Beneficial Mitochondrial Biogenesis in Gastrocnemius Muscle Promoted by High-Intensity Interval Training in Elderly Female Rats

Document Type : Original Article

Authors

1 Department of Basic Sciences, Chabahar Maritime University, Chabahar, Iran

2 Department of Physical Education and Sport Sciences of Tehran University, Tehran, Iran

3 Department of Physical Education and Sport Sciences, University of Kurdistan, Sanandaj, Iran

Abstract

Objective:
Exercise can attenuate mitochondrial dysfunction caused by aging. Our study aimed to compare 12
weeks of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on the expression
of mitochondria proteins [e.g., AMP-activated protein kinase (AMPK), Estrogen-related receptor alpha (ERRα), p38
mitogen-activated protein kinase (P38MAPK), and Peroxisome proliferator-activated receptor gamma coactivator
1-alpha (PGC1-α)] in gastrocnemius muscle of old female rats.

Materials and Methods:
In this experimental study, thirty six old female Wistar rats (18-month-old and 270-310 g) were
divided into three groups: i. HIIT, ii. MICT, and iii. Control group (C). The HIIT protocol was performed for 12 weeks with
16-28 minutes (2 minutes training with 85-90% VO2max in high intensity and 2 minutes training with 45-75% VO2max low intensity). The MICT was performed for 30-60 minutes with the intensity of 65-70% VO2max. The gastrocnemius muscle expression of AMPK, ERRα, P38MAPK, and PGC1α proteins were determined by Western blotting.

Results:
The expression of AMPK (P=0.004), P38MAPK (P=0.003), PGC-1α (P=0.028), and ERRα (P=0.006) in HIIT
was higher than C group. AMPK (P=0.03), P38MAPK (P=0.032), PGC-1α (P=0.015), and ERRα (P=0.028) in MICT
was higher than the C group. Also expression of AMPK (P=0.008), P38MAPK (P=0.009), PGC-1α (P=0.020) and ERRα
(P=0.014) in MICT was higher than MICT group.

Conclusion:
It seems that exercise training has beneficial effects on mitochondrial biogenesis, but the HIIT training
method is more effective than MICT in improving mitochondrial function in aging.

Keywords

Main Subjects

References

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