It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
The molecular responses to acute resistance exercise are well characterized. However, how cellular signals change over time to modulate chronic adaptations to more prolonged exercise training is less well understood. We investigated anabolic signaling and muscle protein synthesis rates at several time points after acute and chronic eccentric loading. Adult rat tibialis anterior muscle was stimulated for six sets of ten repetitions, and the muscle was collected at 0 h, 6 h, 18 h and 48 h. In the last group of animals, 48 h after the first exercise bout a second bout was conducted, and the muscle was collected 6 h later (54 h total). In a second experiment, rats were exposed to four exercise sessions over the course of 2 weeks. Anabolic signaling increased robustly 6 h after the first bout returning to baseline between 18 and 48 h. Interestingly, 6 h after the second bout mTORC1 activity was significantly lower than following the first bout. In the chronically exercised rats, we found baseline anabolic signaling was decreased, whereas myofibrillar protein synthesis (MPS) was substantially increased, 48 h after the last bout of exercise. The increase in MPS occurred in the absence of changes to muscle fiber size or mass. In conclusion, we find that anabolic signaling is already diminished after the second bout of acute resistance type exercise. Further, chronic exposure to resistance type exercise training results in decreased basal anabolic signaling but increased overall MPS rates.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Universitätsmedizin Berlin, Charité, Berlin, Germany (GRID:grid.6363.0) (ISNI:0000 0001 2218 4662); University of California, Department of Physiology and Membrane Biology, Davis, USA (GRID:grid.27860.3b) (ISNI:0000 0004 1936 9684)
2 University of California, Department of Physiology and Membrane Biology, Davis, USA (GRID:grid.27860.3b) (ISNI:0000 0004 1936 9684); University Health Network, KITE Research Institute, Toronto, Canada (GRID:grid.231844.8) (ISNI:0000 0004 0474 0428); University of Toronto, Faculty of Kinesiology and Physical Education, Toronto, Canada (GRID:grid.17063.33) (ISNI:0000 0001 2157 2938)
3 Maastricht University Medical Centre+, Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht, The Netherlands (GRID:grid.412966.e) (ISNI:0000 0004 0480 1382)
4 Universitätsmedizin Berlin, Charité, Berlin, Germany (GRID:grid.6363.0) (ISNI:0000 0001 2218 4662)
5 University of California, Department of Physiology and Membrane Biology, Davis, USA (GRID:grid.27860.3b) (ISNI:0000 0004 1936 9684); University of California, Neurobiology, Physiology and Behavior, Davis, USA (GRID:grid.27860.3b) (ISNI:0000 0004 1936 9684); VA Northern California Health Care System, Mather, USA (GRID:grid.413933.f) (ISNI:0000 0004 0419 2847)