Single Bout Of Exercise Research Articles

The Effect of Physical Activity on Neurotrophin Concentrations and Cognitive Control in Patients With a Depressive Episode.

BackgroundCognitive deficits occur in most patients with affective disorders. The role of neurotrophic factors (e.g., BDNF) as modulators of brain plasticity affecting neurocognitive abilities has been emphasized. Neurotrophin concentrations may change under the influence of various interventions, including physical activity. Selected studies have shown that cognitive function may also be affected by exercise.AimThe aim of the study was to determine whether physical activity changes the concentration of neurotrophins and their receptors in patients with an episode of depression. It was also examined how one session of aerobic exercise affects cognitive control.MethodsThe study included 41 participants. The subjects were asked to exercise on a cycloergometer for 40 min with individually selected exercise loads (70% VO2max). Before and shortly after the exercise blood samples were acquired to perform blood assays (proBDNF, BDNF, TrkB, NGFR). The participants also performed a Stroop test twice—before the exercise and 10 min after its cessation.ResultsThe single bout of physical exercise did not cause any significant changes in the concentration of neurotrophic factors. The SCWT results: both the mean reading time (29.3 s vs. 47.8 s) and the color naming time (36.7 s vs. 50.7 s) increased. The patients made more mistakes after physical exercise, both in part A (0.2 vs. 1.5) and B (0.6 vs. 1.5). The so-called interference effect decreased—the difference between naming and reading times was smaller after exercise (6.2 s vs. 2.4 s). No significant correlations were found between the concentrations of the studied neurotrophic factors and the Stroop test results.ConclusionsThe results did not confirm changes in neurotrophin concentration under the influence of a single session of physical activity. The shortening of the interference time after exercise may be caused by practice effects. A significant limitation of the study is the use of the Stroop test twice in short intervals.

Potato Protein Ingestion Increases Muscle Protein Synthesis Rates at Rest and during Recovery from Exercise in Humans.

ABSTRACTIntroductionPlant-derived proteins have received considerable attention as an alternative to animal-based proteins and are now frequently used in both plant-based diets and sports nutrition products. However, little information is available on the anabolic properties of potato-derived protein. This study compares muscle protein synthesis rates after the ingestion of 30 g potato protein versus 30 g milk protein at rest and during recovery from a single bout of resistance exercise in healthy, young males.MethodsIn a randomized, double-blind, parallel-group design, 24 healthy young males (24 ± 4 yr) received primed continuous l-[ring-13C6]-phenylalanine infusions while ingesting 30 g potato-derived protein or 30 g milk protein after a single bout of unilateral resistance exercise. Blood and muscle biopsies were collected for 5 h after protein ingestion to assess postprandial plasma amino acid profiles and mixed muscle protein synthesis rates at rest and during recovery from exercise.ResultsIngestion of both potato and milk protein increased mixed muscle protein synthesis rates when compared with basal postabsorptive values (from 0.020% ± 0.011% to 0.053% ± 0.017%·h−1 and from 0.021% ± 0.014% to 0.050% ± 0.012%·h−1, respectively; P < 0.001), with no differences between treatments (P = 0.54). In the exercised leg, mixed muscle protein synthesis rates increased to 0.069% ± 0.019% and 0.064% ± 0.015%·h−1 after ingesting potato and milk protein, respectively (P < 0.001), with no differences between treatments (P = 0.52). The muscle protein synthetic response was greater in the exercised compared with the resting leg (P < 0.05).ConclusionsIngestion of 30 g potato protein concentrate increases muscle protein synthesis rates at rest and during recovery from exercise in healthy, young males. Muscle protein synthesis rates after the ingestion of 30 g potato protein do not differ from rates observed after ingesting an equivalent amount of milk protein.

Sex differences in monocyte CCR2 expression and macrophage polarization following acute exercise

