Flashcards in Training Interference 2 Deck (7):
Discuss the work of Kawagushi and Finkel (2014)??
They stated that ROS⬆️ leads to ⬆️protein aggregation, ⬆️organelle damage and activation of host defences. Antioxidants are said to inhibit these pathways, also showed that environmental insults, ageing and genetic alterations leads to ⬆️ROS.
What did Reid et al (2011) propose??
Found cellular redox stars to be closely associated with fatigue.
See inverted U diagram, where fully oxidised lead to fatigue and poor isometric force, and fully reduced leads to antioxidant and poor isometric force.
Discuss the key literature from Gomez-Cabrera et al (2008)??? In rats
Found exercise activates antioxidant systems in skeletal muscle which is suppressed by vitamin C -> mnSOD and GPx expression is significantly higher in trained vs untrained, trained +vitC.
Also found that antioxidant supplementation blocks the ex induced increases in PGC-1a. Trained and Vit C lower than both other groups.
Also found that antioxidant supplementation blocks the ex induced increases in NRF-1 and mTFA. Trained sig higher than untrained and trained and Vit-C.
Antioxidant supplementation only slightly suppressed CytC post training and did affect whole body endurance adaptations to endurance exercise.
Discuss Ristow et al (2009)?? In humans
Found that antioxidants prevent induction of PGC-1a and SoD1 gene expression post training.
Proposed the concept of 'mitohormesis' which links physical exercise and subsequent of ROS to insulin sensitivity and antioxidant defence.
See slides for diagram linking physical exercise to a reduced disease risk.
Discuss the key points to be gained from the Ristow et al (2009) paper??
Exercise induced oxidative stress ameliorates insulin resistance and causes and adaptive response promoting endogenous antioxidant defence capacity - supplementation with antioxidants may preclude these health promoting effects of exercise in humans
Disuss yFanti et al (2010)?? On well trained humans
Looked at whether antioxidant supplementation alters endurance training adaptations.
Found that vitamin C and E supplementation had no effect on training induced increases in VO2 max and maximal power output.
Also showed that vitamin C and E had no effect on training induced increases in CS and HAD activity .
Thus contradicting data when studies in well trained individuals.