Plasma Proteomic Kinetics in Response to Acute Exercise.

Regular exercise has many favorable effects on human health, which may be mediated in part by the release of circulating bioactive factors during each bout of exercise. Limited data exist regarding the kinetic responses of plasma proteins during and after acute exercise. Proteomic profiling of 4163 proteins was performed using a large-scale, affinity-based platform in 75 middle-aged adults who were referred for treadmill exercise stress testing. Plasma proteins were quantified at baseline, peak exercise, and 1-h postexercise, and those with significant changes at both exercise timepoints were further examined for their associations with cardiometabolic traits and change with aerobic exercise training in the Health, Risk Factors, Exercise Training and Genetics Family Study, a 20-week exercise intervention study. A total of 765 proteins changed (false discovery rate < 0.05) at peak exercise compared to baseline, and 128 proteins changed (false discovery rate < 0.05) at 1-h postexercise. The 56 proteins that changed at both timepoints included midkine, brain-derived neurotrophic factor, metalloproteinase inhibitor 4, and coiled-coil domain-containing protein 126 and were enriched for secreted proteins. The majority had concordant direction of change at both timepoints. Across all proteins assayed, gene set enrichment analysis showed increased abundance of coagulation-related proteins at 1-h postexercise. Forty-five proteins were associated with at least one measure of adiposity, lipids, glucose homeostasis, or cardiorespiratory fitness in Health, Risk Factors, Exercise Training and Genetics Family Study, and 20 proteins changed with aerobic exercise training. We identified hundreds of novel proteins that change during acute exercise, most of which resolved by 1 h into recovery. Proteins with sustained changes during exercise and recovery may be of particular interest as circulating biomarkers and pathways for further investigation in cardiometabolic diseases. These data will contribute to a biochemical roadmap of acute exercise that will be publicly available for the entire scientific community.

Exercise-induced cortical disinhibition mediates the relationship between fitness and memory in older adults.

Regular exercise benefits learning and memory in older adults, but the neural mechanisms mediating these effects remain unclear. Evidence in young adults indicates that acute exercise creates a favourable environment for synaptic plasticity by enhancing cortical disinhibition. As such, we investigated whether plasticity-related disinhibition mediated the relationship between cardiorespiratory fitness and memory function in healthy older adults (n = 16, mean age = 66.06). Participants completed a graded maximal exercise test and assessments of visual and verbal memory, followed by two counterbalanced sessions involving 20 min of either high-intensity interval training exercise or rest. Disinhibition was measured following intermittent theta burst stimulation via paired-pulse transcranial magnetic stimulation. In line with our hypotheses, we observed a positive correlation between cardiorespiratory fitness and verbal memory, which was mediated by plasticity-related cortical disinhibition. Our novel finding implicates cortical disinhibition as a mechanism through which the effects of acute bouts of exercise may translate to improved memory in older adults. This finding extends current understanding of the physiological mechanisms underlying the positive influence of cardiorespiratory fitness for memory function in older adults, and further highlights the importance of promoting exercise engagement to maintain cognitive health in later life. KEY POINTS: There are well established benefits of regular exercise for memory function in older adults, but the mechanisms are unclear. Cortical disinhibition is important for laying down new memories, and is enhanced following acute exercise in young adults, suggesting it is a potential mechanism underlying these benefits in ageing. Older adults completed a fitness test and assessments of memory, followed by two sessions involving either 20 min of exercise or rest. Disinhibition was measured following intermittent theta burst stimulation via paired-pulse transcranial magnetic stimulation. Cardiorespiratory fitness was positively associated with memory performance. Higher fitness was associated with enhanced cortical disinhibition following acute exercise. Cortical disinhibition completely mediated the relationship between fitness and memory. This novel finding provides a mechanistic account for the positive influence of cardiorespiratory fitness on memory in later life, and emphasises the importance of regular exercise for cognitive health in older populations.

The neuromodulatory role of dopamine in improved reaction time by acute cardiovascular exercise.

