High-intensity high-volume swimming induces more robust signaling through PGC-1α and AMPK activation than sprint interval swimming in m. triceps brachii

PLoS One . 2017 Oct 3;12(10):e0185494. doi: 10.1371/journal.pone.0185494. eCollection 2017.

Fecha de la publicación: 03/10/2017

Autor: Rafael A Casuso (1, 2), Julio Plaza-Díaz (2, 3), Francisco J Ruiz-Ojeda (2, 3), Jerónimo Aragón-Vela (1, 2), Cándido Robles-Sanchez (2, 3), Nikolai B Nordsborg (4), Marina Hebberecht (5), Luis M Salmeron (5), Jesus R Huertas (1, 2)



1Department of Physiology, School of Pharmacy, University of Granada, Granada, Spain.

2Institute of Nutrition and Food Technology «José Mataix,» Biomedical Research Center, University of Granada, Granada, Spain.

3Department of Biochemistry and Molecular Biology II, School of Pharmacy, University of Granada, Granada, Spain.

4Department of Nutrition, Exercise and Sports, Section of Human Physiology, University of Copenhagen, Copenhagen, Denmark.

5San Cecilio University Hospital, Granada, Spain.


We aimed to test whether high-intensity high-volume training (HIHVT) swimming would induce more robust signaling than sprint interval training (SIT) swimming within the m. triceps brachii due to lower metabolic and oxidation. Nine well-trained swimmers performed the two training procedures on separate randomized days. Muscle biopsies from m. triceps brachii and blood samples were collected at three different time points: a) before the intervention (pre), b) immediately after the swimming procedures (post) and c) after 3 h of rest (3 h). Hydroperoxides, creatine kinase (CK), and lactate dehydrogenase (LDH) were quantified from blood samples, and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) and the AMPKpTHR172/AMPK ratio were quantified by Western blot analysis. PGC-1α, sirtuin 3 (SIRT3), superoxide-dismutase 2 (SOD2), and vascular endothelial growth factor (VEGF) mRNA levels were also quantified. SIT induced a higher release of LDH (p < 0.01 at all time points) and CK (p < 0.01 at post) than HIHVT, but neither SIT nor HIHVT altered systemic hydroperoxides. Additionally, neither SIRT3 nor SOD2 mRNA levels increased, while PGC-1α transcription increased at 3 h after SIT (p < 0.01) and after HIHVT (p < 0.001). However, PGC-1α protein was higher after HIHVT than after SIT (p < 0.05). Moreover, the AMPKpTHR172/AMPK ratio increased at post after SIT (p < 0.05), whereas this effect was delayed after HIHVT as it increased after 3 h (p < 0.05). In addition, VEGF transcription was higher in response to HIHVT (p < 0.05). In conclusion, SIT induces higher muscular stress than HIHVT without increasing systemic oxidation. In addition, HIHVT may induce more robust oxidative adaptations through PGC-1α and AMPK.