scholarly journals Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

2002 ◽  
Vol 93 (4) ◽  
pp. 1301-1309 ◽  
Author(s):  
Ole Johan Kemi ◽  
Jan P. Loennechen ◽  
Ulrik Wisløff ◽  
Øyvind Ellingsen
Keyword(s):  
Skeletal Muscle ◽  
Muscle Hypertrophy ◽  
Molecular Mechanisms ◽  
Maximal Oxygen Consumption ◽  
Posterior Wall ◽  
Running Economy ◽  
Treadmill Running ◽  
Future Studies ◽  
Skeletal Muscle Hypertrophy ◽  
Posterior Wall Thickness

Whereas novel pathways of pathological heart enlargement have been unveiled by thoracic aorta constriction in genetically modified mice, the molecular mechanisms of adaptive cardiac hypertrophy remain virtually unexplored and call for an effective and well-characterized model of physiological mechanical loading. Experimental procedures of maximal oxygen consumption (V˙o 2 max) and intensity-controlled treadmill running were established in 40 female and 36 male C57BL/6J mice. An inclination-dependent V˙o 2 maxwith 0.98 test-retest correlation was found at 25° treadmill grade. Running for 2 h/day, 5 days/wk, in intervals of 8 min at 85–90% of V˙o 2 max and 2 min at 50% (adjusted to weekly V˙o 2 max testing) increasedV˙o 2 max to a plateau 49% above sedentary females and 29% in males. Running economy improved in both sexes, and echocardiography indicated significantly increased left ventricle posterior wall thickness. Ventricular weights increased by 19–29 and 12–17% in females and males, respectively, whereas cardiomyocyte dimensions increased by 20–32, and 17–23% in females and males, respectively; skeletal muscle mass increased by 12–18%. Thus the model mimics human responses to exercise and can be used in future studies of molecular mechanisms underlying these adaptations.

scholarly journals The ROS scavenger PDTC affects adaptation to treadmill running in mice: distinct effects on murine body mass, resting heart rate and skeletal muscle fiber type composition

2021 ◽  
Vol 224 (6) ◽  
pp. jeb234237
Author(s):  
Franziska Röchner ◽  
Angelika Schmitt ◽  
Anne-Lena Brändle ◽  
Annunziata Fragasso ◽  
Barbara Munz
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Muscle Hypertrophy ◽  
Muscle Fibers ◽  
Treadmill Running ◽  
Moderate Intensity ◽  
Resting Heart Rate ◽  
Skeletal Muscle Hypertrophy ◽  
Skeletal Muscle Fibers ◽  
Ros Scavenger

ABSTRACTRegular exercise induces a broad spectrum of adaptation reactions in a variety of tissues and organs. However, the respective mechanisms are incompletely understood. In the context of their analysis, animal model systems, specifically rodent treadmill running protocols, play an important role. However, few researchers have studied different aspects of adaptation, such as cardiorespiratory and skeletal muscle training effects, within one set of experiments. Here, we analyzed physiological adaptation to 10 weeks of regular, moderate-intensity, uphill treadmill running in mice, a widely used model for endurance exercise training. To study the effects of reactive oxygen species (ROS), which have been suggested to be major regulators of training adaptation, a subgroup of mice was treated with the ROS scavenger PDTC (pyrrolidine dithiocarbamate). We found that mass gain in mice that exercised under PDTC treatment lagged behind that of all other experimental groups. In addition, both exercise and PDTC significantly and additively decreased resting heart rate. Furthermore, there was a trend towards an enhanced proportion of type 2A skeletal muscle fibers and differential expression of metabolism-associated genes, indicating metabolic and functional adaptation of skeletal muscle fibers. By contrast, there were no effects on grip strength and relative mass of individual muscles, suggesting that our protocol of uphill running did not increase skeletal muscle hypertrophy and strength. Taken together, our data suggest that a standard protocol of moderate-intensity uphill running induces adaptation reactions at multiple levels, part of which might be modulated by ROS, but does not enhance skeletal muscle hypertrophy and force.

scholarly journals p21-Activated Kinase 1 Is Permissive for the Skeletal Muscle Hypertrophy Induced by Myostatin Inhibition

