Effect of acute transcranial magnetic stimulation on intracellular signalling in human skeletal muscle

To investigate the potential of an acute bout of transcranial electrical stimulation to induce anabolic signalling. Experimental intervention on healthy subjects. Ten healthy subjects, 5 women and 5 men (mean age (standard deviation (SD) 32 years (SD 4)). The quadriceps muscle was stimulated at a fr...

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Published inJournal of rehabilitation medicine Vol. 52; no. 2; p. jrm00022
Main Authors von Walden, F, Gidlund, E, Liu, C, Ramstrand, N, Norrbom, J, von Wachenfelt, N, Kjellgren, H, Sundberg, C, Pontén, E, Alkner, B
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Published Sweden Medical Journals Sweden 2020
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Abstract To investigate the potential of an acute bout of transcranial electrical stimulation to induce anabolic signalling. Experimental intervention on healthy subjects. Ten healthy subjects, 5 women and 5 men (mean age (standard deviation (SD) 32 years (SD 4)). The quadriceps muscle was stimulated at a frequency of 10 Hz for 10 s, followed by 20 s of rest, repeated 40 times over 20 min. Electromyography and force data were collected for all transcranial electrical stimulation sequences. Muscle biopsies were obtained from the vastus lateralis muscle before and 1 and 3 h after stimulation. One bout of transcranial electrical stimulation decreased phosphorylation of AKT at Thr308 (1 h: -29%, 3 h: -38%; p < 0.05) and mTOR phosphorylation at Ser2448 (1 h: -10%; ns, 3 h: -21%; p < 0.05), both in the anabolic pathway. Phosphorylation of AMPK, ACC and ULK1 were not affected. c-MYC gene expression was unchanged following transcranial electrical stimulation, but rDNA transcription decreased (1 h: -28%, 3 h: -19%; p < 0.05). PGC1α-ex1b mRNA increased (1 h: 2.3-fold, 3 h: 2.6-fold; p < 0.05), which also correlated with vastus lateralis electromyography activity, while other PGC-1α variants were unchanged. Acute transcranial electrical stimulation of skeletal muscle in weight-bearing healthy individuals did not induce anabolic signalling, and some signs of impaired muscle anabolism were detected, suggesting limited potential in preventing muscle wasting.
AbstractList OBJECTIVE: To investigate the potential of an acute bout of transcranial electrical stimulation to induce anabolic signalling. DESIGN: Experimental intervention on healthy subjects. SUBJECTS: Ten healthy subjects, 5 women and 5 men (mean age (standard deviation (SD) 32 years (SD 4)). METHODS: The quadriceps muscle was stimulated at a frequency of 10 Hz for 10 s, followed by 20 s of rest, repeated 40 times over 20 min. Electromyography and force data were collected for all transcranial electrical stimulation sequences. Muscle biopsies were obtained from the vastus lateralis muscle before and 1 and 3 h after stimulation. RESULTS: One bout of transcranial electrical stimulation decreased phosphorylation of AKT at Thr308 (1 h: -29%, 3 h: -38%; p &lt; 0.05) and mTOR phosphorylation at Ser2448 (1 h: -10%; ns, 3 h: -21%; p &lt; 0.05), both in the anabolic pathway. Phosphorylation of AMPK, ACC and ULK1 were not affected. c-MYC gene expression was unchanged following transcranial electrical stimulation, but rDNA transcription decreased (1 h: -28%, 3 h: -19%; p &lt; 0.05). PGC1α-ex1b mRNA increased (1 h: 2.3-fold, 3 h: 2.6-fold; p &lt; 0.05), which also correlated with vastus lateralis electromyography activity, while other PGC-1α variants were unchanged. CONCLUSION: Acute transcranial electrical stimulation of skeletal muscle in weight-bearing healthy individuals did not induce anabolic signalling, and some signs of impaired muscle anabolism were detected, suggesting limited potential in preventing muscle wasting.
