title: The order of exercise during concurrent training for rehabilitation does not alter acute genetic expression, mitochondrial enzyme activity or improvements in muscle function.
abstract: Concurrent exercise combines different modes of exercise (e.g., aerobic and resistance) into one training protocol, providing stimuli meant to increase muscle strength, aerobic capacity and mass. As disuse is associated with decrements in strength, aerobic capacity and muscle size concurrent training is an attractive modality for rehabilitation. However, interference between the signaling pathways may result in preferential improvements for one of the exercise modes. We recruited 18 young adults (10 ♂, 8 ♀) to determine if order of exercise mode during concurrent training would differentially affect gene expression, protein content and measures of strength and aerobic capacity after 2 weeks of knee-brace induced disuse. Concurrent exercise sessions were performed 3x/week for 6 weeks at gradually increasing intensities either with endurance exercise preceding (END>RES) or following (RES>END) resistance exercise. Biopsies were collected from the vastus lateralis before, 3 h after the first exercise bout and 48 h after the end of training. Concurrent exercise altered the expression of genes involved in mitochondrial biogenesis (PGC-1α, PRC, PPARγ), hypertrophy (PGC-1α4, REDD2, Rheb) and atrophy (MuRF-1, Runx1), increased electron transport chain complex protein content, citrate synthase and mitochondrial cytochrome c oxidase enzyme activity, muscle mass, maximum isometric strength and VO 2peak. However, the order in which exercise was completed (END>RES or RES>END) only affected the protein content of mitochondrial complex II subunit. In conclusion, concurrent exercise training is an effective modality for the rehabilitation of the loss of skeletal muscle mass, maximum strength, and peak aerobic capacity resulting from disuse, regardless of the order in which the modes of exercise are performed.
authors.affiliation: Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada.
authors.forename: Lauren G
authors.initials: LG
authors.lastname: MacNeil
authors.affiliation: Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada.
authors.forename: Elisa
authors.initials: E
authors.lastname: Glover
authors.affiliation: Department of Health Sciences, McMaster University, Hamilton, Ontario, Canada.
authors.forename: T Graham
authors.initials: TG
authors.lastname: Bergstra
authors.affiliation: Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada.
authors.forename: Adeel
authors.initials: A
authors.lastname: Safdar
authors.affiliation: Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada; Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
authors.forename: Mark A
authors.initials: MA
authors.lastname: Tarnopolsky
mesh_terms: D000293:Adolescent; D000328:Adult; D015444:Exercise; D005260:Female; D015870:Gene Expression; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D008931:Mitochondria, Muscle / Q000201:enzymology / Q000378:metabolism*; D063269:Mitochondrial Turnover; D018482:Muscle, Skeletal / Q000033:anatomy & histology / Q000378:metabolism*; D009142:Musculoskeletal Physiological Phenomena; D009929:Organ Size; D015398:Signal Transduction; D013997:Time Factors; D055815:Young Adult