Loaded wheel running and muscle adaptation in the mouse

2005 ◽  
Vol 289 (1) ◽  
pp. H455-H465 ◽  
Author(s):  
John P. Konhilas ◽  
Ulrika Widegren ◽  
David L. Allen ◽  
Angelika C. Paul ◽  
Allison Cleary ◽  
...  
Keyword(s):  
Exercise Training ◽  
Wheel Running ◽  
Glycogen Synthase ◽  
Physiological Adaptation ◽  
Muscle Adaptation ◽  
Differential Impact ◽  
Cross Sectional ◽  
Biochemical Adaptation ◽  
Physiological Cardiac Hypertrophy ◽  
Exercise Induced

Voluntary cage wheel exercise has been used extensively to determine the physiological adaptation of cardiac and skeletal muscle in mice. In this study, we tested the effect of different loading conditions on voluntary cage wheel performance and muscle adaptation. Male C57Bl/6 mice were exposed to a cage wheel with no-resistance (NR), low-resistance (LR), or high-resistance (HR) loads for 7 wk. Power output was elevated (3-fold) under increased loading (LR and HR) conditions compared with unloaded (NR) exercise training. Only unloaded (NR) exercise induced an increase in heart mass, whereas only loaded (LR and HR) exercise training induced an increase in skeletal (soleus) muscle mass. Moreover, unloaded and loaded exercise training had a differential impact on the cross-sectional area of muscle fibers, depending on the type of myosin heavy chain expressed by each fiber. The biochemical adaptation of the heart was characterized by a decrease in genes associated with pathological (but not physiological) cardiac hypertrophy and a decrease in calcineurin expression in all exercise groups. In addition, transcriptional activity of myocyte enhancer factor-2 (MEF-2) was significantly decreased in the hearts of the LR group as determined by a MEF-2-dependent transgene driving the expression of β-galactosidase. Phosphorylation of glycogen synthase kinase-3β, protein kinase B (Akt), and p70 S6 kinase was increased only in the hearts of the NR group, consistent with the significant increase in cardiac mass. In conclusion, unloaded and loaded cage wheel exercise have a differential impact on cage wheel performance and muscle (cardiac and skeletal) adaptation.

scholarly journals Animal models in the study of exercise-induced cardiac hypertrophy

2010 ◽  
pp. 633-644 ◽  
Author(s):  
Y Wang ◽  
U Wisloff ◽  
OJ Kemi
Keyword(s):  
Animal Models ◽  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Wheel Running ◽  
Experimental Models ◽  
Laboratory Animals ◽  
Training Models ◽  
Advantages And Disadvantages ◽  
Experimental Approaches ◽  
Exercise Induced

Exercise training-induced cardiac hypertrophy occurs following a program of aerobic endurance exercise training and it is considered as a physiologically beneficial adaptation. To investigate the underlying biology of physiological hypertrophy, we rely on robust experimental models of exercise training in laboratory animals that mimic the training response in humans. A number of experimental strategies have been established, such as treadmill and voluntary wheel running and swim training models that all associate with cardiac growth. These approaches have been applied to numerous animal models with various backgrounds. However, important differences exist between these experimental approaches, which may affect the interpretation of the results. Here, we review the various approaches that have been used to experimentally study exercise training-induced cardiac hypertrophy; including the advantages and disadvantages of the various models.

Abstract 1509: Exercise Training Started Before Myocardial Infarction Improves Survival but Aggravates Left Ventricular Dysfunction

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Monique C de Waard ◽  
Dirk J Duncker
Keyword(s):  
Myocardial Infarction ◽  
Exercise Training ◽  
Wheel Running ◽  
Left Ventricular ◽  
Lv Function ◽  
Cardiac Events ◽  
Cross Sectional ◽  
Voluntary Wheel Running ◽  
Lv Dysfunction ◽  
Voluntary Wheel

