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.

Treadmill running causes significant fiber damage in skeletal muscle of KATP channel-deficient mice

2005 ◽  
Vol 22 (2) ◽  
pp. 204-212 ◽  
Author(s):  
M. Thabet ◽  
T. Miki ◽  
S. Seino ◽  
J.-M. Renaud
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Treadmill Running ◽  
Wild Type ◽  
Connective Tissues ◽  
Fiber Damage ◽  
Hindlimb Muscles ◽  
Skeletal Muscle Fibers ◽  
And Function ◽  
Deficient Mice

Although it has been suggested that the ATP-sensitive K+ (KATP) channel protects muscle against function impairment, most studies have so far given little evidence for significant perturbation in the integrity and function of skeletal muscle fibers from inactive mice that lack KATP channel activity in their cell membrane. The objective was, therefore, to test the hypothesis that KATP channel-deficient skeletal muscle fibers become damaged when mice are subjected to stress. Wild-type and KATP channel-deficient mice (Kir6.2−/− mice) were subjected to 4–5 wk of treadmill running at either 20 m/min with 0° inclination or at 24 m/min with 20° uphill inclination. Muscles of all wild-type mice and of nonexercised Kir6.2−/− mice had very few fibers with internal nuclei. After 4–5 wk of treadmill running, there was little evidence for connective tissues and mononucleated cells in Kir6.2−/− hindlimb muscles, whereas the number of fibers with internal nuclei, which appear when damaged fibers are regenerated by satellite cells, was significantly higher in Kir6.2−/− than wild-type mice. Between 5% and 25% of the total number of fibers in Kir6.2−/− extensor digitum longus, plantaris, and tibialis muscles had internal nuclei, and most of such fibers were type IIB fibers. Contrary to hindlimb muscles, diaphragms of Kir6.2−/− mice that had run at 24 m/min had few fibers with internal nuclei, but mild to severe fiber damage was observed. In conclusion, the study provides for the first time evidence 1) that the KATP channels of skeletal muscle are essential to prevent fiber damage, and thus muscle dysfunction; and 2) that the extent of fiber damage is greater and the capacity of fiber regeneration is less in Kir6.2−/− diaphragm muscles compared with hindlimb muscles.

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 ATP-Induced Increase in Intracellular Calcium Levels and Subsequent Activation of mTOR as Regulators of Skeletal Muscle Hypertrophy

2018 ◽  
Vol 19 (9) ◽  
pp. 2804 ◽  
Author(s):  
Naoki Ito ◽  
Urs Ruegg ◽  
Shin’ichi Takeda
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Muscle Hypertrophy ◽  
Mapk Pathway ◽  
Muscle Fibers ◽  
Dependent Manner ◽  
Intracellular Signaling Pathways ◽  
Skeletal Muscle Hypertrophy ◽  
Subsequent Activation

Intracellular signaling pathways, including the mammalian target of rapamycin (mTOR) and the mitogen-activated protein kinase (MAPK) pathway, are activated by exercise, and promote skeletal muscle hypertrophy. However, the mechanisms by which these pathways are activated by physiological stimulation are not fully understood. Here we show that extracellular ATP activates these pathways by increasing intracellular Ca2+ levels ([Ca2+]i), and promotes muscle hypertrophy. [Ca2+]i in skeletal muscle was transiently increased after exercise. Treatment with ATP induced the increase in [Ca2+]i through the P2Y2 receptor/inositol 1,4,5-trisphosphate receptor pathway, and subsequent activation of mTOR in vitro. In addition, the ATP-induced increase in [Ca2+]i coordinately activated Erk1/2, p38 MAPK and mTOR that upregulated translation of JunB and interleukin-6. ATP also induced an increase in [Ca2+]i in isolated soleus muscle fibers, but not in extensor digitorum longus muscle fibers. Furthermore, administration of ATP led to muscle hypertrophy in an mTOR- and Ca2+-dependent manner in soleus, but not in plantaris muscle, suggesting that ATP specifically regulated [Ca2+]i in slow muscles. These findings suggest that ATP and [Ca2+]i are important mediators that convert mechanical stimulation into the activation of intracellular signaling pathways, and point to the P2Y receptor as a therapeutic target for treating muscle atrophy.

The “KIMWIPE” Effect in Ultra-Thin Cryosections

1985 ◽  
Vol 43 ◽  
pp. 458-459
Author(s):  
I. Taylor ◽  
P. Ingram ◽  
J.R. Sommer
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Fibers ◽  
Ice Crystals ◽  
Crystal Formation ◽  
Ice Crystal ◽  
Thin Sections ◽  
Skeletal Muscle Fibers ◽  
Freeze Dried ◽  
Ice Crystal Formation

In studying quick-frozen single intact skeletal muscle fibers for structural and microchemical alterations that occur milliseconds, and fractions thereof, after electrical stimulation, we have developed a method to compare, directly, ice crystal formation in freeze-substituted thin sections adjacent to all, and beneath the last, freeze-dried cryosections. We have observed images in the cryosections that to our knowledge have not been published heretofore (Figs.1-4). The main features are that isolated, sometimes large regions of the sections appear hazy and have much less contrast than adjacent regions. Sometimes within the hazy regions there are smaller areas that appear crinkled and have much more contrast. We have also observed that while the hazy areas remain still, the regions of higher contrast visibly contract in the beam, often causing tears in the sections that are clearly not caused by ice crystals (Fig.3, arrows).

Effect of External Calcium and other Divalent Cations on K+ Contractures in Denervated Slow Skeletal Muscle Fibers of the Frog

2019 ◽  
Author(s):  
Leonardo Hernández
Keyword(s):  
Skeletal Muscle ◽  
Binding Capacity ◽  
Divalent Cations ◽  
Muscle Fibers ◽  
Free Calcium ◽  
Slow Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Free Calcium Concentration ◽  
Chronic Denervation ◽  
Denervated Muscles

The influence of Ca2+ and other divalent cations on contractile responses of slow skeletal muscle fibers of the frog (Rana pipiens) under conditions of chronic denervation was investigated.Isometric tension was recorded from slow bundles of normal and denervated cruralis muscle in normal solution and in solutions with free calcium concentration solution or in solutions where other divalent cations (Sr2+, Ni2+, Co2+ or Mn2+) substituted for calcium. In the second week after nerve section, in Ca2+-free solutions, we observed that contractures (evoked from 40 to 80 mM-K+) of non-denervated muscles showed significantly higher tensions (p<0.05), than those from denervated bundles. Likewise, in solutions where calcium was substituted by all divalent cations tested, with exception of Mn2+, the denervated bundles displayed lower tension than non-denervated, also in the second week of denervation. In this case, the Ca2+ substitution by Sr2+ caused the higher decrease in tension, followed by Co2+ and Ni2+, which were different to non-denervated bundles, as the lowest tension was developed by Mn2+, followed by Co2+, and then Ni2+ and Sr2+. After the third week, we observed a recovery in tension. These results suggest that denervation altering the binding capacity to divalent cations of the voltage sensor.

scholarly journals Development of a human neuromuscular tissue-on-a-chip model on a 24-well-plate-format compartmentalized microfluidic device

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Kazuki Yamamoto ◽  
Nao Yamaoka ◽  
Yu Imaizumi ◽  
Takunori Nagashima ◽  
Taiki Furutani ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Microfluidic Device ◽  
Motor Neurons ◽  
Muscle Fibers ◽  
Three Dimensional ◽  
Tissue Model ◽  
Skeletal Muscle Fibers

A three-dimensional human neuromuscular tissue model that mimics the physically separated structures of motor neurons and skeletal muscle fibers is presented.

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