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Molecular, Genetic, and Biochemical Nutrition Commons

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Full-Text Articles in Molecular, Genetic, and Biochemical Nutrition

Resistance Training In Humans And Mechanical Overload In Rodents Do Not Elevate Muscle Protein Lactylation, Madison L. Mattingly, Auburn University A. Ruple, Casey L. Sexton, Joshua S. Godwin, Mason C. Mcintosh, Morgan A. Smith, Daniel L. Plotkin, J. Max Michel, Derick A. Anglin, Nicholas J. Kontos, Shengyi Fei, Stuart M. Phillips, C. Brooks Mobley, Ivan Jose Vechetti Jr, Christopher G. Vann, Michael D. Roberts Sep 2023

Resistance Training In Humans And Mechanical Overload In Rodents Do Not Elevate Muscle Protein Lactylation, Madison L. Mattingly, Auburn University A. Ruple, Casey L. Sexton, Joshua S. Godwin, Mason C. Mcintosh, Morgan A. Smith, Daniel L. Plotkin, J. Max Michel, Derick A. Anglin, Nicholas J. Kontos, Shengyi Fei, Stuart M. Phillips, C. Brooks Mobley, Ivan Jose Vechetti Jr, Christopher G. Vann, Michael D. Roberts

Department of Nutrition and Health Sciences: Faculty Publications

Although several reports have hypothesized that exercise may increase skeletal muscle protein lactylation, empirical evidence in humans is lacking. Thus, we adopted a multifaceted approach to examine if acute and subchronic resistance training (RT) altered skeletal muscle protein lactylation levels. In mice, we also sought to examine if surgical ablation-induced plantaris hypertrophy coincided with increases in muscle protein lactylation. To examine acute responses, participants’ blood lactate concentrations were assessed before, during, and after eight sets of an exhaustive lower body RT bout (n = 10 trained college-aged men). Vastus lateralis biopsies were also taken before, 3-h post, and 6-h post-exercise …


An Intron Variant Of The Gli Family Zinc Finger 3 (Gli3) Gene Differentiates Resistance Training-Induced Muscle Fiber Hypertrophy In Younger Men, Christopher G. Vann, Robert W. Morton, Christopher B. Mobley, Ivan J. Vechetti, Brian K. Ferguson, Cody T. Haun, Shelby C. Osburn, Casey L. Sexton, Carlton D. Fox, Matthew A. Romero, Paul A. Roberson, Sara Y. Oikawa, Chris Mcglory, Kaelin C. Young, John J. Mccarthy, Stuart M. Phillips, Michael D. Roberts May 2021

An Intron Variant Of The Gli Family Zinc Finger 3 (Gli3) Gene Differentiates Resistance Training-Induced Muscle Fiber Hypertrophy In Younger Men, Christopher G. Vann, Robert W. Morton, Christopher B. Mobley, Ivan J. Vechetti, Brian K. Ferguson, Cody T. Haun, Shelby C. Osburn, Casey L. Sexton, Carlton D. Fox, Matthew A. Romero, Paul A. Roberson, Sara Y. Oikawa, Chris Mcglory, Kaelin C. Young, John J. Mccarthy, Stuart M. Phillips, Michael D. Roberts

Department of Nutrition and Health Sciences: Faculty Publications

We examined the association between genotype and resistance training-induced changes (12 wk) in dual x-ray energy absorptiometry (DXA)-derived lean soft tissue mass (LSTM) as well as muscle fiber cross-sectional area (fCSA; vastus lateralis; n = 109; age = 22 ± 2 y, BMI = 24.7 ± 3.1 kg/m2). Over 315 000 genetic polymorphisms were interrogated from muscle using DNA microarrays. First, a targeted investigation was performed where single nucleotide polymorphisms (SNP) identified from a systematic literature review were related to changes in LSTM and fCSA. Next, genome-wide association (GWA) studies were performed to reveal associations between novel SNP targets with …


Programming Heart Disease: Does Poor Maternal Nutrition Alter Expression Of Cardiac Markers Of Proliferation, Hypertrophy, And Fibrosis In Offspring?, Cathy Chun May 2016

Programming Heart Disease: Does Poor Maternal Nutrition Alter Expression Of Cardiac Markers Of Proliferation, Hypertrophy, And Fibrosis In Offspring?, Cathy Chun

Honors Scholar Theses

Maternal malnutrition can affect fetal organogenesis, metabolic processes, and factors involved in developmental regulation. Of the many physiological effects poor maternal nutrition can induce in offspring, one of the most important organs affected is the heart. Cardiovascular disease has been associated with poor maternal diet. It also been suggested that hypertension can originate during impaired intrauterine growth and development. Hypertension can trigger hypertensive heart disease and is associated with numerous heart complications. We hypothesized that poor maternal nutrition would alter critical growth factors associated with normal heart development, specifically, insulin-like growth factor (IGF)-1, IGF-2, transforming growth factor (TGF)β, and connective …