Monocyte chemokine receptor 2 (CCR2) and phosphorylated extra-cellular regulated kinase 1 & 2 (ERK1/2) impact macrophage differentiation and progression of atherosclerosis. Whereas aerobic exercise favorably modulates the immune system and reduces atherosclerotic risk, it is unknown whether sex differences exist in the monocyte/macrophage response to acute aerobic exercise. AimsTo determine the impact of an acute bout of moderate intensity aerobic exercise on monocyte and macrophage CCR2 expression, ERK1/2 phosphorylation, and macrophage polarization in pre-menopausal women and men. Materials and methodsBlood samples were collected in 24 people (Women/Men; n = 12) prior to (PRE), immediately after a bout of moderate intensity cycle ergometry (POST), and 2 h (2H) following exercise. Monocyte and macrophage CCR2 and phosphorylated ERK1/2 as well as macrophage CD86 and CD206 were analyzed by flow cytometry. Key findingsPRE classical monocyte CCR2 expression was greater in women compared to men (Women: 20546.2 ± 2306.4 vs. Men: 14437.6 ± 1201.9 AUF; p = 0.028) and was reduced in women at 2H (PRE: 20546.2 ± 2306.4 vs. 2H: 15856.9 ± 1314.4 AUF; p = 0.027). POST classical monocyte CCR2 expression was inversely associated (r = −0.697, p = 0.012) with POST classical monocyte ERK1/2 phosphorylation in women only. The percentage of CCR2+ macrophages was lower in women at POST (Women: 62.0 ± 8.9 vs. Men: 83.6 ± 3.1; p = 0.031) and at 2H (Women: 60.3 ± 8.4 vs. Men: 83.5 ± 3.0%; p = 0.016). SignificanceThese data suggest that a single bout of moderate intensity aerobic exercise differentially impacts monocyte CCR2 expression and macrophage polarization in women compared to men.

Nestin and osteocrin mRNA increases in human semitendinosus myotendinous junction 7days after a single bout of eccentric exercise.

The myotendinous junction (MTJ), a specialized interface for force transmission between muscle and tendon, has a unique transcriptional activity and is highly susceptible to muscle strain injury. Eccentric exercise training is known to reduce this risk of injury, but knowledge of the influence of exercise on the MTJ at the molecular and cellular levels is limited. In this study, 30 subjects were randomized to a single bout of eccentric exercise 1week prior to tissue sampling (exercised) or no exercise (control). Samples were collected from the semitendinosus as part of reconstruction of the anterior cruciate ligament and divided into fractions containing muscle, MTJ and tendon, respectively. The concentrations of macrophages and satellite cells were counted, and the expression of genes previously known to be active at the MTJ were analyzed by real-time-quantitative PCR. An effect of the single bout of exercise was found on the expression of nestin (NES) and osteocrin (OSTN) mRNA in the MTJ and tendon fractions. Genes earlier identified at the MTJ (COL22A1, POSTN, ADAMTS8, MNS1, NCAM1) were confirmed to be expressed at a significantly higher level in the MTJ compared to muscle and tendon but were unaffected by exercise. In the exercise group a higher concentration of macrophages, but not of satellite cells, was seen in muscle close to the MTJ. The expression of NES and OSTN was higher in human semitendinosus MTJ 1week after a single session of heavy eccentric exercise. Based on these results, NES and OSTN could have a part in explaining how the MTJ adapts to eccentric exercise.

The effect of active vs passive recovery and use of compression garments following a single bout of muscle-damaging exercise

BACKGROUND: Some recovery strategies are needed to reduce or eliminate the effect of negative symptoms caused by exercise. OBJECTIVE: The aim of this study was to determine the effect of different types of recovery after single-bout strength exercises on biomarkers of muscle damage, cytokine release and lactate elimination. METHODS: Following familiarization, 10 male volunteers performed four randomized recovery protocols (passive or active recovery with or without compression garments) following a single bout of resistance exercise (squat and deadlift exercises). The blood creatine kinase (CK), lactate dehydrogenase (LDH), interleukine-6 (IL-6), and tumor necrosis factor-alfa (TNF-α) values were measured before and after exercise, and after 24, 48, 72 hours. RESULTS: The CK analysis showed that all protocols significantly increased (p&lt; 0.05) CK activity compared to the pre and 24 h post time points. Interestingly, protocol 3 and 4 significantly decreased (p&lt; 0.05) CK activity compared 24 and 72 h post-exercise. LDH, IL-6, and TNF values did not show significant difference (p&gt; 0.05) at the time points tested. CONCLUSIONS: Active recovery is an effective method for reducing the severity and duration of muscle damage and for accelerating the clearance of blood lactate (BLa) following a single bout of strength training. There is no added benefit of using compression garments.