Acute cardiovascular physical exercise improves cognitive performance, as evidenced by a reduction in reaction time (RT). However, the mechanistic understanding of how this occurs is elusive and has not been rigorously investigated in humans. Here, using positron emission tomography (PET) with [11 C]raclopride, in a multi-experiment study we investigated whether acute exercise releases endogenous dopamine (DA) in the brain. We hypothesized that acute exercise augments the brain DA system, and that RT improvement is correlated with this endogenous DA release. The PET study (Experiment 1: n = 16) demonstrated that acute physical exercise released endogenous DA, and that endogenous DA release was correlated with improvements in RT of the Go/No-Go task. Thereafter, using two electrical muscle stimulation (EMS) studies (Experiments 2 and 3: n = 18 and 22 respectively), we investigated what triggers RT improvement. The EMS studies indicated that EMS with moderate arm cranking improved RT, but RT was not improved following EMS alone or EMS combined with no load arm cranking. The novel mechanistic findings from these experiments are: (1) endogenous DA appears to be an important neuromodulator for RT improvement and (2) RT is only altered when exercise is associated with central signals from higher brain centres. Our findings explain how humans rapidly alter their behaviour using neuromodulatory systems and have significant implications for promotion of cognitive health. KEY POINTS: Acute cardiovascular exercise improves cognitive performance, as evidenced by a reduction in reaction time (RT). However, the mechanistic understanding of how this occurs is elusive and has not been rigorously investigated in humans. Using the neurochemical specificity of [11 C]raclopride positron emission tomography, we demonstrated that acute supine cycling released endogenous dopamine (DA), and that this release was correlated with improved RT. Additional electrical muscle stimulation studies demonstrated that peripherally driven muscle contractions (i.e. exercise) were insufficient to improve RT. The current study suggests that endogenous DA is an important neuromodulator for RT improvement, and that RT is only altered when exercise is associated with central signals from higher brain centres.

Phosphorylation of AS160-serine 704 is not essential for exercise-increase in insulin-stimulated glucose uptake by skeletal muscles from female or male rats.

One exercise session can increase subsequent insulin-stimulated glucose uptake (ISGU) by skeletal muscle from rodents and humans of both sexes. We recently found that concurrent mutation of three key sites to prevent their phosphorylation (Ser588, Thr642, and Ser704) on Akt substrate of 160 kDa (AS160; also known as TBC1D4) reduced the magnitude of the enhancement of postexercise ISGU (PEX-ISGU) by muscle from male, but not female rats. However, we did not test the role of individual phosphorylation sites on PEX-ISGU. Accordingly, our current aim was to test whether AS160 Ser704 phosphorylation (pSer704) is required for elevated PEX-ISGU by muscle. AS160-knockout (AS160-KO) rats (female and male) were studied when either in sedentary or 3 h after acute exercise. Adeno-associated virus (AAV) vectors were used to enable muscle expression of wild-type AS160 (AAV-WT-AS160) or AS160 mutated Ser704 to alanine to prevent phosphorylation (AAV-1P-AS160). Paired epitrochlearis muscles from each rat were injected with AAV-WT-AS160 or AAV-1P-AS160. We discovered that regardless of sex 1) AS160 abundance in AS160-KO rats was similar in paired muscles expressing WT-AS160 versus 1P-AS160; 2) muscles from exercised versus sedentary rats had greater ISGU, and PEX-ISGU was slightly greater for muscles expressing 1P-AS160 versus contralateral muscles expressing WT-AS160; and 3) pAS160Thr642 was lower in muscles expressing 1P-AS160 versus paired muscles expressing WT-AS160. These results indicate that pAS160Ser704 was not essential for elevated PEX-ISGU by skeletal muscle from rats of either sex. Furthermore, elimination of the postexercise increase in pAS160Thr642 did not lessen the postexercise effect on ISGU.NEW & NOTEWORTHY The current study evaluated the role of Akt substrate of 160 kDa (AS160) phosphorylation on Ser704 in increased insulin-stimulated glucose uptake by skeletal muscle after exercise. Adeno-associated virus vectors were engineered to express either wild-type-AS160 or AS160 mutated so that it could not be phosphorylated on Ser704 in paired muscles from AS160-knockout rats. The results demonstrated that AS160 phosphorylation on Ser704 was not essential for exercise-induced elevation in insulin-stimulated glucose uptake by rats of either sex.

AS160 expression, but not AS160 Serine-588, Threonine-642, and Serine-704 phosphorylation, is essential for elevated insulin-stimulated glucose uptake by skeletal muscle from female rats after acute exercise.

