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Ex & Diet > Authors & Dates > Flashcards

Authors & Dates Flashcards

Know the shit out of them

1
Q

Gomez-Cabrera et al 2008

A

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.

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2
Q

McArdle et al 2000

A

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).

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3
Q

Zerba et al 1990

A

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

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4
Q

Van der Mulen 1997

A

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.

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5
Q

Ji 1993

A

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.

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6
Q

Renaud 1992

A

The French Paradox

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7
Q

Hollenberg et al 1997

A

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

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8
Q

Taubert 2003

A

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

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9
Q

Heiss 2003 and Schtoeter 2006

A

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 .

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10
Q

Sansone et all 2015

A

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.

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11
Q

Letenneur et al 2007

A

Intake of cocoa flavanols reduces cognitive decline with age. compared high, to mid and low cocoa flavanol intake

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12
Q

Francis et al 2006

A

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

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13
Q

Rendeiro et al 2013

A

Animal evidence. Showed flavanol intake lead to increased cognitive function an a better speed of learning and improved memory

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14
Q

Green et al 2004

A

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.

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15
Q

Berry et al 2010

A

Investigated flavanol interaction with exercise.

High flavanols reduced BP responses to exercise but not at rest in obese subjects.

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16
Q

Davison et al 2008

A

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

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17
Q

Decroix 2016

A

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.

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18
Q

Decroix 2017

A

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

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19
Q

Taub 2016

A

Flavanol intake on performance in sedentary subjects.

Increase in VO2 & max watts output (exercise capacity) and muscle metabolism ( AMPK, PGC-1a)

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20
Q

Bailey 2009 /2010

A

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

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21
Q

Richards et al 2018

A

Beetroot intervention with hand grip test. significant increases in forearm blood flow and vasodilation

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22
Q

Lansely et al 2011

A

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.

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23
Q

Higashida et al 2011

A

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

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24
Q

Yfani et al 2010

A

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.

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25
Q

Gomez-Cabrera et al 2005

A

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.

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26
Q

Logan & Spriet 2015

A

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

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27
Q

Fisher et al 2011

A

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

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28
Q

Bloomer et al 2007

A

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

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29
Q

Gomez-Cabrera et al 2003

A

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.

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30
Q

Radak et al 1995

A

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.

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31
Q

Bogdanis et al 2013

A

HIIT sessions as training and took blood samples around a spring test.
Significant main effect in training for lipid oxidation over time. - TBARS
PC increases post exercise to a peak at 24h after exercise and blood sample values around the sprint tests decrease post-training
Post-training programme saw an increase in GPx, CAT and TAC (increased activity of AOs)

32
Q

Ogonovsky et al 2005

A

OS markers, DNA repair, memory via levels of reactive carbonyl derivatives (RCD) - in rats
Compared these in groups that trained moderately, strenuous, and over-trained.
Most RCD in control group. there is a decrease in oxidation levels in all training groups but the most in the strenuous training group

33
Q

Neubauer et al 2008

A

Ironman triathlon
No indication of persistent oxidative stress.
Most OS markers values in plasma were significantly elevated 1d post race compared to prerace. Most had returned to normal values or below baseline by 5d post race.
Levels of antioxidant enzymes also increased post race.
TEAC (measure of soluble antioxidants) increases significantly post race and doesn’t return to baseline until 5d post. this sig increases because AOs are released into the fluid tp prepare the body for the next bout of OS

34
Q

Babior et al 2000

A

oxidation of LDL and its role in inflammation and causing macrophages to turn into foam cells

35
Q

Reichhold et al 2009

A

DNA damage in response to an ironman
Graph is tail DNA so shows that the more oxidised DNA the more it’ll run down the gel during electrophoresis so a longer tail.
Most oxidation was occurring 1day post race

36
Q

Machefer et al 2004

A

Marathon des sables
GSH and GPx - more post competition but decreased levels of SOD
Significant increase in lipid peroxidation 72 hrs post race (may be linked to the low levels of SOD)

37
Q

Turner et al 2011

A

great union canal race
prolonged depletion of AO capacity after ultra endurance exercise
Plasma protein peroxidation showed sig increase post race, and then this continued to decrease up to 7 days later. back to normal after 28 days
plasma lipid peroxidation, there was an overcompensation for the amount of lipid in the blood, they had less baseline peroxidation when before the race by 28days post race

38
Q

Beckman and Ames 1998

A

review of the FRTA
It argues that generation of oxidants, antioxidant defense and repair of oxidative damage all interact to affect ageing.
If you have a poor repair system then you’re going to age quicker

39
Q

Roberts et al 2001

A

Increased markers of OS with age - through radical interaction with lipids in old and young rats. however there is also a v wide spread of oxidative status at old age - some people age better than others

40
Q

Muller et al 2006

A

Knockout of CuZnSOD in mice. compared the mice that had SOD to the ones that didn’t.
Significantly more isoprostanes in the plasma and also elevated levels of lipid peroxidation in the tissue with the absence of CuZnSOD

