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What did Yeo et al (2008) find when looking at twice every second day endurance regimes??

- muscle glycogen was significantly lower going into the second HIT session in the LOW group compared to the HIGH group.
- showed following training, the LOW group had significantly improved their ability to utilise FFA as a fuel during steady state exercise.
- also showed various metabolic enzymes increasing in LOW compared to HIGH, including CS, B-had p, CYTC


Discuss what Hulston et al (2010) found?

Looked at relative contributions, found following training, the low group had significantly improved their ability to utilise IMTG as a fuel during steady state ex. -i.e. Low enhances fat metabolism

Backed up by the LOW group having significant increases in metabolic enzyme activity (CD36% change and HAD%change) and mitochondrial ETC protein content compared to HIGH.


What did Philp et aL (2012) conclude from his review??

That exercise in a glycogen depleted state leads to a greater capacity to utilise FFA during exercise via a few potential mechanisms (such as AMPK, PGC-1a and PPARs)


Discuss the work of Bartlett et al (2013)??

Wanted to test Philps 2012 hypothesis.
Demonstrated a clear glycogen depletion being achieved in the low vs high exercise groups.
- showed an enhanced transcriptional response of genes involved in mitochondrial remodelling in the LOW vs HIGH (what?)
- also showed an enhanced activity of AMPK (assessed via ACC phosphorylation) in LOW vs HIGH.


What did both Yeo (2008) and Hulston (2010) find regarding HIGH intensity work??

The low glycogen groups produced a significantly lower % of PPO during each HIT training session

Concluding low should be used with caution.


What did Barish et al (2006) and Wu et al (2004) state about PPAR-o ??

Barish et al (2006) showed that PPAR-o remodels skeletal muscle to an oxidative phenotype in heart, muscle and adidas tissue.

Wu et al (2004) showed that PPAR-o over-expression in skeletal muscle leads to metabolic remodelling


Discuss the key study of Narber et al (2008) at length?

Review this study.

Demonstrated that AMPK and PPARo agonists are exercise mimetics.

In transgenic PPARd mice, more T1 fibre proportion, more mitochondrial content, also increased the time and distance of a treadmill run following 5 weeks of training .
Also showed that PPAR-o activation and exercise training increase similar patterns of gene expression in SM.

Observed that AMPK is activated by endurance training and PPAR-o overexpression (more phosphorylated AMPK and total AMPK in sed/TG on western blot than sed/wt mice.


What did Narber et al (2008) conclude?

Given that the pharmalogical activators reproduced many of the genetic characteristics of exercise, a GW/AICAR pill may be a viable treatment for human chronic disease.


What did Goodyear (2009) state about Narbers work?

Rebutted the idea of an exercise pill by stating its lack of effects in comparison with just regular exercise, and also stating an unknown on health benefits in multiple organs.


What did Canto et al (2012) suggest about nicotinamide riboside??

Showed that NR increases NAD+ content in numerous organs following supplementation in mice.
This enhances oxidative metabolism and protects against high fat diet induced obesity.
NR also increases oxidative capacity and mitochondrial biogenesis in brown adipose tissue.
NR induces mitochondrial biogenesis in SM. (Mice had more CS mRNA and mtDNA copy number).


What did Khan et al (2014) state about NR??

NR induces skeletal mitochondrial mass and prevents the development of mitochondrial ultrastructural abnormalities in mitochondrial myopathy


Discuss the work of Nogueira et al (2011) on epicatechins??

Stated epicatechins enhance fatigue resistance and oxidative capacity in mouse muscle (substance found in cocoa beans and dark chocolate)
Found that epi increases the isolated time to fatigue (i.e. Increased oxidative capacity) compared to water
Further showed for the quads, epi increases mitochondrial protein complexes (Cox 1-4)
Demonstrated an increase in Mito volume density and cristae membrane surface area with epi use


Discuss the Hutteman et al (2012) work on epicatechins?

Epicatechins maintain endurance training adaptation in mice after a 14 day retraining period.

Also found a higher capillary to fibre ratio in the detrained epi group compared to the detrained water group.
The epi treatment during detraining maintained exercise improvements in mitochondrial ETC proteins


What did Taub et al (2012) find??

Found that epicatechin supplementation increases SIRT1 protein content in human skeletal muscle (in 5 patients).

Also, the epicatechin supplementation successfully increased PGC-1a content and deacetlylation in human skeletal muscle, alongside also increasing mito ETC content (COmplex 1 oxphos + complex V oxphos).
Finally they showed the epi supplementation to remodel mitochondrial structure (i.e. Cristae/outer membrane ratio, mito volume density) both increased.