Neutrophils accumulate and contribute to skeletal muscle dysfunction after ischemia-reperfusion

1990 ◽  
Vol 259 (6) ◽  
pp. H1809-H1812 ◽  
Author(s):  
D. L. Walden ◽  
H. J. McCutchan ◽  
E. G. Enquist ◽  
J. R. Schwappach ◽  
P. F. Shanley ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Gastrocnemius Muscle ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Contractile Dysfunction ◽  
Skeletal Muscle Dysfunction ◽  
Blood Neutrophils ◽  
Muscle Edema ◽  
Gastrocnemius Muscles ◽  
Muscle Contractile

Skeletal muscles subjected to ischemia and then reperfusion develop contractile dysfunction for reasons that are unclear. We found that rats pretreated with vinblastine 4 days before study had decreased numbers of blood neutrophils and increased gastrocnemius muscle function after ischemia (3h) and reperfusion (4 h) compared with untreated rats or rats treated 4 days before study with saline. By comparison, rats pretreated with vinblastine or saline 1 day before study had increased blood neutrophils and decreased gastrocnemius muscle contractile function after ischemia-reperfusion compared with untreated rats. In addition, numbers of neutrophils in gastrocnemius muscles paralleled numbers of blood neutrophils and correlated with gastrocnemius muscle edema and contractile function after ischemia and reperfusion. The results indicate that neutrophils accumulate and may play an important role in the genesis of skeletal muscle contractile dysfunction after ischemia-reperfusion.

scholarly journals Dysfunction of muscle contraction with impaired intracellular Ca2+ handling in skeletal muscle and the effect of exercise training in male db/db mice

2019 ◽  
Vol 126 (1) ◽  
pp. 170-182 ◽  
Author(s):  
Hiroaki Eshima ◽  
Yoshifumi Tamura ◽  
Saori Kakehi ◽  
Kyoko Nakamura ◽  
Nagomi Kurebayashi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Contraction ◽  
Contractile Function ◽  
Contractile Force ◽  
Contractile Dysfunction ◽  
Muscle Contractile ◽  
Type 2 Diabetic

Type 2 diabetes is characterized by reduced contractile force production and increased fatigability of skeletal muscle. While the maintenance of Ca2+ homeostasis during muscle contraction is a requisite for optimal contractile function, the mechanisms underlying muscle contractile dysfunction in type 2 diabetes are unclear. Here, we investigated skeletal muscle contractile force and Ca2+ flux during contraction and pharmacological stimulation in type 2 diabetic model mice ( db/db mice). Furthermore, we investigated the effect of treadmill exercise training on muscle contractile function. In male db/db mice, muscle contractile force and peak Ca2+ levels were both lower during tetanic stimulation of the fast-twitch muscles, while Ca2+ accumulation was higher after stimulation compared with control mice. While 6 wk of exercise training did not improve glucose tolerance, exercise did improve muscle contractile dysfunction, peak Ca2+ levels, and Ca2+ accumulation following stimulation in male db/db mice. These data suggest that dysfunctional Ca2+ flux may contribute to skeletal muscle contractile dysfunction in type 2 diabetes and that exercise training may be a promising therapeutic approach for dysfunctional skeletal muscle contraction. NEW & NOTEWORTHY The purpose of this study was to examine muscle contractile function and Ca2+ regulation as well as the effect of exercise training in skeletal muscle in obese diabetic mice ( db/db). We observed impairment of muscle contractile force and Ca2+ regulation in a male type 2 diabetic animal model. These dysfunctions in muscle were improved by 6 wk of exercise training.

