December 1, 2014BMC PhysiologyOpen Access

Co-overexpression of alpha- and beta-CaMKII in regenerating skeletal muscle reduced time-to-peak-twitch force by 16% and half-relaxation time by 15%, but did not stimulate mitochondrial biogenesis.

Q: What is the clinical evidence from this study?

Study design: Other. Population: Healthy (skeletal muscle plasticity) (n=13). Intervention: Co-overexpression of native alpha- and beta-CaMKII isoforms vs. Control-transfected contralateral muscle. Primary outcome: Time-to-peak-twitch force and half-relaxation time (-16% for time-to-peak-twitch force and -15% for half-relaxation time, p=<0.05).

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Population

3-month old rats (fast-twitch muscle m. gastrocnemius and slow-twitch muscle m. soleus)

Comparison

Transfection via electro-transfer of injected… vs Control-transfected muscles of the contralateral…

Design

Preclinical

Follow-up

7 days

Key result

Co-overexpression of alpha- and beta-CaMKII in regenerating skeletal muscle reduced time-to-peak-twitch force by 16% and half-relaxation time by 15%, but did not stimulate mitochondrial biogenesis.

Authors

WEWouter Eilers RJRichard T. Jaspers AHA. de Haan

Discussion

Member takes

Overview

Elevated CaMKII may promote slow-to-fast fiber shifts in regenerating muscle; leaves open its role in mitochondrial biogenesis.

Structured PICO

Population

13 three-month-old female Wistar rats subjected to in vivo electro-transfer of CaMKII expression plasmids in skeletal muscle to study muscle plasticity.

Intervention

Transfection via electro-transfer of injected expression plasmids for native α/β CaMKII in the right leg

Comparator

Control-transfected muscles of the contralateral leg and non-transfected muscles

Outcome

Contractile and mitochondrial phenotype (excitation-contraction coupling, relaxation, SERCA2, ANXV, fast myosin type IIA/X content, mitochondrial protein content)surrogate

Main Result

Effect estimate: -16% for time-to-peak-twitch force and -15% for half-relaxation time

p-value: p=<0.05

Elevated CaMKII content promotes a slow-to-fast type fibre shift in regenerating skeletal muscle but does not stimulate mitochondrial biogenesis without an endurance stimulus.

Limitations

Muscle regeneration and damage are inherent to the selected mode of transfection (electroporation), which may mask or alter physiological responses.
The study was conducted under normal cage activity without an imposed endurance contraction protocol, which may be required for mitochondrial biogenesis.

Cite This Study

Eilers et al. (2014) studied Healthy (skeletal muscle plasticity) (n=13). Co-overexpression of native alpha- and beta-CaMKII isoforms vs. Control-transfected contralateral muscle was evaluated on Time-to-peak-twitch force and half-relaxation time (-16% for time-to-peak-twitch force and -15% for half-relaxation time, p=<0.05). Co-overexpression of alpha- and beta-CaMKII in regenerating skeletal muscle reduced time-to-peak-twitch force by 16% and half-relaxation time by 15%, but did not stimulate mitochondrial biogenesis.

synapsesocial.com/papers/6a656af62d34c0d4ae2d69b2 https://doi.org/10.1186/s12899-014-0007-z

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December 1, 2014BMC PhysiologyOpen Access

Co-overexpression of alpha- and beta-CaMKII in regenerating skeletal muscle reduced time-to-peak-twitch force by 16% and half-relaxation time by 15%, but did not stimulate mitochondrial biogenesis.

View Full Paper

Ask AI

Bookmark

Population

3-month old rats (fast-twitch muscle m. gastrocnemius and slow-twitch muscle m. soleus)

Comparison

Transfection via electro-transfer of injected… vs Control-transfected muscles of the contralateral…

Design

Preclinical

Follow-up

7 days

Key result

Co-overexpression of alpha- and beta-CaMKII in regenerating skeletal muscle reduced time-to-peak-twitch force by 16% and half-relaxation time by 15%, but did not stimulate mitochondrial biogenesis.

Authors

WEWouter Eilers RJRichard T. Jaspers AHA. de Haan

Discussion

Member takes

Overview

Elevated CaMKII may promote slow-to-fast fiber shifts in regenerating muscle; leaves open its role in mitochondrial biogenesis.

Structured PICO

Population

13 three-month-old female Wistar rats subjected to in vivo electro-transfer of CaMKII expression plasmids in skeletal muscle to study muscle plasticity.

Intervention

Transfection via electro-transfer of injected expression plasmids for native α/β CaMKII in the right leg

Comparator

Control-transfected muscles of the contralateral leg and non-transfected muscles

Outcome

Contractile and mitochondrial phenotype (excitation-contraction coupling, relaxation, SERCA2, ANXV, fast myosin type IIA/X content, mitochondrial protein content)surrogate

Main Result

Effect estimate: -16% for time-to-peak-twitch force and -15% for half-relaxation time

p-value: p=<0.05

Elevated CaMKII content promotes a slow-to-fast type fibre shift in regenerating skeletal muscle but does not stimulate mitochondrial biogenesis without an endurance stimulus.

Limitations

Muscle regeneration and damage are inherent to the selected mode of transfection (electroporation), which may mask or alter physiological responses.
The study was conducted under normal cage activity without an imposed endurance contraction protocol, which may be required for mitochondrial biogenesis.

Cite This Study

synapsesocial.com/papers/6a656af62d34c0d4ae2d69b2 https://doi.org/10.1186/s12899-014-0007-z

Also Consider

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