Authors & Dates Flashcards
Know the shit out of them
Gomez-Cabrera et al 2008
Moderate exercise produces antioxidants in the natural signalling pathway
Exercise produces ROS through the pathway that involves NFkB.
The paper shows an increase in GPx and MnSOD, as a consequence of this, antioxidants work to remove the SO or hydrogen peroxide produced.
McArdle et al 2000
Showed SO over a time course, and that exercise triggers it to be released. (in the case of this paper it what when the contraction was induced)
They then went on to look at SOD and showed that when SOD was introduced you could decrease the spike of SO that was produced. Immediately after contraction, SOD halved SO, proving that super oxide is produced during muscle contraction and can be quenched vie SOD (the antioxidant).
Zerba et al 1990
Showed that damage produced in flat running and downhill running. More radical species are produced when running downhill.
The same paper also showed that most damaged is completely SOD
Van der Mulen 1997
Looks at Vitamin E. at this time they thought it was a radical inhibitor
They compared plyometric contractions to isometric contractions and then supplemented with Vit E,
They found that Vit E helped protect against radical production (lowered this) but didn’t protect against the force deficit.
They also looked at CK and pyruvate damage, both involved in muscle damage. When taking vitamin E the activity of these 2 were reduced so vitamin E helped protect against muscle damage.
Ji 1993
Measured different levels of antioxidant molecules and compared the level of these in trained and untrained athletes. The only ones that were significantly elevated in athletes were the GPx ones, this indicates that when you train there is adaptation to muscle damage and it is required more to help prevent oxidative damage in athletes compared to untrained people.
Renaud 1992
The French Paradox
Hollenberg et al 1997
Cocoa and the Kuna Amerinds The people in Kuna had higher nitric oxide levels than people in Panama.
This was due to the high levels of cocoa flavanols that the ate, this meant significantly lower blood pressure and lower rates of heart disease
Taubert 2003
This was a 2 week intervention for people eating polyphenol rich chocolate compared to low polyphenol rich chocolate. The study showed the people in the high polyphenol groups diastolic and systolic blood pressures both decreased when they were consuming the chocolate however, when they stopped eating it, their blood pressure returned back to baseline
Heiss 2003 and Schtoeter 2006
Both investigated endothelial function with a diet high in cocoa flavanols. Both showed significant increases in flow mediated dilation once the flavanols get into the blood stream, and this peaks about 2 hours after consumption. Flavanols improve endothelial function.
Schtoeter even then isolated the epicatechin (the active ingredient in the flavanols) and gave just that - this also improved FMD to show that it was the active part of the flavanol .
Sansone et all 2015
Compared chronic effects of flavanols to acute.
After each intake of flavanols there was an increase in FMD (there began an acute effect), however as the effects became chronic, less of an increase in FMD was seen due to the baseline gradually increasing each time of measurement. You see an adaptation with less of a relative and absolute change as time goes on.
Letenneur et al 2007
Intake of cocoa flavanols reduces cognitive decline with age. compared high, to mid and low cocoa flavanol intake
Francis et al 2006
Showed an increase in mean cerebral blood flow across the grey matter 2 hours after consumption of high flavanol concentrated drink, compared to low.
However the effects weren’t seen for everyone, there were some individual declines, but an overall mean increase. Also showed increased cognitive function
Rendeiro et al 2013
Animal evidence. Showed flavanol intake lead to increased cognitive function an a better speed of learning and improved memory
Green et al 2004
Shows a time course of NO activity with training.
NO bioavailability changes can occur in the first 7 days of training and training exposes blood vessels to higher levels of stress which increases NO production through the activation of eNOS.
This initiates adaptation of an increase in vessel diameter. Stress levels then return to normal as blood flow is not putting stress on a larger vessel. NO bioavailability then returns to normal again.
Berry et al 2010
Investigated flavanol interaction with exercise.
High flavanols reduced BP responses to exercise but not at rest in obese subjects.
