Irisin/FNDC5 influences myogenic markers on skeletal muscle following high and moderate-intensity exercise training in STZ-diabetic rats
In the present study, we investigated the effects of high-intensity interval training (HIIT) versus moderate-intensity continuous training (MICT) on irisin and expression of myogenic markers (paired box 7 (Pax7), myogenic differentiation 1 (MyoD), myogenin) in skeletal muscle of diabetic rats. Eight...
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Veröffentlicht in: | 3 Biotech 2022-09, Vol.12 (9), p.193-193, Article 193 |
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Zusammenfassung: | In the present study, we investigated the effects of high-intensity interval training (HIIT) versus moderate-intensity continuous training (MICT) on irisin and expression of myogenic markers (paired box 7 (Pax7), myogenic differentiation 1 (MyoD), myogenin) in skeletal muscle of diabetic rats. Eighty-four male Wistar rats (6 weeks of age) were randomly divided into seven groups (
n
= 12): basic control (Co Basic), 8 weeks control (Co 8w), diabetes mellitus (DM), HIIT, DM + HIIT, MICT, and DM + MICT groups. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ). The
V
˙
o
2
max
protocol was characterized by running on a rodent treadmill with moderate intensity (60–70%
V
˙
o
2
max
), 60 min per session, 5 days/week, for 6 weeks. HIIT consisted of six 3-min runs at a high intensity (80–90%
V
˙
o
2
max
) alternated with 2-min running at low intensity (50%
V
˙
o
2
max
), 30 min per session, 5 days/week, for 6 weeks. Results showed that DM decreased myoblast markers compared to Co Basic and Co 8w groups. Fibronectin type III domain-containing protein 5 (FNDC5) mRNA decrease was correlated with myoblast markers (Pax7
r
= 0.632,
p
= 0.027; MyoD
r
= 0.999,
p
= 0.001; myogenin
r
= 1.000,
p
= 0.001) in DM group. DM + MICT significantly increased gene expression of MyoD, myogenin, and FNDC5 compared to DM and DM + HIIT. The results also showed that the intensity and duration of exercise on the treadmill were effective in stimulating irisin and myogenic markers after DM. |
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ISSN: | 2190-572X 2190-5738 |
DOI: | 10.1007/s13205-022-03253-9 |