scholarly journals Impact of Different Physical Exercises on the Expression of Autophagy Markers in Mice

2021 ◽  
Vol 22 (5) ◽  
pp. 2635
Author(s):  
Ana P. Pinto ◽  
Alisson L. da Rocha ◽  
Bruno B. Marafon ◽  
Rafael L. Rovina ◽  
Vitor R. Muñoz ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Gastrocnemius Muscle ◽  
Acute Exercise ◽  
Colchicine Treatment ◽  
Heart Tissue ◽  
Beclin 1 ◽  
Liver Protein ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Exercise Induced

Although physical exercise-induced autophagy activation has been considered a therapeutic target to enhance tissue health and extend lifespan, the effects of different exercise models on autophagy in specific metabolic tissues are not completely understood. This descriptive investigation compared the acute effects of endurance (END), exhaustive (ET), strength (ST), and concurrent (CC) physical exercise protocols on markers of autophagy, genes, and proteins in the gastrocnemius muscle, heart, and liver of mice. The animals were euthanized immediately (0 h) and six hours (6 h) after the acute exercise for the measurement of glycogen levels, mRNA expression of Prkaa1, Ppargc1a, Mtor, Ulk1, Becn1, Atg5, Map1lc3b, Sqstm1, and protein levels of Beclin 1 and ATG5. The markers of autophagy were measured by quantifying the protein levels of LC3II and Sqstm1/p62 in response to three consecutive days of intraperitoneal injections of colchicine. In summary, for gastrocnemius muscle samples, the main alterations in mRNA expressions were observed after 6 h and for the ST group, and the markers of autophagy for the CC group were increased (i.e., LC3II and Sqstm1/p62). In the heart, the Beclin 1 and ATG5 levels were downregulated for the ET group. Regarding the markers of autophagy, the Sqstm1/p62 in the heart tissue was upregulated for the END and ST groups, highlighting the beneficial effects of these exercise models. The liver protein levels of ATG5 were downregulated for the ET group. After the colchicine treatment, the liver protein levels of Sqstm1/p62 were decreased for the END and ET groups compared to the CT, ST, and CC groups. These results could be related to diabetes and obesity development or liver dysfunction improvement, demanding further investigations.

scholarly journals Physical exercise increases overall brain oscillatory activity but does not influence inhibitory control in young adults

2018 ◽  
Author(s):  
Luis F. Ciria ◽  
Pandelis Perakakis ◽  
Antonio Luque-Casado ◽  
Daniel Sanabria
Keyword(s):  
Physical Exercise ◽  
Inhibitory Control ◽  
Frequency Band ◽  
Brain Function ◽  
Acute Exercise ◽  
Brain Activity ◽  
Oscillatory Activity ◽  
Power Increase ◽  
Oscillatory Brain Activity ◽  
Exercise Induced

AbstractExtant evidence suggests that acute exercise triggers a tonic power increase in the alpha frequency band at frontal locations, which has been linked to benefits in cognitive function. However, recent literature has questioned such a selective effect on a particular frequency band, indicating a rather overall power increase across the entire frequency spectrum. Moreover, the nature of task-evoked oscillatory brain activity associated to inhibitory control after exercising, and the duration of the exercise effect, are not yet clear. Here, we investigate for the first time steady state oscillatory brain activity during and following an acute bout of aerobic exercise at two different exercise intensities (moderate-to-high and light), by means of a data-driven cluster-based approach to describe the spatio-temporal distribution of exercise-induced effects on brain function without prior assumptions on any frequency range or site of interest. We also assess the transient oscillatory brain activity elicited by stimulus presentation, as well as behavioural performance, in two inhibitory control (flanker) tasks, one performed after a short delay following the physical exercise and another completed after a rest period of 15’ post-exercise to explore the time course of exercise-induced changes on brain function and cognitive performance. The results show that oscillatory brain activity increases during exercise compared to the resting state, and that this increase is higher during the moderate-to-high intensity exercise with respect to the light intensity exercise. In addition, our results show that the global pattern of increased oscillatory brain activity is not specific to any concrete surface localization in slow frequencies, while in faster frequencies this effect is located in parieto-occipital sites. Notably, the exercise-induced increase in oscillatory brain activity disappears immediately after the end of the exercise bout. Neither transient (event-related) oscillatory activity, nor behavioral performance during the flanker tasks following exercise showed significant between-intensity differences. The present findings help elucidate the effect of physical exercise on oscillatory brain activity and challenge previous research suggesting improved inhibitory control following moderate-to-high acute exercise.

scholarly journals Exhaustive acute exercise-induced ER stress is attenuated in IL-6-knockout mice

