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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

Serum insulin concentration and blood glucose disposal rate in control and statin user groupsA, serum insulin area under the curve (AUC) (μIU ml−1 min−1) during the period of steady-state glucose disposal of the fed state clamp (40 mU m−2 min−1 insulin and 10 g h−1 mixed amino acids); B, rate of steady-state whole body glucose disposal (mg kg−1 min−1) during the fed state clamp; C, rate of steady-state leg glucose uptake during the fed state clamp (mg kg−1 leg lean mass min−1); D, relationship between whole body glucose disposal (mg kg−1 min−1) and trunk fat mass (kg). Closed circles = control, open circles = statin myalgic subjects. All values are expressed as mean ± SEM. **P < 0.01 compared to control.
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fig04: Serum insulin concentration and blood glucose disposal rate in control and statin user groupsA, serum insulin area under the curve (AUC) (μIU ml−1 min−1) during the period of steady-state glucose disposal of the fed state clamp (40 mU m−2 min−1 insulin and 10 g h−1 mixed amino acids); B, rate of steady-state whole body glucose disposal (mg kg−1 min−1) during the fed state clamp; C, rate of steady-state leg glucose uptake during the fed state clamp (mg kg−1 leg lean mass min−1); D, relationship between whole body glucose disposal (mg kg−1 min−1) and trunk fat mass (kg). Closed circles = control, open circles = statin myalgic subjects. All values are expressed as mean ± SEM. **P < 0.01 compared to control.

Mentions: When serum insulin was clamped at a fasting concentration for 2 h (insulin infusion rate of 0.6 mU m2 min−1), no difference in steady-state serum insulin concentration was seen when comparing control and statin user groups (data not shown). Similarly, when the insulin infusion rate was increased to 40 mU m2 min−1, along with AA infusion at 10 g h−1 to create a fed state condition, no difference in steady-state serum insulin concentration was observed, although there was a trend for the area under the steady-state insulin curve to be greater in the statin user group (Fig. 4A, P = 0.07), probably reflecting blunted insulin clearance in statin myalgic subjects, given that endogenous insulin production was suppressed by octreotide infusion (see Methods). The rate of whole body glucose disposal during the fed state insulin clamp was 30% lower in the statin user group compared to control (Fig. 4B, P = 0.05) and was accompanied by leg glucose uptake being 45% lower in the statin group (Fig. 4C, P < 0.01). A negative correlation was seen between whole body glucose disposal and trunk fat mass (Fig. 4D, r = –0.70, P < 0.01). The fed state insulin clamp tended to increase muscle PDC activity, but this was not significantly different from baseline or between groups (Table 4). Muscle PDK4 protein expression was not different between control and statin myalgic subjects at baseline or after both fasted and fed state insulin clamps (Table 4).


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)

Serum insulin concentration and blood glucose disposal rate in control and statin user groupsA, serum insulin area under the curve (AUC) (μIU ml−1 min−1) during the period of steady-state glucose disposal of the fed state clamp (40 mU m−2 min−1 insulin and 10 g h−1 mixed amino acids); B, rate of steady-state whole body glucose disposal (mg kg−1 min−1) during the fed state clamp; C, rate of steady-state leg glucose uptake during the fed state clamp (mg kg−1 leg lean mass min−1); D, relationship between whole body glucose disposal (mg kg−1 min−1) and trunk fat mass (kg). Closed circles = control, open circles = statin myalgic subjects. All values are expressed as mean ± SEM. **P < 0.01 compared to control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4358682&req=5

fig04: Serum insulin concentration and blood glucose disposal rate in control and statin user groupsA, serum insulin area under the curve (AUC) (μIU ml−1 min−1) during the period of steady-state glucose disposal of the fed state clamp (40 mU m−2 min−1 insulin and 10 g h−1 mixed amino acids); B, rate of steady-state whole body glucose disposal (mg kg−1 min−1) during the fed state clamp; C, rate of steady-state leg glucose uptake during the fed state clamp (mg kg−1 leg lean mass min−1); D, relationship between whole body glucose disposal (mg kg−1 min−1) and trunk fat mass (kg). Closed circles = control, open circles = statin myalgic subjects. All values are expressed as mean ± SEM. **P < 0.01 compared to control.
Mentions: When serum insulin was clamped at a fasting concentration for 2 h (insulin infusion rate of 0.6 mU m2 min−1), no difference in steady-state serum insulin concentration was seen when comparing control and statin user groups (data not shown). Similarly, when the insulin infusion rate was increased to 40 mU m2 min−1, along with AA infusion at 10 g h−1 to create a fed state condition, no difference in steady-state serum insulin concentration was observed, although there was a trend for the area under the steady-state insulin curve to be greater in the statin user group (Fig. 4A, P = 0.07), probably reflecting blunted insulin clearance in statin myalgic subjects, given that endogenous insulin production was suppressed by octreotide infusion (see Methods). The rate of whole body glucose disposal during the fed state insulin clamp was 30% lower in the statin user group compared to control (Fig. 4B, P = 0.05) and was accompanied by leg glucose uptake being 45% lower in the statin group (Fig. 4C, P < 0.01). A negative correlation was seen between whole body glucose disposal and trunk fat mass (Fig. 4D, r = –0.70, P < 0.01). The fed state insulin clamp tended to increase muscle PDC activity, but this was not significantly different from baseline or between groups (Table 4). Muscle PDK4 protein expression was not different between control and statin myalgic subjects at baseline or after both fasted and fed state insulin clamps (Table 4).

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