2021 ◽  
Vol 12 ◽  
Author(s):  
Caroline Barbé ◽  
Audrey Loumaye ◽  
Pascale Lause ◽  
Olli Ritvos ◽  
Jean-Paul Thissen
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Hypertrophy ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
The Body ◽  
Negative Regulator ◽  
Skeletal Muscle Hypertrophy ◽  
Myostatin Inhibition

Skeletal muscle, the most abundant tissue in the body, plays vital roles in locomotion and metabolism. Understanding the cellular processes that govern regulation of muscle mass and function represents an essential step in the development of therapeutic strategies for muscular disorders. Myostatin, a member of the TGF-β family, has been identified as a negative regulator of muscle development. Indeed, its inhibition induces an extensive skeletal muscle hypertrophy requiring the activation of Smad 1/5/8 and the Insulin/IGF-I signaling pathway, but whether other molecular mechanisms are involved in this process remains to be determined. Using transcriptomic data from various Myostatin inhibition models, we identified Pak1 as a potential mediator of Myostatin action on skeletal muscle mass. Our results show that muscle PAK1 levels are systematically increased in response to Myostatin inhibition, parallel to skeletal muscle mass, regardless of the Myostatin inhibition model. Using Pak1 knockout mice, we investigated the role of Pak1 in the skeletal muscle hypertrophy induced by different approaches of Myostatin inhibition. Our findings show that Pak1 deletion does not impede the skeletal muscle hypertrophy magnitude in response to Myostatin inhibition. Therefore, Pak1 is permissive for the skeletal muscle mass increase caused by Myostatin inhibition.

scholarly journals Molecular Mechanisms of Skeletal Muscle Hypertrophy

2020 ◽  
pp. 1-15
Author(s):  
Stefano Schiaffino ◽  
Carlo Reggiani ◽  
Takayuki Akimoto ◽  
Bert Blaauw
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Hypertrophy ◽  
Molecular Mechanisms ◽  
Muscle Growth ◽  
Transcriptional Level ◽  
Ribosomal Biogenesis ◽  
Skeletal Muscle Hypertrophy ◽  
Positive Regulators ◽  
Exercise Muscle

Skeletal muscle hypertrophy can be induced by hormones and growth factors acting directly as positive regulators of muscle growth or indirectly by neutralizing negative regulators, and by mechanical signals mediating the effect of resistance exercise. Muscle growth during hypertrophy is controlled at the translational level, through the stimulation of protein synthesis, and at the transcriptional level, through the activation of ribosomal RNAs and muscle-specific genes. mTORC1 has a central role in the regulation of both protein synthesis and ribosomal biogenesis. Several transcription factors and co-activators, including MEF2, SRF, PGC-1α4, and YAP promote the growth of the myofibers. Satellite cell proliferation and fusion is involved in some but not all muscle hypertrophy models.

Hypoxia transiently affects skeletal muscle hypertrophy in a functional overload model

2012 ◽  
Vol 302 (5) ◽  
pp. R643-R654 ◽  
Author(s):  
Thomas Chaillou ◽  
Nathalie Koulmann ◽  
Nadine Simler ◽  
Adélie Meunier ◽  
Bernard Serrurier ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Muscle Hypertrophy ◽  
Molecular Mechanisms ◽  
Muscle Growth ◽  
Female Rats ◽  
Mrna Levels ◽  
Hypertrophic Response ◽  
Protein Levels ◽  
Skeletal Muscle Hypertrophy