One exercise session can increase subsequent insulin-stimulated glucose uptake (ISGU) by skeletal muscle in both sexes. We recently found that muscle expression and phosphorylation of key sites of Akt substrate of 160 kDa (AS160; also called TBC1D4) are essential for the full-exercise effect on postexercise-ISGU (PEX-ISGU) in male rats. In striking contrast, AS160's role in increased PEX-ISGU has not been rigorously tested in females. Our rationale was to address this major knowledge gap. Wild-type (WT) and AS160-knockout (KO) rats were either sedentary or acutely exercised. Adeno-associated virus (AAV) vectors were engineered to express either WT-AS160 or AS160 mutated on key serine and threonine residues (Ser588, Thr642, and Ser704) to alanine to prevent their phosphorylation. AAV vectors were delivered to the muscle of AS160-KO rats to determine if WT-AS160 or phosphorylation-inactivated AS160 would influence PEX-ISGU. AS160-KO rats have lower skeletal muscle abundance of the GLUT4 glucose transporter protein. This GLUT4 deficit was rescued using AAV delivery of GLUT4 to determine if eliminating muscle GLUT4 deficiency would normalize PEX-ISGU. The novel results were as follows: (1) AS160 expression was required for greater PEX-ISGU; (2) rescuing muscle AS160 expression in AS160-KO rats restored elevated PEX-ISGU; (3) AS160's essential role for the postexercise increase in ISGU was not attributable to reduced muscle GLUT4 content; and (4) AS160 phosphorylation on Ser588, Thr642, and Ser704 was not essential for greater PEX-ISGU. In conclusion, these novel findings revealed that three phosphosites widely proposed to influence PEX-ISGU are not required for this important outcome in female rats.

Changes in the reactive hyperemia index after continuous and interval exercise.

INTRODUCTION: High-intensity interval exercise (HIIE) is more effective than moderate-intensity interval exercise (MICE) for improving macrovascular function (e.g., flow-mediated dilation), but less is known regarding the effect of HIIE on microvascular function. We used peripheral artery tonometry to measure the reactive hyperemia index (RHI) and examine the acute effects of HIIE and MICE on microvascular function. METHODS: Ten healthy participants (50% men, age: 26 ± 5 years, mass: 75.6 ± 15.1 kg, height: 170 ± 10 cm, body mass index: 26.0 ± 3.1 kg∙m-2) performed single bouts of HIIE and MICE cycling on separate occasions. The MICE protocol was 20 min at 60% of maximum power output. The HIIE protocol was a 12-min warm up at 50% of maximum power output immediately followed by an 8-min Tabata protocol where participants alternated between cycling at ⩾ 100% max power (20 sec) and rest (10 sec). The RHI was measured before, immediately after, and 1 h after exercise and compared by two-way repeated measures analysis of variance (condition [MICE, HIIE] and time [pre-, post-, and 1-h postexercise]). RESULTS: Compared to baseline, RHI increased 1 h after MICE only (p = 0.02). Heart rate was higher during MICE at 5 and 10 min (p = 0.02) and higher during HIIE at min 20 (p < 0.01). CONCLUSION: Within a sample of healthy adults, the RHI was improved 1 h after a single session of MICE but not HIIE. Future research is needed to determine the significance of the differential effects of exercise regimens on the macro- and microvasculature.

Time-course and muscle-specific gene expression of matrix metalloproteinases and inflammatory cytokines in response to acute treadmill exercise in rats.

