Condensed nutrition deck for exam Flashcards
How is vitamin D made?
In our skin by converting UVB light, 30 mins per day is enough
Can also be found in lots of food
Cellular effects of vitamin D?
Classical actions -
Calcium homeostasis
Bone metabolism
Neuromuscular function
Non-classical actions - Immune function Cardiovascular function Mitochondrial function Cellular proliferation and differentitation
Roles of vitamin D?
Bone health:
Increases calcium and phosphate absorption
Bone mineral density increases with vitamin D
Muscle function:
Calcium kinetics
myoblast differentiation - muscle regeneration
Muscle weakness evident with vitamins D deficiency
Immune function:
Improved macrophage and monocyte function
Increased upper respiratory tract infection (URTI) rate with a poor fit D status
Vitamin D conclusions?
Deficiency or inadequacy is prevalent amongst athletes
Poor vitamin D status is associated with impaired bone health, exercise performance and immune function
Not sure if casual
Vit D3 supplementation may be helpful for those who are deficient, reaching a target serum of 75nmol.L^-1 which is done by having 4000 IU per day
Carbohydrate digestion?
In mouth broken down by salivary amylase
Down the oesophagus into the stomach
High levels of acid stop amylase action - no carb breakdown
Move to small intestine where there is pancreatic amylase which breaks carbs down into disaccharides
Sucrase, Lactase and Maltase then break the carbs down into monosaccharides
Monosaccharides transported into the blood and the liver
Monosaccharide absorption for glucose and galactose?
Co transported with Na+ from the intestinal lumen via SGLT 1, through the intestinal wall and into the blood via GLUT 2
Monosaccharide absorption for fructose?
Intestinal lumen through the intestinal wall via GLUT 5, then into the blood via GLUT 2
Is muscle glycogen essential for endurance capacity and obtained from a high carb diet, and features of this?
yes
It also depletes quicker with more intense exercise
Same with liver glycogen
Therefore muscle glycogen is essential for short duration exercise, gets used up so not utilised in longer bouts of exercise
Classical super compensation protocol?
Week before a race you would do one hard bout of training, followed by no training at all and 3 days of low CHO intake, then 3 days of high CHO intake before race day
Problems:
Hypoglycaemia in low CHO = low blood blood sugar
Difficult to find food with no carbs
GI distress
Poor recovery
Poor mental state from no training
Moderate super compensation protocol?
Slowly decrease training, whilst slowly increasing CHO intake
No difference compared to the classical after 60 minutes of exercise
Is carb loading worth it?
Yes for:
Repeated sprints
Intermittent sports lasting greater than an hour
Exercise lasting more than 90 minutes
No for:
Short and explosive
Kess apparent if ingesting CHO during exercise
Practical guidelines for carb loading?
Start exercise with sufficient muscle glycogen, don’t need way more
Eating CHO rich for 2 days prior to a race decrease training
EE reduced so not just ear more
A carbohydrate intake of 5-7 g/kg per day seems to be sufficient in the majority of cases (with low EE)
GI athletes need to be careful
CHO intake hours pre exercise?
Maximise glycogen in liver and muscle
Improves performance
CHO are most important 1-4g/kgBM - lower if very close to the event
Avoid low GI and avoid fat, need to get all food out of stomach before running to avoid runners trots
Practice the routine
Physiological effects of CHO intake hours pre exercise?
Transient fall in plamsa glucose at exercise onset
Increased CHO oxidation and accelerated glycogen breakdown
Blunting of Fatty acid mobilisation and fat oxidation - good for short exercise as want to prioritise carbs
Important if cannot take CHO in during exercise
Physiological effects of CHO intake 30-60 min pre exercise?
Causes large rise in plasma glucose and insulin
Which may then lead to hypoglycaemia during exercise
This is due to large rise in plasma glucose and insulin, which can then lead to reactive/rebound hypoglycaemia during exercise
Can manipulate of ingested CHO to help tis (lower are better), also low GI food and just don’t eat
This is hypothetical and performance should be fine
Goals and considerations when taking in CHO during exercise?
