Abstract
[Purpose]The purpose of this study was to determine whether exercise or/and cold exposure regulate mitochondria biogenesis-related gene expression in soleus and inguinal adipose tissue of mice. [Methods]Forty ICR 5-week old male mice were divided into four groups: thermoneutrality-untrained (23 ± 1 °C in room temperature, n=10), cold-water immersion (24 ± 1 °C, n=10), exercise in neutral temperature (34 ± 1 °C, n=10), and exercise in cold temperature (24 ± 1 °C, n=10). The mice performed swimming exercise (30 min to 60 min, 5 times) for 8 weeks. After 8 weeks, we confirmed mitochondrial biogenesis-related gene expression changes for peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), nuclear respiratory factors 1 (NRF1), and mitochondrial transcription factor A (Tfam) in soleus muscle and inguinal adipose tissue, and the related protein expression in soleus muscle. [Results]In soleus muscle, PGC-1α expression significantly increased in response to cold exposure (p = 0.006) and exercise (p = 0.05). There was also significant interaction between exercise and cold exposure (p = 0.005). Only exercise had a significant effect on NRF1 relative expression (p=0.001). Neither cold exposure nor the interaction showed significant effects (p = 0.1222 and p = 0.875, respectively). Relative Tfam expression did not show any significant effect from exercise. In inguinal adipose tissue, relative PGC-1α expression did not significantly change in any group. NRF1 expression showed a significant change from exercise (p = 0.01) and cold exposure (p = 0.011). There was also a significant interaction between exercise and cold exposure (p = 0.000). Tfam mRNA expression showed a significant effect from exercise (p=0.000) and an interaction between exercise and cold exposure (p=0.001). Only temperature significantly affected PGC-1α protein levels (p=0.045). Neither exercise nor the interaction were significant (p = 0.397 and p = 0.292, respectively). NRF1 protein levels did not show a significant effect in any experimental treatments. Tfam protein levels showed a significant effect in the exercise group (p=0.012), but effects of neither cold exposure nor the interaction were significant (p = 0.085 and p=0.374, respectively). [Conclusion]Exercise and cold exposure promoted increased expression of mitochondrial biogenesis- related genes in soleus muscle. Only cold exposure had a significant effect on PGC-1α protein expression and only exercise had a significant effect on Tfam protein expression. In inguinal adipose tissue, there was interaction between exercise and cold exposure in expression of mitochondrial biogenesis-related genes.
Highlights
Mitochondrial dysfunction has been recognized as an important contributor to an array of human pathologies[1,2,3,4,5]
Animals that exercised in neutral temperature water had a lower body weight than animals used as controls, those immersed in cold water, and those exercised in cold water
Only temperature had a significant effect on PGC-1α protein expression and only exercise had a significant effect on nuclear respiratory factors 1 (NRF1) protein expression
Summary
Mitochondrial dysfunction has been recognized as an important contributor to an array of human pathologies[1,2,3,4,5]. Exercise increases cellular energy demand, which increases intracellular AMP, Ca2+ concentrations, free phosphate groups (Pi), and reactive oxygen species (ROS)[15] These substances are potent signaling transducers and activate calcium/ calmodulin-dependent protein kinases (CaMK), AMP-activated protein kinase (AMPK), and p38 mitogen-activated kinase (p38MAPK), which trigger transcription and activation of PGC-1α and mitochondrial biogenesis[16]. There are multiple changes within the adipose tissue, increased mitochondrial content[17,18] It is unclear whether exercise and cold exposure act independently or dependently, because previous studies have reported only the effect of exercise[6,8,16] or cold exposure[9,10,11,19].
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