BACKGROUND: The extracellular matrix (ECM) of skeletal muscle plays a pivotal role in tissue repair and growth, and its remodeling tightly regulated by matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), and inflammatory cytokines. This study aimed to investigate changes in the mRNA expression of MMPs (Mmp-2 and Mmp-14), TIMPs (Timp-1 and Timp-2), and inflammatory cytokines (Il-1ß, Tnf-α, and Tgfß1) in the soleus (SOL) and extensor digitorum longus (EDL) muscles of rats following acute treadmill exercise. Additionally, muscle morphology was examined using hematoxylin and eosin (H&E) staining. METHODS AND RESULTS: Male rats were subjected to acute treadmill exercise at 25 m/min for 60 min with a %0 slope. The mRNA expression of ECM components and muscle morphology in the SOL and EDL were assessed in both sedentary and exercise groups at various time points (immediately (0) and 1, 3, 6, 12, and 24 h post-exercise). Our results revealed a muscle-specific response, with early upregulation of the mRNA expression of Mmp-2, Mmp-14, Timp-1, Timp-2, Il-1ß, and Tnf-α observed in the SOL compared to the EDL. A decrease in Tgfß1 mRNA expression was evident in the SOL at all post-exercise time points. Conversely, Tgfß1 mRNA expression increased at 0 and 3 h post-exercise in the EDL. Histological analysis also revealed earlier cell infiltration in the SOL than in the EDL following acute exercise. CONCLUSIONS: Our results highlight how acute exercise modulates ECM components and muscle structure differently in the SOL and EDL muscles, leading to distinct muscle-specific responses.

Inverted U-shape-like functional connectivity alterations in cognitive resting-state networks depending on exercise intensity: An fMRI study.

Acute physical activity influences cognitive performance. However, the relationship between exercise intensity, neural network activity, and cognitive performance remains poorly understood. This study examined the effects of different exercise intensities on resting-state functional connectivity (rsFC) and cognitive performance. Twenty male athletes (27.3 ± 3.6 years) underwent cycling exercises of different intensities (high, low, rest/control) on different days in randomized order. Before and after, subjects performed resting-state functional magnetic resonance imaging and a behavioral Attention Network Test (ANT). Independent component analysis and Linear mixed effects models examined rsFC changes within ten resting-state networks. No significant changes were identified in ANT performance. Resting-state analyses revealed a significant interaction in the Left Frontoparietal Network, driven by a non-significant rsFC increase after low-intensity and a significant rsFC decrease after high-intensity exercise, suggestive of an inverted U-shape relationship between exercise intensity and rsFC. Similar but trend-level rsFC interactions were observed in the Dorsal Attention Network (DAN) and the Cerebellar Basal Ganglia Network. Explorative correlation analysis revealed a significant positive association between rsFC increases in the right superior parietal lobule (part of DAN) and better ANT orienting in the low-intensity condition. Results indicate exercise intensity-dependent subacute rsFC changes in cognition-related networks, but their cognitive-behavioral relevance needs further investigation.

Mindfulness induction and executive function after high-intensity interval training with and without mindful recovery intervals.

OBJECTIVES: Determine the effect of incorporating mindfulness-based activities into the recovery intervals of high-intensity interval training (HIIT) on mindfulness induction and subsequent executive function performance. DESIGNS: A within-subject crossover trial. METHODS: Forty adults participated in two experimental conditions, including a 30-min bout of HIIT involving mindfulness recovery intervals (Mindful) and a 30-min bout of HIIT without mindfulness recovery intervals (Non-mindful), on two separate days in counterbalanced order. Before and after each condition, participants completed the flanker task, switch-flanker task, and n-back task to measure inhibitory control, cognitive flexibility, and working memory, respectively. RESULTS: A higher level of mindfulness state was observed following the Mindful condition than the Non-mindful condition. Dispositional mindfulness was positively correlated with the level of the mindful state only during the Mindful condition but not the Non-mindful condition. The switch-flanker response accuracy was improved from the pretest to posttest during the Non-mindful condition but remained unchanged over time during the Mindful condition. Time-related improvements in the flanker and n-back task outcomes were observed for both the Mindful and Non-mindful conditions and did not differ between conditions. CONCLUSION: Although incorporating mindfulness-based activities during the recovery intervals of HIIT successfully led to greater state-related mindfulness, such a heightened mindful state did not correspond with additional modulation in inhibitory control and working memory performance while attenuating HIIT-related positive changes in task performance requiring cognitive flexibility.

Post-acute exercise cardiovagal modulation in older male adults with and without type 2 diabetes.