Hypoxia induces a loss of skeletal muscle mass, but the signaling pathways and molecular mechanisms involved remain poorly understood. We hypothesized that hypoxia could impair skeletal muscle hypertrophy induced by functional overload (Ov). To test this hypothesis, plantaris muscles were overloaded during 5, 12, and 56 days in female rats exposed to hypobaric hypoxia (5,500 m), and then, we examined the responses of specific signaling pathways involved in protein synthesis (Akt/mTOR) and breakdown (atrogenes). Hypoxia minimized the Ov-induced hypertrophy at days 5 and 12 but did not affect the hypertrophic response measured at day 56. Hypoxia early reduced the phosphorylation levels of mTOR and its downstream targets P70S6K and rpS6, but it did not affect the phosphorylation levels of Akt and 4E-BP1, in Ov muscles. The role played by specific inhibitors of mTOR, such as AMPK and hypoxia-induced factors (i.e., REDD1 and BNIP-3) was studied. REDD1 protein levels were reduced by overload and were not affected by hypoxia in Ov muscles, whereas AMPK was not activated by hypoxia. Although hypoxia significantly increased BNIP-3 mRNA levels at day 5, protein levels remained unaffected. The mRNA levels of the two atrogenes MURF1 and MAFbx were early increased by hypoxia in Ov muscles. In conclusion, hypoxia induced a transient alteration of muscle growth in this hypertrophic model, at least partly due to a specific impairment of the mTOR/P70S6K pathway, independently of Akt, by an undefined mechanism, and increased transcript levels for MURF1 and MAFbx that could contribute to stimulate the proteasomal proteolysis.

scholarly journals Hypertrophy of Rat Skeletal Muscle Is Associated with Increased SIRT1/Akt/mTOR/S6 and Suppressed Sestrin2/SIRT3/FOXO1 Levels

2021 ◽  
Vol 22 (14) ◽  
pp. 7588
Author(s):  
Zoltan Gombos ◽  
Erika Koltai ◽  
Ferenc Torma ◽  
Peter Bakonyi ◽  
Attila Kolonics ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Hypertrophy ◽  
Male Rats ◽  
Cellular Interactions ◽  
Molecular Signaling ◽  
Protein Breakdown ◽  
Rat Skeletal Muscle ◽  
Plantaris Muscle ◽  
Skeletal Muscle Hypertrophy ◽  
Intensive Investigation

Despite the intensive investigation of the molecular mechanism of skeletal muscle hypertrophy, the underlying signaling processes are not completely understood. Therefore, we used an overload model, in which the main synergist muscles (gastrocnemius, soleus) of the plantaris muscle were surgically removed, to cause a significant overload in the remaining plantaris muscle of 8-month-old Wistar male rats. SIRT1-associated pro-anabolic, pro-catabolic molecular signaling pathways, NAD and H2S levels of this overload-induced hypertrophy were studied. Fourteen days of overload resulted in a significant 43% (p < 0.01) increase in the mass of plantaris muscle compared to sham operated animals. Cystathionine-β-synthase (CBS) activities and bioavailable H2S levels were not modified by overload. On the other hand, overload-induced hypertrophy of skeletal muscle was associated with increased SIRT1 (p < 0.01), Akt (p < 0.01), mTOR, S6 (p < 0.01) and suppressed sestrin 2 levels (p < 0.01), which are mostly responsible for anabolic signaling. Decreased FOXO1 and SIRT3 signaling (p < 0.01) suggest downregulation of protein breakdown and mitophagy. Decreased levels of NAD+, sestrin2, OGG1 (p < 0.01) indicate that the redox milieu of skeletal muscle after 14 days of overloading is reduced. The present investigation revealed novel cellular interactions that regulate anabolic and catabolic processes in the hypertrophy of skeletal muscle.

scholarly journals Is an Energy Surplus Required to Maximize Skeletal Muscle Hypertrophy Associated With Resistance Training

2019 ◽  
Vol 6 ◽  
Author(s):  
Gary John Slater ◽  
Brad P. Dieter ◽  
Damian James Marsh ◽  
Eric Russell Helms ◽  
Gregory Shaw ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy ◽  
Energy Surplus

scholarly journals Skeletal muscle hypertrophy and structure and function of skeletal muscle fibres in male body builders

2006 ◽  
Vol 570 (3) ◽  
pp. 611-627 ◽  
Author(s):  
Giuseppe D'Antona ◽  
Francesca Lanfranconi ◽  
Maria Antonietta Pellegrino ◽  
Lorenza Brocca ◽  
Raffaella Adami ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Hypertrophy ◽  
Structure And Function ◽  
Muscle Fibres ◽  
Male Body ◽  
Skeletal Muscle Hypertrophy ◽  
And Function ◽  
Skeletal Muscle Fibres
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