2019 ◽  
Vol 240 (2) ◽  
pp. 181-193 ◽  
Author(s):  
Ana P Pinto ◽  
Alisson L da Rocha ◽  
Eike B Kohama ◽  
Rafael C Gaspar ◽  
Fernando M Simabuco ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Er Stress ◽  
Knockout Mice ◽  
Acute Exercise ◽  
Stress Proteins ◽  
Serum Levels ◽  
Exercise Protocol ◽  
Caspase 12 ◽  
Exercise Induced ◽  
Eif2 Alpha

The endoplasmic reticulum (ER) stress and inflammation relationship occurs at different levels and is essential for the adequate homeostatic function of cellular systems, becoming harmful when chronically engaged. Intense physical exercise enhances serum levels of interleukin 6 (IL-6). In response to a chronic exhaustive physical exercise protocol, our research group verified an increase of the IL-6 concentration and ER stress proteins in extensor digitorium longus (EDL) and soleus. Based on these results, we hypothesized that IL-6-knockout mice would demonstrate a lower modulation in the ER stress proteins compared to the wild-type mice. To clarify the relationship between exercise-induced IL-6 increased and ER stress, we studied the effects of an acute exhaustive physical exercise protocol on the levels of ER stress proteins in the skeletal muscles of IL-6-knockout (KO) mice. The WT group displayed a higher exhaustion time compared to the IL-6 KO group. After 1 h of the acute exercise protocol, the serum levels of IL-6 and IL-10 were enhanced in the WT group. Independent of the experimental group, the CHOP and cleaved caspase 12/total caspase 12 ratio in EDL as well as ATF6 and CHOP in soleus were sensitive to the acute exercise protocol. Compared to the WT group, the oscillation patterns over time of BiP in EDL and soleus as well as of peIF2-alpha/eIF2-alpha ratio in soleus were attenuated for the IL-6 KO group. In conclusion, IL-6 seems to be related with the ER stress homeostasis, once knockout mice presented attenuation of BiP in EDL and soleus as well as of pEiF2-alpha/EiF2-alpha ratio in soleus after the acute exhaustive physical exercise protocol.

scholarly journals IL-15 Is Required for Postexercise Induction of the Pro-Oxidative Mediators PPARδ and SIRT1 in Male Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (1) ◽  
pp. 143-155 ◽  
Author(s):  
LeBris S. Quinn ◽  
Barbara G. Anderson ◽  
Jennifer D. Conner ◽  
Tami Wolden-Hanson ◽  
Taylor J. Marcell
Keyword(s):  
Physical Exercise ◽  
Gastrocnemius Muscle ◽  
Sirtuin 1 ◽  
Treadmill Running ◽  
Separate Experiment ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Protein Levels ◽  
Deficient Mice

Physical exercise induces transient upregulation of the pro-oxidative mediators peroxisome proliferator-activated receptor-δ (PPARδ), silent information regulator of transcription (sirtuin)-1 (SIRT1), PPARγ coactivator 1α (PGC-1α), and PGC-1β in skeletal muscle. To determine the role of the cytokine IL-15 in acute postexercise induction of these molecules, expression of these factors after a bout of exhaustive treadmill running was examined in the gastrocnemius muscle of untrained control and IL-15–knockout (KO) mice. Circulating IL-15 levels increased transiently in control mice after exercise. Control mice, but not IL-15–KO mice, upregulated muscle PPARδ and SIRT1 protein after exercise, accompanied by a complex pattern of mRNA expression for these factors. However, in exhaustive exercise, control mice ran significantly longer than IL-15–KO mice. Therefore, in a second experiment, mice were limited to a 20-minute run, after which a similar pattern of induction of muscle PPARδ and SIRT1 protein by control mice only was observed. In a separate experiment, IL-15–KO mice injected systemically with recombinant IL-15 upregulated muscle PPARδ and SIRT1 mRNA within 30 minutes and also exhibited increased muscle PPARδ protein levels by 3 hours. After exercise, both control and IL-15–KO mice downregulated IL-15 receptor-α (IL-15Rα) mRNA, whereas IL-15Rα–deficient mice exhibited constitutively elevated circulating IL-15 levels. These observations indicate IL-15 release after exercise is necessary for induction of PPARδ and SIRT1 at the protein level in muscle tissue and suggest that exercise releases IL-15 normally sequestered by the IL-15Rα in the resting state. These findings could be used to develop an IL-15–based strategy to induce many of the metabolic benefits of physical exercise.

scholarly journals Habitual physical activity mediates the acute exercise-induced modulation of anxiety-related amygdala functional connectivity