Prevention of the depletion of blood glucose, and muscle and liver glycogen
Maintain hydration
Duration of event?
How much CHO? (duration, intensity, GI ability)
Type and form of CHO? (gel /solid/ monosachharide
Oxidation of ingested carbohydrate?
It doesn’t keep on getting bigger the more carbs you eat, maxes out round 1g/min can’t digest it quick enough, or absorb it
Rapidly oxidised: (up to 1g/min) - Glucose Sucrose Maltose Maltodextrins Amylopectin
Oxidised at lower rates (up to 0.5g/min)
Fructose (liver) Galactose (liver) AMyose Isomalutose Trehalose
What can be done to increase ingested carb oxidation rate?
Combined ingestion - means that different transporters are utilised
This means there is now very rapidly oxidised carbohydrate mixes ( >1g/min) which are?
Glucose and fructose (>60g/h glucose)
Maltodextrin and fructose (>60g/h maltodextrin)
Glucose, sucrose and fructose (>60g/h glucose and sucrose)
If you can tolerate higher levels of carbs (120g/h) then during hard exercise can reduce exercise induced muscle damage markers such as creatine kinase, lactate dehydrogenase, GOT
Also performance is enhanced by using combinations
Conclusions on CHO use on exercise performance?
CHO can improve endurance capacity over 2 hours, but also high intensity exercise lasting around 75 min
CHO ingested during exercise will spare liver glycogen and can completely block hepatic glucose output
Exogenous CHO oxidation rates of a single CHO peaks at 1-1.1 g.min^-1
Ingestion of multiple transportable CHO can increase exogenous carbohydrate oxidation rates by 20-50%
Features of triglycerides?
Major storage from of fats in the body
3 fatty acids react with one glycerol molecule to produce a triglyceride molecule
This is done via a condensation reaction = esterification (water is removed)
n-3 and n-6 polyunsaturated fatty acids are incorporated into cell membranes, what effect does this have on cell function?
The ratio of n-3/n-6 PUFA in cell membranes leads to different set of intracellular mediators produced
Higher n-3 leads to less inflammatory mediators produced
Studies in illness, disease in human and animal confirm this effect, which is modulated by dietary intake
Features of adipose tissue?
Provides a basically infinite store of energy during exercise
Can you generate ATP from fat anaerobically?
NO
Fat must go through complex set of regulatory reactions to get into the mitochondria, then can enter the TCA cycle to produce ATP
So its slower than producing energy from carbs
Describe long chain fatty acids getting into the mitochondria and therefore being able to produce ATP?
Fatty acid translocase/CD36 and fatty acid binding protein take the long chain fatty acids from circulation into the cytosol
Join a pool from the intramuscular triglyceride store as well
The long chain fatty acids are very inert so become activated by Co enzyme A (CoASH), forming Acyl-CoA
This can now enter the mitochondria through the carnitine shuttle, achieved through the CPT1, CACT, and CPT2 enzymes
Ready to undergo beta oxidation to make ATP
This is why fat can’t sustain contractions at 75% VO2 max, it is too sluggish
The athletes paradox?
As we exercise we reduce the amount of adipose tissue we have
Oxidative capacity and insulin sensitivity are markers of good metabolic health
as we exercised more, restricted calories, are metabolic health increases, and if we are inactive, obese and on high fat diets it would decrease
The more fat we get the more is stored as intra myocellular lipids as expected at one end of the scale
As you get leaner the intra myocellular lipids levels drops, but when you keep on training on the scale of athlete they increase above what someone who is obese or type 2 diabetic
In athletes how is the intra myocellular lipids stored in the muscle compared to that of an obese person?
