0.01) suggests that IHE promotes erythropoiesis to increase the hemoglobin concentration. Furthermore, the addition of IHE after the intense exercise training sessions also significantly increased the concentration of renal EPO (P < 0.05), although the increase of the serum EPO level was statistically insignificant (P > 0.05). The different IHE protocols were similarly effective at increasing renal EPO and preventing the training-induced decreases in [Hb], RBCs, and Hct. Collectively, this study suggests that IHE may be used as a new strategy to prevent intense exercise training-induced reductions in [Hb], and deserves future exploration in athletes.

Exercise Reverses the Alterations in Gut Microbiota Upon Cold Exposure and Promotes Cold-Induced Weight Loss.

Gut microbiota has been reported to contribute to reduced diet-induced obesity upon cold exposure. Furthermore, gut microbiome fermentation determines the efficacy of exercise for diabetes prevention and enhances exercise performance. However, there have been no systematic examinations of changes in gut microbiome composition in relation to exercise performed under low-temperature conditions. In this study, we investigated the effects of exercise performed under different conditions (room temperature, acute cold, intermittent cold, and sustained cold) in obese rats maintained on a high-fat diet at four time points during experimental trials (days 0, 1, 3, and 35), including observations on white fat browning, weight loss, cardiovascular effects, and changes in gut microbiota among treatment groups. We found that exercise under sustained cold conditions produced a remarkable shift in microbiota composition. Unexpectedly, exercise was found to reverse the alterations in gut microbiota alpha-diversity and the abundance of certain bacterial phyla observed in response to cold exposure (e.g., Proteobacteria decreased upon cold exposure but increased in response to exercise under cold conditions). Moreover, exercise under cold conditions (hereafter referred to "cold exercise") promoted a considerably higher level of white fat browning and greater weight loss and protected against the negative cardiovascular effects of cold exposure. Correlation analysis revealed that cold exercise-related changes in gut microbial communities were significantly correlated with white fat browning and cardiovascular phenotypes. These results could reveal novel mechanisms whereby additional health benefits attributable to both cold and exercise are mediated via altered gut microbes differently compared with either of them alone.

Identification of Urinary Biomarkers for Exercise-Induced Immunosuppression by iTRAQ Proteomics.

PURPOSE: To identify noninvasive immune biomarkers of exercise-induced immunosuppression using the iTRAQ proteomics technique. METHODS: Fifteen healthy males were recruited and subjected to a four-week incremental treadmill running training program. After each week of training, WBC counts and CD4+ and CD8+ lymphocytes were measured to monitor the immune function status. iTRAQ proteomics technology was used to identify differential proteins and their characteristics in urine. RESULTS: Our data showed that the WBC counts, CD4+ lymphocytes, and CD4+/CD8+ ratio decreased by more than 10% after four weeks of training, suggesting exercise-induced immunosuppression. A total of 1854 proteins were identified in urine during the incremental running using the iTRAQ technology. Compared with the urine before training, there were 89, 52, 77, and 148 proteins significantly upregulated and 66, 27, 68, and 114 proteins significantly downregulated after each week, respectively. Among them, four upregulated proteins, SEMG-1, PIP, PDGFRL, and NDPK, increased their abundance with the increased exercise intensity. Bioinformatics analysis indicates that these proteins are involved in stress response and immune function. CONCLUSION: Four weeks of incremental treadmill running induced immunosuppression in healthy males. By using iTRAQ proteomics, four proteins in the urine, SEMG-1, PIP, PDGFRL, and NDPK, were found to increase incrementally with the increased exercise intensity, which have the potential to be used as noninvasive immune biomarkers of exercise-induced immunosuppression.