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yu-Chun Chen ◽  
Chenyi Chen ◽  
Róger Marcelo Martínez ◽  
Jennifer L. Etnier ◽  
Yawei Cheng
Keyword(s):  
Physical Activity ◽  
Functional Connectivity ◽  
Acute Exercise ◽  
Neural Mechanism ◽  
Habitual Physical Activity ◽  
Treadmill Running ◽  
Beneficial Effects ◽  
Fmri Study ◽  
Exercise Induced ◽  
Amygdala Reactivity

AbstractAerobic exercise, in relation to physical activity, has been shown to have beneficial effects on anxiety. However, the underlyig neural mechanism remains elusive. Using a within-subject crossover design, this fMRI study examined how exercise (12-min treadmill running versus walking) mediated amygdala reactivity to explicit and implicit (backward masked) perception of emotional faces in young adults (N = 40). Results showed that acute exercise-induced differences of state anxiety (STAI-S) varied as a function of individual’s habitual physical activity (IPAQ). Subjects with high IPAQ levels showed significant STAI-S reduction (P < 0.05). Path analyses indicated that IPAQ explained 14.67% of the variance in acute exercise-induced STAI-S differences. Running elicited stronger amygdala reactivity to implicit happiness than fear, whereas walking did the opposite. The exercise-induced amygdala reactivity to explicit fear was associated with the IPAQ scores and STAI-S differences. Moreover, after running, the amygdala exhibited a positive functional connectivity with the orbitofrontal cortex and insula to implicit happiness, but a negative connectivity with the parahippocampus and subgenual cingulate to implicit fear. The findings suggest that habitual physical activity could mediate acute exercise-induced anxiolytic effects in regards to amygdala reactivity, and help establish exercise training as a form of anxiolytic therapy towards clinical applications.

Coping with Exercise Induced Spatial Memory Improvement in Morphine Dependent Rats by Inhibiting Brain Derived Neurotrophic Factor (BDNF)

2021 ◽  
Author(s):  
Aboozar Zare ◽  
Vali Nowzari ◽  
Tahereh Karimi-Jashni
Keyword(s):  
Spatial Memory ◽  
Learning And Memory ◽  
Potential Method ◽  
Voluntary Exercise ◽  
Morphine Dependence ◽  
Spatial Learning And Memory ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Neurotropic Factor ◽  
Exercise Induced

Background: Addiction as a chronic disorder that requires long treatment. One way to treating this chronic disease is exercise. Chronic exposure to opiates impairs spatial learning and memory. Given the well-known beneficial effects of voluntary exercise on cognitive functions, we investigated whether voluntary exercise would ameliorate the cognitive deficits that are induced by morphine dependence. If an effect of exercise was observed, we aimed to investigate the possible role of hippocampal brain-derived neurotropic factor (BDNF) in the exercise-induced enhancement of learning and memory in morphine-dependent rats. Methods: The rats were injected with bi-daily doses (10 mg/kg, at 12 hr. intervals) of morphine over a period of 10 days of voluntary exercise. Following these injections, a water maze task was performed twice a day for 5 consecutive days, followed by a probe trial 2 days later. A specific BDNF inhibitor (TrkB-IgG chimera) was used to block the hippocampal BDNF action during the 10 days of voluntary exercise. Results: The voluntary exercise diminished the severity of the rats’ dependency on morphine. A blockade of the BDNF action blunted the exercise-induced improvement of spatial memory, hippocampal neuron counting and BDNF protein levels in the dependent rats. Our results indicate that voluntary exercise could be increase the expression of LTP by lowering the induction threshold for LTP in the DG of morphine-dependent rats. Conclusion: Thus, voluntary exercise might be considered as a potential method to ameliorate some of the deleterious behavioral consequences of the abuse of morphine and other opiates.

Effect of birth weight and 12 weeks of exercise training on exercise-induced AMPK signaling in human skeletal muscle

2013 ◽  
Vol 304 (12) ◽  
pp. E1379-E1390 ◽  
Author(s):  
Brynjulf Mortensen ◽  
Janne R. Hingst ◽  
Nicklas Frederiksen ◽  
Rikke W. W. Hansen ◽  
Caroline S. Christiansen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Birth Weight ◽  
Exercise Training ◽  
Acute Exercise ◽  
Mrna Levels ◽  
Ampk Activation ◽  
Ampk Signaling ◽  
Protein Levels ◽  
Before And After ◽  
Exercise Induced