The Acute Effects of Single or Repeated Bouts of Vigorous-Intensity Exercise on Insulin and Glucose Metabolism during Postprandial Sedentary Behavior

Fitness and exercise may counteract the detrimental metabolic and mood adaptations during prolonged sitting. This study distinguishes the immediate effects of a single bout vs. work-load and intensity-matched repeated exercise breaks on subjective well-being, blood glucose, and insulin response (analyzed as area under the curve) during sedentary time; and assesses the influence of fitness and caloric intake on metabolic alterations during sedentariness. Eighteen women underwent cardiopulmonary exercise testing and three 4 h sitting interventions: two exercise interventions (70% VO2max, 30 min, cycle ergometer: (1) cycling prior to sitting; (2) sitting interrupted by 5 × 6 min cycling), and one control condition (sitting). Participants consumed one meal with ad libitum quantity (caloric intake), but standardized macronutrient proportion. Exercise breaks (4057 ± 2079 μU/mL·min) reduced insulin values compared to a single bout of exercise (5346 ± 5000 μU/mL·min) and the control condition (6037 ± 3571 μU/mL·min) (p ≤ 0.05). ANCOVA revealed moderating effects of caloric intake (519 ± 211 kilocalories) (p ≤ 0.01), but no effects of cardiorespiratory fitness (41.3 ± 4.2 mL/kg/min). Breaks also led to lower depression, but higher arousal compared to a no exercise control (p ≤ 0.05). Both exercise trials led to decreased agitation (p ≤ 0.05). Exercise prior to sitting led to greater peace of mind during sedentary behavior (p ≤ 0.05). Just being fit or exercising prior to sedentary behavior are not feasible to cope with acute detrimental metabolic changes during sedentary behavior. Exercise breaks reduce the insulin response to a meal. Despite their vigorous intensity, breaks are perceived as positive stimulus. Detrimental metabolic changes during sedentary time could also be minimized by limiting caloric intake.

A Single Bout of Ultra-Endurance Exercise Reveals Early Signs of Muscle Aging in Master Athletes.

Middle-aged and master endurance athletes exhibit similar physical performance and long-term muscle adaptation to aerobic exercise. Nevertheless, we hypothesized that the short-term plasticity of the skeletal muscle might be distinctly altered for master athletes when they are challenged by a single bout of prolonged moderate-intensity exercise. Six middle-aged (37Y) and five older (50Y) master highly-trained athletes performed a 24-h treadmill run (24TR). Vastus lateralis muscle biopsies were collected before and after the run and assessed for proteomics, fiber morphometry, intramyocellular lipid droplets (LD), mitochondrial oxidative activity, extracellular matrix (ECM), and micro-vascularisation. Before 24TR, muscle fiber type morphometry, intramyocellular LD, oxidative activity, ECM and micro-vascularisation were similar between master and middle-aged runners. For 37Y runners, 24TR was associated with ECM thickening, increased capillary-to-fiber interface, and an 89% depletion of LD in type-I fibers. In contrast, for 50Y runners, 24TR did not alter ECM and capillarization and poorly depleted LDs. Moreover, an impaired succinate dehydrogenase activity and functional class scoring of proteomes suggested reduced oxidative phosphorylation post-24TR exclusively in 50Y muscle. Collectively, our data support that middle-aged and master endurance athletes exhibit distinct transient plasticity in response to a single bout of ultra-endurance exercise, which may constitute early signs of muscle aging for master athletes.

Fasting potentiates insulin-mediated glucose uptake in rested and prior-contracted rat skeletal muscle.

A single bout of exercise can potentiate the effect of insulin on skeletal muscle glucose uptake via activation of the AMPK-TBC1 domain family member 4 (TBC1D4) pathway, which suggests a positive correlation between AMPK activation and insulin sensitization. In addition, prolonged fasting in rodents is known to upregulate and thereby synergistically enhance the effect of exercise on muscle AMPK activation. Therefore, fasting may potentiate the insulin-sensitizing effect of exercise. In the present study, we mimicked exercise by in situ muscle contraction and evaluated the effect of a 36-h fast on muscle contraction-induced insulin sensitization. Male Wistar rats weighing 150-170 g were allocated to either a 36-h fasting or feeding group. The extensor digitorum longus (EDL) muscles were electrically contracted via the common peroneal nerve for 10 min followed by a 3-h recovery period. EDL muscles were dissected and incubated in the presence or absence of submaximal insulin. Our results demonstrated that acute muscle contraction and 36 h of fasting additively upregulated AMPK pathway activation. Insulin-stimulated muscle glucose uptake and site-specific TBC1D4 phosphorylation were enhanced by prior muscle contraction in 36-h-fasted rats, but not in fed rats. Moreover, enhanced insulin-induced muscle glucose uptake and Akt phosphorylation due to 36 h of fasting were associated with a decrease in tribbles homolog 3 (TRB3), a negative regulator of Akt activation. In conclusion, fasting and prior muscle contraction synergistically enhance insulin-stimulated TBC1D4 phosphorylation and glucose uptake, which is associated with augmented AMPK pathway activation in rodents.NEW & NOTEWORTHY In this study, we revealed that 36 h of fasting additively upregulated acute muscle contraction-induced AMPK pathway activation in rats. Besides, fasting and muscle contraction synergistically enhanced insulin-stimulated site-specific TBC1D4 phosphorylation and glucose uptake, which was associated with augmented AMPK pathway activation. These results contribute to understanding the regulation of muscle insulin sensitivity.

