Abstract
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.
Highlights
It is well-established that sprint interval training (SIT), conducted as cycling or running, induces mitochondrial biogenesis in human m. vastus lateralis [1,2]
No differences were found for heart rate (HR) between SIT and high-volume training (HIHVT) (Fig 1B), but rating of the perceived exertion (RPE) was higher (p < 0.05) in response to SIT throughout the protocol (Fig 1C)
We used a randomized crossover design to study molecular signaling in m. triceps brachii
Summary
It is well-established that sprint interval training (SIT), conducted as cycling or running, induces mitochondrial biogenesis in human m. vastus lateralis [1,2]. Recent findings suggest that two weeks of SIT arm cycling apparently fails to do so in the m. Triceps brachii of untrained subjects despite marked elevations of arm-cranking VO2peak and work capacity [3]. Triceps brachii maladaptability exists as a result of excessive generation of mitochondrial reactive oxygen species (ROS) specific to the muscle group as indicated by the marked increase of catalase, which elevates the capacity for H2O2 decomposition as well as a reduction of the redox sensitive tricarboxylic acid cycle enzyme aconitase, resulting in inhibited maximal mitochondrial respiration [3]. Deltoideus mitochondrial content can be increased in untrained women after 12 weeks of highintensity swimming [4], which is in apparent contrast to the m. Analysis of the response to both high-intensity high-volume training (HIHVT) swimming and SIT swimming exercise provides the possibility to evaluate the effect on markers of muscular stress, systemic increased oxidation, and the associated molecular signaling. Systemic oxidative stress can be monitored by determining plasma hydroperoxides (HPx) [6,7]
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