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Statin myalgia is not associated with reduced muscle strength, mass or protein turnover in older male volunteers, but is allied with a slowing of time to peak power output, insulin resistance and differential muscle mRNA expression.

Mallinson JE, Marimuthu K, Murton A, Selby A, Smith K, Constantin-Teodosiu D, Rennie MJ, Greenhaff PL - J. Physiol. (Lond.) (2015)

Bottom Line: Statins are associated with muscle myalgia and myopathy, which probably reduce habitual physical activity.Statin myalgic subjects had reduced whole body (P = 0.05) and leg (P < 0.01) glucose disposal, greater abdominal adiposity (P < 0.05) and differential expression of 33 muscle mRNAs (5% false discovery rate (FDR)), six of which, linked to mitochondrial dysfunction and apoptosis, increased at 1% FDR.Statin myalgia was associated with impaired muscle function, increased abdominal adiposity, whole body and leg insulin resistance, and evidence of mitochondrial dysfunction and apoptosis.

View Article: PubMed Central - PubMed

Affiliation: MRC/Arthritis Research UK Centre for Musculoskeletal Ageing Research, University of Nottingham, Nottingham, NG7 2UH, UK.

No MeSH data available.


Related in: MedlinePlus

Muscle mRNA expression normalised to HMBS in the statin user group relative to control at baseline (fold change)A–E, SAM analysis, using an FDR of 5%, revealed these genes to be significantly up-regulated in statin myalgic subjects. Values are expressed as mean ± SEM. Control values are set at 1 and are represented as a dotted line. F, muscle creatine kinase mRNA expression normalised to HMBS (fold change relative to control). Values are expressed as mean ± SEM (black horizontal bar) and individual fold difference in statin myalgic subjects (black spots). ***P < 0.001 when compared to control.
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fig07: Muscle mRNA expression normalised to HMBS in the statin user group relative to control at baseline (fold change)A–E, SAM analysis, using an FDR of 5%, revealed these genes to be significantly up-regulated in statin myalgic subjects. Values are expressed as mean ± SEM. Control values are set at 1 and are represented as a dotted line. F, muscle creatine kinase mRNA expression normalised to HMBS (fold change relative to control). Values are expressed as mean ± SEM (black horizontal bar) and individual fold difference in statin myalgic subjects (black spots). ***P < 0.001 when compared to control.

Mentions: Following SAM analysis, mRNA expression of 33 genes was significantly (P < 0.05) up-regulated in the muscle of the statin myalgic subjects compared to control when employing a 5% FDR, and no genes were found to be down-regulated. The major pathways up-regulated were proteolysis and apoptosis (Fig. 7A), CHO and fat metabolism (Fig. 7B), cell migration and proliferation (Fig. 7C), transcription factors (Fig. 7D) and insulin signalling (Fig. 7E). The magnitude of the fold increase was generally modest (ranging from 1.1- to 1.8-fold greater than control), but six genes were found to be up-regulated using a 1% FDR. These genes were MMP2, RhoB, BCL2, SREBF2, myostatin (MSTN) and CK. In the case of CK, a profound mean increase in mRNA expression (89-fold) was evident compared to control, with all statin myalgic subjects displaying a striking increase in muscle CK mRNA expression relative to control, which ranged from ∼55- to 130-fold (Fig. 7F).


Statin myalgia is not associated with reduced muscle strength, mass or protein turnover in older male volunteers, but is allied with a slowing of time to peak power output, insulin resistance and differential muscle mRNA expression.

Mallinson JE, Marimuthu K, Murton A, Selby A, Smith K, Constantin-Teodosiu D, Rennie MJ, Greenhaff PL - J. Physiol. (Lond.) (2015)

Muscle mRNA expression normalised to HMBS in the statin user group relative to control at baseline (fold change)A–E, SAM analysis, using an FDR of 5%, revealed these genes to be significantly up-regulated in statin myalgic subjects. Values are expressed as mean ± SEM. Control values are set at 1 and are represented as a dotted line. F, muscle creatine kinase mRNA expression normalised to HMBS (fold change relative to control). Values are expressed as mean ± SEM (black horizontal bar) and individual fold difference in statin myalgic subjects (black spots). ***P < 0.001 when compared to control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC4358682&req=5

fig07: Muscle mRNA expression normalised to HMBS in the statin user group relative to control at baseline (fold change)A–E, SAM analysis, using an FDR of 5%, revealed these genes to be significantly up-regulated in statin myalgic subjects. Values are expressed as mean ± SEM. Control values are set at 1 and are represented as a dotted line. F, muscle creatine kinase mRNA expression normalised to HMBS (fold change relative to control). Values are expressed as mean ± SEM (black horizontal bar) and individual fold difference in statin myalgic subjects (black spots). ***P < 0.001 when compared to control.
Mentions: Following SAM analysis, mRNA expression of 33 genes was significantly (P < 0.05) up-regulated in the muscle of the statin myalgic subjects compared to control when employing a 5% FDR, and no genes were found to be down-regulated. The major pathways up-regulated were proteolysis and apoptosis (Fig. 7A), CHO and fat metabolism (Fig. 7B), cell migration and proliferation (Fig. 7C), transcription factors (Fig. 7D) and insulin signalling (Fig. 7E). The magnitude of the fold increase was generally modest (ranging from 1.1- to 1.8-fold greater than control), but six genes were found to be up-regulated using a 1% FDR. These genes were MMP2, RhoB, BCL2, SREBF2, myostatin (MSTN) and CK. In the case of CK, a profound mean increase in mRNA expression (89-fold) was evident compared to control, with all statin myalgic subjects displaying a striking increase in muscle CK mRNA expression relative to control, which ranged from ∼55- to 130-fold (Fig. 7F).

Bottom Line: Statins are associated with muscle myalgia and myopathy, which probably reduce habitual physical activity.Statin myalgic subjects had reduced whole body (P = 0.05) and leg (P < 0.01) glucose disposal, greater abdominal adiposity (P < 0.05) and differential expression of 33 muscle mRNAs (5% false discovery rate (FDR)), six of which, linked to mitochondrial dysfunction and apoptosis, increased at 1% FDR.Statin myalgia was associated with impaired muscle function, increased abdominal adiposity, whole body and leg insulin resistance, and evidence of mitochondrial dysfunction and apoptosis.

View Article: PubMed Central - PubMed

Affiliation: MRC/Arthritis Research UK Centre for Musculoskeletal Ageing Research, University of Nottingham, Nottingham, NG7 2UH, UK.

No MeSH data available.


Related in: MedlinePlus