Increased cortisol levels caused by acute resistance physical exercise impair memory and learning ability.

Acute physical exercise works as an activator of the responses of the human organism to stress. This is based on the activation of the hypothalamic–pituitary–adrenal (HPA) axis, affecting physical, physiological and psychological levels. This study aimed to analyse the effects of a single bout of high-intensity resistance exercise on cognitive-behavioural responses: visuo-spatial path learning and memory, as well as physiological responses (salivary cortisol levels). Nineteen healthy male military-trained powerlifting subjects were tested in a within-subject design on two experimental days with an interval of 48 h. The stress and cognitive variables were measured by cortisol levels and Ruff–Light trail-learning test (RULIT) test scores, respectively. The results showed the immediate influence of acute exercise on cortisol, with significantly higher cortisol levels found in subjects after completion of the acute resistance exercise. In addition, this study found a significant deterioration of memory and learning ability after a dose of intense resistance exercise. In conclusion, the study highlights the relative effects of resistance exercise on cortisol and cognitive performance depending on the intensity and type of the exercise, the moment of measurement and the cerebral areas implicated.

Eccentric Exercise Causes Specific Adjustment in Pyruvate Oxidation by Mitochondria.

The impact of eccentric exercise on mitochondrial function has only been poorly investigated and remains unclear. This study aimed to identify the changes in skeletal muscle mitochondrial respiration, specifically triggered by a single bout of eccentric treadmill exercise. Male adult mice were randomly divided into eccentric (ECC; downhill running), concentric (CON; uphill running), and unexercised control groups ( n = 5/group). Running groups performed 18 bouts of 5 min at 20 cm·s -1 on an inclined treadmill (±15° to 20°). Mice were sacrificed 48 h after exercise for blood and quadriceps muscles collection. Deep proximal (red) and superficial distal (white) muscle portions were used for high-resolution respirometric measurements. Plasma creatine kinase activity was significantly higher in the ECC compared with CON group, reflecting exercise-induced muscle damage ( P < 0.01). The ECC exercise induced a significant decrease in oxidative phosphorylation capacity in both quadriceps femoris parts ( P = 0.032 in proximal portion, P = 0.010 in distal portion) in comparison with the CON group. This observation was only made for the nicotinamide adenine dinucleotide (NADH) pathway using pyruvate + malate as substrates. When expressed as a flux control ratio, indicating a change related to mitochondrial quality rather than quantity, this change seemed more prominent in distal compared with proximal portion of quadriceps muscle. No significant difference between groups was found for the NADH pathway with glutamate or glutamate + malate as substrates, for the succinate pathway or for fatty acid oxidation. Our data suggest that ECC exercise specifically affects pyruvate mitochondrial transport and/or oxidation 48 h after exercise, and this alteration mainly concerns the distal white muscle portion. This study provides new perspectives to improve our understanding of the mitochondrial adaptation associated with ECC exercise.

Effects of low load exercise with and without blood-flow restriction on microvascular oxygenation, muscle excitability and perceived pain