41
Q

Donato et al 2007

A

Human study. Old vs young levels of NADPH and 3-NT significantly elevated levels of both in the old subjects compared to the young
therefore increased baseline levels of oxidation in old vessels

42
Q

Meocci et al 2000

A

Natural levels of antioxidants decrease as you get older. If you then look at vitamin E and vitamin A the centenarians then have higher levels of these vitamins compared to the young

43
Q

Okiwana centenarians

A

Okiwana has 4-5 times as many centenarians in its population than any other industrialised country.
they consume 17% less calories
Lower on protein
rich in veg, fruits, sweet potatoes soy and fish

44
Q

Leoni et al 2009

A

Calorie restriction on biomarkers of longevity. in overweight people - 6 month
- Most weight lost in very low calorie diet
- All groups on calorie restriction has decreased in circulating insulin
Calorie restriction and exercise lose weight at the same rate because they’re essentially having the same effect

45
Q

Ravussin et al 2015

A

Calorie restriction in humans - all health marks for predictors of disease decrease in the 2 year caloric restriction groups. including total cholesterol

46
Q

Holloszy et al 1997

A

Rat study - A=runners, B=sedentary, C=calorie restricted runners, D=calorie restricted sedentary
calorie restricted rats ran further than the rats who just ran with normal amount of food
most survival rate in rats that were calorie restricted groups

47
Q

Harman et al 2006

A

Mitochondrial importance in the FRTA

  • ROS production by the ETC contributes to DNA damage
  • Malfunctioning mitochondrial genome is directly correlated with impairs mitochondrial physiology and lowered ATP synthesis
48
Q

Sanz 2004/2005/2006

A

2004 - Protein restriction - in rats. sig less hydrogen peroxide (so less oxidation). less mitochondrial and DNA oxidative damage.
2005 - calorie restriction - old ctrl, old cal restricted, young ctrl… significant reduction in free radical leak in the OR group.
OC = sig increase in oxidative damage, not seen in the cal restricted group. the OR also have less DNA damage
2006 - Lipid restriction, then carbohydrate restriction s well… both found no change in hydrogen peroxide production, radical leak did not change and DNA damage did not change either. lipid restriction -

49
Q

Meijer et al 2001

A

2 Antipyrine markers measured for OS split into exercise and control. Old age people
no real significant results found. no significant trends ad large data spreads. No other studies to compare to so cant compare for validation

50
Q

Jessup et al 1990

A

Sed and exercise with or without vit E in old aged people
Vitamin E concs increase after the programme in both control and exercise group.
Lipid peroxidation fell, most in exercise with vitamin E

51
Q

Fatouros et al 2004

A

32 weeks of endurance training for old aged people
MDA - increase after exercise but overall concentrations at baseline
3-NT - change from rest to exercise isn’t as much post training
GPx - levels increase post exercise.
TAC - increase overall. shows adaptation with training.
When you stop training adaptation decreases and goes back to normal

52
Q

Johnson et al 2014

A

Endurance training - in older aged people.
Measured mitochondrial function. exercise causes better ability to clear out adducts with regards to SOD and catalase in old and young

53
Q

Murray et al 2016

A

Ketone diet enhances physical and cognitive performance
rat study - treadmill perf and cognitive ability
ketone = greatest distance on the treadmill. Quicker decision making. Greater number or correct decisions in cog task

54
Q

Greene et al 2018

A

in powerlifters and oly lifters - ketone diet reduced body mass without reducing performance
Lean mass and fat mass decrease. Power to weight ratio go up

55
Q

Pinckaers et al 2017

A

How ketones interact with performance. interaction with metabolic process?

56
Q

PREDIMED (Estruch et al 2013)

A

Mediterranean diet in attempts to be a primary prevention for cardiovascular disease
3 groups: control diet, med diet with olive oil, med diet with mixed nuts
measured the end point at rate of major CV events.
hazard ratio were 0.7 and 0.72 for olive oil and nuts compared to control.
Med diet with olive oil is the best for prolonging mortality rate.
Med diet associated with: moderate wine consumption, low meat and meat products consumption, high veg, fruit, legumes, fish, olive oil consumption

57
Q

FINGER study (Ngandu et al)

A

Control vs intervention group - intervention group had diet control and exercise as well as cognitive training and vascular risk monitoring
Intervention group came out with better neuropsychological test battery, better executive function, better processing speed and slightly better memory (change is not as much)

58
Q

Shakersain et al 2018

A

Nordic Prudent diet reduces risk of cognitive decline. When you then pair this with an active lifestyle this risk decreases further

59
Q

Ceriello et al 2004

A

the imbalance of oxidants in the ETC and the common soil hypothesis

You have more SO being produced. The proton balance change causes inhibition of complex 3 (uncoupling) which drive O2 to be produced as SO instead of the process carrying on producing atp.
this is due to excess FFA and glucose driving the TCA cycle to make lots of electrons going into the ETC

60
Q

Morihiro et al 2013

A

high glucose, insulin fatty acids and inflammatory cytokines. these al lead to increased ROS.
which then causes insulin resistance, increased inflammation of adipose tissues from increase IL-6 etc, and decreased adiponectin.
this all leads to the metabolic syndrome.
the paper shows that even though this cascade has occurred in the adipose tissue, it can become a whole body issue, with it triggering other pathways

61
Q

Paolisso et al 1993

A

Baseline levels of antioxidants of control vs T2D sufferers
Shows decreased levels of antioxidants in the diabetes people.
However snapshots of AOs are hard, what were they like before? are they low because of the disease or because they’re not needed in the disease or increased in the control because they’re doing lots
The paper then goes on to do an oral glucose tolerance test. The T2D people were either in the control group or supplemented with vitamin E. When given vit E, their plasma glucose doesn’t increase as much as the control. therefor there is a quicker glucose uptake.