Increased Ischemia-Reperfusion Blood Flow Impairs the Skeletal Muscle Contractile Function

2001 ◽  
Vol 99 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Kenshiro Ikebe ◽  
Teiji Kato ◽  
Makio Yamaga ◽  
Jun Hirose ◽  
Toru Tsuchida ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Muscle Contractile

Effects ofS-nitroso-N-acetylcysteine on contractile function of reperfused skeletal muscle

1998 ◽  
Vol 274 (3) ◽  
pp. R822-R829 ◽  
Author(s):  
Long-En Chen ◽  
Anthony V. Seaber ◽  
Rima M. Nasser ◽  
Jonathan S. Stamler ◽  
James R. Urbaniak
Keyword(s):  
Skeletal Muscle ◽  
Reperfusion Injury ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Control Group ◽  
Group Vi ◽  
No Donor ◽  
Early Reperfusion ◽  
Reconstructive Operations

The ultimate goal of replantation and microsurgical reconstructive operations is to regain or improve impaired function of the tissue. However, the data related to the influence of NO on tissue function are limited. This study evaluated the effects of the NO donor S-nitroso- N-acetylcysteine (SNAC) on contractile function of skeletal muscle during reperfusion. Forty-nine rats were divided into six groups. The extensor digitorum longus (EDL) muscles in groups I and II were not subjected to ischemia-reperfusion but were treated with a low (100 nmol/min) or high (1 μmol/min) dose of SNAC. In groups III- V, the EDL underwent 3 h of ischemia and 3 h of reperfusion and was also treated with low (100 nmol/min) or high doses (1 or 5 μmol/min) of SNAC. Group VI was a phosphate-buffered saline (PBS)-treated control group. Twenty additional animals were used to document systemic effects of SNAC and PBS only. SNAC or PBS was infused for 6.5 h, beginning 30 min before ischemia and continuing throughout the duration of reperfusion. Contractile testing compared the maximal twitch force, isometric tetanic contractile forces, fatigue, and fatigue half time of the experimental EDL and the contralateral nontreated EDL. The findings indicate that 1) SNAC does not influence contractile function of EDL muscle not subjected to ischemia-reperfusion, 2) SNAC significantly protects the contractile function of ischemic skeletal muscle against reperfusion injury in the early reperfusion period, and 3) the protective role of SNAC is critically dosage dependent; protection is lost at higher doses. The conclusion from this study is that supplementation with exogenous NO exerts a protective effect on the tissue against reperfusion injury.

scholarly journals Targeted overexpression of mitochondrial catalase protects against cancer chemotherapy-induced skeletal muscle dysfunction

2016 ◽  
Vol 311 (2) ◽  
pp. E293-E301 ◽  
Author(s):  
Laura A. A. Gilliam ◽  
Daniel S. Lark ◽  
Lauren R. Reese ◽  
Maria J. Torres ◽  
Terence E. Ryan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cancer Chemotherapy ◽  
Protein Oxidation ◽  
Muscle Function ◽  
Contractile Function ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Dysfunction ◽  
Whole Muscle ◽  
Loss Of Strength ◽  
Mitochondrial Respiratory

The loss of strength in combination with constant fatigue is a burden on cancer patients undergoing chemotherapy. Doxorubicin, a standard chemotherapy drug used in the clinic, causes skeletal muscle dysfunction and increases mitochondrial H2O2. We hypothesized that the combined effect of cancer and chemotherapy in an immunocompetent breast cancer mouse model (E0771) would compromise skeletal muscle mitochondrial respiratory function, leading to an increase in H2O2-emitting potential and impaired muscle function. Here, we demonstrate that cancer chemotherapy decreases mitochondrial respiratory capacity supported with complex I (pyruvate/glutamate/malate) and complex II (succinate) substrates. Mitochondrial H2O2-emitting potential was altered in skeletal muscle, and global protein oxidation was elevated with cancer chemotherapy. Muscle contractile function was impaired following exposure to cancer chemotherapy. Genetically engineering the overexpression of catalase in mitochondria of muscle attenuated mitochondrial H2O2 emission and protein oxidation, preserving mitochondrial and whole muscle function despite cancer chemotherapy. These findings suggest mitochondrial oxidants as a mediator of cancer chemotherapy-induced skeletal muscle dysfunction.

scholarly journals Effects of fasting on isolated murine skeletal muscle contractile function during acute hypoxia

PLoS ONE ◽  
2020 ◽  
Vol 15 (4) ◽  
pp. e0225922
Author(s):  
Cameron A. Schmidt ◽  
Emma J. Goldberg ◽  
Tom D. Green ◽  
Reema R. Karnekar ◽  
Jeffrey J. Brault ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Contractile Function ◽  
Acute Hypoxia ◽  
Murine Skeletal Muscle ◽  
Muscle Contractile