Subjects with a low birth weight (LBW) display increased risk of developing type 2 diabetes (T2D). We hypothesized that this is associated with defects in muscle adaptations following acute and regular physical activity, evident by impairments in the exercise-induced activation of AMPK signaling. We investigated 21 LBW and 21 normal birth weight (NBW) subjects during 1 h of acute exercise performed at the same relative workload before and after 12 wk of exercise training. Multiple skeletal muscle biopsies were obtained before and after exercise. Protein levels and phosphorylation status were determined by Western blotting. AMPK activities were measured using activity assays. Protein levels of AMPKα1 and -γ1 were significantly increased, whereas AMPKγ3 levels decreased with training independently of group. The LBW group had higher exercise-induced AMPK Thr172 phosphorylation before training and higher exercise-induced ACC2 Ser221 phosphorylation both before and after training compared with NBW. Despite exercise being performed at the same relative intensity (65% of V̇o2peak), the acute exercise response on AMPK Thr172, ACC2 Ser221, AMPKα2β2γ1, and AMPKα2β2γ3 activities, GS activity, and adenine nucleotides as well as hexokinase II mRNA levels were all reduced after exercise training. Increased exercise-induced muscle AMPK activation and ACC2 Ser221 phosphorylation in LBW subjects may indicate a more sensitive AMPK system in this population. Long-term exercise training may reduce the need for AMPK to control energy turnover during exercise. Thus, the remaining γ3-associated AMPK activation by acute exercise after exercise training might be sufficient to maintain cellular energy balance.

Detrimental effect of combined exercise training and eNOS overexpression on cardiac function after myocardial infarction

2009 ◽  
Vol 296 (5) ◽  
pp. H1513-H1523 ◽  
Author(s):  
Monique C. de Waard ◽  
Jolanda van der Velden ◽  
Nicky M. Boontje ◽  
Dick H. W. Dekkers ◽  
Rien van Haperen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Exercise Training ◽  
Left Ventricular ◽  
Lv Function ◽  
Enos Expression ◽  
Beneficial Effects ◽  
Protein Levels ◽  
Enos Uncoupling ◽  
Lv Remodeling ◽  
Exercise Induced

It has been reported that exercise after myocardial infarction (MI) attenuates left ventricular (LV) pump dysfunction by normalization of myofilament function. This benefit could be due to an exercise-induced upregulation of endothelial nitric oxide synthase (eNOS) expression and activity. Consequently, we first tested the hypothesis that the effects of exercise after MI can be mimicked by elevated eNOS expression using transgenic mice with overexpression of human eNOS (eNOSTg). Both exercise and eNOSTg attenuated LV remodeling and dysfunction after MI in mice and improved cardiomyocyte maximal force development (Fmax). However, only exercise training restored myofilament Ca2+-sensitivity and sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)2a protein levels and improved the first derivative of LV pressure at 30 mmHg. Conversely, only eNOSTg improved survival. In view of these partly complementary actions, we subsequently tested the hypothesis that combining exercise and eNOSTg would provide additional protection against LV remodeling and dysfunction after MI. Unexpectedly, the combination of exercise and eNOSTg abolished the beneficial effects on LV remodeling and dysfunction of either treatment alone. The latter was likely due to perturbations in Ca2+ homeostasis, as myofilament Fmax actually increased despite marked reductions in the phosphorylation status of several myofilament proteins, whereas the exercise-induced increases in SERCA2a protein levels were lost in eNOSTg mice. Antioxidant treatment with N-acetylcysteine or supplementation of tetrahydrobiopterin and l-arginine prevented these detrimental effects on LV function while partly restoring the phosphorylation status of myofilament proteins and further enhancing myofilament Fmax. In conclusion, the combination of exercise and elevated eNOS expression abolished the cardioprotective effects of either treatment alone after MI, which appeared to be, at least in part, the result of increased oxidative stress secondary to eNOS “uncoupling.”

scholarly journals Road to exercise mimetics: targeting nuclear receptors in skeletal muscle

2013 ◽  
Vol 51 (3) ◽  
pp. T87-T100 ◽  
Author(s):  
Weiwei Fan ◽  
Annette R Atkins ◽  
Ruth T Yu ◽  
Michael Downes ◽  
Ronald M Evans
Keyword(s):  
Skeletal Muscle ◽  
Physical Exercise ◽  
Nuclear Receptors ◽  
Beneficial Effects ◽  
The Metabolic Syndrome ◽  
Bona Fide ◽  
Exercise Mimetics ◽  
Exercise Induced ◽  
Muscle Energy Metabolism ◽  
Clinical Conditions

