Sport Nutrition second half Flashcards
Define micro-nutrients
Essential nutrients (can’t synth all that we need), required in small amounts for health
Difference between vitamins and minerals
Organic micronutrients essential for a specific organism
Cannot be synth so must be obtained from the diet
Minerals
Essential inorganic micronutrients
Which vitmains can be synthesised by the body?
D can be synth in skin from cholesterol with exposure to UV
Vitamin K synthesised by some gut bacteria
Water soluble vitamins?
B complex (12 different vitmaines C
Fat soluble vitmamins?
A (found in lliver, known as retinoids)
E,D,K
Functions of vitamins
Energy metab
B complex - lots of citric acid cycle components, part of NAD and B5 CoA? Antioxidants A,C,E Synthesis of body components
Collagen Vit C Hormones Vit C (norepinephrine) Bone Vit D, A Blood clotting factors Vit K Visual pigment Vit A
How many minerals, classification?
15 inorganic elements Minerals - required in amounts >100mg.day Ca, P, Mg, K, Fe, Na, Zn, Cl Trace Elements - required in <20mg.day (others)
Function of minerals?
Structure
Bone and teeth
Most abundant - Ca, P, Mg
Function
Soluble salts responsible for body fluid osmolality and determination of ICF and ECF volume
Na, K (more ICF), Cl, Mg, Ca
Maintain normal heart rhythm, muscle contractibility, neural conductivity
Regulation
Components of proteins (hormones and enzymes)
I and thryroxine
Fe, Cu, Zn components of enzymes/ cofactors
What do antioxidants do?
Prevent of limit damaging effects of free radicals in the body (intra and intercellularly)
Atoms or molecules with 1 or more unpaired electron
Most common are reactive oxygen species (ROS)
How are ROS formed?
Aerobic resp - intermediates in normal reactions WBCs-ROS for invading pathogens Hypoxia e.g. HIIT Radiation and pollution Smoking UV Inflammation
Describe enzyme control of radicals e.g. O2-
SOD (o2 -> H2O2)
Catalase (h2O2 = H2O and O2)
Gluathione peroxidase
Describe non-enzyme control of radicals
Non enzyme
Vit E - major lipid soluble antioxidant
Protects membranes from oxidative damage
Vit C
Aqueous components of body
Flavonoids and carotenoids
Role of antioxidants in skeletal muscle fatigue?
Antioxidants in skeletal muscle fatigue
=Inability of muscle to generate force
Radical production may play a role
ROS increases in contracting skeletal muscle
Excessive ROS induces oxidative damage to muscle proteins and reduces force production
Mostly from animal studies - antioxidants protect skeletal muscle from damage and delay fatigue during prolonged submax exercise
No effect on high intensity
Study that an antioxidant can prolong fatigue?
Exercise can be prolonged with N-acetylcysteine infusion (NAC) - antioxidant
70% VO2 max at 45 min then fatigue at 92% VO2max - time increases by miunutes
Little evidence that dietary antioxidants could make a difference e,g, E, C, betacarotene
Arguments for Vitamin C/E supplementation?
Most common are not toxic so no harm
Radicals promote fatigue in skeletal msucel
NAX attenuates
Inadequate dietary intake e.g. Restriction, poor diet, increased training
Arguments against vitamin supplementation?
Exercise oxidative stress -no evidence it harms health
Exercise increases antiocidants (both kinds) in skeletal muscle)
If dietary intake sufficient, supplementation likely not needed
Might impair adaptation of muscle to exercise
ROS signal to promote expression of skeletal muscle proteins
Antioxidant enzymes, mitochondiral proteins and heat shock proteins
Explain the Golman dilemma
198 US olympic athletes asked 2 questions
Would they take performance enhancing drugs if,
Guarenteed to win every comp for 5 years
Guaranteed notto get caught
98% yes
Would they take performance enhancing frugs if:
Same
But guarenteed death from side effects
52% said yes
1992
Findings from the Gooldman dilema revisited?
Athletes more concerned about legality than death
What is Maughan’s rule for supplements
If it works, its banned
If it doesnt work, its not banned
Few exceptions
Why do athletes supplement?
Aid recovery Health Improve performance Prevent. Treat illness. Compensate poor diet Most high level take 80-90% track and field
Why may an athlete have a poor diet and need supplements?