ABSTRACT This paper aimed to examine the acute effect of low-load (LL) exercise with blood-flow restriction (LL-BFR) on microvascular oxygenation and muscle excitability of the vastus medialis (VM) and vastus lateralis (VL) muscles during a single bout of unilateral knee extension exercise performed to task failure. Seventeen healthy recreationally resistance-trained males were enrolled in a within-group randomized cross-over study design. Participants performed one set of unilateral knee extensions at 20% of one-repetition maximum (1RM) to task failure, using a LL-BFR or LL free-flow (LL-FF) protocol in a randomized order on separate days. Changes in microvascular oxygenation and muscle excitability in VL and VM were assessed using near-infrared spectroscopy (NIRS) and surface electromyography (sEMG), respectively. Pain measures were collected using the visual analog scale (VAS) before and following set completion. Within- and between- protocol comparisons were performed at multiple time points of set completion for each muscle. During LL-BFR, participants performed 43% fewer repetitions and reported feeling more pain compared to LL-FF (p<0.05). Normalized to time to task failure, LL-BFR and LL-FF generally demonstrated similar progression in microvascular oxygenation and muscle excitability during exercise to task failure. The present results demonstrate that LL-BFR accelerates time to task failure, compared with LL-FF, resulting in a lower dose of mechanical work to elicit similar levels of oxygenation, blood-pooling, and muscle excitability. LL-BFR may be preferable to LL-FF in clinical settings where high workloads are contraindicated, although increased pain experienced during BFR may limit its application. Highlights Compared to free flow (FF), neuromuscular fatigue mechanisms are accelerated during blood flow restricted (BFR) training. This can be observed as changes in microvascular oxygenation and muscle excitability occurring at a ∼43% faster mean rate during BFR compared to FF. BFR exercise seems to elicit the same level of neuromuscular fatigue as FF training within a shorter timeframe. This reduces total joint load and may be especially helpful in cases where high training volumes may be contraindicated (e.g. recovering from a sports injury or orthopedic surgery).

The Effect of a Single Bout of Resistance Exercise with Blood Flow Restriction on Arterial Stiffness in Older People with Slow Gait Speed: A Pilot Randomized Study.

Purpose: Low-intensity resistance exercise with moderate blood-flow restriction (LIRE-BFR) is a new trending form of exercises worldwide. The purpose of this study was to compare the acute effect of a single bout of traditional resistance exercise (TRE) and LIRE-BFR on arterial stiffness in older people with slow gait speeds. Methods: This was a randomized, controlled clinical study. Seventeen older adults (3 men; 14 women; 82 ± 5 years old) completed a session of TRE (n = 7) or LIRE-BFR (n = 10). At baseline and after 60 min post-exercise, participants were subject to blood pressure measurement, heart rate measurements and a determination of arterial stiffness parameters. Results: There was no significant difference between the TRE and LIRE-BFR group at baseline. Pulse-wave velocity increased in both groups (p < 0.05) post-exercise with no between-group differences. Both exercise modalities did not produce any adverse events. The increase in systolic blood pressure, pulse pressure, augmentation pressure and pulse wave velocity (all p > 0.05) were similar after both TRE and LIRE-BFR. Conclusion: TRE and LIRE-BFR had similar responses regarding hemodynamic parameters and pulse-wave velocity in older people with slow gait speed. Long-term studies should assess the cardiovascular risk and safety of LIRE-BFR training in this population.

12 Inflammatory Response Following a Single Bout of Exercise Is More Prominent Is Young Horses Compared to Older Horses

Abstract Horses experience a post-exercise inflammatory response to damaged tissues that is part of the mechanism of recovery and is indicated by heat and muscle soreness (MS). Further, old horses (OH) are at a greater risk of prolonged MS, lameness, and injury than are young horses (YH). Therefore, the objective of this study was to compare heat and MS of unconditioned young (14-16 months) and old (19-24 years) Quarter Horses after the completion of an incremental exercise test (IET: counterclockwise at 3 min at 6.44 kph, 10 min at 16.09 kph, 2 min each at 19.31 and 22.53 kph). MS evaluations were performed on neck, shoulder, back, and hip for both sides at pre, 12, 36, 60, and 84 hours post IET. FLIR images of the shoulder, forearm, back, hip, and gaskin were taken on the left side at day 0, pre-IET, 15 min, and 12, 24, 48, 72 h post-IET. Data were analyzed by repeated measures ANOVA using the MIXED procedure of SAS. There was a main effect of age on gaskin temperature, whereby YH (32.3±17.5°C) had higher temperatures than OH (31.4±17.5°C; P = 0.043). There was a tendency for an interaction of age and time for shoulders (P = 0.063) and an interaction for forearm (P = 0.03) and back (P = 0.046). At 12 h post IET, YH shoulders were higher (34.6±17.1°C) than OH (31.8±17.1°C), YH forearms were higher (34.1±17.3°C) than OH (30.4±17.1°C), and YH backs (33.4±17.3°C) were higher than OH (32±17.3°C). Necks were sorer on the right side 36 h post-IET compared to pre-exercise (P = 0.033) and 60 hours compared to 12 hours post IET (P = 0.033). Muscle soreness increased in the right hip from pre-IET to 36 h post-IET (P = 0.037). No other differences were observed. Our results suggest that YH have higher surface temperatures than OH but this was not associated with MS.

