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Neuronal nitric oxide synthase is dislocated in type I fibers of myalgic muscle but can recover with physical exercise training.

Jensen L, Andersen LL, Schrøder HD, Frandsen U, Sjøgaard G - Biomed Res Int (2015)

Bottom Line: Distribution of fiber type, cross-sectional area, and sarcolemmal nNOS expression did not differ between MYA and CON.However, MYA showed increased sarcoplasmic nNOS localization (18.8 ± 12 versus 12.8 ± 8%, P = 0.049) compared with CON.SST resulted in a decrease of sarcoplasm-localized nNOS following training (before 18.1 ± 12 versus after 12.0 ± 12%; P = 0,027).

View Article: PubMed Central - PubMed

Affiliation: Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, 5000 Odense C, Denmark ; Institute of Clinical Research, Pathology and SDU Muscle Research Cluster, University of Southern Denmark, 5230 Odense M, Denmark.

ABSTRACT
Trapezius myalgia is the most common type of chronic neck pain. While physical exercise reduces pain and improves muscle function, the underlying mechanisms remain unclear. Nitric oxide (NO) signaling is important in modulating cellular function, and a dysfunctional neuronal NO synthase (nNOS) may contribute to an ineffective muscle function. This study investigated nNOS expression and localization in chronically painful muscle. Forty-one women clinically diagnosed with trapezius myalgia (MYA) and 18 healthy controls (CON) were included in the case-control study. Subsequently, MYA were randomly assigned to either 10 weeks of specific strength training (SST, n = 18), general fitness training (GFT, n = 15), or health information (REF, n = 8). Distribution of fiber type, cross-sectional area, and sarcolemmal nNOS expression did not differ between MYA and CON. However, MYA showed increased sarcoplasmic nNOS localization (18.8 ± 12 versus 12.8 ± 8%, P = 0.049) compared with CON. SST resulted in a decrease of sarcoplasm-localized nNOS following training (before 18.1 ± 12 versus after 12.0 ± 12%; P = 0,027). We demonstrate that myalgic muscle displays altered nNOS localization and that 10 weeks of strength training normalize these disruptions, which supports previous findings of impaired muscle oxygenation during work tasks and reduced pain following exercise.

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Intermyofibrillar network changes in muscle fibers lacking sarcolemmal nNOS. Enlarged type I fiber (#) with decreased sarcolemmal nNOS protein shows alterations in the intermyofibrillar network demonstrated by irregular NADH-TR staining ((a) and (b): arrow head). Note also a subsarcolemmal accumulation of cellular material or mitochondria seen as dark areas below the fiber membrane ((b): dark arrow). Type II fibers appear normal. NADH-TR (mitochondria) is blue, MHC-I is green, and nNOS is red. # marks identical fibers on serial sections. Scale bar: 50 μm.
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fig4: Intermyofibrillar network changes in muscle fibers lacking sarcolemmal nNOS. Enlarged type I fiber (#) with decreased sarcolemmal nNOS protein shows alterations in the intermyofibrillar network demonstrated by irregular NADH-TR staining ((a) and (b): arrow head). Note also a subsarcolemmal accumulation of cellular material or mitochondria seen as dark areas below the fiber membrane ((b): dark arrow). Type II fibers appear normal. NADH-TR (mitochondria) is blue, MHC-I is green, and nNOS is red. # marks identical fibers on serial sections. Scale bar: 50 μm.

Mentions: NADH-TR staining showed alterations in the intermyofibrillar network and clustering of cellular material in the sarcoplasm of some type I muscle fibers. Most of these same fibers showed loss of sarcolemmal nNOS (Figure 4).


Neuronal nitric oxide synthase is dislocated in type I fibers of myalgic muscle but can recover with physical exercise training.

Jensen L, Andersen LL, Schrøder HD, Frandsen U, Sjøgaard G - Biomed Res Int (2015)

Intermyofibrillar network changes in muscle fibers lacking sarcolemmal nNOS. Enlarged type I fiber (#) with decreased sarcolemmal nNOS protein shows alterations in the intermyofibrillar network demonstrated by irregular NADH-TR staining ((a) and (b): arrow head). Note also a subsarcolemmal accumulation of cellular material or mitochondria seen as dark areas below the fiber membrane ((b): dark arrow). Type II fibers appear normal. NADH-TR (mitochondria) is blue, MHC-I is green, and nNOS is red. # marks identical fibers on serial sections. Scale bar: 50 μm.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4380094&req=5

fig4: Intermyofibrillar network changes in muscle fibers lacking sarcolemmal nNOS. Enlarged type I fiber (#) with decreased sarcolemmal nNOS protein shows alterations in the intermyofibrillar network demonstrated by irregular NADH-TR staining ((a) and (b): arrow head). Note also a subsarcolemmal accumulation of cellular material or mitochondria seen as dark areas below the fiber membrane ((b): dark arrow). Type II fibers appear normal. NADH-TR (mitochondria) is blue, MHC-I is green, and nNOS is red. # marks identical fibers on serial sections. Scale bar: 50 μm.
Mentions: NADH-TR staining showed alterations in the intermyofibrillar network and clustering of cellular material in the sarcoplasm of some type I muscle fibers. Most of these same fibers showed loss of sarcolemmal nNOS (Figure 4).

Bottom Line: Distribution of fiber type, cross-sectional area, and sarcolemmal nNOS expression did not differ between MYA and CON.However, MYA showed increased sarcoplasmic nNOS localization (18.8 ± 12 versus 12.8 ± 8%, P = 0.049) compared with CON.SST resulted in a decrease of sarcoplasm-localized nNOS following training (before 18.1 ± 12 versus after 12.0 ± 12%; P = 0,027).

View Article: PubMed Central - PubMed

Affiliation: Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, 5000 Odense C, Denmark ; Institute of Clinical Research, Pathology and SDU Muscle Research Cluster, University of Southern Denmark, 5230 Odense M, Denmark.

ABSTRACT
Trapezius myalgia is the most common type of chronic neck pain. While physical exercise reduces pain and improves muscle function, the underlying mechanisms remain unclear. Nitric oxide (NO) signaling is important in modulating cellular function, and a dysfunctional neuronal NO synthase (nNOS) may contribute to an ineffective muscle function. This study investigated nNOS expression and localization in chronically painful muscle. Forty-one women clinically diagnosed with trapezius myalgia (MYA) and 18 healthy controls (CON) were included in the case-control study. Subsequently, MYA were randomly assigned to either 10 weeks of specific strength training (SST, n = 18), general fitness training (GFT, n = 15), or health information (REF, n = 8). Distribution of fiber type, cross-sectional area, and sarcolemmal nNOS expression did not differ between MYA and CON. However, MYA showed increased sarcoplasmic nNOS localization (18.8 ± 12 versus 12.8 ± 8%, P = 0.049) compared with CON. SST resulted in a decrease of sarcoplasm-localized nNOS following training (before 18.1 ± 12 versus after 12.0 ± 12%; P = 0,027). We demonstrate that myalgic muscle displays altered nNOS localization and that 10 weeks of strength training normalize these disruptions, which supports previous findings of impaired muscle oxygenation during work tasks and reduced pain following exercise.

Show MeSH
Related in: MedlinePlus