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MITOCHONDRIAL MRNA ACUTE RESPONSE TO BOUTS OF HIGH- AND LOW-LOAD RESISTANCE TRAINING

Abstract

BACKGROUND: The effects of high-load (HL ~80% of 1-RM) versus low-load (LL ~30% of 1-RM) resistance training (RT) on various molecular outcomes has proven to be similar between the two paradigms. However, the mitochondrial response to such training paradigms remains understudied. Therefore, the purpose of this study was to interrogate the transcriptional response of HL and LL RT in mRNAs related to mitochondrial biogenesis and remodeling. METHODS: Eleven resistance trained males completed two acute bouts of either HL or LL barbell back squats and seated leg extensions to failure. Each session was completed in randomized order and separated by 7 days. Vastus lateralis muscle biopsies were collected at PRE, 3 hours post- (3h), and 6 hours post-exercise (6h). Ten mRNAs related to mitochondrial biogenesis and remodeling were investigated using the Clariom S Assay Human mRNA array, and two-way ANOVAS were performed to detect any interactions or main effects of timepoint and condition. RESULTS: NRF1 was statistically significantly higher in the LL condition (p = 0.040), but no other markers of mitochondrial biogenesis demonstrated statistically significant differences. However, there was a statistically significant main effect of timepoint for multiple markers of mitochondrial biogenesis. This included NRF1 (p = 0.049) decreasing at 3h and both PGC1-a (p = < 0.001) and TFAM (p= 0.030) increasing at 6h compared to PRE. There was a main effect of timepoint, but not condition, in markers of mitochondrial remodeling with MFN2 (p = 0.021) and Parkin (p= 0.006) showing decreased mRNA expression from PRE to 3h. CONCLUSION: Resistance training load had little effect on mRNA markers of mitochondrial biogenesis and remodeling. However, it appears that acute resistance exercise uniquely affects markers of mitochondrial biogenesis and remodeling at 3h and 6h timepoints. Further investigation is warranted to delineate the time course of the transcriptional response of each marker of mitochondrial biogenesis and remodeling.

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