Mendham 2015 Abstract MiPschool Cape Town 2015
|Cycling and small-sided games similarly stimulates mitochondrial gene expression and signalling in middle-aged sedentary men.|
Event: MiPschool Cape Town 2015
An acute bout of exercise activates downstream signaling cascades that ultimately result in mitochondrial biogenesis . Elucidating the molecular signaling cascades that stimulate exercise-induced mitochondrial biogenesis carries significance for the prevention of physical-inactivity related diseases . Traditionally, research investigating exercise-induced mitochondrial biogenesis has employed continuous aerobic exercise as the experimental model . An alternative to these more traditional training modes is intermittent running in the form of football-based small-sided games (SSG), which has been reported to improve metabolic health in clinical populations . Accordingly, this study aimed to assess changes in molecular signaling cascades that stimulate mitochondria biogenesis in response to an acute bout of SSG and continuous cycling (CYC) in sedentary, middle-aged men.
Nine middle-aged, sedentary but disease-free men completed two respective 40 min exercise bouts (CYC and SSG) in a randomized, cross-over order. Heart rate (HR) and Rating of Perceived Exertion (RPE) were collected during each bout. Venous blood was collected at fasting, immediately, 30, 60 and 240 min post-exercise for measurement of glucose, insulin, cortisol and lactate. Muscle samples were collected at rest, 30 and 240 min post-exercise for the analysis of total PGC-1α, SIRT1, p38MAPK, CAMKIIα and p53, and phosphorylated proteins, p53Ser15, p38Thr180, CAMKIIThr286, AMPKThr172 and p38MAPKThr180/Tyr182. mRNA expression included, PGC-1α, p53, NRF1, NRF2, Tfam and cytochrome c.
• O2k-Network Lab: AU Melbourne Stepto NK
Organism: Human Tissue;cell: Skeletal muscle
No significant differences existed between conditions for HR, RPE, lactate and cortisol (p>0.05). Both conditions significantly increased PGC-1α protein content, including, PGC-1α mRNA expression at 240 min (p<0.05), without differences between conditions (p>0.05). AMPK Thr172 increased at 30 min post in CYC (p<0.05), with no change in SSG and no difference between conditions (p>0.05). CYC significantly increased p53 total protein content at 240 min than SSG (p<0.05). NRF2 mRNA expression significantly decreased in both conditions (p<0.05), despite no changes in NRF-1 or cytochrome c (p>0.05). Finally, only SSG significantly decreased Tfam mRNA at 30 min (p<0.05). No significant exercise-induced changes were evident for SIRT1, p38MAPK and CAMKII (p>0.05).
PGC-1α regulates mitochondrial biogenesis via a regulating transcription of nuclear-encoded mitochondrial gene . Accordingly, the similar PGC-1α response between conditions suggests that both conditions are of similar benefit for stimulating mitochondrial biogenesis. Phosphorylation of p53ser15 is enhanced in association with upstream signalling through AMPK, which collectively converge on the regulation of PGC-1α . Thus, the increase of p53 and AMPK within CYC may potentially relate to the differences between conditions in energy contributions and contraction type stimulating these signalling cascades at different time-points.
1-Div Exercise Sc and Sports Med, Dept Human Biol Univ Cape Town, South Africa. - email@example.com
2-Univ Bathurst, Australia
3-Univ Technology, Sydney, Australia
4-Victoria Univ, Melbourne, Australia
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