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Stand-up exercise training facilitates muscle recovery from disuse atrophy by stimulating myogenic satellite cell proliferation in mice.

Itoh Y, Hayakawa K, Mori T, Agata N, Inoue-Miyazu M, Murakami T, Sokabe M, Kawakami K - Physiol Rep (2014)

Bottom Line: Seven days after the training, average myofiber cross-sectional area (CSA) of the soleus muscle was significantly greater in the SE-trained group than in the non-SE-trained group (1843 ± 194 μm(2) vs. 1315 ± 153 μm(2)).Mean soleus muscle CSA in the SE trained group was not different from that in the CON group subjected to neither TS nor SE training (2005 ± 196 μm(2)), indicating that SE training caused nearly complete recovery from muscle atrophy.The number of myonuclei per myofiber was increased by ~60% in the SE-trained group compared with the non-SE-trained and CON groups (0.92 ± 0.03 vs. 0.57 ± 0.03 and 0.56 ± 0.11, respectively).

View Article: PubMed Central - PubMed

Affiliation: Physical and Occupational Therapy Program, Nagoya University Graduate School of Medicine, Nagoya, Japan Faculty of Rehabilitation Science, Nagoya Gakuin University, Seto, Japan.

No MeSH data available.


Related in: MedlinePlus

SE‐training‐induced increases in myonuclei are due to the proliferation and fusion of myogenic satellite cells. (A) Typical section stained by 5‐ethynyl‐2’‐deoxyuridine (EdU), antidystrophin, and 4’,6‐diamidino‐2‐phenylindole. (B) Numbers of myonuclei per myofiber and EdU‐positive myonuclei (A, arrow). The number of myonuclei per myofiber was highest in the group administered EdU on day 2 of SE training. *P <0.05 for total myonuclei counts, #P <0.05 for EdU‐positive myonuclei counts. (C) Photomicrographs of muscle samples stained with an anti‐Pax7 antibody (red, arrowheads), a marker of myogenic satellite cells, from mice subjected to TS and then SE training (SE‐trained group). Immunoreactivity to Pax7 was observed in EdU‐positive nuclei (green, arrows).
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fig05: SE‐training‐induced increases in myonuclei are due to the proliferation and fusion of myogenic satellite cells. (A) Typical section stained by 5‐ethynyl‐2’‐deoxyuridine (EdU), antidystrophin, and 4’,6‐diamidino‐2‐phenylindole. (B) Numbers of myonuclei per myofiber and EdU‐positive myonuclei (A, arrow). The number of myonuclei per myofiber was highest in the group administered EdU on day 2 of SE training. *P <0.05 for total myonuclei counts, #P <0.05 for EdU‐positive myonuclei counts. (C) Photomicrographs of muscle samples stained with an anti‐Pax7 antibody (red, arrowheads), a marker of myogenic satellite cells, from mice subjected to TS and then SE training (SE‐trained group). Immunoreactivity to Pax7 was observed in EdU‐positive nuclei (green, arrows).

Mentions: To confirm that newly proliferated cells had fused with atrophied myofibers, EdU, a nucleoside analogue used to detect de novo DNA synthesis, was administered to SE trained or non‐SE mice on day 0, 1, or 2 of the SE‐training period (Figs 1B, 5A), and the numbers of EdU‐positive myonuclei were determined 48 h later (on day 2, 3, or 4 of SE training, respectively). There was a significant increase in EdU‐positive myonuclei when EdU was administered on day 2 of SE training. On day 4, EdU‐positive myonuclei accounted for 11.1% of the total myonuclei per myofiber (Fig. 5B). The number of myonuclei on day 4 SE‐trained mice was nearly the same on day 7 SE‐trained mice. (Figs 4B, 5B). These results suggested that myogenic precursor cells had begun to proliferate as early as 2 days after the SE‐training onset, and then fused with existing myofibers within 2 days (between 2 and 4 days of SE training). The EdU‐positive myonuclei was hardly detected in the non‐SE‐trained mice at any time point (0.0003, 0.01, 0.02% on day 2, 3, or 4, respectively).


