title: Similar skeletal muscle angiogenic and mitochondrial signalling following 8 weeks of endurance exercise in mice: discontinuous versus continuous training.
abstract: Little is known about skeletal muscle adaptation to discontinuous endurance training. It has been suggested that accumulating 30 min of endurance exercise daily may result in similar adaptations in the working muscle to a 30 min exercise bout. The purposes of the present investigation, therefore, were to conduct an 8 week continuous or discontinuous endurance training regimen and determine the following: (i) whether treadmill exercise capacity differs between the two training regimens; and (ii) whether the angiogenic and mitochondrial signalling pathways are differentially activated in the two training regimens. Twenty-four young adult male FVB/NJ mice were randomized into the following three groups: control; continuous treadmill endurance training for 30 min five times a week; or discontinuous treadmill endurance training for a total of 30 min five times per week for three 10 min intervals with 2 h rest between intervals. After the intervention, endurance capacity increased by 60% (P < 0.001) in both exercise groups compared to control animals. For the quadriceps muscle, anti-angiogenic regulators (thrombospondin-1 and ADAMTS1) were reduced by 50-70% (P < 0.001) with either exercise regimen. In addition, phosphorylation of p38 mitogen-activated protein kinase signalling increased by 50-300% (P < 0.001), which corresponded to an increase in peroxisome proliferator-activated receptor γ coactivator 1 β (PGC-1β) protein expression. These findings suggest that accumulating 30 min of endurance exercise in 10 min sessions results in similar endurance training adaptations in skeletal muscle to a 30 min exercise bout.
authors.affiliation: Wayne State University, Eugene Applebaum College of Pharmacy & Health Sciences, 259 Mack Avenue, Room 2248, Detroit, MI 48201, USA. en7488@wayne.edu
authors.forename: Moh H
authors.initials: MH
authors.lastname: Malek
authors.forename: Maik
authors.initials: M
authors.lastname: Hüttemann
authors.forename: Icksoo
authors.initials: I
authors.lastname: Lee
authors.forename: Jared W
authors.initials: JW
authors.lastname: Coburn
mesh_terms: D051722:ADAM Proteins / Q000096:biosynthesis; D000071097:ADAMTS1 Protein; D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D008297:Male; D051379:Mice; D018482:Muscle, Skeletal / Q000502:physiology*; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D010766:Phosphorylation; D010805:Physical Conditioning, Animal / Q000502:physiology*; D010807:Physical Endurance / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D019700:Thrombospondin 1 / Q000096:biosynthesis; D015534:Trans-Activators / Q000096:biosynthesis; D014157:Transcription Factors; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; C485290:Ppargc1a protein, mouse; D019700:Thrombospondin 1; D015534:Trans-Activators; D014157:Transcription Factors; D048051:p38 Mitogen-Activated Protein Kinases; D051722:ADAM Proteins; D000071097:ADAMTS1 Protein; C486323:Adamts1 protein, mouse