PURPOSE: We examined heart rate variability (HRV) and baroreflex sensitivity (BRS) disease- and age-related response at 10-and 60-min after an acute high-intensity interval (HIIE) and moderate continuous exercise (MICE) in older adults with and without type 2 diabetes mellitus (T2DM) and healthy young adults. METHODS: Twelve older male adults with (57-84 years) and without T2DM (57-76 years) and 12 healthy young male adults (20-40 years) completed an isocaloric acute bout of HIIE, MICE, and a non-exercise condition in a randomized order. Time and Wavelets-derived frequency domain indices of HRV and BRS were obtained in a supine position and offline over 2-min time-bins using Matlab. RESULTS: HIIE but not MICE reduced natural logarithm root mean square of successive differences (Ln-RMSSD) (d = - 0.85; 95% CI - 1.15 to - 0.55 ms, p < 0.001), Ln-high-frequency power (d = - 1.60; 95% CI - 2.24 to - 0.97 ms2; p < 0.001), and BRS (d = - 6.32; 95% CI - 9.35 to - 3.29 ms/mmHg, p < 0.001) in adults without T2DM (averaged over young and older adults without T2DM), returning to baseline 60 min into recovery. These indices remained unchanged in older adults with T2DM after HIIE and MICE. Older adults with T2DM had lower resting Ln-RMSSD and BRS than aged-matched controls (Ln-RMSSD, d = - 0.71, 95% CI - 1.16 to - 0.262 ms, p = 0.001; BRS d = - 3.83 ms/mmHg), 95% CI - 6.90 to - 0.76, p = 0.01). CONCLUSIONS: Cardiovagal modulation following acute aerobic exercise is intensity-dependent only in adults without T2DM, and appears age-independent. These findings provide evidence of cardiac autonomic impairments in older adults with T2DM at rest and following aerobic exercise.

Acute exercise might not affect subsequent appetite responses to a fixed meal in adolescents with obesity: The SMASH exploratory study.

While an intensity-dependent post-exercise decrease in energy intake (EI) has been described in adolescents with obesity, studies invariably used ad libitum meals, limiting then any conclusions regarding the effect of exercise on post-meal appetitive responses that can be also impacted by the ad libitum nature of the meal. This study analyses appetite and food-reward related responses to a fixed meal after an acute exercise, also exploring the associations between substrate use during exercise and overall daily EI in adolescents with obesity. Thirteen adolescents with obesity (12-16 years, 5 males) randomly complete 2 experimental sessions: (i) a control condition (CON); (ii) a 30-min moderate intensity (65% VO2peak) cycling condition (EX). Energy expenditure and substrate oxidation were measured during both 30 min of rest (CON) or exercise (EX). Ad libitum EI, macronutrient intake and relative EI were assessed at dinner, subjective appetite sensations taken at regular intervals and food reward measured before and after lunch as well as before dinner. Energy and macronutrient intake did not differ between conditions, as well as appetite feelings. A time effect (p = 0.012) was observed between pre and post meal for choice fat bias in both conditions but was only significant within the CON condition (p = 0.004). CHO oxidation during exercise was found correlated with both EI (r = 0.586, p = 0.045), pre-lunch hunger (r = 0.624, p = 0.030), daily AUC for hunger and DTE (r = 0.788, p = 0.002 and r = 0.695; p = 0.012 respectively). This exploratory study highlights that acute exercise might not affect subsequent appetite responses when using a fixed test meal in adolescents with obesity.

Acute Effects of Cadence-Controlled Walking on Cognition and Vascular Function in Physically Inactive Older Adults: A Randomized Crossover Study.

BACKGROUND: Cadence-controlled walking may be a desirable approach for older adults to self-monitor exercise intensity and achieve physical activity guidelines. We examined the acute effects of cadence-controlled walking on cognition and vascular function in physically inactive older adults. METHODS: In a randomized crossover design, 26 participants (65% females, 67.8 ± 11.3 years) underwent 30-min acute exercise (walking at 100 steps/min) and control (sitting) conditions. We measured cognition, central blood pressure (BP), and arterial stiffness before, and immediately, after each condition. RESULTS: We observed significant Time × Condition interactions in the Flanker Inhibitory Control and Attention (Flanker) test and Dimensional Change Card Sort (DCCS) test scores, and in central systolic BP, central pulse pressure, and carotid to femoral pulse wave velocity (p < .05). The Flanker and DCCS scores significantly increased after walking (d = 0.4 and 0.5, respectively), but not after sitting. Central systolic BP, central pulse pressure, and carotid to femoral pulse wave velocity significantly increased after sitting but remained unchanged after acute walking (d = 0.4-0.2), with p-values < .05. After walking, significant correlations were observed between DCCS and diastolic BP and central pulse pressure change scores and change scores in central pulse wave velocity, Flanker, and DCCS (rs = -0.45 to -0.52). CONCLUSION: These findings suggest that a single bout of cadence-controlled walking elicited an immediate improvement in cognition and might have mitigated increases in arterial stiffness and central BP observed in the seated control condition. Further research is needed to examine the association between cognition and vascular function following acute exercise compared to control conditions. SIGNIFICANCE: Our findings may have practical implications for developing daily physical activity recommendations for improving the cognitive health for successful aging.