Short‐term exercise‐induced protection of cardiovascular function and health: why and how fast does the heart benefit from exercise?

Regular exercise training has potent and powerful protective effects against the development of cardiovascular disease. These cardioprotective effects of regular exercise training are partly explained through the effects of exercise on traditional cardiovascular risk factors and improvement in cardiac and vascular health, which take several weeks to months to develop. This review focuses on the observation that single bouts of exercise may also possess an underrecognized, clinically useful form of immediate cardioprotection. Studies, performed in both animals and humans, demonstrate that single or short‐term exercise‐induced protection (SEP) attenuates the magnitude of cardiac and/or vascular damage in response to prolonged ischaemia and reperfusion injury. This review highlights preclinical evidence supporting the hypothesis that SEP activates multiple pathways to confer immediate protection against ischaemic events, reduce the severity of potentially lethal ischaemic myocardial injury, and therefore act as a physiological first line of defence against injury. Given the fact that the extent of SEP could be modulated by exercise‐related and subject‐related factors, it is important to recognize and consider these factors to optimize future clinical implications of SEP. This review also summarizes potential effector signalling pathways (i.e. communication between exercising muscles to vascular/cardiac tissue) and intracellular pathways (i.e. reducing tissue damage) that ultimately confer protection against cardiac and vascular injury. Finally, we discuss potential future directions for designing adequate human and animal studies that will support developing effective SEP strategies for the (multi‐)diseased and aged individual.Key points Single or short‐term exercise‐induced protection (SEP) attenuates the magnitude of cardiac and/or vascular damage in response to prolonged ischaemia and reperfusion injury (IR injury).SEP activates multiple pathways to confer cardiac protection, which develops remotely at the site of the activated muscle by release of circulating molecules, which transfer towards activation of intramyocardial signalling that promotes cell survival during episodes of IR injury.SEP represents an attractive intervention in aged individuals and in those with co‐morbidities. The immediate protection, low cost and simplicity to increase the ‘dose’ of SEP offers unique opportunities in the clinical applications of SEP.

Effect of PKC inhibitor on renal podocyte slit diaphragm protein expression in exhausted rats

Objective: To investigate the expression level of podocyte slit diaphragm protein in rats after one-time exhaustive exercise, to explore the effect of PKC inhibitor on the protein expression level, and to reveal the mechanism of PKC in the formation of exercise-induced proteinuria. Methods: Thirty male SD rats were randomly divided into control group (C), exercise group (E) and exercise combining with PKC inhibitor group (EPI), with 10 rats in each group. Rats in group E and EPI performed one single bout of exhaustive exercise (25 m/min), rats in group EPI were intraperitoneally injected with a PKC inhibitor (chelerythrine, 5 mg/kg) 1 day and 1 hour before exercise respectively, while rats in group C and E were injected with the same volume of saline. Results: ①Compared with group C, the levels of urine protein, uric acid, urine sugar, blood urea, and blood uric acid of rats in group E were increased significantly (P＜0.05), the level of blood glucose was reduced significantly (P＜0.01), and renal ROS production was increased significantly (P＜0.01). The expressions of nephrin and podocin protein in renal tissue were decreased significantly (P＜ 0.05), while the expressions of PKC, Nox2, and Nox4 protein were increased significantly (P＜0.05). ②Compared with group E, the levels of urinary protein,urine glucose and blood urea in EPI group were decreased significantly (P＜0.05), the level of blood glucose was increased significantly (P＜0.01), renal ROS production was reduced significantly (P＜0.01). the expressions of nephrin and podocin protein in renal tissues of the EPI group were increased significantly (P＜0.05), while the expressions of PKC and Nox2 protein was reduced significantly (P＜0.05, P＜0.01). Conclusion: One-time exhaustive exercise can down-regulate the expressions of nephrin and podocin through PKC/Nox/ROS pathways in the kidney of rats; PKC inhibitor alleviates the decrease in the expression of podocyte slit diaphragm protein caused by exhaustive exercise, and prevents the occurrence of exercise-induced proteinuria.

