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Am J Physiol Regul Integr Comp Physiol. 2017 Mar 1;312(3):R426-R433. doi: 10.1152/ajpregu.00356.2016. Epub 2016 Dec 30.

Short-term intense exercise training reduces stress markers and alters the transcriptional response to exercise in skeletal muscle.

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Human Performance Laboratory, Ball State University, Muncie, Indiana.
Human Performance Laboratory, Ball State University, Muncie, Indiana


The purpose of this investigation was to examine the influence of short-term intense endurance training on cycling performance, along with the acute and chronic signaling responses of skeletal muscle stress and stability markers. Ten recreationally active subjects (25 ± 2 yr, 79 ± 3 kg, 47 ± 2 ml·kg-1·min-1) were studied before and after a 12-day cycling protocol to examine the effects of short-term intense (70-100% V̇o2max) exercise training on resting and exercise-induced regulation of molecular factors related to skeletal muscle cellular stress and protein stability. Skeletal muscle biopsies were taken at rest and 3 h following a 20-km cycle time trial on days 1 and 12 to measure mRNA expression and protein content. Training improved (P < 0.05) cycling performance by 5 ± 1%. Protein oxidation was unaltered on day 12, while resting SAPK/JNK phosphorylation was reduced (P < 0.05), suggesting a reduction in cellular stress. The maintenance in the myocellular environment may be due to synthesis of cytoprotective markers, along with enhanced degradation of damage proteins, as training tended (P < 0.10) to increase resting protein content of manganese superoxide dismutase and heat shock protein 70 (HSP70), while mRNA expression of MuRF-1 was elevated (P < 0.05). Following training (day 12), the acute exercise-induced transcriptional response of TNF-α, NF-κB, MuRF-1, and PGC1α was attenuated (P < 0.05) compared with day 1 Collectively, these data suggest that short-term intense training enhances protein stability, creating a cellular environment capable of resistance to exercise-induced stress, which may be favorable for adaptation.


MuRF-1; SAPK/JNK; myostatin; proliferator-activated receptor gamma coactivator 1-α; protein oxidation

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