Introduction: Regular physical activity in patients with established coronary heart disease not only reduces the incidence of cardiac events, but also reduces the risk of all-cause mortality. Recently, we showed in mice that exercise training (EX) started immediately after myocardial infarction (MI) ameliorates left ventricular (LV) dysfunction. Here we tested the hypothesis that additional exercise training prior to an acute MI, i.e. a higher level of physical fitness at the time of MI, is associated with improved survival and attenuated LV dysfunction after MI. Methods and Results: MI was induced by permanent coronary ligation in 128 C57Bl/6 mice and subsequently followed by 8 weeks of voluntary wheel running (MI-EX) or sedentary housing (MI). In a third group, voluntary wheel running was started two weeks before induction of MI (EX-MI-EX). Sham operated mice served as controls. EX after MI had no effect on survival, infarct size, LV hypertrophy or dilation (Table ). However, EX improved LV function, reflected in enhanced LV fractional shortening (FS), rate of rise in LV pressure at 30 mmHg (LVdP/dt P30 ), and decreased pulmonary congestion and right ventricular weight (RVW). When EX was started prior to MI, post-MI survival nearly doubled and mice ran an average post-MI distance of ~7km/d compared to ~5km/d in MI-EX mice. Infarct cross-sectional area was larger, which was principally due to an increased infarct thickness (0.15±0.02mm EX-MI-EX vs 0.11±0.01mm MI; P =0.06). Surprisingly, however, LV hypertrophy and dysfunction were aggravated in the EX-MI-EX group compared to MI-EX. Conclusion: In line with our hypothesis, EX started prior to MI improved survival. However, contrary to our hypothesis, the improved survival was associated with a deterioration of LV dysfunction. The latter may have been the result of survival and hence inclusion of mice with the most severe LV dysfunction.

scholarly journals Variability in training-induced skeletal muscle adaptation

2011 ◽  
Vol 110 (3) ◽  
pp. 846-853 ◽  
Author(s):  
James A. Timmons
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Gene Networks ◽  
Endurance Performance ◽  
Transcript Abundance ◽  
Physiological Adaptation ◽  
Muscle Adaptation ◽  
Genetic And Environmental Factors ◽  
Response To Exercise ◽  
Molecular Bases

When human skeletal muscle is exposed to exercise training, the outcomes, in terms of physiological adaptation, are unpredictable. The significance of this fact has long been underappreciated, and only recently has progress been made in identifying some of the molecular bases for the heterogeneous response to exercise training. It is not only of great medical importance that some individuals do not substantially physiologically adapt to exercise training, but the study of the heterogeneity itself provides a powerful opportunity to dissect out the genetic and environmental factors that limit adaptation, directly in humans. In the following review I will discuss new developments linking genetic and transcript abundance variability to an individual's potential to improve their aerobic capacity or endurance performance or induce muscle hypertrophy. I will also comment on the idea that certain gene networks may be associated with muscle “adaptability” regardless the stimulus provided.

scholarly journals Contribution of IL-6 to the Hsp72, Hsp25, and αβ-crystallin responses to inflammation and exercise training in mouse skeletal and cardiac muscle

2008 ◽  
Vol 105 (6) ◽  
pp. 1830-1836 ◽  
Author(s):  
Kimberly A. Huey ◽  
Benjamin M. Meador
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Cardiac Muscle ◽  
Wheel Running ◽  
Protein Levels ◽  
Cardiac Muscles ◽  
Exercise Induced ◽  
Shock Proteins ◽  
Dependent Mechanism

The heat shock proteins (Hsps) Hsp72, Hsp25, and αβ-crystallin (αβC) may protect tissues during exercise and/or inflammatory insults; however, no studies have investigated whether exercise training increases both basal and inflammation-induced expression of these Hsps in skeletal or cardiac muscle. IL-6 is produced by muscle during both exercise and inflammation and has been shown to modulate Hsp expression. These studies tested the hypothesis that voluntary wheel running (RW) increases basal and inflammation-induced Hsp72, Hsp25, and αβC protein through an IL-6-dependent mechanism. We compared Hsp72, Hsp25, αβC, and IL-6 protein levels 4 h after systemic inflammation induced by lipopolysaccharide (LPS) in skeletal and cardiac muscles of wild-type (IL-6+/+) and IL-6 deficient (IL-6−/−) mice after 2 wk of RW or normal cage activity (Sed). LPS significantly increased skeletal Hsp72 and Hsp25 relative to saline in Sed IL-6+/+, but not IL-6−/− mice. LPS increased Hsp72 relative to saline in Sed IL-6+/+ cardiac muscle. RW increased basal Hsp72, Hsp25, and αβC in skeletal muscle in IL-6+/+ and IL-6−/− mice. However, LPS was not associated with increases in any Hsp in RW IL-6+/+ or IL-6−/− mice. LPS increased IL-6 protein in skeletal muscle and plasma in Sed and RW groups, with a significantly greater response in RW. The major results provide the first in vivo evidence that the absence of IL-6 is associated with reduced skeletal muscle Hsp72 and Hsp25 responses to LPS, but that IL-6 is not required for exercise-induced Hsp upregulation in skeletal or cardiac muscle.