In athletes stored directly proximal to the mitochondria
Also in athlete normally in smaller droplets = larger SA to volume ratio so can be used quicker
Therefore most readily available fat store in the body
Obese individual harder to access the fat and use it effectively
What happens when you go over 65%-80% of VO2 max?
Before that use carbs and fats equally
After that fats drops massively and carbs is increased
What are the possible limitations to fat oxidation during exercise?
Want fatty acids that can be transported to the muscle for fuel
These are made from lipoprotein lipase breaking triglycerides, or Adrenaline released by exercise causing lipolysis through hormone sensitive lipase causing triglycerides to turn into fatty acids
Increase in insulin (released after a meal) causes lipogenesis, fatty acids turned into triglycerides
Problem is actually that fewer fats actually being able to get into the muscle cell - even though the supply of fats is enough
The ability of the cell to take them up is not actually impaired, so the decline must be intracellular
Co enzyme A exists in small amounts in the cytosol and mitochondria to form Acyl-CoA, but it is also needed for beta oxidation of Acyl-CoA to Acetyl-CoA
Co enzyme A also needed in the carbohydrate pathway, when this increases so does this demand
Same problem with Carnitine which takes Acyl-CoA across the mitochondrial membrane, it is also required on the carbohydrate side to form acetlycarnitine
The more trained we get do we utilise fat more?
yes. it enhances fat oxidation
What can a nutritionist potentially do?
Increase endogenous fat availability, increasing fat oxidation and spare carbohydrate - good for performance
Can we increase this in the diet and should we?
What happens when pre exercise fat feeding (+heparin which helps them to be converted to fatty free acids) occurs?
Increases fat oxidation, and spares muscle glycogen use
Without heparin does not help, as only triglyceride levels have increased as not being converted quickly to fatty free acids
Overall pre exercise fat feeding does not help exercise performance
Take home points on acute fat feeding?
It’s not easy to increase fatty acid availability
When increased you do increase fatty acid oxidation
This doesn’t help with exercise performance
Regardless of the length of chain of fat feeding
Why doesn’t it help? and if supplementing is not possible can chronic feeding be used as a practical strategy
3 day high fat diet on cyclists has what effect?
Favourable changes in substrate use with high fat diet
They have adapted to be able to utilise fat more effectively
Does more fat in diet result in more optimal storage of intramuscular triglyceride stores and glycogen stores?
No, need a set amount in the diet to maintain IMTG stores, and too much and impair glycogen storage
Does a low fat diet result in more glycogen utilisation?
yes
Over 7 weeks what improved cycling performance more, the high carb or high fat diet?
High carb by far
Baseline knowledge on low fat intake and high fat intake?
If too low:
There is progressive depletion of IMTG
Minimum fat intake is required to maintain IMTG stores ( a key energy source for endurance performance)
If too high:
Results in greater fat oxidation
Also results in lower muscle glycogen storage
This reduces performance, particularly during higher intensity events which rely on carbohydrate oxidation
This could also be due to a decrease in the efficiency of CHO use during more intense exercise
A theory on how to get the best out of both high CHO diet and high Fat diet?
Have people of high fat diet in weeks leading up to performance so adapt to be able to perform more fat oxidation
Then before performance have a high CHO diet to replenish glycogen stores
Because:
Potentially elevated ketones are shown that they increase RPE
High fat diet make it difficult to reach a ‘top gear’, as their ability to move carbohydrate through the rate limiting step of pyruvate dehydrogenase is reduced
The high fat diet has deprimed the carbohydrate adaptations the body has
Conclusions on should you have a high fat diet or high carb diet?
High carb is better, good endurance exercise is also normally performed higher than 75% VO2 max as this is strongly CHO dependant
So under most conditions Fat adaptation is not useful for exercise performance
Caffeine mechanisms to improve exercise performance?
Blood:
Increased free fatty acids, means less carbohydrate stores used
Muscle:
Altered {K+}
Blood lactate concentration
Increasing Ca handling = increasing the power of muscle contractions
Brain:
Increased motor unit recruitment
Adenosone antagonism = decreased rpe and pain
Increases reaction time, alertness and mood = anti fatigue effect
What are the factors that limit repeated sprint performance?