Skeletal muscle is the largest organ in the human body and is the major site for energy expenditure. It exhibits remarkable plasticity in response to physiological stimuli such as exercise. Physical exercise remodels skeletal muscle and enhances its capability to burn calories, which has been shown to be beneficial for many clinical conditions including the metabolic syndrome and cancer. Nuclear receptors (NRs) comprise a class of transcription factors found only in metazoans that regulate major biological processes such as reproduction, development, and metabolism. Recent studies have demonstrated crucial roles for NRs and their co-regulators in the regulation of skeletal muscle energy metabolism and exercise-induced muscle remodeling. While nothing can fully replace exercise, development of exercise mimetics that enhance or even substitute for the beneficial effects of physical exercise would be of great benefit. The unique property of NRs that allows modulation by endogenous or synthetic ligands makes them bona fide therapeutic targets. In this review, we present an overview of the current understanding of the role of NRs and their co-regulators in skeletal muscle oxidative metabolism and summarize recent progress in the development of exercise mimetics that target NRs and their co-regulators.

scholarly journals Effects of acute and chronic exercise on sarcolemmal MCT1 and MCT4 contents in human skeletal muscles: current status

2012 ◽  
Vol 302 (1) ◽  
pp. R1-R14 ◽  
Author(s):  
Claire Thomas ◽  
David J. Bishop ◽  
Karen Lambert ◽  
Jacques Mercier ◽  
George A. Brooks
Keyword(s):  
Skeletal Muscle ◽  
Acute Exercise ◽  
Contractile Activity ◽  
Current Status ◽  
Chronic Exercise ◽  
Lactate Transport ◽  
Cross Sectional ◽  
Protein Levels ◽  
General Exercise ◽  
Exercise Induced

Two lactate/proton cotransporter isoforms (monocarboxylate transporters, MCT1 and MCT4) are present in the plasma (sarcolemmal) membranes of skeletal muscle. Both isoforms are symports and are involved in both muscle pH and lactate regulation. Accordingly, sarcolemmal MCT isoform expression may play an important role in exercise performance. Acute exercise alters human MCT content, within the first 24 h from the onset of exercise. The regulation of MCT protein expression is complex after acute exercise, since there is not a simple concordance between changes in mRNA abundance and protein levels. In general, exercise produces greater increases in MCT1 than in MCT4 content. Chronic exercise also affects MCT1 and MCT4 content, regardless of the initial fitness of subjects. On the basis of cross-sectional studies, intensity would appear to be the most important factor regulating exercise-induced changes in MCT content. Regulation of skeletal muscle MCT1 and MCT4 content by a variety of stimuli inducing an elevation of lactate level (exercise, hypoxia, nutrition, metabolic perturbations) has been demonstrated. Dissociation between the regulation of MCT content and lactate transport activity has been reported in a number of studies, and changes in MCT content are more common in response to contractile activity, whereas changes in lactate transport capacity typically occur in response to changes in metabolic pathways. Muscle MCT expression is involved in, but is not the sole determinant of, muscle H+and lactate anion exchange during physical activity.

scholarly journals Myocardial NADPH oxidase-4 regulates the physiological response to acute exercise

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Matthew Hancock ◽  
Anne D Hafstad ◽  
Adam A Nabeebaccus ◽  
Norman Catibog ◽  
Angela Logan ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Exercise Capacity ◽  
Exercise Performance ◽  
Acute Exercise ◽  
Contractile Function ◽  
Beneficial Effects ◽  
Nadph Oxidase 4 ◽  
Endogenous Antioxidants ◽  
Exercise Induced ◽  
Nrf2 Activator

Regular exercise has widespread health benefits. Fundamental to these beneficial effects is the ability of the heart to intermittently and substantially increase its performance without incurring damage, but the underlying homeostatic mechanisms are unclear. We identify the ROS-generating NADPH oxidase-4 (Nox4) as an essential regulator of exercise performance in mice. Myocardial Nox4 levels increase during acute exercise and trigger activation of the transcription factor Nrf2, with the induction of multiple endogenous antioxidants. Cardiomyocyte-specific Nox4-deficient (csNox4KO) mice display a loss of exercise-induced Nrf2 activation, cardiac oxidative stress and reduced exercise performance. Cardiomyocyte-specific Nrf2-deficient (csNrf2KO) mice exhibit similar compromised exercise capacity, with mitochondrial and cardiac dysfunction. Supplementation with an Nrf2 activator or a mitochondria-targeted antioxidant effectively restores cardiac performance and exercise capacity in csNox4KO and csNrf2KO mice respectively. The Nox4/Nrf2 axis therefore drives a hormetic response that is required for optimal cardiac mitochondrial and contractile function during physiological exercise.

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