Impact of acute dynamic exercise on vascular stiffness in the retinal arteriole in healthy subjects

Acute exercise can improve vascular stiffness in the conduit artery, but its effect on the retinal arterioles is unknown. The present study investigated the effects of acute dynamic exercise on retinal vascular stiffness. In experiment 1, we measured the cardio-ankle vascular index (CAVI), carotid artery intima-media thickness (carotid IMT), and retinal blood velocity by laser speckle flowgraphy in 28 healthy old and 28 young men (69 ± 3 and 23 ± 3 years, respectively). Pulse waveform variables, which were used as an index of retinal vascular stiffness, were assessed by retinal blood flow velocity profile analysis. In experiment 2, 18 healthy old and 18 young men (69 ± 3 and 23 ± 3 years, respectively) underwent assessment of pulse waveform variables after a 30-min bout of moderate cycling exercise at an intensity of 60% heart rate reserve. There was a significant difference in the baseline pulse waveform variables between the old and young groups. Pulse waveform variables in the retinal arteriole did not significantly change after acute dynamic exercise, whereas CAVI significantly decreased. These findings suggest that retinal vascular stiffness does not change by acute exercise. The effect of exercise on vascular stiffness in the retinal arterioles might be different from that in the conduit artery.

A Bayesian Network Meta-analysis of the Effect of Acute Exercise on Executive Function in Middle-aged and Senior People

Review question / Objective: Objective: To compare the intervention effect of multiple acute movement formulas on the executive function in middle-aged and senior people and to provide references for the discussion of the plans for precise movements. P: middle-aged and senior people elderly people; I: acute exercise; C: reading or sitting; O: Executive Function; S: RCT/crossover. Information sources: Randomized searches were carried out in Chinese databases such as CNKI, Wanfang Database, VTTMS, SinoMed and foreign databases such as PubMed, EMBASE, Cochrane Library, Web of Science. The retrieval period is from the beginning of each database to August 2021, supplemented with manual searches for gray literature and references traced back to previous systematic reviews.

CHOP is Dispensable for Exercise-Induced Increases in GDF15

Growth differentiating factor-15 (GDF15) is expressed, and secreted, from a wide range of tissues and serves as a marker of cellular stress. A key transcriptional regulator of this hormone is the endoplasmic reticulum stress protein, CHOP (C/EBP Homologous Protein). Exercise increases GDF15 levels but the underlying mechanisms of this are not known. To test whether CHOP regulates GDF15 during exercise we used various models of altered ER stress. We examined the effects of acute exercise on circulating GDF15 and GDF15 mRNA expression in liver, triceps skeletal muscle, and epididymal white adipose tissue and examined the GDF15 response to acute exercise in lean and high-fat diet-induced obese mice, sedentary and exercise trained mice, and CHOP deficient mice. We found that obesity augments exercise-induced circulating GDF15 although ER stress markers were similar in lean and obese mice. Exercise-induced GDF15 was increased in trained and sedentary mice that ran at the same relative exercise intensity, despite trained mice being protected against increased markers of ER stress. Finally, exercise-induced increases in GDF15 at the tissue and whole-body level were intact in CHOP deficient mice. Together, these results provide evidence that exercise-induced GDF15 expression and secretion occurs independent of ER stress/CHOP.

EXPRESS: Effects of Acute Exercise Intensity on Source Episodic Memory and Metamemory Accuracy

Prior research suggests that behavioral (e.g., exercise) and psychological factors (e.g., metamemory; monitoring and control of one’s memory processes) may influence memory function. However, there is conflicting results on the optimal intensity of acute exercise to enhance memory and whether acute exercise can also enhance metamemory. Further, very limited research has evaluated whether acute exercise can influence source episodic memory. The objective of this study was to evaluate whether there is an intensity-specific effect of acute aerobic exercise on source episodic memory and metamemory accuracy. Thirty young adults participated in a three condition (Control/Moderate/Vigorous-Intensity Exercise), within-subject counterbalanced experimental study. After each intervention, participants completed source episodic memory and metamemory tasks. Results demonstrated that acute exercise, relative to control, was effective in enhancing source episodic memory, but not metamemory accuracy. Vigorous-intensity acute exercise was the most optimal intensity to enhance source episodic memory. Overall, our findings suggest that there is an intensity-specific effect of acute exercise on source episodic memory. Further, when exercise-related improvements in memory occur, young adults may be unaware of these memory benefits from exercise.

