scholarly journals Fasting increases 18:2-containing phosphatidylcholines to complement the decrease in 22:6-containing phosphatidylcholines in mouse skeletal muscle

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0255178
Author(s):  
Nanami Senoo ◽  
Takumi Akahori ◽  
Hiyori Ichida ◽  
Noriyuki Miyoshi ◽  
Akihito Morita ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Structural Diversity ◽  
Compensatory Mechanism ◽  
Liquid Chromatography Mass Spectrometry ◽  
Cellular Functions ◽  
Environmental Status ◽  
Muscle Phospholipid ◽  
Muscle Adaptations ◽  
Acyl Chains ◽  
Deficient Mice

Fasting stimulates catabolic reactions in skeletal muscle to survive nutrient deprivation. Cellular phospholipids have large structural diversity due to various polar-heads and acyl-chains that affect many cellular functions. Skeletal muscle phospholipid profiles have been suggested to be associated with muscle adaptations to nutritional and environmental status. However, the effect of fasting on skeletal muscle phospholipid profiles remains unknown. Here, we analyzed phospholipids using liquid chromatography mass spectrometry. We determined that fasting resulted in a decrease in 22:6-containing phosphatidylcholines (PCs) (22:6-PCs) and an increase in 18:2-containing PCs (18:2-PCs). The fasting-induced increase in 18:2-PCs was sufficient to complement 22:6-PCs loss, resulting in the maintenance of the total amount of polyunsaturated fatty acid (PUFA)-containing PCs. Similar phospholipid alterations occurred in insulin-deficient mice, which indicate that these observed phospholipid perturbations were characteristic of catabolic skeletal muscle. In lysophosphatidic acid acyltransferase 3-knockout muscles that mostly lack 22:6-PCs, other PUFA-containing PCs, mainly 18:2-PCs, accumulated. This suggests a compensatory mechanism for skeletal muscles to maintain PUFA-containing PCs.

scholarly journals Lack of Skeletal Muscle Serotonin Impairs Physical Performance

2021 ◽  
Vol 14 ◽  
pp. 117864692110031
Author(s):  
Marion Falabrègue ◽  
Anne-Claire Boschat ◽  
Romain Jouffroy ◽  
Marieke Derquennes ◽  
Haidar Djemai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Physical Performance ◽  
Depressive Disorders ◽  
Tryptophan Metabolism ◽  
Long Distance ◽  
Positive Effects ◽  
Tryptophan Metabolites ◽  
The Brain ◽  
Deficient Mice

Low levels of the neurotransmitter serotonin have been associated with the onset of depression. While traditional treatments include antidepressants, physical exercise has emerged as an alternative for patients with depressive disorders. Yet there remains the fundamental question of how exercise is sensed by the brain. The existence of a muscle–brain endocrine loop has been proposed: according to this scenario, exercise modulates metabolization of tryptophan into kynurenine within skeletal muscle, which in turn affects the brain, enhancing resistance to depression. But the breakdown of tryptophan into kynurenine during exercise may also alter serotonin synthesis and help limit depression. In this study, we investigated whether peripheral serotonin might play a role in muscle–brain communication permitting adaptation for endurance training. We first quantified tryptophan metabolites in the blood of 4 trained athletes before and after a long-distance trail race and correlated changes in tryptophan metabolism with physical performance. In parallel, to assess exercise capacity and endurance in trained control and peripheral serotonin–deficient mice, we used a treadmill incremental test. Peripheral serotonin–deficient mice exhibited a significant drop in physical performance despite endurance training. Brain levels of tryptophan metabolites were similar in wild-type and peripheral serotonin–deficient animals, and no products of muscle-induced tryptophan metabolism were found in the plasma or brains of peripheral serotonin–deficient mice. But mass spectrometric analyses revealed a significant decrease in levels of 5-hydroxyindoleacetic acid (5-HIAA), the main serotonin metabolite, in both the soleus and plantaris muscles, demonstrating that metabolization of tryptophan into serotonin in muscles is essential for adaptation to endurance training. In light of these findings, the breakdown of tryptophan into peripheral but not brain serotonin appears to be the rate-limiting step for muscle adaptation to endurance training. The data suggest that there is a peripheral mechanism responsible for the positive effects of exercise, and that muscles are secretory organs with autocrine-paracrine roles in which serotonin has a local effect.

scholarly journals Novel metabolic disorders in skeletal muscle of Lipodystrophic Bscl2/Seipin deficient mice

2019 ◽  
Vol 482 ◽  
pp. 1-10 ◽  
Author(s):  
Wenqiong Xu ◽  
Hongyi Zhou ◽  
Hongzhuan Xuan ◽  
Pradip Saha ◽  
Gongxian Wang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Disorders ◽  
Deficient Mice

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 Exercise-induced alterations and loss of sarcomeric M-line organization in the diaphragm muscle of obscurin knockout mice

2017 ◽  
Vol 312 (1) ◽  
pp. C16-C28 ◽  
Author(s):  
D. Randazzo ◽  
B. Blaauw ◽  
C. Paolini ◽  
E. Pierantozzi ◽  
S. Spinozzi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Detailed Examination ◽  
Diaphragm Muscle ◽  
Hindlimb Muscles ◽  
Skeletal Muscle Fibers ◽  
Exercise Induced ◽  
Old Mice ◽  
Ankyrin B ◽  
Deficient Mice

We recently reported that skeletal muscle fibers of obscurin knockout (KO) mice present altered distribution of ankyrin B (ankB), disorganization of the subsarcolemmal microtubules, and reduced localization of dystrophin at costameres. In addition, these mice have impaired running endurance and increased exercise-induced sarcolemmal damage compared with wild-type animals. Here, we report results from a combined approach of physiological, morphological, and structural studies in which we further characterize the skeletal muscles of obscurin KO mice. A detailed examination of exercise performance, using different running protocols, revealed that the reduced endurance of obscurin KO animals on the treadmill depends on exercise intensity and age. Indeed, a mild running protocol did not evidence significant differences between control and obscurin KO mice, whereas comparison of running abilities of 2-, 6-, and 11-mo-old mice exercised at exhaustion revealed a progressive age-dependent reduction of the exercise tolerance in KO mice. Histological analysis indicated that heavy exercise induced leukocyte infiltration, fibrotic connective tissue deposition, and hypercontractures in the diaphragm of KO mice. On the same line, electron microscopy revealed that, in the diaphragm of exercised obscurin KO mice, but not in the hindlimb muscles, both M-line and H-zone of sarcomeres appeared wavy and less defined. Altogether, these results suggest that obscurin is required for the maintenance of morphological and ultrastructural integrity of skeletal muscle fibers against damage induced by intense mechanical stress and point to the diaphragm as the skeletal muscle most severely affected in obscurin-deficient mice.

Skeletal Muscle Adaptations to Prolonged Exposure to Extreme Altitude: A Role of Physical Activity?

2008 ◽  
Vol 9 (4) ◽  
pp. 311-317 ◽  
Author(s):  
Masao Mizuno ◽  
Gabrielle K Savard ◽  
Nils-Holger Areskog ◽  
Carsten Lundby ◽  
Bengt Saltin
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Prolonged Exposure ◽  
Muscle Adaptations ◽  
Extreme Altitude ◽  
Skeletal Muscle Adaptations
Sign in / Sign up

Export Citation Format

Share Document