Russell Hepple's lab examines the mechanisms causing muscle atrophy and dysfunction with aging, and is working to identify strategies for attenuating those declines to promote mobility and extend health-span. Russell is a professor in the College of Public Health and Health Professions department of physical therapy.
Areas of Expertise (6)
Media Appearances (1)
Will you keep winning races into old age? Your cells hold clues
In 2011, Fauja Singh became the oldest person to run a marathon when he completed all 42 kilometers of a Toronto race in just over eight hours. Singh—100 at the time (and still active today)—is exceptional, but he’s not alone. People train and compete in athletic events well into their 70s, 80s, and 90s.
Integrating Mechanisms of Exacerbated Atrophy and Other Adverse Skeletal Muscle Impact in COPD.Frontiers in Physiology
Tanja Taivassalo, et. al
The normal decline in skeletal muscle mass that occurs with aging is exacerbated in patients with chronic obstructive pulmonary disease (COPD) and contributes to poor health outcomes, including a greater risk of death. There has been controversy about the causes of this exacerbated muscle atrophy, with considerable debate about the degree to which it reflects the very sedentary nature of COPD patients vs. being precipitated by various aspects of the COPD pathophysiology and its most frequent proximate cause, long-term smoking.
Unbiased proteomics, histochemistry, and mitochondrial DNA copy number reveal better mitochondrial health in muscle of high-functioning octogenariansEpidemiology and Global Health
Ceereena Ubaida-Mohien, et. al
Master athletes (MAs) prove that preserving a high level of physical function up to very late in life is possible, but the mechanisms responsible for their high function remain unclear. We performed muscle biopsies in 15 octogenarian world-class track and field MAs and 14 non-athlete age/sex-matched controls (NA) to provide insights into mechanisms for preserving function in advanced age.
NMR Spectroscopy Identifies Chemicals in Cigarette Smoke Condensate That Impair Skeletal Muscle Mitochondrial Function.Toxics
Ram B. Khattri, et. al
Tobacco smoke-related diseases such as chronic obstructive pulmonary disease (COPD) are associated with high healthcare burden and mortality rates. Many COPD patients were reported to have muscle atrophy and weakness, with several studies suggesting intrinsic muscle mitochondrial impairment as a possible driver of this phenotype.
Chronic aryl hydrocarbon receptor activity phenocopies smoking‐induced skeletal muscle impairmentJournal of Cachexia, Sarcopenia and Muscle
Trace Thome, et. al
Chronic obstructive pulmonary disease (COPD) patients exhibit skeletal muscle atrophy, denervation and reduced mitochondrial oxidative capacity. Whilst chronic tobacco smoke exposure is implicated in COPD muscle impairment, the mechanisms involved are ambiguous. The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that activates detoxifying pathways with numerous exogenous ligands, including tobacco smoke.