Effects of an acute exercise bout in hypoxia on extracellular vesicle release in healthy and prediabetic subjects

Purpose: To investigate exosome-like vesicle (ELV) plasma concentrations and markers of multivesicular body (MVB) biogenesis in skeletal muscle in response to acute exercise. Methods: Seventeen healthy (BMI: 23.5±0.5kg·m-2) and fifteen prediabetic (BMI: 27.3±1.2kg·m-2) men were randomly assigned to two groups performing an acute cycling bout in normoxia or hypoxia (FiO2 14.0%). Venous blood samples were taken before (T0), during (T30) and after (T60) exercise and biopsies from m. vastus lateralis were collected before and after exercise. Plasma ELVs were isolated by size exclusion chromatography, counted by nanoparticle tracking analysis (NTA), and characterized according to international standards, followed by expression analyses of canonical ELV markers in skeletal muscle. Results: In the healthy normoxic group, the total number of particles in the plasma increased during exercise from T0 to T30 (+313%) followed by a decrease from T30 to T60 (-53%). In the same group, an increase in TSG101, CD81 and HSP60 protein expression was measured after exercise in plasma ELVs; however, in the prediabetic group, the total number of particles in the plasma was not affected by exercise. The mRNA content of TSG101, ALIX and CD9 were upregulated in skeletal muscle after exercise in normoxia; whereas, CD9 and CD81 were downregulated in hypoxia. Conclusions: ELV plasma abundance increased in response to acute aerobic exercise in healthy subjects in normoxia, but not in prediabetic subjects, nor in hypoxia. Skeletal muscle analyses suggested that this tissue did not likely play a major role of the exercise-induced increase in circulating ELVs.

A Systematic Review of the Effects of Football Playing on Changes in Serum Brain-Derived Neurotrophic Factor Level

Background: Consistent evidence suggests that exercise improves cognition and decision making, with preliminary evidence suggesting that brain-derived neurotrophic factors (BDNFs) may mediate these effects on high-intensity interval activities, such as in football playing. We conducted a systematic review of studies on football players or football task interventions that evaluated the causality of exercise or its relationship with changes in the basal BDNF level. Methods: The search was conducted in PubMed, SPORTDiscus, Cochrane, and FECYT (Web of Sciences, CCC, DIIDW, KJD, MEDLINE, RSCI, and SCIELO) according to the guidelines for performing systematic reviews in the sport sciences field. Results: From the 44 studies initially identified, seven studies were fully reviewed, and their outcome measures were extracted and analysed. In the scientific study of football, the studies published thus far have explored the relationship of serum BDNF levels and other cognitive function factors with the genetic expression of polymorphisms, the anthropometric and fitness conditions, the acute exercise effect of the match, and the typical actions of the match such as heading. Conclusions: The heterogeneity of designs and variables evaluated in studies related to BDNF exercise or interaction and football playing does not allow us to conclusively determine that there is a relationship with the cause or effect of genetic, anthropometric, or conditional factors that derive from an increase in BDNF due to actions during the playing of football.

MiRNA126 – RGS16 – CXCL12 Cascade as a Potential Mechanism of Acute Exercise-Induced Precursor Cell Mobilization

Acute exercise enhances circulating stem and precursor cells (CPCs) in the peripheral blood. The responsible mechanisms and molecular pathways, however, have not been fully identified. The aim of the present study was to investigate a pathway related to elevated levels of apoptotic peripheral blood mononuclear cells (MNCs) and their secretome. An increased uptake of miRNA126 in MNCs was suggested to lead to reduced levels of RGS16 mRNA and, in turn, an enhanced translation and secretion of CXCL12. Eighteen healthy, young men underwent two identical incremental cycling exercises of which the first served as control while the second was preceded by a 7-day-long antioxidative supplementation. Blood samples were collected at baseline (−10min) and several time points after exercise (0, 30, 90, 180, and 270min). Relative concentrations of miRNA126 in MNCs and CXCL12 levels in plasma were determined at all time points while RGS16 mRNA was assessed in MNCs at baseline and 30min after exercise. CXCL12 increased after exercise and strongly correlated with CPC numbers. MiRNA126 increased 30min and, to a lesser extent, also 180 and 270min after exercise but only with supplementation. RGS16 mRNA decreased 30min after exercise independent of the intervention. The amount of RGS16 mRNA inversely correlated with levels of miRNA126, but not with plasma CXCL12. In conclusion, even though plasma CXCL12 correlated with CPC numbers, the increase in CXCL12 cannot be explained by the increased concentration of miRNA126 and lower RGS16 mRNA in MNCs that would have allowed for an enhanced translation of CXCL12.Clinical Trial Registration: ClinicalTrials.gov, NCT03747913. Registered 20 November 2018, https://clinicaltrials.gov/ct2/show/NCT03747913.