Phosphocreatine supply
Low muscle pH - acidosis
Extracellular potassium accumulation - altered excitability
Central fatigue
Why do we care about the integration of fuel metabolism?
The integration of fuel metabolism is crucial to generating large amounts of ATP
Important in the current day
What do we mean by the intergration of fuel metabolism?
At any time point the energy required by the cells of our body (metabolic rate) is almost always provided by both fat and CHO utilisation
Different circumstances can require different amounts of energy
At any given energy expenditure there can be a different contribution of dat and CHO to this energy expenditure
Importance of skeletal muscle in fuel metabolism?
Skeletal muscle is 40-50@ of body mass
Responsible for 20-30% of resting oxygen consumption
Mediates over 75% of all insulin mediated glucose disposal under normal physiological conditions
Primary depot for this disposal of nutrients
What’s the Randle cycle?
Fat is boss in the integration of fuel metabolism - under most conditions it’s what regulates metabolism over carbohydrates
Fatty-acid pathway can inhibit the glucose pathway
The acceleration of fat metabolism happens over carbs when we are fasting
End product inhibition, fatty acid cycle produces Acetyl-CoA, which is also the end product of glucose metabolism, so if the glucose pathway isn’t even working hard there is an imbalance between pyruvate which should be converted into the abundant acetyl-CoA which has now been made harder
Acetyl-CoA also enters the TCA cycle and one of the products it produces is Citrate, which in excess diffuses across the mitochondrial membrane into the cytosol, where it inhibits phospofructokinsase, and essential enzyme is glycolysis
This results in a build up of glucose-6-phosphate, which inhibits hexokinase which is required to activate the glucose molecule
Empirical data supports all of this
Empirical evidence supporting the randle cycle?
Increasing plasma FFA (via lipid and heparin infusion):
(Odland et al, 1998, 2000).
• Suggests regulation at PFK.
33% ↓ thigh glucose uptake during moderate intensity knee extensor exercise
(Hargreaves et al, 1991).
• Suggests regulation at GLUT4.
↑ fat oxidation by 15% and ↓glycogenolysis by 50% at >80% VO2max. ↔ PDC activity and muscle contents of acetyl-CoA, citrate, and G-6-P. ↓ free ADP and AMP. (Dyck et al, 1993, 1996; Romijn et al, 1995).
• Suggests regulation at Glycogen phosphorylase.
Insulin stimulated glucose uptake?
Eat carbs meal
Carbs digested and absorbed as glucose which is distributed in circulation
As glucose passes by the pancreas, pancreatic beta cells release insulin
Glucose is impermeable so needs an active transporter (insulin)
More simple carbs = quick insulin peak (easier to breakdown)
More complex carbs = more prolonged peak (harder to breakdown)
Insulin attached to insulin receptor on cell membrane
Phosphorylation and therefore activation of IRS-1
IRS-1 stimulates PI3kinase, this stimulates GLUT4 (a muscle specific transporter) to go from vesicles within the cell into the cell membrane
PI3kinase also stimulates the protein AKt, which stimulates GLUT4 as well
GLUT4 makes the cell membrane essentially permeable to glucose
Akt also directly regulates the pyruvatedehydrogenase comple
3 routes the initial glucose molecule can take?
Aerobically converted from pyruvate into acetyl-CoA
Anaerobically converted from Pyruvate into lactate
Stored as glycogen
Does the feeding of glucose ( so not being in a fasted state) disrupt the randle cycle?
Yes, it helps to reverse the randle cycle
But it only impairs oxidation of long chain fatty acids, not medium chain
This switch is controlled by CPT1
Molecular mechanism how the fed state reverses the randle cycle?