scholarly journals An inducible knockout of Dicer in adult mice does not affect endurance exercise-induced muscle adaptation

2019 ◽  
Vol 316 (2) ◽  
pp. C285-C292 ◽  
Author(s):  
Satoshi Oikawa ◽  
Minjung Lee ◽  
Norio Motohashi ◽  
Seiji Maeda ◽  
Takayuki Akimoto
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Citrate Synthase ◽  
Wheel Running ◽  
Fiber Type ◽  
Tamoxifen Treatment ◽  
Muscle Adaptation ◽  
Adult Skeletal Muscle ◽  
Significant Difference ◽  
Exercise Induced

The contractile and metabolic properties of adult skeletal muscle change in response to endurance exercise. The mechanisms of transcriptional regulation in exercise-induced skeletal muscle adaptation, including fiber-type switching and mitochondrial biogenesis, have been investigated intensively, whereas the role of microRNA (miRNA)-mediated posttranscriptional gene regulation is less well understood. We used tamoxifen-inducible Dicer1 knockout (iDicer KO) mice to reduce the global expression of miRNAs in adult skeletal muscle and subjected these mice to 2 wk of voluntary wheel running. Dicer mRNA expression was completely depleted in fast-twitch plantaris muscle after tamoxifen injection. However, several muscle-enriched miRNAs, including miR-1 and miR-133a, were reduced by only 30–50% in both the slow and fast muscles. The endurance exercise-induced changes that occurred for many parameters (i.e., fast-to-slow fiber-type switch and increases in succinate dehydrogenase, respiratory chain complex II, and citrate synthase activity) in wild type (WT) also occurred in the iDicer KO mice. Protein expression of myosin heavy chain IIa, peroxisome proliferator-activated receptor-γ coactivator-1α, and cytochrome c complex IV was also increased in the iDicer KO mice by the voluntary running. Furthermore, there was no significant difference in oxygen consumption rate in the isolated mitochondria between the WT and iDicer KO mice. These data indicate that muscle-enriched miRNAs were detectable even after 4 wk of tamoxifen treatment and there was no apparent specific endurance-exercise-induced muscle phenotype in the iDicer KO mice.

scholarly journals Molecular Mechanisms of Nigella sativa- and Nigella sativa Exercise-Induced Cardiac Hypertrophy in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Lubna Ibrahim Al Asoom
Keyword(s):  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Molecular Mechanisms ◽  
Nigella Sativa ◽  
Male Rats ◽  
Cell Diameter ◽  
Vigorous Exercise ◽  
Physiological Cardiac Hypertrophy ◽  
Igf I ◽  
Exercise Induced

Background. In our lab, we demonstrated cardiac hypertrophy induced by long-term administration of Nigella sativa (Ns) with enhanced function. Therefore, we aim to investigate the molecular mechanisms of Ns-induced cardiac hypertrophy, compare it with that induced by exercise training, and explore any possible synergistic effect of these two interventions. Method. Twenty adult Wistar male rats were divided into control (C), Ns-fed (N.s.), exercise-trained (Ex.), Ns-fed exercise-trained (N.s.Ex.) groups. 800 mg/kg of Ns was administered orally to N.s. rats. Ex. rats were trained on a treadmill with speed 18 m/min and grade 32° for two hours daily, and the N.s.Ex. group underwent both interventions. After 8 weeks, Immunohistochemical slides of the left ventricles were prepared using rat growth hormone (GH), insulin-like growth factor I (IGF-I), angiotensin-II receptors 1 (AT-I), endothelin-I (ET-1), Akt-1, and Erk-1. Cell diameter and number of nuclei were measured. Results. Cardiomyocyte diameter, number of nuclei, GH, and Akt were significantly higher in N.s, Ex., and N.s.Ex groups compared with the controls. IGF-I, AT-1, and ET-1 were significantly higher in Ex. rats only compared with the controls. Erk-1 was lower in N.s., Ex., and N.s.Ex. compared with the controls. Conclusion. We can conclude that Ns-induced cardiac hypertrophy is mediated by the GH-IGF I-PI3P-Akt pathway. Supplementation of Ns to exercise training protocol can block the upregulation of AT-I and ET-1. The combined N.s. exercise-induced cardiac hypertrophy might be a superior model of physiological cardiac hypertrophy and be used as a prophylactic therapy for athletes who are engaged in vigorous exercise activity.