Objective: To investigate the potential of an acute bout of transcranial magnetic stimulation to induce anabolic signalling. Design: Experimental intervention on healthy subjects. Subjects: Ten healthy subjects, 5 women and 5 men (mean age 32 years; standard deviation (SD) 4). Methods: Transcranial magnetic stimulation, resulting in contraction of the quadriceps muscles, was applied at a frequency of 10 Hz for 10 s followed by 20 s of rest, repeated 40 times over 20 min. Electromyography and force data were collected for all transcranial magnetic stimulation sequences. Muscle biopsies were obtained from the vastus lateralis muscle before and 1 and 3 h after stimulation for evaluation of the molecular response of the muscle. Results: The described stimulation decreased phosphorylation of AKT at Thr308 (1 h: -29%, 3 h: -38%; p&amp;lt;0.05) and mTOR phosphorylation at Ser2448 (1 h: -10%; ns, 3 h: -21%; p &amp;lt; 0.05), both in the anabolic pathway. Phosphorylation of AMPK, ACC and ULK1 were not affected. c-MYC gene expression was unchanged following transcranial magnetic stimulation, but rDNA transcription decreased (1 h: -28%, 3 h: -19%; p&amp;lt;0.05). PGC1 alpha-exlb mRNA increased (1 h: 2.3-fold, 3 h: 2.6-fold; p&amp;lt;0.05), which also correlated with vastus lateralis electromyography activity, while other PGC-1 alpha variants were unchanged. Conclusion: Acute transcranial magnetic stimulation of skeletal muscle in weight-bearing healthy individuals did not induce anabolic signalling, but some signs of impaired muscle anabolism were detected. Therefore, these results do not support the use of acute transcranial magnetic stimulation in preventing muscle wasting.
Objective: To investigate the potential of an acute bout of transcranial magnetic stimulation to induce anabolic signalling. Design: Experimental intervention on healthy subjects. Subjects: Ten healthy subjects, 5 women and 5 men (mean age 32 years; standard deviation (SD) 4). Methods: Transcranial magnetic stimulation, resulting in contraction of the quadriceps muscles, was applied at a frequency of 10 Hz for 10 s followed by 20 s of rest, repeated 40 times over 20 min. Electromyography and force data were collected for all transcranial magnetic stimulation sequences. Muscle biopsies were obtained from the vastus lateralis muscle before and 1 and 3 h after stimulation for evaluation of the molecular response of the muscle. Results: The described stimulation decreased phosphorylation of AKT at Thr308 (1 h: –29%, 3 h: –38%; p < 0.05) and mTOR phosphorylation at Ser2448 (1 h: –10%; ns, 3 h: –21%; p < 0.05), both in the anabolic pathway. Phosphorylation of AMPK, ACC and ULK1 were not affected. c-MYC gene expression was unchanged following transcranial magnetic stimulation, but rDNA transcription decreased (1 h: –28%, 3 h: –19%; p < 0.05). PGC1α-ex1b mRNA increased (1 h: 2.3-fold, 3 h: 2.6-fold; p < 0.05), which also correlated with vastus lateralis electromyography activity, while other PGC-1α variants were unchanged. Conclusion: Acute transcranial magnetic stimulation of skeletal muscle in weight-bearing healthy individuals did not induce anabolic signalling, but some signs of impaired muscle anabolism were detected. Therefore, these results do not support the use of acute transcranial magnetic stimulation in preventing muscle wasting.
To investigate the potential of an acute bout of transcranial electrical stimulation to induce anabolic signalling. Experimental intervention on healthy subjects. Ten healthy subjects, 5 women and 5 men (mean age (standard deviation (SD) 32 years (SD 4)). The quadriceps muscle was stimulated at a frequency of 10 Hz for 10 s, followed by 20 s of rest, repeated 40 times over 20 min. Electromyography and force data were collected for all transcranial electrical stimulation sequences. Muscle biopsies were obtained from the vastus lateralis muscle before and 1 and 3 h after stimulation. One bout of transcranial electrical stimulation decreased phosphorylation of AKT at Thr308 (1 h: -29%, 3 h: -38%; p < 0.05) and mTOR phosphorylation at Ser2448 (1 h: -10%; ns, 3 h: -21%; p < 0.05), both in the anabolic pathway. Phosphorylation of AMPK, ACC and ULK1 were not affected. c-MYC gene expression was unchanged following transcranial electrical stimulation, but rDNA transcription decreased (1 h: -28%, 3 h: -19%; p < 0.05). PGC1α-ex1b mRNA increased (1 h: 2.3-fold, 3 h: 2.6-fold; p < 0.05), which also correlated with vastus lateralis electromyography activity, while other PGC-1α variants were unchanged. Acute transcranial electrical stimulation of skeletal muscle in weight-bearing healthy individuals did not induce anabolic signalling, and some signs of impaired muscle anabolism were detected, suggesting limited potential in preventing muscle wasting.
