The current study aims to investigate if the overexpression of the mitochondrial transcription factor A (TFAM) gene in a transgenic mouse model diminishes soleus and gastrocnemius atrophy occurring with hindlimb suspension (HLS). Additionally, we aim to observe if combining concurrent, treadmill exercise training with TFAM transgenic mice prior to HLS has a synergistic effect in preventing skeletal muscle atrophy. Male transgenic mice aged 12–14 weeks old overexpressing the TFAM gene were assigned to a control (T‐Control), 7‐day HLS (T‐HLS), and 14 exercise sessions prior to 7‐day HLS (T‐Ex+HLS) groups and compared to male C57BL/6 (WT) mice (all wild‐type data from prior work currently in submission) aged 12–14 weeks old assigned to Control, 7‐day HLS (HLS), 14 exercise sessions prior to 7‐day HLS (Ex+HLS), and 14 exercise sessions (Ex). Results indicate overexpressing TFAM results in a decrease of 8.3% in soleus weight/bodyweight ratio and 2.6% in gastrocnemius weight/bodyweight ratio after HLS compared to losses in wild‐type mice of 27.1% in soleus weight/bodyweight ratio and 21.5% in gastrocnemius weight/bodyweight ratio after HLS. Our data indicates TFAM may play a critical role in protecting skeletal muscle from disuse atrophy and is correlated with increased expression of antioxidants (SOD‐2) and potential redox balance. Our results also indicate combining exercise with TFAM overexpression had no significant increase compared to wild‐type Ex+HLS. TFAM may be a molecule of interest for future pharmaceutical and therapeutic targeting to treat skeletal muscle atrophy.Support or Funding InformationThe study was supported by NIH Grant HL74185 to SCT.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

To study the influence of genetics and feeding strategy, we measured growth and mRNA expression of protein degradation markers in growth‐selected and control rainbow trout that were either fed to satiation or limit‐fed. Fish were limit fed to 90–95% of the feed required to reach maximal growth. Length and weight of 1600 trout were measured every six weeks for 24 weeks. After 24 weeks of dietary treatment there was an interaction (p<0.05) between genetics and feeding strategy for both length and weight. The least squares means ± the standard error of the means for weight of satiation/control, limit‐fed/control, satiation/selected and limit‐fed/selected fish were 371 ± 6, 350 ± 4, 544 ± 24, and 426 ± 16 grams and for length 299 ± 2, 291 ± 2, 347 ± 2 and 330 ± 2 mm, respectively. mRNA expression of 4 components of the ubiquitin/proteasome machinery were decreased (p<0.05) by an average of 17% in muscle of the growth‐selected fish consistent with a reduced capacity to degrade protein. No effect of feeding strategy was seen for mRNA expression nor was an interaction detected. No differences in IGF‐1 concentrations were detected due to feeding strategy or genetics. This suggests decreased degradation of protein through proteasomes and caspases could be the cause for increased weight and length of the growth‐selected trout. Support: Aquaculture Product and Marketing Development Project.