scholarly journals Expression of phospholemman and its association with Na+-K+-ATPase in skeletal muscle: effects of aging and exercise training

2005 ◽  
Vol 99 (4) ◽  
pp. 1508-1515 ◽  
Author(s):  
Justin Reis ◽  
Lianqin Zhang ◽  
Steve Cala ◽  
Korinne N. Jew ◽  
Lisa C. Mace ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Treadmill Exercise ◽  
Accessory Protein ◽  
Dependent Manner ◽  
Muscle Type ◽  
Effects Of Aging ◽  
High Level ◽  
Reduced Activity ◽  
Α Subunits

Phospholemman (PLM) is a recently identified accessory protein of the Na+-K+-ATPase (NKA), with a high level of expression in skeletal muscle. The objectives of this study are to characterize the PLM in skeletal muscle and to test the hypothesis that, as an accessory protein of NKA, expression of PLM and its association with the α-subunits of NKA is regulated during aging and with exercise training. PLM was characterized in skeletal muscle of 6- and 16-mo-old sedentary middle-aged rats (Ms), and the effects of aging and exercise training were studied in Ms, 29-mo-old sedentary senescent, and 29-mo-old treadmill-exercised senescent rats. Expression of PLM was muscle-type dependent, and immunofluorescence study showed that PLM distributed predominantly on the sarcolemmal membrane of the muscle fibers. Anti-PLM antibody reduced activity of NKA, and thus PLM appears to be required for NKA to express its full activity in skeletal muscle. Expression of PLM was not altered with aging but increased after exercise training. Coimmunoprecipitation studies demonstrated that PLM associates with both the α1- and α2-subunit isoforms of NKA. Compared with Ms rats, levels of PLM-associated α1-subunit increased in 29-mo-old sedentary senescent rats, and treadmill exercise has a tendency to partially reverse it. There was no significant change in PLM-associated α2-subunit with age, and exercise training has a tendency to increase that level. It is concluded that, in skeletal muscle, PLM appears to be a protein integral to the NKA complex and that PLM has the potential to modulate NKA in an isoform-specific and muscle type-dependent manner in aging and after exercise training.

Effects of aging and exercise training on the dynamics of vasoconstriction in skeletal muscle resistance vessels

2017 ◽  
Vol 117 (3) ◽  
pp. 397-407 ◽  
Author(s):  
Elizabeth M. Gittemeier ◽  
Tyler Ericson ◽  
Payal Ghosh ◽  
Steven W. Copp ◽  
Alexander B. Opoku-Acheampong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Resistance Vessels ◽  
Effects Of Aging

Short-term exercise training augments sympathetic vasoconstrictor responsiveness and endothelium-dependent vasodilation in resting skeletal muscle

2012 ◽  
Vol 303 (3) ◽  
pp. R332-R339 ◽  
Author(s):  
Nicholas G. Jendzjowsky ◽  
Darren S. DeLorey
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Training Session ◽  
Dependent Manner ◽  
Sympathetic Stimulation ◽  
Training Intensity ◽  
Sprague Dawley ◽  
Short Term ◽  
Time Control ◽  
40 Hz

We tested the hypotheses that 4 wk of exercise training would diminish the magnitude of vasoconstriction in response to sympathetic nerve stimulation and augment endothelium-dependent vasodilation (EDD) in resting skeletal muscle in a training intensity-dependent manner. Sprague-Dawley rats were randomly assigned to sedentary time-control (S), mild- (M; 20 m/min, 5% grade), or heavy-intensity (H; 40 m/min, 5% grade) treadmill exercise groups. Animals trained 5 days/wk for 4 wk with training volume matched between groups. Rats were anesthetized and instrumented for study 24 h after the last training session. Arterial pressure and femoral artery blood flow were measured, and femoral vascular conductance (FVC) was calculated. Lumbar sympathetic chain stimulation was delivered continuously at 2 Hz and in patterns at 20 and 40 Hz. EDD was assessed by the vascular response to intra-arterial bolus injections of ACh. The response (% change FVC) to sympathetic stimulation increased ( P < 0.05) in a training intensity-dependent manner at 2 Hz (S: −20.2 ± 9.8%, M: −34.0 ± 6.7%, and H: −44.9 ± 2.0%), 20 Hz (S: −22.0 ± 10.6%, M: −31.2 ± 8.4%, and H: −42.8 ± 5.9%), and 40 Hz (S: H −24.5 ± 8.5%, M: −35.1 ± 8.9%, H: −44.9 ± 6.5%). The magnitude of EDD also increased in a training intensity-dependent manner ( P < 0.05). These data demonstrate that short-term exercise training augments the magnitude of vasoconstriction in response to sympathetic stimulation and EDD in resting skeletal muscle in a training intensity-dependent manner.