scholarly journals Housing temperature influences exercise training adaptations in mice

2019 ◽  
Author(s):  
Steffen H. Raun ◽  
Carlos Henriquez Olguín ◽  
Iuliia Karavaeva ◽  
Mona Ali ◽  
Lisbeth L. V. Møller ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Exercise Training ◽  
Wheel Running ◽  
Voluntary Exercise ◽  
List Type ◽  
Training Adaptations ◽  
Housing Temperature ◽  
Voluntary Running ◽  
Protein Expressions ◽  
Exercise Induced

AbstractExercise training is a powerful means to combat metabolic pathologies. Mice are extensively used to describe the benefits of exercise, but mild cold stress induced by housing temperatures may confound translation to humans. Thermoneutral housing is a strategy to make mice more metabolically similar to humans but its effects on exercise adaptations are unknown. Using voluntary wheel running, we show that thermoneutral housing blunted exercise-induced improvements in insulin action in muscle and adipose tissue. Moreover, thermoneutrality reduced the effects of training on energy expenditure, body composition, muscle and adipose tissue protein expressions, and the gut microbiome. The majority of these thermoneutral-dependent training adaptations could not be ascribed to a lower voluntary running volume. Thus, we conclude that organismal adaptations to exercise training in mice critically depend upon housing temperature. Our findings underscore the importance of housing temperature as an important parameter in the design and interpretation of murine exercise studies.HighlightsHousing at 30°C blunts several adaptations to exercise training in miceExercise-sensitive protein induction is dampened at 30°C in skeletal muscle30°C-housing blunts training-induced increase in insulin-stimulated glucose uptakeGlucose tolerance is not improved by voluntary exercise training at 30°C housingDecreased running in 30°C housing is not due to overheatingGraphical abstract

scholarly journals Transcriptomic adaptation during skeletal muscle habituation to eccentric or concentric exercise training

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Craig R. G. Willis ◽  
Colleen S. Deane ◽  
Ryan M. Ames ◽  
Joseph J. Bass ◽  
Daniel J. Wilkinson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Transcriptional Control ◽  
Muscle Adaptation ◽  
Transcriptional Responses ◽  
Gene Level ◽  
Elevated Expression ◽  
Specific Muscle ◽  
Exercise Induced ◽  
Functional Profiles

AbstractEccentric (ECC) and concentric (CON) contractions induce distinct muscle remodelling patterns that manifest early during exercise training, the causes of which remain unclear. We examined molecular signatures of early contraction mode-specific muscle adaptation via transcriptome-wide network and secretome analyses during 2 weeks of ECC- versus CON-specific (downhill versus uphill running) exercise training (exercise ‘habituation’). Despite habituation attenuating total numbers of exercise-induced genes, functional gene-level profiles of untrained ECC or CON were largely unaltered post-habituation. Network analysis revealed 11 ECC-specific modules, including upregulated extracellular matrix and immune profiles plus downregulated mitochondrial pathways following untrained ECC. Of 3 CON-unique modules, 2 were ribosome-related and downregulated post-habituation. Across training, 376 ECC-specific and 110 CON-specific hub genes were identified, plus 45 predicted transcription factors. Secreted factors were enriched in 3 ECC- and/or CON-responsive modules, with all 3 also being under the predicted transcriptional control of SP1 and KLF4. Of 34 candidate myokine hubs, 1 was also predicted to have elevated expression in skeletal muscle versus other tissues: THBS4, of a secretome-enriched module upregulated after untrained ECC. In conclusion, distinct untrained ECC and CON transcriptional responses are dampened after habituation without substantially shifting molecular functional profiles, providing new mechanistic candidates into contraction-mode specific muscle regulation.