If eliminated food group e.g. Vegan
If put into energy deficit - may need supplements
Need extra valories/ carbs
Why is taking lots of supps potentially detrimental?
Risk of contamination increases
Potential detriment to performance
describe types of nutritional supplements
Ergogenic Ergo=work Genic=making Creatine - from meat, veges better Beta-alanine/carnosine - only is turkey (eat lots for sufficient amount) Biocarbonate Caffeine? - some from foods Nitrate? - some foods e.g. beetroot Sports food Protein Carb - tablets, drinks
which group may benefit from creatine supps the most?
Females
In 2008 how many sipplements contained WADA banned steroids or prohormones?
14.8%
How do banned supps get into legal supps?
Often raw materials cross contaminated at source
Manufacturing process cross contamination of line
Outsorced manufacturer
Inadequate cleaning of machinery
Not because they want their product to better
How sesnitive are anti doping tests in 2009?
0.00005% can detect
2.5ug 25% would fail
5ug 50% would fail
-level has been found
How can a practicitioner know if a supp is clean? drawbacks?
informed-sport.com logo
Means batch has been tested
Often on site but not always on product
How much and why for muscle biopsy
.1g
Used for glycogen, protein synthesis
3 questions to ask when considering supplements?
Is there an underpinning biological rationale?
If i was to provide this, does it reach desired location? Does it change plasma conc?
If it reaches muscle, is it taken up and does it change anything?
Difference between rates of ATP turnover and physiological mechanism for this
In cells with low rate of ATP turnover e.g. Skin cell and plant cell
ATP produced in mito, travells to muscle, used to fuel muscle contraction/ biological process
In cells with high rate of ATP turnover e.g. Muscle and brain
ATP synesised, dephosphorylates and phosphate transferead to Cr (creatine)
Creating phosphate suttles across to site of biological process/ muscle, Forms ATP. Acts as a shuttle.
Describe the biological roles of creatine
Plays a role in resynthesis of ATP from ADP
1) Directly rephosphorylate ADP to form ATP
2) Shuttle phosphates from site where nutriets are synthesised e.g. Mito to muscle
(H+ role)
describe variation in creatine loading
Different starting points for total creatinine
Start from a lower level, see a bigger increase
(ceiling effect)
Some people with higher levels don’t really change
Vegetarians maybe have lower creatine
Normal loading dose and maintainence of cretine
5x4/day one week
followed by 2g/day
Hultman et al 1996 methods
Active males
4 groups
1- 20 for 6, muscle biopsies at day 0,7,21 and 35
2- 20 for 6 then 2 for 28, 0,7,21,35
3- 3 for 28days, days 0,15,29
4- 20g of placebo for 5 days, 24h urine sample multiple times until (day 25 after). Same subjects then injgested placebo and Cr for 5 days (same as 6). (24 hr).
Hultman et al 1996 key findings
Muscle total creatine conc increased by 20% after 6 days of supp at a rate of 20g/day
Maintain if supp continued at 2g/day for a further 30 days
Without, total creatine gradually decline over next 30 days until there there was no diff to presupp value
Correspondingly urine increased with increased creatine up to day 5, decline afterwards compared woth placebo
More gradual increas if 3g/day supp over 28 days
Conc
20g a day for 6 days= rapid creatine load
3g a day, same effect in long term
Hultman et al 1996 main aim
The effect of dietary creatine supplementation on skeletal muscle creatine accumulation and subsequent degradation and on urinary creatinine
Sale et al 2009 main aim
to compare the effect of two creatine monohydrate supplementation regimes (4x5 g day and 20 x1 g day for 5 days) on urinary creatine and methylamine excretion. (methylamine = potential toxic compound)
Sale et al 2009 methods
9 males each completing 2 trials separated by 9 weeks
1- 4x5xday for 5 days
2-20x1xday for 5 days
Collected 24h urine days 1-2 (baseline) and day 5 and 2 post supp days (days 8-9)
Urine assayed for creatine and methylamine
Sale et al 2009 key findings
Less creatine and methylamine excreted following the 20x1gxday regime
Suggests a greater retention in body and likely in the muscle.
