Complex training where a high-load conditioning stimulus (CS) is performed prior to a biomechanically similar plyometric movement has been demonstrated to acutely enhance the performance of the plyometric movement in a phenomenon called post-activation performance enhancement (PAPE). Despite the positive influence PAPE can have on power production, the abundance of research has only investigated PAPE locally while comparing biomechanically similar movements. The purpose of this study was to determine if a heavy barbell bench press could elicit PAPE in a lower body plyometric movement. Eight (n = 8) resistance-trained males performed one set of countermovement jumps (CMJs) before (pre-CS) and three sets of CMJs after (post-CS) a heavy bench press set. Changes in muscle activation, jump height, work, power output, and rate of force development (RFD) during the early (E-RFD) and late (L-RFD) stages were compared between pre-CS and post-CS. The level of significance was set at p < .05. There were no significant differences in muscle activation, jump height, work, power output, or E-RFD (p > .05). There was a significant increase in L-RFD between pre-CS and the final set of jumps post-CS (p = .01). These results suggest that an upper body CS may not influence PAPE in the lower body. However, pairing a high-load upper body exercise with a lower body plyometric does not seem disadvantageous, and could be implemented as a strategy to maximize workout time efficiency with proper fatigue management incorporation.

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Nutrient consumption and mechanical overload influence skeletal muscle metabolism and function. These metabolic and functional outcomes are mediated at least in part by changes to the types of genes that are expressed in skeletal muscle. The extent to which nutrient consumption and mechanical overload act synergistically or independent of each other to change the skeletal muscle gene expression signature remains ill defined. Therefore, the purpose of this study was to define the differential and conserved gene expression responses to either nutrient consumption or mechanical overload as well as the combination of these stimuli. Published RNA‐Seq data sets generated from the muscle of humans subjected to acute resistance exercise were uploaded into the Database for Annotation Visualization and Integrated Discovery (DAVID) to define important functional gene categories related to muscle metabolism and/or function. Genes from the functional categories of ‘cell cycle’, ‘FoxO pathway’, and ‘transcription’ were marked for analysis in a mouse model of acute feeding and mechanical overload. For this model, C57BL/6 mice were initially fasted beginning at 1700 hr. The next morning (0800‐1000 hr), mice were randomized to remain fasted or allowed access to food for 30 min. Then, a mechanical overload was placed upon the left tibialis anterior (TA) muscle of all mice by subjecting the muscle to 10 sets of 6 eccentric muscle contractions by unilateral electrical stimulation of the sciatic nerve. The contralateral TA served as the non‐overloaded control muscle. All mice were deprived of food following the contractions protocol until euthanasia 4 hr later. The relative mRNA expression of Gadd45a, Usp2, Foxo1, Foxo3,and Myod1 were determined by RT‐PCR. Feeding and contractions each decreased the mRNA expression of Gadd45a(cell cycle), Foxo1, and Foxo3(FoxO pathway), with the combination of feeding and contractions acting to synergistically decrease the expression of each gene. Conversely, the mRNA expression of Usp2 (cell cycle) was decreased in response to muscle contractions, with no effect of feeding noted. Finally, the mRNA expression of Myod1 (transcription) was significantly increased in response to feeding, with contractions causing a differential change in direction of Myod1 mRNA expression depending upon the fasting/feeding state. These data show that nutrient consumption and mechanical overload have shared and differential effects on the skeletal muscle gene expression signature. A more thorough understanding of the genetic changes regulated by each stimulus alone, as well as the combination of stimuli, will provide novel insight for how nutrients and mechanical overload alter metabolism and function in muscle.

Adaptations to the skeletal muscle following long term aerobic exercise training are mediated at least in part by transcriptional changes that occur in response to each bout of exercise. There is evidence that glucocorticoids induce transcriptional changes in the skeletal muscle in response to a bout of aerobic exercise, but the extent of these changes and whether time of day exercise affects the glucocorticoid transcriptional response is unknown. The purpose of this study was to define changes to the skeletal muscle glucocorticoid transcriptome in response to acute aerobic exercise at different times of day. A secondary purpose was to define the role of Regulated in Development and DNA Damage 1 (REDD1) in mediating these changes as REDD1 is not only a transcriptional target of the glucocorticoid receptor, but it can also modulate glucocorticoid receptor transcriptional activity. A list of glucocorticoid target genes whose expression is altered in the skeletal muscle at various times of day in response to acute exercise was generated by comparing published genomic data sets from rodents subjected to acute aerobic exercise in the light or dark cycles to published genomic data sets from C2C12 myotubes treated with Dexamethasone. The role of glucocorticoid receptor signaling to the genomic changes was assessed in exercised mice treated with RU‐486. The role of REDD1 in mediating the changes to the glucocorticoid transcriptome was assessed in mice lacking REDD1. Glucocorticoids modulated expression of numerous genes in the skeletal muscle in response to acute aerobic exercise in the light and dark cycles, including those that are a target of, or contribute to, ubiquitin conjugation. The extent of changes to the glucocorticoid transcriptome was greater when exercise was conducted in the dark cycle compared to the light cycle. Only some genes encoding proteins involved in ubiquitin conjugation were induced by exercise at both times of day. REDD1 is required for the induction of these genes, whereas those only induced in the light cycle did not require REDD1. The time of day at which aerobic exercise is conducted dictates the extent of changes to the glucocorticoid transcriptome in skeletal muscle. REDD1 is a transducer mediating the time‐of‐day changes to the glucocorticoid transcriptome in skeletal muscle.

In males, the factors that decrease limb muscle mass and strength in response to androgen deprivation are largely unknown. Sirtuin1 (SIRT1) protein levels are lower in the limb muscle of male mice subjected to androgen deprivation. The present study aimed to assess whether SIRT1 induction preserved limb muscle mass and force production in response to androgen deprivation. Physically mature male mice containing an inducible muscle‐specific SIRT1 transgene were subjected to a sham or castration surgery and compared to sham and castrated male mice where the SIRT1 transgene was not induced. SIRT1 induction partially preserved whole‐body lean mass, tibialis anterior (TA) mass and triceps surae muscle mass in response to castration. Further analysis of the TA muscle showed that muscle‐specific SIRT1 induction partially preserved limb muscle soluble protein content and fibre cross‐sectional area. Unilateral AAV9‐mediated SIRT1 induction in the TA muscle showed that SIRT1 partially preserved mass by acting directly in the muscle. Despite those positive outcomes to limb muscle morphology, muscle‐specific SIRT1 induction did not preserve the force generating capacity of the TA or triceps surae muscles. Interestingly, SIRT1 induction in females did not alter limb muscle mass or limb muscle strength even though females have naturally low androgen levels. SIRT1 also did not alter the androgen‐mediated increase in limb muscle mass or strength in females. In all, these data suggest that decreases in SIRT1 protein in the limb muscle of males may partially contribute to the loss of limb muscle mass in response to androgen deprivation. imageKey points SIRT1 induction in skeletal muscle of male mice subjected to androgen deprivation partially preserved limb muscle mass and fibre cross‐sectional area. SIRT1 induction in skeletal muscle of male mice subjected to androgen deprivation did not prevent preserve limb muscle force generating capacity. SIRT1 induction in skeletal muscle of females did not alter baseline limb muscle mass, nor did it affect the androgen‐mediated increase in limb muscle mass.