The relationship between neurotransmission-related amino acid blood concentrations and neuropsychological performance following acute exercise

Amino acid neurotransmitters, including glutamate, phenylalanine, tyrosine, alanine, and glycine, underlie the majority of the excitatory and inhibitory neurotransmission in the nervous system, and acute exercise has been shown to modulate their concentrations. We aimed to determine whether any correlation exists between the above-mentioned amino acid blood concentrations and the neuropsychological performance after an acute exercise intervention. Sixty basketball players were randomly assigned to one of two experimental conditions: exercise or inactive resting. All participants underwent a comprehensive neuropsychological assessment and blood samples were taken on a Guthrie card before and after the end of the experimental conditions. Amino acid blood concentrations were significantly elevated and cognitive performance significantly improved post-exercise on specific neuropsychological assessments. Significant intervention × group interaction effects were apparent for Trail Making Test part-B [F(1,58) = 20.46, p < .0001, η 2 = .26] and Digit Span Backwards [F(1,58) = 15.47, p < .0001, η 2 = .21] neuropsychological assessments. Additionally, regression analysis indicated that tyrosine accounted for 38.0% of the variance in the Trail Making Test part-A test. These results suggest that elevated blood concentrations of neurotransmission-related amino acids are associated with improved neuropsychological performance after a single bout of high-intensity exercise.

Acute effects of aerobic exercise on conflict suppression, response inhibition, and processing efficiency underlying inhibitory control processes: An ERP and SFT study.

Aerobic exercise has been identified as an effective strategy for transiently enhancing inhibitory control, an ability to suppress irrelevant distractors while focusing on relevant information in facilitating the implementation of goal-directed behavior. The purpose of this study was to employ a go/no-go version of the redundant-target task and event-related potential to further determine whether inhibitory control at the perceptual and response levels as well as their underlying processing capacity and neuroelectric alterations are differentially affected by a single bout of aerobic exercise. Twenty-seven young adults completed the redundant-target task while electroencephalogram was recorded before and after one 20-min bout of moderate-intensity aerobic exercise and a sitting control condition on separate days in counterbalanced order. Although behavioral outcomes of mean-level performance did not differ between intervention conditions, time-related decreases in processing capacity for the faster responses were only observed following rest. Aerobic exercise resulted in maintained P3b amplitude from pretest to posttest for all trial types while decreased P3b amplitude from pretest to posttest during single-target and redundant-target trials was observed following rest. Further, the time-related changes in P3b amplitude were positively correlated with improvements in task performance following exercise. These findings suggest that a short bout of aerobic exercise selectively counteracts the time-related decrements in processing capacity as well as neuroelectric processing of attention and conflict suppression that contribute to behavioral outcomes of inhibitory control.

Impact of 12-Week Moderate-Intensity Aerobic Training on Inflammasome Complex Activation in Elderly Women.

Aging often associates with a chronic low-grade inflammatory status that can be consequent to the activation of Toll-like receptors (TLRs) and the downstream NLR family pyrin domain containing 3 (NLRP3) inflammasome and causes a chronic secretion of pro-inflammatory cytokines. Since exercise has known anti-inflammatory effects, we investigated the effect of Nordic walking training on inflammasome activation and downstream effectors in elderly women. A population of elderly women was divided into EXP (n = 29) that completed 12 weeks of the moderate-intensity aerobic training program and CTRL (n = 29), performing no activity. Blood samples were taken before and after the first (T1-pre and T1-post, respectively) and last (T2-pre and T2-post, respectively) exercise unit. Inflammasome activation status was assessed by whole blood NLRP3 and TLR4 expression by RT-qPCR. Serum levels of IL-1β, IL-6, TNFα, and IL-18 cytokines were assayed by multiplex fluorescent beads-based immunoassays or ELISA. NLRP3 and TLR4 levels were reduced 2 folds between T1-pre and T2-pre and induced at T2-post, compared to T2-pre, by 2.6- and 2.9-fold, respectively. A single exercise bout elicited a 1. 38-, 1. 5-, and 1.36-fold rise of IL-1β, TNFα, and IL-6 concentration, respectively, although not significant, at the beginning of the training (T1-pre vs. T1-post), a 1.4-fold decrease for IL-1β and TNFα at the end of the training (T1-pre vs. T2-pre), and a 2-, 1.8- and 1.26-fold increase after the last exercise session (T2-pre vs. T2-post) for the three cytokines. When stratifying the population based on BMI in normal weight (NW) and overweight (OW), NLRP3 and TLR4 expression was affected only in NW. As for inflammatory cytokines, IL-1β was modulated in NW at the beginning of the training, whereas in OW at the end of the training; for TNFα, this time-dependent modulation was significant only in OW. Applied aerobic training affected the resting expression of inflammasome constituents (NLRP3 and TLR4) and levels of downstream effectors (IL-1β, TNFα, and IL-6). However, at the end of the program, participants acquire an acute inflammatory response to exercise that was absent at baseline. Future studies would have to define the molecular mechanisms associated with, and how to potentiate, the exercise-associated inflammatory response.