Rise in glucose results in an increase Acetyl-CoA
Produced in excess to what the TCA cycle can handle
So it is converted by the ACC enzyme into Malonyl-CoA which inhibits CPT1
Data saying that malonyl-CoA is not involved?
> 2fold ↑ in fat oxidation (due to depleted pre-exercise muscle glycogen content) during exercise at 65% VO2,peak. ↔ muscle malonyl-CoA compared to control.
(Roepstorff et al, 2005)
No association between muscle malonyl-CoA content and fat oxidation rates during
prolonged moderate-intensity exercise or graded-intensity exercise. (Odland et al, 1996, 1998; Dean et al, 2000)
so doesn’t work in humans
Free carnitine hypothesis?
Acetyl-CoA converted into acetylcarnitine and moved into the cytosol by CAT and CACT reacting acetyl-CoA and Carnitine
Acetyl-CoA can act as a metabolic sink
CoA is also produced which can be used by the mitochondria
This overall causes a decrease in free Carnitine, so can’t act as a cofactor for CPT1 to shuttle fatty acids (acetyl-CoA) into the mitochondria -this is the limiting step everyone believes right now
Claims around carnitine supplementation?
Broad et al. (2005) found no effect of oral L-carnitine supplementation for 4 weeks (3g/day) on carbohydrate and fat metabolism or on exercise performance
Vukovich et al. (1994) reported no significant effects on fat or carbohydrate metabolism during exercise at 70% VO2max after 14 days (6g/day) supplementation of L-carnitine.
Wächter et al. (2002) also concluded that oral L-carnitine supplementation for 3 months (4g/day) did not affect exercise performance.
Importantly, Wächter et al. (2002) and Vukovich et al. (1994) reported that L- carnitine supplementation did not alter muscle carnitine content.
Does not work from these studies, it works basically only in the muscle, so when you digest it there is an unfavourable concentration to get more in the muscle
So you need molecules that bring the carnitine into the muscle, can use carbohydrates to do this
Ben wall and colleagues shows it can work when it is up taken, can alter fat and carb oxidation, and can increase exercise performance by saving glycogen stores through driving fat oxidation (only lower intensities), but at higher % of Vo2 max where carnitine is a limiting factor for fat oxidation, it didn’t actually help, what it did was reduce lactate accumulation
What carnitine did was change its role from being used in CPT1 translation to the mitochondria, or it’s role as a acetyl buffer depending on glycolytic flux
So higher glycolytic flux (higher work intensity) drove carnitine to help form a metabolic sink for acetyl coA, more of it means it can be done in larger quantities, reducing pyruvate quantities and therefore lactate accumulation
What is insulin resistance?
The reduced responsiveness of skeletal muscle glucose uptake to normal circulating levels of insulin
Can also be viewed as…
Impaired ability of insulin to stimulate glucose oxidation (via PDC) Impaired ability of insulin to stimulate microvascular perfusion
Impaired ability of insulin to stimulate amino acid uptake into muscle cells Impaired ability of insulin to inhibit muscle protein breakdown.
Makes it harder to get glucose into the cell, therefore results in it being harder to use it to generate energy
Some techniques at measuring insulin resistance?
Single blood sample
Ratio of insulin to glucose in your blood using an equation
Healthy in fasted = low in both
Diabetes type 2 = high insulin and high glucose as it just isn’t enough to get the glucose in the cell
Or high glucose low insulin, as the pancreas has been stimulated so much it can’t release much anymore
One technique is looking at glucose disposal rate
Gold standard is hyperinsulianemic clamp technique
Measuring insulin resistance, the hyperinsulianemic clamp technique?
Induce artificial high levels of insulin pumped into the body
Glucose chased away into peripheral cells, so you inject glucose as well and look at the rate in which it gets put into cells
Athlete will have fast rate
Obese will have slow rate
What is metabolic inflexibility?
Obese people suffer from it
From fasting to insulin stimulated they can’t oxidise the glucose they have digested
Can’t switch between fat and carb oxidation
Lipid overspill theory (following on from Randle cycle)?
