Abstract
Reduced activation of exercise responsive signalling pathways have been reported in response to acute exercise after training; however little is known about the adaptive responses of the mitochondria. Accordingly, we investigated changes in mitochondrial gene expression and protein abundance in response to the same acute exercise before and after 10-d of intensive cycle training. Nine untrained, healthy participants (mean±SD; VO2peak 44.1±17.6 ml/kg/min) performed a 60 min bout of cycling exercise at 164±18 W (72% of pre-training VO2peak). Muscle biopsies were obtained from the vastus lateralis muscle at rest, immediately and 3 h after exercise. The participants then underwent 10-d of cycle training which included four high-intensity interval training sessions (6×5 min; 90–100% VO2peak) and six prolonged moderate-intensity sessions (45–90 min; 75% VO2peak). Participants repeated the pre-training exercise trial at the same absolute work load (64% of pre-training VO2peak). Muscle PGC1-α mRNA expression was attenuated as it increased by 11- and 4- fold (P<0.001) after exercise pre- and post-training, respectively. PGC1-α protein expression increased 1.5 fold (P<0.05) in response to exercise pre-training with no further increases after the post-training exercise bout. RIP140 protein abundance was responsive to acute exercise only (P<0.01). COXIV mRNA (1.6 fold; P<0.01) and COXIV protein expression (1.5 fold; P<0.05) were increased by training but COXIV protein expression was decreased (20%; P<0.01) by acute exercise pre- and post-training. These findings demonstrate that short-term intensified training promotes increased mitochondrial gene expression and protein abundance. Furthermore, acute indicators of exercise-induced mitochondrial adaptation appear to be blunted in response to exercise at the same absolute intensity following short-term training.
Highlights
Acute and chronic exercise models have been used to investigate mitochondrial adaptations in skeletal muscle
PGC-1a protein expression was increased after the first exercise bout pretraining and was sustained at this level for the post-training exercise bout and recovery
Our most surprising finding was acute reduction in the protein expression of COXI and COXIV by acute moderate intensity exercise both before and after exercise training. These data highlight the effects of high intensity short-term exercise training and acute exercise on selected genes and proteins involved in muscle mitochondrial biogenesis and function, suggesting the importance of relative exercise intensity for continued muscle mitochondrial adaptation
Summary
Acute and chronic exercise models have been used to investigate mitochondrial adaptations in skeletal muscle. The activation of AMP-activated protein kinase (AMPK), calcium/calmodulin-dependent protein kinase (CaMK) II and p38 mitogen-activated protein kinase (p38 MAPK) signalling cascades are well characterized upstream modulators of peroxisome proliferator activated receptor c co-activator -1a (PGC-1a) gene expression in skeletal muscle [15,16,17]. These cascades activate downstream regulatory factors [15,17], and in the case of AMPK [16] and p38 [18], directly phosphorylate PGC-1a, thereby increasing transcriptional activation of the PGC1a. We hypothesized that there will be an increase in mitochondrial protein abundance after training with no effects of acute exercise both before and after training
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