The Acute, Short-, and Long-Term Effects of Endurance Exercise on Skeletal Muscle Transcriptome Profiles.

A better understanding of the cellular and molecular mechanisms that are involved in skeletal muscle adaptation to exercise is fundamentally important to take full advantage of the enormous benefits that exercise training offers in disease prevention and therapy. The aim of this study was to elucidate the transcriptional signatures that distinguish the endurance-trained and untrained muscles in young adult males (24 ± 3.5 years). We characterized baseline differences as well as acute exercise-induced transcriptome responses in vastus lateralis biopsy specimens of endurance-trained athletes (ET; n = 8; VO2max, 67.2 ± 8.9 mL/min/kg) and sedentary healthy volunteers (SED; n = 8; VO2max, 40.3 ± 7.6 mL/min/kg) using microarray technology. A second cohort of SED volunteers (SED-T; n = 10) followed an 8-week endurance training program to assess expression changes of selected marker genes in the course of skeletal muscle adaptation. We deciphered differential baseline signatures that reflected major differences in the oxidative and metabolic capacity of the endurance-trained and untrained muscles. SED-T individuals in the training group displayed an up-regulation of nodal regulators of oxidative adaptation after 3 weeks of training and a significant shift toward the ET signature after 8 weeks. Transcriptome changes provoked by 1 h of intense cycling exercise only poorly overlapped with the genes that constituted the differential baseline signature of ETs and SEDs. Overall, acute exercise-induced transcriptional responses were connected to pathways of contractile, oxidative, and inflammatory stress and revealed a complex and highly regulated framework of interwoven signaling cascades to cope with exercise-provoked homeostatic challenges. While temporal transcriptional programs that were activated in SEDs and ETs were quite similar, the quantitative divergence in the acute response transcriptomes implicated divergent kinetics of gene induction and repression following an acute bout of exercise. Together, our results provide an extensive examination of the transcriptional framework that underlies skeletal muscle plasticity.

A study on the impact of acute exercise on cognitive function in Alzheimer's disease or mild cognitive impairment patients: A narrative review.

This narrative review follows the JBI approach and comprehensively explores the effects and mechanisms of acute exercise on cognitive function in Alzheimer's disease (AD) and Mild cognitive impairment (MCI) patients. The results showed that the combination of acute exercise and cognitive training improved the cognitive function of AD patients better than aerobic exercise or resistance training alone. For patients with MCI, moderate intensity acute aerobic exercise and resistance exercise were beneficial to enhance Inhibitory control (IC), but high-intensity acute exercise was adverse to improve IC; Brain-derived neurotrophic factor (BDNF) and Insulin-like growth factor 1 (IGF-1) may assume the potential mediating mechanism of acute exercise on cognitive function in AD and MCI patients, but more research is needed to further confirm this mechanism.

Acute exercise increases the contact between lipid droplets and mitochondria independently of obesity and type 2 diabetes.