Acute exercise decreases insulin-stimulated extracellular vesicles in conjunction with augmentation index in adults with obesity.

Extracellular vesicles (EVs) are often elevated in obesity and may modulate disease risk. Although acute exercise reduces fasting EVs in adults with obesity, no data exist on insulin-mediated EV responses. This study evaluated the effects of exercise on EV responses to insulin in relation to vascular function. Ten (5M/5F) sedentary adults with obesity (34.3±3.7kg/m2 ) completed an evening control and acute exercise condition (70% to expend 400kcal). Following an overnight fast, participants underwent a 2h euglycaemic-hyperinsulinaemic clamp (90mg/dl; 40mU/m2 /min) to determine metabolic insulin sensitivity (M-value), phenotypes of medium- to large-sized EVs, and aortic waveform measures. Endothelial (CD105+ , CD41- /CD31+ )-, leukocyte (CD45+ )-, platelet (CD41+ , CD41+ /31+ )- and tetraspanin (TX+ )-derived EVs, as well as platelet endothelial cell adhesion molecule (CD31+ ), were determined before and after the clamp using high resolution spectral flow cytometry. Although exercise did not alter fasting haemodynamics, it lowered the augmentation index (AIx75, P=0.024) and increased the M-value (P=0.042). Further, exercise decreased all fasting EVs (P<0.01) and decreased insulin-stimulated TX+ (P=0.060), CD31+ (P=0.060) and CD41- /31+ (P=0.045) compared to rest. Interestingly, greater insulin-stimulated decreases in CD41- /31+ were associated with reduced AIx75 during the clamp (r=0.62, P=0.059), while insulin-stimulated decreases in CD41+ (r=-0.68, P=0.031), CD41+ /31+ (r=-0.69, P=0.262), TX+ (r=-0.66, P=0.037) and CD31+ (r=-0.69, P=0.028) correlated with M-value following exercise. Thus, acute exercise may decrease fasting and insulin-stimulated medium- to large-size EVs in conjunction with improved M-value and AIx75. More research is needed to understand effects of exercise on EVs in the regulation of glucose homeostasis and vascular function. KEY POINTS: Extracellular vesicles (EVs) are increased in states of obesity and may play a role in altered insulin sensitivity and blood pressure; aerobic exercise decreases fasting EV concentrations the following day in adults with obesity. This study directly tested the effects of insulin on EVs and how a single bout of exercise impacts these responses. Together, these data highlight the positive effects of a single bout of exercise on fasting and insulin-stimulated EVs, with the latter relating to increased insulin sensitivity and decreased augmentation index. These results support future research identifying EVs as mechanistic factors in glucose regulation and vascular function as well as clinical use of exercise to reduce cardiovascular disease risk.

A single bout of exhaustive treadmill exercise increased AMPK activation associated with enhanced autophagy in mice skeletal muscle.

Previous studies reported inconsistent findings on autophagy activation in skeletal muscles after acute exercise. In this study, we investigated the effect of a single bout of exhaustive treadmill exercise on AMPK and autophagy activations in mice gastrocnemius muscle in vivo. Male ICR/CD-1mice were randomly divided into the control and exercise groups. The later was subjected to a single bout of exhaustive treadmill exercise. Changes of AMPK, phosphorylation of AMPKThr172 (pAMPKThr172 ), and autophagy markers including Beclin1, LC3II/LC3I and p62mRNA and protein expressions in gastrocnemius muscle at different times (0, 6, 12, 24h) after the exercise were analysed by quantitative real-time PCR and western blot. Our results demonstrated that a single bout of exhaustive treadmill exercise significantly induced AMPK content and AMPK activity at 0, 6 and 12h after the exercise, and changed the expressions of autophagy markers at different time points in the recovery period, respectively. Moreover, we observed positive correlations between expressions of LC3II/LC3I ratio and pAMPKThr172 or AMPK, and a negative correlation between expressions of p62 and AMPK or pAMPKThr172 . In conclusion, a single bout of exhaustive treadmill exercise in mice caused a prolonged activation of AMPK and improved autophagy in the gastrocnemius muscle. The regulation of autophagic markers were related to enhanced AMPK activity. The findings indicate that acute exercise enhanced AMPK-related autophagy activation may be the underlying molecular mechanism that regulates cellular energy metabolism during exercise.