Stand-up exercise training facilitates muscle recovery from disuse atrophy by stimulating myogenic satellite cell proliferation in mice.

Itoh Y, Hayakawa K, Mori T, Agata N, Inoue-Miyazu M, Murakami T, Sokabe M, Kawakami K - Physiol Rep (2014)

SE‐training‐induced increases in myonuclei are due to the proliferation and fusion of myogenic satellite cells. (A) Typical section stained by 5‐ethynyl‐2’‐deoxyuridine (EdU), antidystrophin, and 4’,6‐diamidino‐2‐phenylindole. (B) Numbers of myonuclei per myofiber and EdU‐positive myonuclei (A, arrow). The number of myonuclei per myofiber was highest in the group administered EdU on day 2 of SE training. *P <0.05 for total myonuclei counts, #P <0.05 for EdU‐positive myonuclei counts. (C) Photomicrographs of muscle samples stained with an anti‐Pax7 antibody (red, arrowheads), a marker of myogenic satellite cells, from mice subjected to TS and then SE training (SE‐trained group). Immunoreactivity to Pax7 was observed in EdU‐positive nuclei (green, arrows).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255801&req=5

fig05: SE‐training‐induced increases in myonuclei are due to the proliferation and fusion of myogenic satellite cells. (A) Typical section stained by 5‐ethynyl‐2’‐deoxyuridine (EdU), antidystrophin, and 4’,6‐diamidino‐2‐phenylindole. (B) Numbers of myonuclei per myofiber and EdU‐positive myonuclei (A, arrow). The number of myonuclei per myofiber was highest in the group administered EdU on day 2 of SE training. *P <0.05 for total myonuclei counts, #P <0.05 for EdU‐positive myonuclei counts. (C) Photomicrographs of muscle samples stained with an anti‐Pax7 antibody (red, arrowheads), a marker of myogenic satellite cells, from mice subjected to TS and then SE training (SE‐trained group). Immunoreactivity to Pax7 was observed in EdU‐positive nuclei (green, arrows).
Mentions: To confirm that newly proliferated cells had fused with atrophied myofibers, EdU, a nucleoside analogue used to detect de novo DNA synthesis, was administered to SE trained or non‐SE mice on day 0, 1, or 2 of the SE‐training period (Figs 1B, 5A), and the numbers of EdU‐positive myonuclei were determined 48 h later (on day 2, 3, or 4 of SE training, respectively). There was a significant increase in EdU‐positive myonuclei when EdU was administered on day 2 of SE training. On day 4, EdU‐positive myonuclei accounted for 11.1% of the total myonuclei per myofiber (Fig. 5B). The number of myonuclei on day 4 SE‐trained mice was nearly the same on day 7 SE‐trained mice. (Figs 4B, 5B). These results suggested that myogenic precursor cells had begun to proliferate as early as 2 days after the SE‐training onset, and then fused with existing myofibers within 2 days (between 2 and 4 days of SE training). The EdU‐positive myonuclei was hardly detected in the non‐SE‐trained mice at any time point (0.0003, 0.01, 0.02% on day 2, 3, or 4, respectively).

Bottom Line: Seven days after the training, average myofiber cross-sectional area (CSA) of the soleus muscle was significantly greater in the SE-trained group than in the non-SE-trained group (1843 ± 194 μm(2) vs. 1315 ± 153 μm(2)).Mean soleus muscle CSA in the SE trained group was not different from that in the CON group subjected to neither TS nor SE training (2005 ± 196 μm(2)), indicating that SE training caused nearly complete recovery from muscle atrophy.The number of myonuclei per myofiber was increased by ~60% in the SE-trained group compared with the non-SE-trained and CON groups (0.92 ± 0.03 vs. 0.57 ± 0.03 and 0.56 ± 0.11, respectively).

View Article: PubMed Central - PubMed

Affiliation: Physical and Occupational Therapy Program, Nagoya University Graduate School of Medicine, Nagoya, Japan Faculty of Rehabilitation Science, Nagoya Gakuin University, Seto, Japan.

No MeSH data available.


Related in: MedlinePlus