Big lipid droplets form in muscle
Broken down to acyl-CoA
Athlete can turn these over
Obese can’t, resulting in an accumulation of fatty acid intermediates, such as Ceramide and Diacylglycerol
These stimulate the JNK pathway which can directly inhibit the IRS-1 which is needed for to pathway of insulin creating an effect within the muscle cell
The IkKB and PKC pathways do the same to IRS-1
Overall this exacerbates the cycle build up of lipids
What’s the inflammation theory?
Excess lipid and adipose tissue release Il-6 and TNF-a cytokines can interfere with insulin signalling
Interacts with JNK pathway as well
What can’t obese individuals oxidise?
Muscle and plasma triglyceride
Can do endogenous carbohydrate and plasma FFA
When we do exercise without insulin being present (haven’t just had a meal) is glucose still used?
yes, so it is contraction stimulated glucose uptake
Contraction increases concentration of Ca2+
and turns ATP broken down into AMP and ADP, this changes the charge of the cell, this ratio tells AMPK what to do
AMP accumulates, AMPK tells the cell to breakdown Glycogen to provide ATP
AMPK also tells GLUT4 to go to the membrane, and stimulates CPT1 to shuttle fats into the mitochondria
Ca2+ increase stimulates PDC increase activity, as well as the enzyme CaMK which increases GLUT4 translocation the cell membrane
Amino acid oxidation?
The breakdown of intracellular amino acids for energy production
If oxidised not available for protein synthesis
Leucine oxidation?
The enzyme KIC via transamination and decarboxylation turns Leucine into isovaleryl - CoA with the byproducts glutamate and Co2
This then turns into Acetyl CoA or Acetoacetate
Protein turnover described?
Intake protein through diet (50-100g a day) which forms plasma amino acid pool via digestion and absorption
These amino acids are uptake by cells forming an intracellular amino acid pool
This is when protein synthesis now occurs, (350g/day)
Protein breakdown is also occurring going into the intracellular amino acid pool
Inter-organ nitrogen transfer?
Amino acids and ammonia go from the GI tract to the liver
Amino acids go from the GI tract to skeletal muscle, breakdown of proteins here produces alanine which turns into glutamine and goes to the kidneys where glujconeogeneis occurs and glucose is formed which goes to the liver
Liver excretes urea, glucose, triglycerides, and proteins
2 major methods to look at protein metabolism?
Nitrogen balance:
Nitrogen excretion = nitrogen intake
Need to know exactly what’s being eaten, and what is being excreted (Sweat, urine, faecaes)
You don’t know what tissues storage is occurring in or what time
Stables isotopes:
Label a specific amino acid can trace where it is in the body eg. 13C-Leucine
Can see how much is uptake from plasma amino acid pool into the intracellular amino acid pool
Can see how much undergoes oxidation
Can see how much incorporated into muscle protein through synthesis
Can also see how much of this protein is then broke down
Factors influencing protein turnover?
Habitual diet Protein intake Energy intake Hormones - insulin, steroids such as testosterone Exercise
Potential roles of dietary protein in sports and exercise?
Muscle hypertrophy Muscle strength Immune function Central fatigue Glycogen re-synthesis Additional energy during exercise Specific function of individual amino acids Effects on muscle damage Oxidative damage Increasing the synthesis of specific proteins? Mitochondrial/oxidative proteins?
What does endurance exercise do to muscle protein metabolism?
During exercise amino acid metabolism increases (still low compared to carb and fat metabolism, it’s 1-10%) to produce energy, it’s lower pre and post exercise
Therefore whole body protein synthesis is higher pre and post exercise
When we begin endurance exercise the priority of the tissue is to produce energy = catabolic state
Same showed on a training day in which nitrogen balance goes negative
Effect of endurance exercise and CHO/Protein feeding during exercise?