scholarly journals Oxidative stress and mitochondrial function in skeletal muscle: Effects of aging and exercise training

AGE ◽  
1998 ◽  
Vol 21 (3) ◽  
pp. 109-117 ◽  
Author(s):  
Raj Chandwaney ◽  
Steve Leichtweis ◽  
Christiaan Leeuwenburgh ◽  
Li Li Ji
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Mitochondrial Function ◽  
Effects Of Aging

scholarly journals Effects of aging, TNF-α, and exercise training on angiotensin II-induced vasoconstriction of rat skeletal muscle arterioles

2012 ◽  
Vol 113 (7) ◽  
pp. 1091-1100 ◽  
Author(s):  
Yoonjung Park ◽  
Rhonda D. Prisby ◽  
Brad J. Behnke ◽  
James M. Dominguez ◽  
Lisa A. Lesniewski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Angiotensin Ii ◽  
Exercise Training ◽  
Old Age ◽  
Physical Exertion ◽  
Ang Ii ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Effects Of Aging

Skeletal muscle vascular resistance during physical exertion is higher with old age. The purpose of this study was to determine whether 1) aging enhances angiotensin II (ANG II)-induced vasoconstriction; 2) the proinflammatory cytokine tumor necrosis factor (TNF)-α contributes to alterations in ANG II-mediated vasoconstriction with aging; 3) exercise training attenuates putative age-associated increases in ANG II-mediated vasoconstriction; and 4) the mechanism(s) through which aging and exercise training alters ANG II-induced vasoconstriction in skeletal muscle arterioles. Male Fischer 344 rats were assigned to four groups: young sedentary (4 mo), old sedentary (24 mo), young trained, and old trained. In a separate group of young sedentary and old sedentary animals, a TNF type 1 receptor inhibitor was administered subcutaneously for 10 wk. First-order arterioles were isolated from soleus and gastrocnemius muscles for in vitro experimentation. Old age augmented ANG II-induced vasoconstriction in both soleus (young: 27 ± 3%; old: 38 ± 4%) and gastrocnemius (young: 42 ± 6%; old: 64 ± 9%) muscle arterioles; this augmented vasoconstriction was abolished with the removal of the endothelium, NG-nitro-l-arginine methyl ester, and chronic inhibition of TNF-α. In addition, exercise training ameliorated the age-induced increase in ANG II vasoconstriction. These findings demonstrate that old age enhances and exercise training diminishes ANG II-induced vasoconstrictor responses in skeletal muscle arterioles through an endothelium-dependent nitric oxide synthase signaling pathway. In addition, the enhancement of ANG II vasoconstriction with old age appears to be related to a proinflammatory state.

scholarly journals Exercise Training Attenuates Obesity-Induced Skeletal Muscle Remodeling and Mitochondria-Mediated Apoptosis in the Skeletal Muscle

2018 ◽  
Vol 15 (10) ◽  
pp. 2301 ◽  
Author(s):  
Jun-Won Heo ◽  
Su-Zi Yoo ◽  
Mi-Hyun No ◽  
Dong-Ho Park ◽  
Ju-Hee Kang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
High Fat Diet ◽  
Skeletal Muscles ◽  
Treadmill Exercise ◽  
Sectional Area ◽  
High Fat ◽  
Cross Sectional ◽  
Muscle Remodeling ◽  
Protective Intervention

Obesity is characterized by the induction of skeletal muscle remodeling and mitochondria-mediated apoptosis. Exercise has been reported as a positive regulator of skeletal muscle remodeling and apoptosis. However, the effects of exercise on skeletal muscle remodeling and mitochondria-mediated apoptosis in obese skeletal muscles have not been clearly elucidated. Four-week-old C57BL/6 mice were randomly assigned into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and HFD plus exercise groups (HFD + EX). After obesity was induced by 20 weeks of 60% HFD feeding, treadmill exercise was performed for 12 weeks. Exercise ameliorated the obesity-induced increase in extramyocyte space and a decrease in the cross-sectional area of the skeletal muscle. In addition, it protected against increases in mitochondria-mediated apoptosis in obese skeletal muscles. These results suggest that exercise as a protective intervention plays an important role in regulating skeletal muscle structure and apoptosis in obese skeletal muscles.

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