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

Abstract

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% V̇o_2max) 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 <i>days 1</i> and <i>12</i> to measure mRNA expression and protein content. Training improved (<i>P</i> < 0.05) cycling performance by 5 ± 1%. Protein oxidation was unaltered on <i>day 12</i>, while resting SAPK/JNK phosphorylation was reduced (<i>P</i> < 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 (<i>P</i> < 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 (<i>P</i> < 0.05). Following training (<i>day 12</i>), the acute exercise-induced transcriptional response of TNF-α, NF-κB, MuRF-1, and PGC1α was attenuated (<i>P</i> < 0.05) compared with <i>day 1</i> 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.