Intramuscular lipid droplets (LDs) and mitochondria are essential organelles in cellular communication and metabolism, supporting local energy demands during muscle contractions. While insulin resistance impacts cellular functions and systems within the skeletal muscle, it remains unclear whether the interaction of LDs and mitochondria is affected by exercise and the role of obesity and type 2 diabetes. By employing transmission electron microscopy (TEM), we aimed to investigate the effects of 1 h of ergometry cycling on LD morphology, subcellular distribution and mitochondrial contact in skeletal muscle fibres of patients with type 2 diabetes and glucose-tolerant lean and obese controls, matched for equal exercise intensities. Exercise did not change LD volumetric density, numerical density, profile size or subcellular distribution. However, evaluated as the magnitude of inter-organelle contact, exercise increased the contact between LDs and mitochondria with no differences between the three groups. This effect was most profound in the subsarcolemmal space of type 1 muscle fibres, and here the absolute contact length increased on average from ∼275 to ∼420 nm. Furthermore, the absolute contact length before exercise (ranging from ∼140 to ∼430 nm) was positively associated with the fat oxidation rate during exercise. In conclusion, we showed that acute exercise did not mediate changes in the LD volume fractions, numbers or size but increased the contact between LDs and mitochondria, irrespective of obesity or type 2 diabetes. These data suggest that the increased LD-mitochondria contact with exercise is not disturbed in obesity or type 2 diabetes. KEY POINTS: Type 2 diabetes is associated with altered interactivity between lipid droplets (LDs) and mitochondria in the skeletal muscle. Physical contact between the surface of LDs and the surrounding mitochondrial network is considered favourable for fat oxidation. We show that 1 h of acute exercise increases the length of contact between LDs and mitochondria, irrespective of obesity or type 2 diabetes. This contact length between LDs and mitochondria is not associated with a net decrease in the LD volumetric density after the acute exercise. However, it correlates with the fat oxidation rate during exercise. Our data establish that exercise mediates contact between LDs and the mitochondrial network and that this effect is not impaired in individuals with type 2 diabetes or obesity.

Maximal Exercise Improves the Levels of Endothelial Progenitor Cells in Heart Failure Patients.

The impact of exercise on the levels of endothelial progenitor cells (EPCs), a marker of endothelial repair and angiogenesis, and circulating endothelial cells (CECs), an indicator of endothelial damage, in heart failure patients is largely unknown. This study aims to evaluate the effects of a single exercise bout on the circulating levels of EPCs and CECs in heart failure patients. Thirteen patients with heart failure underwent a symptom-limited maximal cardiopulmonary exercise test to assess exercise capacity. Before and after exercise testing, blood samples were collected to quantify EPCs and CECs by flow cytometry. The circulating levels of both cells were also compared to the resting levels of 13 volunteers (age-matched group). The maximal exercise bout increased the levels of EPCs by 0.5% [95% Confidence Interval, 0.07 to 0.93%], from 4.2 × 10-3 ± 1.5 × 10-3% to 4.7 × 10-3 ± 1.8 × 10-3% (p = 0.02). No changes were observed in the levels of CECs. At baseline, HF patients presented reduced levels of EPCs compared to the age-matched group (p = 0.03), but the exercise bout enhanced circulating EPCs to a level comparable to the age-matched group (4.7 × 10-3 ± 1.8 × 10-3% vs. 5.4 × 10-3 ± 1.7 × 10-3%, respectively, p = 0.14). An acute bout of exercise improves the potential of endothelial repair and angiogenesis capacity by increasing the circulating levels of EPCs in patients with heart failure.

Acute impact of aerobic exercise on local cutaneous thermal hyperaemia.

Little is known about the acute changes in cutaneous microvascular function that occur in response to exercise, the accumulation of which may provide the basis for beneficial chronic cutaneous vascular adaptations. Therefore, we examined the effects of acute exercise on cutaneous thermal hyperaemia. Twelve healthy, recreationally active participants (11 male, 1 female) performed 30-minute cycling at 50 % (low-intensity exercise, LOW) or 75 % (high-intensity exercise, HIGH) maximum heart rate. Laser Doppler flowmetry (LDF) and rapid local skin heating were used to quantify cutaneous thermal hyperaemia before (PRE), immediately following (IMM) and 1-h (1HR) after exercise. Baseline, axon reflex peak, axon reflex nadir, plateau, maximum skin blood flow responses to rapid local heating (42 °C for 30-min followed by 44 °C for 15-min) at each stage were assessed and indexed as cutaneous vascular conductance [CVC = flux / mean arterial blood pressure (MAP), PU·mm Hg-1], and expressed as a percentage of maximum (%CVCmax). Exercise increased heart rate (HR), MAP and skin blood flow (all P < 0.001), and to a greater extent during HIGH (all P < 0.001). The axon reflex peak and nadir were increased immediately and 1-h after exercise (all comparisons P < 0.01 vs. PRE), which did not differ between intensities (peak: P = 0.34, axon reflex nadir: P = 0.91). The endothelium-dependent plateau response was slightly elevated after exercise (P = 0.06), with no effect of intensity (P = 0.58) nor any interaction effect (P = 0.55). CONCLUSION: Exercise increases cutaneous microvascular axonal responses to local heating for up to 1-h, suggesting an augmented sensory afferent function post-exercise. Acute exercise may only modestly affect endothelial function in cutaneous microcirculation.