To investigate the potential of an acute bout of transcranial electrical stimulation to induce anabolic signalling.OBJECTIVETo investigate the potential of an acute bout of transcranial electrical stimulation to induce anabolic signalling.Experimental intervention on healthy subjects.DESIGNExperimental intervention on healthy subjects.Ten healthy subjects, 5 women and 5 men (mean age (standard deviation (SD) 32 years (SD 4)).SUBJECTSTen healthy subjects, 5 women and 5 men (mean age (standard deviation (SD) 32 years (SD 4)).The quadriceps muscle was stimulated at a frequency of 10 Hz for 10 s, followed by 20 s of rest, repeated 40 times over 20 min. Electromyography and force data were collected for all transcranial electrical stimulation sequences. Muscle biopsies were obtained from the vastus lateralis muscle before and 1 and 3 h after stimulation.METHODSThe quadriceps muscle was stimulated at a frequency of 10 Hz for 10 s, followed by 20 s of rest, repeated 40 times over 20 min. Electromyography and force data were collected for all transcranial electrical stimulation sequences. Muscle biopsies were obtained from the vastus lateralis muscle before and 1 and 3 h after stimulation.One bout of transcranial electrical stimulation decreased phosphorylation of AKT at Thr308 (1 h: -29%, 3 h: -38%; p < 0.05) and mTOR phosphorylation at Ser2448 (1 h: -10%; ns, 3 h: -21%; p < 0.05), both in the anabolic pathway. Phosphorylation of AMPK, ACC and ULK1 were not affected. c-MYC gene expression was unchanged following transcranial electrical stimulation, but rDNA transcription decreased (1 h: -28%, 3 h: -19%; p < 0.05). PGC1α-ex1b mRNA increased (1 h: 2.3-fold, 3 h: 2.6-fold; p < 0.05), which also correlated with vastus lateralis electromyography activity, while other PGC-1α variants were unchanged.RESULTSOne bout of transcranial electrical stimulation decreased phosphorylation of AKT at Thr308 (1 h: -29%, 3 h: -38%; p < 0.05) and mTOR phosphorylation at Ser2448 (1 h: -10%; ns, 3 h: -21%; p < 0.05), both in the anabolic pathway. Phosphorylation of AMPK, ACC and ULK1 were not affected. c-MYC gene expression was unchanged following transcranial electrical stimulation, but rDNA transcription decreased (1 h: -28%, 3 h: -19%; p < 0.05). PGC1α-ex1b mRNA increased (1 h: 2.3-fold, 3 h: 2.6-fold; p < 0.05), which also correlated with vastus lateralis electromyography activity, while other PGC-1α variants were unchanged.Acute transcranial electrical stimulation of skeletal muscle in weight-bearing healthy individuals did not induce anabolic signalling, and some signs of impaired muscle anabolism were detected, suggesting limited potential in preventing muscle wasting.CONCLUSIONAcute transcranial electrical stimulation of skeletal muscle in weight-bearing healthy individuals did not induce anabolic signalling, and some signs of impaired muscle anabolism were detected, suggesting limited potential in preventing muscle wasting.
Author Alkner, B
Ramstrand, N
von Walden, F
Norrbom, J
von Wachenfelt, N
Gidlund, E
Liu, C
Sundberg, C
Kjellgren, H
Pontén, E
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electromyography
transcranial magnetic stimulation
anabolic signalling
muscle wasting
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Snippet To investigate the potential of an acute bout of transcranial electrical stimulation to induce anabolic signalling. Experimental intervention on healthy...
To investigate the potential of an acute bout of transcranial electrical stimulation to induce anabolic signalling.OBJECTIVETo investigate the potential of an...
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Objective: To investigate the potential of an acute bout of transcranial magnetic stimulation to induce anabolic signalling. Design: Experimental intervention...
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SubjectTerms electromyography
skeletal muscle
transcranial magnetic stimulation
Title Effect of acute transcranial magnetic stimulation on intracellular signalling in human skeletal muscle
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