62
Q

Garcia-Bailo et al 2011

A

seeing if you can reduce insulin resistance by protecting against oxidative stress.
In the normal oxidant pathway for T2D NFkB and Ap-1 are triggered which drive cytokines in the body, which can inhibit IRS-1 (an enzyme that drives insulin action). If you were able to reduce the action of NFkB and AP-1 then not as much IRS-1 would be inhibited.

63
Q

Miller et al 2010

A

Superoxide production reduced the NO availability. This means there is less vessel efficiency and dilation. Decreased NO availability is linked to CV disease, hypertension, strokes, AD etc

64
Q

Strobel et al 2010

A

Review papers on oxidative stress markers in CV disease

16 papers found OxLDL to be an independent predictor of CVD

65
Q

Wadey et al 2012

A

time scale of disease development against levels of oxidative stress markers

iNOS increases with age
SO increases at onset of disease due to a decrease in L-argenine and BH4 being capable of producing SO. @ disease the availability of NO + co-factor goes down. eNOS levels remain constant.
all the while Ox Stress is increasing

66
Q

Douglas et al 2011

A

Vessel composition old vs young.
In the old vessels there is elevated levels of eNOS, 3-NT, phosphorylated eNOS and also lower FMD change when there is high levels of 3-NT

67
Q

Nedeljkovic et al 2003

A

when the number of ROS outweighs NO-mediated actions, this leads to endothelial dysfunction causing other issues in the body such as inflammation and vasoconstriction

68
Q

Sindler et al 2009

A

decreases in factors such as BH4, L-argenine and inflammatory cytokines can lead to the uncoupling of eNOS, this can then cause a decrease in NO and elevated levels of SO. In the normal situation you should see SOD pathway occur to alter this however this doesn’t and this cause a build up of ONOO (peroxinitrite)

69
Q

Markesbery et al 1997

A

Hypothesis for OS in alzheimers disease

  1. increase in brain metal ions - thatll stimulate free radicals
  2. Increased lipid peroxidation
  3. Increased protein and DNA oxidation in AD brain
  4. Decreased cytochrome C oxidase in the AD brain
  5. SOD1 levels are different
  6. Amyloid beta capable of generating free radicals
70
Q

Hensley et al 1998

A

shows brain regions affected by AD and tyrosine oxidation products
Cerebellum isn’t much affected by AD
Hippocampus, inferior parietal lobe and superior temporal gyrus are affected
in hippocampus - more expressed proteins in AD. Pin 1 is present but not in an oxidised state in control patients but is oxidised in AD patients

71
Q

Aldred et al 2009

A

increased LDL oxidation, but not total plasma protein oxidation in AD patients

72
Q

Nunomura et al 2001

A

Oxidative stress is part of the initial kick which then causes other issues in AD development.
- looked into amyloid beta deposition in brain tissue - AD patient showing limited amyloid deposition shows prominent 8OHG (oxidation product) but AD patient with abundant amyloid beta deposition shows limited 8OHG

AD - can use FINGER STUDY as well

73
Q

Seven et al 2008

A

control vs rheumatoid arthritis group
TBARS - lipid oxidation = significantly higher in RA patients
T-SH = antioxidant capacity would decrease in a situation of oxidation so therefore decreases in RA patients

74
Q

Henrotin et al 2003

A

Shows that there is a continuous degrading cycle of OS in RA patients.
oxidative stress occurs in the cartilage causes oxidative molecules to lead to inflammation in the synovial membrane, which round circles back to releasing radicals into the synovial fluid, thus causing oxidative stress of the cartilage

The paper showed increased incidence of CVD in RA patients due to the link between oxidative stress and the inflammation. Increased mortality in people with RA and the mortality is due to CVD

75
Q

St Clair et al 1996

A

RA patients have shown elevated levels of NO production indicated by iNOS expression.

76
Q

Popa et al 2005

A

Anti TNF-a therapy for RA patients
HDL cholesterol levels increased with anti TNF-a
No change in LDL but when considering ratios, the HDL:LDL increased
Inflammatory markers of CRP and IL-6 significantly decreased

77
Q

Wadley et al 2014

A

3 months exercise intervention of RA sufferers
Looking into acute exercise effects
NO metabolites increase (can assume NO has become available)
Carbonyls increased significantly
Saw a decrease in 3-NT in the exercise group over the 3 months from baseline but an increase in the controls. this suggests an improvement in NO availability as NO is not reacting with SO

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