Short-Term Intensified Cycle Training Alters Acute and Chronic Responses of PGC1α and Cytochrome C Oxidase IV to Exercise in Human Skeletal Muscle

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.

High-Intensity Exercise Causes Greater Irisin Response Compared with Low-Intensity Exercise under Similar Energy Consumption

“…A previous study reported that PGC-1α mRNA, an upstream factor of irisin, was significantly elevated at 3 h after exercise (Egan et al 2010;Stepto et al 2012). Hence, we speculated that PGC-1α mRNA expression signal would stimulate irisin production through FNDC 5 in skeletal myocytes 3 h after exercise.…”

Effect of N-acetylcysteine infusion on exercise-induced modulation of insulin sensitivity and signaling pathways in human skeletal muscle

“…Additionally, despite our focus on skeletal muscle, our whole body IS findings should be interpreted with caution since the liver also plays an important role in glucose metabolism, which can be affected by NAC (32,44). Finally, although our small sample size may potentially be a limitation, these sample sizes have been used previously in similarly invasive studies, which include several muscle biopsies and hyperinsulinemic euglycemic clamps, across two sessions for each participant (15,45). In conclusion, this study revealed novel human in vivo data that attenuation of ROS with antioxidant infusion impaired IS 3 h after exercise, which did not occurr not via the Aktsignaling pathway in skeletal muscle.…”

Resistance Exercise Training Alters Mitochondrial Function in Human Skeletal Muscle

“…Similar to previous reports(1), we did not see a pronounced increase in the expression of mRNA”s involved in mitochondrial biogenesis (COX18, MFN1, NDRG2, PPARGC1A (PGC1α) and TFAM), assessed 3 days after the last day of RET. It should be noted that marked improvements in aerobic capacity can be see without chronic increases (31), or even a decrease (16) in markers of mitochondrial biogenesis. It appears that PGC1α, due to its short half-life, may be more reflective of a transcriptional regulation of the acute response, and thus the timing of biopsy (3 days post exercise in the case of the current study), may explain the absence of any transcriptional response.…”