Joshua S. Godwin

This study develops a ribosome enrichment protocol for human muscle tissue and examines ribosomal protein composition differences between higher and lower responders to resistance training.

This study compares mitochondrial mRNA and protein responses to high-load and high-volume resistance training in trained men, finding no differences between the two training paradigms.

This study examines how leg immobilization and recovery resistance training affect skeletal muscle angiogenesis markers in young adults, finding similar molecular responses regardless of prior training experience.

The paper investigates how resistance exercise and mechanical overload upregulate vimentin in skeletal muscle, linking it to hypertrophy and regeneration.

This study examines how resistance training status affects muscle size and molecular markers during leg immobilization and recovery training in young adults.

The paper compares RNA quantification methods for ribosome content in skeletal muscle and evaluates a novel RiboAb antibody cocktail as a surrogate for rRNA levels.

This study examines how resistance exercise and disuse atrophy affect myosin heavy chain (MyHC) protein fragmentation in humans, finding increased fragmentation post-exercise and during atrophy, with adaptive responses after training.

This study examines how resistance training affects denervated myofibers, senescent cells, and related proteins in middle-aged adults, finding increased muscle-nerve communication proteins but no significant changes in senescent cell content or SASP proteins.

This study investigates the relationship between relative rDNA copy number and resistance training-induced skeletal muscle hypertrophy, finding no significant association.

This study develops a novel imaging method (FIM-ID) to show that myofibrillogenesis, not myofibril hypertrophy, drives mechanically induced skeletal muscle growth.

This study examines how resistance training before endurance training affects mitochondrial adaptations, finding that prior resistance training impairs mitochondrial responses to subsequent endurance training.

This study compares DNA methylation and mRNA responses to lower- versus higher-load resistance exercise in trained men, finding similar gene expression and methylation patterns despite differences in exercise intensity.

Resistance training reduces methylation at 63% of mtDNA CpG sites in older males, mimicking a youthful methylome signature and enhancing mitochondrial function.