Cerebrospinal fluid and plasma metabolomics of acute endurance exercise.

Metabolomics has emerged as a powerful new tool in precision medicine. No studies have yet been published on the metabolomic changes in cerebrospinal fluid (CSF) produced by acute endurance exercise. CSF and plasma were collected from 19 young active adults (13 males and 6 females) before and 60 min after a 90-min monitored outdoor run. The median age, BMI, and VO2 max of subjects was 25 years (IQR 22-31), 23.2 kg/m2 (IQR 21.7-24.5), and 47 ml/kg/min (IQR 38-51), respectively. Targeted, broad-spectrum metabolomics was performed by liquid chromatography, tandem mass spectrometry (LC-MS/MS). In the CSF, purines and pyrimidines accounted for 32% of the metabolic impact after acute endurance exercise. Branch chain amino acids, amino acid neurotransmitters, fatty acid oxidation, phospholipids, and Krebs cycle metabolites traceable to mitochondrial function accounted for another 52% of the changes. A narrow but important channel of metabolic communication was identified between the brain and body by correlation network analysis. By comparing these results to previous work in experimental animal models, we found that over 80% of the changes in the CSF correlated with a cascade of mitochondrial and metabolic changes produced by ATP signaling. ATP is released as a co-neurotransmitter and neuromodulator at every synapse studied to date. By regulating brain mitochondrial function, ATP release was identified as an early step in the kinetic cascade of layered benefits produced by endurance exercise.

Meta-Analysis of Electroencephalographic Correlates and Cognitive Performance for Acute Exercise-Induced Modulation.

INTRODUCTION: Although abundant research delving into the acute exercise-induced modulation of cognitive performance and the P300-ERP component has been conducted, there is a lack of consensus regarding whether or not this type of intervention has a beneficial effect on cognition and how it relates to the P300-ERP. METHODS: To examine the possible sources of this discrepancy, we conducted a meta-analysis of ERP results together with cognitive performance that were systemically stratified by relevant demographic and methodological moderators. RESULTS: Our results indicate that while acute exercise exerted an overall stable effect on cognitive improvement, associated with enlarged P300 amplitudes, the effect size varied across factors of age, biological sex, exercise intensity, exercise type, control type, and experimental design. Future research taking into consideration modulating factors as to avoid misestimating the beneficial effects of acute exercise are encouraged. CONCLUSION: All in all, and to our knowledge, this is the first meta-analysis quantitatively summarizing the relevant literature on the associations between P300-ERP correlates, acute exercise, and its positive influence on attention and cognitive performance in healthy individuals.

The effect of acute exercise on attentional control and theta power in young adults.

Exercise has a profound impact on one's health, and it is becoming increasingly accepted that exercise also benefits cognitive functioning. Yet, the neural mechanism for which cognitive enhancement occurs is less understood. Therefore, the purpose of our study was to experimentally test whether an acute exercise activity was able to increase theta power and behavioral performance during an executive functioning attentional control task. Participants were randomly assigned to either a stationary-bike exercise or a resting control condition. Thereafter, they completed the Eriksen flanker task, and most participants completed this while EEG data were recorded. From the flanker task data, we demonstrated an interaction effect from both accuracy and reaction time measurements. Importantly, the exercise group was more accurate than the control group in incongruent trials. From the EEG data, theta power was overall higher in the exercise group, especially during the congruent trials, compared to controls. Our results add to the limited but growing body of research that suggests acute exercise produces a general increase in theta power, which in turn may play a role in enhancing cognitive performance. These results, combined with previous research, could have widespread implications in multiple settings such as in the investigation of a biomarker of physical fitness, neurorehabilitation, and in education.