Exercise Effects on γ3-AMPK Activity, Akt Substrate of 160 kDa Phosphorylation, and Glucose Uptake in Muscle of Normal and Insulin Resistant Female Rats

Previous studies demonstrated that acute exercise can enhance glucose uptake (GU), γ3-AMPK activity, and Akt Substrate of 160 kDa (AS160) phosphorylation in skeletal muscles from low fat diet (LFD) and high fat diet (HFD) fed male rats. Because little is known about exercise-effects on these outcomes in females, we assessed postexercise GU by muscles incubated ±insulin, delta-insulin GU (GU of muscles incubated with insulin minus GU uptake of paired muscles incubated without insulin), and muscle signaling proteins from female rats fed a LFD or brief-HFD (2wk). Rats were sedentary (LFD-SED, HFD-SED) or swim-exercised. Immediately postexercise (IPEX) or 3h postexercise (3hPEX), epitrochlearis muscles were incubated (no insulin IPEX; ±insulin 3hPEX) to determine GU. Muscle γ3-AMPK activity (IPEX, 3hPEX) and phosphorylated AS160 (pAS160; 3hPEX) were also assessed. γ3-AMPK activity and insulin-independent GU of IPEX-rats exceeded sedentary-rats without diet-related differences in either outcome. At 3hPEX, both GU by insulin-stimulated muscles and delta-insulin GU exceeded their respective diet-matched sedentary controls. GU by insulin-stimulated muscles, but not delta-insulin GU for LFD-3hPEX exceeded HFD-3hPEX. LFD-3hPEX versus LFD-SED had greater γ3-AMPK activity and greater pAS160. HFD-3hPEX exceeded HFD-SED for pAS160, but not for γ3-AMPK activity. pAS160 and γ3-AMPK at 3hPEX did not differ between diet-groups. These results revealed that increased γ3-AMPK activity at 3hPEX was not essential for greater GU in insulin-stimulated muscle or greater delta-insulin GU in HFD-female rats. Similarly elevated γ3-AMPK activity in LFD-IPEX versus HFD-IPEX and pAS160 in LFD-3hPEX versus HFD-3hPEX may contribute to the comparable, delta-insulin GU at 3hPEX in both diet groups.

Real-Time Monitoring of Metabolism during Exercise by Exhaled Breath

Continuous monitoring of metabolites in exhaled breath has recently been introduced as an advanced method to allow non-invasive real-time monitoring of metabolite shifts during rest and acute exercise bouts. The purpose of this study was to continuously measure metabolites in exhaled breath samples during a graded cycle ergometry cardiopulmonary exercise test (CPET), using secondary electrospray high resolution mass spectrometry (SESI-HRMS). We also sought to advance the research area of exercise metabolomics by comparing metabolite shifts in exhaled breath samples with recently published data on plasma metabolite shifts during CPET. We measured exhaled metabolites using SESI-HRMS during spiroergometry (ramp protocol) on a bicycle ergometer. Real-time monitoring through gas analysis enabled us to collect high-resolution data on metabolite shifts from rest to voluntary exhaustion. Thirteen subjects participated in this study (7 female). Median age was 30 years and median peak oxygen uptake (VO2max) was 50 mL·/min/kg. Significant changes in metabolites (n = 33) from several metabolic pathways occurred during the incremental exercise bout. Decreases in exhaled breath metabolites were measured in glyoxylate and dicarboxylate, tricarboxylic acid cycle (TCA), and tryptophan metabolic pathways during graded exercise. This exploratory study showed that selected metabolite shifts could be monitored continuously and non-invasively through exhaled breath, using SESI-HRMS. Future studies should focus on the best types of metabolites to monitor from exhaled breath during exercise and related sources and underlying mechanisms.

Mitochondria-targeted antioxidant supplementation augments acute exercise-induced increases in muscle PGC1α mRNA and improves training-induced increases in peak power independent of mitochondrial content and function in untrained middle-aged men

ABSTRACTThe role of mitochondrial ROS production and signalling in muscle adaptations to exercise training has not been explored in detail. Here we investigated the effect of supplementation with the mitochondria-targeted antioxidant MitoQ on a) the skeletal muscle mitochondrial and antioxidant gene transcriptional response to acute high-intensity exercise and b) skeletal muscle mitochondrial content and function following exercise training. In a randomised, double-blind, placebo-controlled, parallel design study, 23 untrained men (age: 44 ± 7 years, VO2peak: 39.6 ± 7.9 ml/kg/min) were randomised to receive either MitoQ (20 mg/d) or a placebo for 10 days before completing a bout of high-intensity interval exercise (cycle ergometer, 10 × 60 s at VO2peak workload with 75 s rest). Blood samples and vastus lateralis muscle biopsies were collected before exercise and immediately and 3 hours after exercise. Participants then completed high-intensity interval training (HIIT; 3 sessions per week for 3 weeks) and another blood sample and muscle biopsy were collected. MitoQ supplementation augmented acute exercise-induced increases in skeletal muscle mRNA expression of the major regulator of proteins involved in mitochondrial biogenesis peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α). Despite this, training-induced increases in skeletal muscle mitochondrial content were unaffected by MitoQ supplementation. HIIT-induced increases in VO2peak and 20 km time trial performance were also unaffected by MitoQ while MitoQ augmented training-induced increases in peak power achieved during the VO2peak test. These data suggest that MitoQ supplementation enhances the effect of training on peak power, which may be related to the augmentation of skeletal muscle PGC1α expression following acute exercise. However, this effect does not appear to be related to an effect of MitoQ supplementation on HIIT-induced mitochondrial biogenesis in skeletal muscle and may therefore be the result of other adaptations mediated by PGC1α.