Lower and more frequent doses of creatine monohydrate attenuate formation of methylamine
Green et al 1996 aim
The effect of carb ingestion on skeletal muscle Cr accumulation during Cr supplementation in human
Green et al 1996 method
Muscle biopsy, urine, plasma from males before and after ingestion of:
1) 5g Cr
2) 5g CR, followed by CHO30 mins later
4x a day for 5 days
Green et al 1996 key findings
Supplementation resulted in an increase in muscle PCr,Cr and TCr in both groups.
60% greater TCr in group B.
Corresponding decrease in urinary Cr excretion in group B
Cr had no effect on insulin conc but Cr and CHO did. Suggests Cr accumulation may be insulin mediated.
Effect of exercise on creating conc
Increased retention of creatine postex, at 6h and 5day in ex leg compared with non ex leg
Effect of creatine on glycogen stores
Slight increase found p=0.06 with exercise
Casey et al 1996 aim
to perform a direct investigation of the effects of Cr supplementation on skeletal muscle energy metabolism and performance during repeated bouts of maximal exercise in humans.
Casey et al 1996 methods
2x 30s maximal isokinetic cycling separated by 4 mins of passive recovery befor and after ingestion of 20g Cr monohydrate/day for 5 days
Muscle biopsies were taken before and after each session of 2 bouts (pre and post Cr)
Measured total work production and peak work production
Casey et al 1996 key finidngs
Increase in TCr conc in muscle
Total work production increased during both bouts
Cumulative increases in both peak and total work production over the 2 bouts were correlated with increase in muscle TCr
Culumative loss of ATP was less after Cr ingestion despite increased work production
Resting PCR increased in type 1&2 fibres, correlated with changes in total work production and PCR breakdown.
Suggests an improvement in ATP resynthesis due to increased PCr availability
Rawson et al 2011 aim
Examine the effects of 6wk of low-dose creatine supp on body comp, muscle function and body creatine retention
Rawson et al 2011 methods
1) Creatine 0.03g/lg/day
2) Placebo
6 week, double blind trial
Tested before and after supplementation
Included
Body composition - electrode bioimpedance analyzer
Maximal strength (3-rep max concentric knee extension at 180deg)
Muscle fatigue (5 sets of 30 concentric knee ex..)
Plasma creatine conc
Rawson et al 2011 key findings
No sig diff in body mass, FFM, FM, total body water or maximal strength in either group.
Plasma creatine increased in creatine group, no diff in placebo
Creatine group more resitent to fatigue during sets 2-5
Describe exercise and pH
Everytime ATP is resynthesised
H+ is produced from glycogolysis, either lactate and H+ or CO2 (more from HI)
Describe the body’s mechanism for H+ buffering
Slows decline in pH
Buffer at muscle and in blood stream
Physico-chemical buffering in the muscle e.g. Phosphate, bicarbonate, petide/protein bound histidine
Dynamic buffering - with sodium bicarbonate in the circulation from diffused H+
Describe creatine and buffering
CK reaction results in the breakdown of PCr and the regeneration of ATP
H+ is consumed as part of the process
PCr breakdown during high-intensity exercise could contribute to intracellular buffering
Might have a small effect on muscle buffering capactiy as well as ATP regen
How is carnosine normally synthesised?
Increases muscle carnosine
Histidine+ B alanine = carnosine
Histidine already high, increase B-alanine which may be lmiting step here
Consume carnosine in diet, broken down into b alanine and hisitidine
Harris et al 2006 aims
x
Harris et al 2006 methods
x
Harris et al 2006 key findings
x
MoA of beta alanine?
Forms more carnosine, acts as pH buffer, delaying fatigue in high intensity exercise
Hill et al 2007 aim
Influence of b-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity
Hill et al 2007 methods
4weeks or 10weeks BA Biopsy of VL at 0,4,10 wks. Cycle capacity test (CCT) to determine (TWD) at 110% of max power Matched subjects receiving placebo Completed CCT at 0,4,8.10 weeks
Hill et al 2007 key findings
Muscle carnosine increased at both 4 and further increase at 10wks BA supp
Carnosine increased equally in type 1,2 over 10 weeks
No increase in control
BA supp resulted in increase TWD at 4 and further increase at 10 weeks
This was associated with increase in muscle carnosine
Taurine unchanged in both groups
Benefit of BA on exercise lasting <60s? when is optimal?
No benefit on exercise lasting <60s
Beetter for 1-4 mins (more H where buffering is more useful)