Davison et al 2008
High vs low flavanol and exercise vs no exercise.
the high flavanol groups resulted in better FMD but had no interactional effect with exercise.
The exercise groups had an increase in fat oxidation during exercise compared to sedentary groups but this had no interaction with exercise
Decroix 2016
2016 - showed no interaction between exercise and acute flavanol intake on cerebral oxygenation in healthy subjects.
Both factors improve cerebral blood flow but used together there is no added effect.
Decroix 2017
Flavanols and performance
added cocoa flavanols had little effect on performance in trained cyclists.
No changes in the mediators of the NO pathway so not better vascular function. not power output changes and minimal improvements in TAC in the plasma
Taub 2016
Flavanol intake on performance in sedentary subjects.
Increase in VO2 & max watts output (exercise capacity) and muscle metabolism ( AMPK, PGC-1a)
Bailey 2009 /2010
2009 - influence of nitrate on moderate exercise - intake as beetroot or placebo. Nitrates reduced the steady state pulmonary VO2, so you’re more efficient with producing power output when intake of nitrates
2010 - Nitrates with the PCr and ATP turnover- drop in PCr is blunted compared to how it would usually drop during exercise without More efficient use of ATP at same time point
these effects are due to reduced calcium ATPase activity and reduced cross-bridge cycling
Richards et al 2018
Beetroot intervention with hand grip test. significant increases in forearm blood flow and vasodilation
Lansely et al 2011
beetroot given 2.5 hours before race in 4km and 16km cycle time tests in comp cyclists. It reduced O2 consumption during moderate intensity exercise. VO2 slowed during high intensity - reduced PCr utilization/accumulation of fatigue metabolites.
Higashida et al 2011
SOD as an antioxidant supplementation.
it showed a plasma lipid oxidation and the effect of it compared to control in sed and exercise groups.
plasma TBARS sig increases during exercise compared to sed. however when given SOD, the TBARS level is reduced. effect of lipid oxidation is reduced
PGC-1a is significantly higher with or without SOD, so more mitochondria are being formed during exercise and the antioxidant doesn’t prevent this adaptation from occurring
Yfani et al 2010
muscle SOD1 study - shows the amount of skeletal muscle pre & post exercise that has the antioxidant in it. See and increase in amount of skeletal muscle in it that has SOD1 in it due to exercise. training adaptation.
Gomez-Cabrera et al 2005
Changes in SOD, iNOS and eNOS at rest, during exercise, and exercise but protected by allopurinol (antioxidant, SO inhibitor). the AO causes the increase that you see during exercise to not occur and match what happens during rest. When you inhibit the radical production then there is a decrease in things that follow.
Logan & Spriet 2015
12 week omega-3 supplementation
omega 3 vs olive oil - similar structure but olive oil doesn’t contain EPA or DHA.
Omega-3 increased metabolic rate. increased the amount of fat oxidation that occurred during exercise so more fat loss
more fat oxidation at rest and exercise. decreased resting HR and exercise HR. Decreased fasted blood triglycerides
Fisher et al 2011
Intense exercise - HIIT, measuring levels of TBARS.
TBARS after exercise increase and then begin to return to baseline 3 hours after. By day 3, TBARS don’t increase by as much, don’t get a significant response because people are beginning to adapt
Bloomer et al 2007
looked into
protein oxidation- significant increase after sprint and squat
8-DG (DNA damage) - more DNA damage and OS after squat and sprint
MDA (lipid oxidation) - Decreases after sprint and squat
Gomez-Cabrera et al 2003
CK and AAT with allopurinol.
Control shows spikes in CK and AAT after the time trials. however when supplemented with allopurinol, these spikes don’t occur in this period of intense exercise.
Radak et al 1995
Xanthine Oxidase and intense exercise
allopurinol inhibits XO.
XO becomes more active the more lactate that is produced. therefore higher intensity means more SO is produced.