Can Bodybuilding Peak Week Manipulations Favorably Affect Muscle Size, Subcutaneous Thickness, and Related Body Composition Variables? A Case Study.

BACKGROUND: The purpose of this case study was to implement an evidence-based dietary approach to peaking for a bodybuilding competition and monitor its impact on body composition, muscle thickness (MT), intra-to-extra-cellular fluid shifts, subcutaneous thickness (ST), and hydration status. Secondarily, to document any adverse events of this peak week approach in a small, controlled setting. Methods Dietary practices were recorded, and laboratory testing was conducted throughout peak week, including competition morning. Assessments included: dual-energy X-ray absorptiometry (DEXA) for body composition, B-mode ultrasound for MT and ST, bioimpedance spectroscopy (BIS) for total body water (TBW)/intracellular water (ICW)/extracellular water (ECW), and raw BIS data (i.e., resistance, reactance, and phase angle), urine specific gravity (USG) for hydration status, and subjective fullness. Sequential dietary manipulations were made (i.e., CHO depletion/fat loading, CHO/water loading, and a refinement phase) with specific physiological goals. This was reflected in changes observed across all assessments throughout the peak week. RESULTS: From the carbohydrate-depleted state (three days out) to competition day, we observed increases in lean body mass, MT, TBW (primarily ICW), and subjective fullness. Kendall's Tau B revealed a strong relationship between carbohydrate intake and ∑MT (τ = 0.733, p = 0.056). Additionally, novel ST data demonstrated a 10% reduction for the summation of all seven sites, with some drastic changes in specific regions (e.g., -43% for triceps ST) from three days out to competition day. CONCLUSIONS: These data suggest that the prototypical goals of bodybuilders' peak week (i.e., increasing muscle fullness, decreasing subcutaneous thickness) to enhance their aesthetics/muscularity presented can be achieved with a drug-free protocol involving dietary manipulations.

Elongator regulates the melanocortin satiety pathway.

This study investigates the function of Elp1 and Elongator in the pituitary gland. Two conditional knockout models were generated where Elp1 was selectively deleted in either somatotropes of the anterior pituitary or Pomc-expressing cells of the anterior and intermediate pituitary. Although loss of Elp1 in somatotropes did not significantly impact murine growth or development, its loss in Pomc-expressing cells resulted in dramatically reduced levels of α-MSH, hyperphagia and obesity. This report provides the first evidence that Elongator plays an essential role in regulating the melanocortin satiety pathway.

Loaded Inter-set Stretching for Muscular Adaptations in Trained Males: Is the Hype Real?

The study examined the effects of adding a loaded stretch in the inter-set rest period (ISS) compared to traditional resistance training (TR) on muscular adaptations in resistance-trained males. Twenty-six subjects were randomly assigned into two groups (ISS: n=12; TR: n=14) and underwent an 8-week training regimen. Subjects in ISS underwent an additional loaded stretch for 30 s at 15% of their working load from the prior set during the inter-set rest periods. Muscle thickness of the pectoralis major at the belly (BMT) and lateral (LMT) portions, One-repetition maximum (1RM) and repetitions-to-failure (RTF) on the bench press exercise were measured at baseline and post 8 weeks of training. Additionally, volume load and perceptual parameters for exertion and recovery were measured. Both groups had similar total volume load and average perceptual parameters (p>0.05). There was a main time effect (p<0.01) for all but one dependent variable indicating that both groups responded similarly across time [(∆BMT: ISS=2.7±1.7 mm; TR = 3.0±2.2 mm), (∆LMT: ISS=3.2±1.6 mm; TR=2.8±1.7 mm, (∆1RM: ISS=6.6±3.8 kg; TR=7.5±5.7 kg). Repetitions-to-failure did not change in either group (∆RTF: ISS=0.0±2.1 repetitions; TR=0.0±2.3 repetitions, p>0.05). Our results suggest that addition of a loaded ISS does not affect muscular adaptations either positively or negatively in resistance-trained males.

Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway.

Elongator dysfunction is increasingly recognized as a contributor to multiple neurodevelopmental and neurodegenerative disorders including familial dysautonomia, intellectual disability, amyotrophic lateral sclerosis, and autism spectrum disorder. Although numerous cellular processes are perturbed in the context of Elongator loss, converging evidence from multiple studies has resolved Elongator's primary function in the cell to the modification of tRNA wobble uridines and the translational regulation of codon-biased genes. Here we characterize H2a.z, encoding the variant H2a histone H2A.Z, as an indirect Elongator target. We further show that canonical Notch signaling, a pathway directed by H2A.Z, is perturbed as a consequence of Elp1 loss. Finally, we demonstrate that hyperacetylation of H2A.Z and other histones via exposure to the histone deacetylase inhibitor Trichostatin A during neurogenesis corrects the expression of Notch3 and rescues the development of sensory neurons in embryos lacking the Elp1 Elongator subunit.

Elongator and codon bias regulate protein levels in mammalian peripheral neurons.

Familial dysautonomia (FD) results from mutation in IKBKAP/ELP1, a gene encoding the scaffolding protein for the Elongator complex. This highly conserved complex is required for the translation of codon-biased genes in lower organisms. Here we investigate whether Elongator serves a similar function in mammalian peripheral neurons, the population devastated in FD. Using codon-biased eGFP sensors, and multiplexing of codon usage with transcriptome and proteome analyses of over 6,000 genes, we identify two categories of genes, as well as specific gene identities that depend on Elongator for normal expression. Moreover, we show that multiple genes in the DNA damage repair pathway are codon-biased, and that with Elongator loss, their misregulation is correlated with elevated levels of DNA damage. These findings link Elongator's function in the translation of codon-biased genes with both the developmental and neurodegenerative phenotypes of FD, and also clarify the increased risk of cancer associated with the disease.

Fast track minimally invasive transmyocardial revascularization.

OBJECTIVE: : We evaluated the initial results of a fast-track discharge protocol for patients undergoing minimally invasive transmyocardial revascularization (MiTMR). METHODS: : Fifteen male patients, aged 64.5 ± 9.2 years, with an ejection fraction of 46.8% ± 9.9%, underwent MiTMR through a mini-left anterior thoracotomy aided by robotic-controlled thoracoscopic assistance. A postoperative management protocol included immediate extubation, early chest tube and pulmonary artery catheter removal, and mobilization within 12 hours. RESULTS: : There were no operative arrhythmias or in-hospital mortalities. Three of 15 patients developed left lower lobe atelectasis, delaying discharge between 2 and 5 days. Overall hospital length of stay was 1.4 ± 1.2 days, although 12 of 15 patients (80%) were discharged to home in 23 hours. Mild-moderate cardiomyopathy (ejection fraction 30%-50%) was not associated with prolonged length of stay. Mean hospital profit margin was $1882.50. One 30-day readmission occurred on day 23 for rapid atrial fibrillation, and one death occurred on day 11. CONCLUSIONS: : Despite these high-risk patients having end-staged, ischemic coronary artery disease, most MiTMR patients can be discharged to home in less than 24 hours. Perioperative morbidity and mortality rates are relatively low, and hospital profit margins are modest.