Role of the motor nerve in activity-induced enzymatic adaptation in skeletal muscle

1982 ◽  
Vol 242 (5) ◽  
pp. C272-C277 ◽  
Author(s):  
J. Henriksson ◽  
H. Galbo ◽  
E. Blomstrand
Keyword(s):  
Skeletal Muscle ◽  
Gastrocnemius Muscle ◽  
Tricarboxylic Acid Cycle ◽  
Motor Nerve ◽  
Oxidative Capacity ◽  
Control Group ◽  
Marker Enzyme ◽  
Muscle Weight ◽  
Enzymatic Adaptation ◽  
Gastrocnemius Muscles

The sciatic nerve was cut on one side in 11 male cats, and a piece of the nerve was removed. The cats were then divided at random into two groups, a stimulation group (S) of five cats and a control group (C) of six cats. Bilateral electrical stimulation (2 Hz) of the gastrocnemius muscle (directly or via the motor nerve) was carried out in the S cats 4 h/day, 3 days/wk for 4 wk. The voltage delivered was adjusted in each cat so that both gastrocnemius muscles lifted identical loads the same distance. The activity of the tricarboxylic acid cycle marker enzyme succinate dehydrogenase (SDH) per unit of muscle weight more than doubled in response to stimulation both in the intact and the denervated gastrocnemius muscle. Stimulation did not affect the activity of the glycolytic marker enzyme 6-phosphofructokinase (PFK) or muscle capillarization. Denervation resulted in pronounced (approx 50%) fiber atrophy, which was not prevented by the stimulation. It is concluded that the presence of the motor nerve per se is not necessary for an activity-induced adaptation of the oxidative capacity of skeletal muscle.

scholarly journals Does Phototherapy Enhance Skeletal Muscle Contractile Function and Postexercise Recovery? A Systematic Review

2013 ◽  
Vol 48 (1) ◽  
pp. 57-67 ◽  
Author(s):  
Paul A. Borsa ◽  
Kelly A. Larkin ◽  
Jerry M. True
Keyword(s):  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Contractile Function ◽  
Placebo Control ◽  
Original Research ◽  
Data Sets ◽  
Electromyographic Activity ◽  
Postexercise Recovery ◽  
Exercise Induced ◽  
Muscle Contractile

Context Recently, researchers have shown that phototherapy administered to skeletal muscle immediately before resistance exercise can enhance contractile function, prevent exercise-induced cell damage, and improve postexercise recovery of strength and function. Objective To critically evaluate original research addressing the ability of phototherapeutic devices, such as lasers and light-emitting diodes (LEDs), to enhance skeletal muscle contractile function, reduce exercise-induced muscle fatigue, and facilitate postexercise recovery. Data Sources We searched the electronic databases PubMed, SPORTDiscus, Web of Science, Scopus, and Rehabilitation & Physical Medicine without date limitations for the following key words: laser therapy, phototherapy, fatigue, exercise, circulation, microcirculation, and photobiomodulation. Study Selection Eligible studies had to be original research published in English as full papers, involve human participants, and receive a minimum score of 7 out of 10 on the Physiotherapy Evidence Database (PEDro) scale. Data Extraction Data of interest included elapsed time to fatigue, total number of repetitions to fatigue, total work performed, maximal voluntary isometric contraction (strength), electromyographic activity, and postexercise biomarker levels. We recorded the PEDro scores, beam characteristics, and treatment variables and calculated the therapeutic outcomes and effect sizes for the data sets. Data Synthesis In total, 12 randomized controlled trials met the inclusion criteria. However, we excluded data from 2 studies, leaving 32 data sets from 10 studies. Twenty-four of the 32 data sets contained differences between active phototherapy and sham (placebo-control) treatment conditions for the various outcome measures. Exposing skeletal muscle to single-diode and multidiode laser or multidiode LED therapy was shown to positively affect physical performance by delaying the onset of fatigue, reducing the fatigue response, improving postexercise recovery, and protecting cells from exercise-induced damage. Conclusions Phototherapy administered before resistance exercise consistently has been found to provide ergogenic and prophylactic benefits to skeletal muscle.

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