Effects of Antioxidant Supplementation and Exercise Training on Erythrocyte Antioxidant Enzymes

2006 ◽  
Vol 76 (5) ◽  
pp. 324-331 ◽  
Author(s):  
Marsh ◽  
Laursen ◽  
Coombes
Keyword(s):  
Antioxidant Enzymes ◽  
Exercise Training ◽  
Endurance Training ◽  
Young Male ◽  
Antioxidant Defenses ◽  
Antioxidant Enzyme Activities ◽  
Antioxidant Supplementation ◽  
Male Wistar Rats ◽  
Exercise Induced ◽  
Antioxidant Supplements

Erythrocytes transport oxygen to tissues and exercise-induced oxidative stress increases erythrocyte damage and turnover. Increased use of antioxidant supplements may alter protective erythrocyte antioxidant mechanisms during training. Aim of study: To examine the effects of antioxidant supplementation (α-lipoic acid and α-tocopherol) and/or endurance training on the antioxidant defenses of erythrocytes. Methods: Young male Wistar rats were assigned to (1) sedentary; (2) sedentary and antioxidant-supplemented; (3) endurance-trained; or (4) endurance-trained and antioxidant-supplemented groups for 14 weeks. Erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activities, and plasma malondialdehyde (MDA) were then measured. Results: Antioxidant supplementation had no significant effect (p > 0.05) on activities of antioxidant enzymes in sedentary animals. Similarly, endurance training alone also had no effect (p > 0.05). GPX (125.9 ± 2.8 vs. 121.5 ± 3.0 U.gHb–1, p < 0.05) and CAT (6.1 ± 0.2 vs. 5.6 ± 0.2 U.mgHb–1, p < 0.05) activities were increased in supplemented trained animals compared to non-supplemented sedentary animals whereas SOD (61.8 ± 4.3 vs. 52.0 ± 5.2 U.mgHb–1, p < 0.05) activity was decreased. Plasma MDA was not different among groups (p > 0.05). Conclusions: In a rat model, the combination of exercise training and antioxidant supplementation increased antioxidant enzyme activities (GPX, CAT) compared with each individual intervention.

scholarly journals The effectiveness of supplemental oxygen during exercise training in patients with chronic obstructive pulmonary disease who show severe exercise-induced desaturation: a protocol for a meta-regression analysis and systematic review

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Shohei Kawachi ◽  
Shuhei Yamamoto ◽  
Kenichi Nishie ◽  
Takayoshi Yamaga ◽  
Manaka Shibuya ◽  
...  
Keyword(s):  
Systematic Review ◽  
Exercise Training ◽  
Exercise Tolerance ◽  
Supplemental Oxygen ◽  
Walking Distance ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Severe Exercise ◽  
Meta Regression ◽  
Exercise Induced

Abstract Background Supplemental oxygen during exercise training is used to increase the training effect of an exercise program in patients with chronic obstructive pulmonary disease (COPD) who show exercise-induced desaturation. Exercise-induced desaturation is not clearly defined in the guidelines; however, it is generally defined in clinical studies as a decrease in SpO2 of more than 4% from rest or a decrease to less than 88% during exercise. Although some meta-analyses examined the effectiveness of supplemental oxygen during exercise training, these studies concluded that it does not further improve exercise tolerance compared to exercise training alone. However, supplemental oxygen during exercise training may be effective in improving exercise tolerance in COPD patients with severe exercise-induced desaturation. Therefore, this study will be performed to elucidate the effectiveness of supplemental oxygen during exercise training and the relationship between its effectiveness and severity of exercise-induced desaturation at baseline. Methods We will first assess the effectiveness of supplemental oxygen during exercise training in COPD. The main outcome is the change in exercise tolerance before and after the intervention, indicated by the 6-min walking distance, the walking distance, or the walking time in incremental shuttle walking test, and analyzed as the standardized mean difference (SMD). The quality and risk of bias in individual studies will be assessed using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system and risk-of-bias tool (RoB ver.2). If statistical heterogeneity in terms of the effectiveness of exercise tolerance is shown, we will conduct meta-regression analyses to examine the association between the effectiveness of exercise training with supplemental oxygen and severity of exercise-induced desaturation at baseline. Discussion One strength of this study is that it is a systematic review with meta-regression analysis to elucidate the effectiveness of supplemental oxygen during exercise training in patients with COPD who show severe exercise-induced desaturation. Furthermore, we will assess the severity of exercise-induced desaturation for which exercise training with supplemental oxygen is effective, the influence of acute effects at baseline, and the effect of supplemental oxygen on adverse events. Systematic review registration Registration number, UMIN000039960.

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