8 physically active overnight fasted young men
2 trials one with and one without protein (both have carbs)
2h rest, 3h exercise at 60% VO2 max, 3h recovery
Leg phenylalanine kinetics, fractional synthetic rate looked at
No decline seen in protein synthesis as both were fed with carbs, but protein showed far larger protein synthesis. Exercise makes protein synthesis increase when having protein, but the breakdown from exercise is still too much that it’s still net negative
Protein breakdown was the same on all conditions
What is the relevance of improving muscle protein balance for the endurance athlete?
Adaptation to the mitochondria within the muscle = improved oxidative capacity
More mitochondria/ better functioning mitochondria
Oxidative enzymes in higher concentrations in endurance athletes compared to resistance trained
What does endurance training cause and what does resistance training cause?
Endurance = increase in mitochondria
Resistance = increase in myofibrillar proteins
Effect of CHO/Protein during recovery from endurance exercise? (Breen et al, 2011)
Was found that protein increases myofibrillar but not mitochondrial protein synthesis - so not as good for the endurance athlete
This evidence is not that researched however, seems still essential to not spend days in negative protein balance,
Overall the findings in meta analysis are conflicting
IN THE EXAM??? What is the relevance of protein balance during exercise for the ultra-endurance athlete
ok
What is central fatigue their?
Theory on how protein improves endurance exercise performance
Its that fatigue may be associated with inadequate central nervous system drive to the working muscle
Main theory is Serotonin Central Fatigue Hypothesis:
Increased brain 5-hydroxytryptamine (5-HT) (Serotonin) concentration causes a deterioration in performance
Serotonin synthesised in the brain from the amino acid tryptophan
Mechanism of Serotonin Central Fatigue Hypothesis? (in reverse)
Serotonin interferes neural drive - causing impaired CNS function, reducing exercise performance
Serotonin is directly affected by Tryptophan (it’s amino acid pre cursor) that arrives at the brain through the blood Brain barrier using a selective transporter
This selective transporter is not very specific, and also allows other amino acid chains to cross the barrier, therefore there is competitive inhibition
So less free tryptophan will get across the blood brain barrier if there are branch chain amino acids present
Tryptophan circulates the body bound to Albumin and free fatty acids
BCAA concentration depends on dietary protein intake and exercise
Exercise causes more FFA to be released from the adipose tissue which binds onto Albumin increases the ratio in favour of tryptophan
We are using the BCAA for exercise, so that makes the ratio worse BCAA’s again
Can you use BCCA for improved exercise performance?
Blomstand et al 1991
Looked runners, only improved slower runners performance, but these slower runs all had lower rates of CHO ingestion as well
What did VAN HALL ET AL 1995 show?
That placebo, tryptophan, and BCAA supplementation all had the same to time to exhaustion during cycling
So does protein help during exercise?
Only if you have insufficient energy from food, and carbohydrate is better and easy to supplement with during exercise
So do endurance athletes require increased protein?
Meredith et al, 1989
Looked at 0.6, 0.9, or 1.2g protein/kg/d in endurance trained athletes
Only when you got to 1.2g per day they were really in a nitrogen positive balance, showing could be making the adaptations
Most endurance athletes surpass this from their diet anyways, so it’s not normally a concern
So RDI = 1.2-2.0 g/kg Dependent on: Mode/intensity/duration of training Protein quality Likely that adequate energy in the diet = adequate protein, without supplementation
Timing relative to exercise is important:
Protein ingestion in close proximity to exercise may facilitate muscle reconditioning
Protein feeding during exercise does not appear to enhance exercise performance assuming adequate CHO is consumed
To lose weight without losing muscle should have higher protein diets
Describe regulation of skeletal muscle mass?
You eat a meal
Muscle protein synthesis goes up
Insulin released which inhibits muscle protein breakdown
Over time this will drop and your fed gains reduces
This goes up and down resulting in a balance that is stable overall in a normal individual (oscillation)
So there is mild anabolism and catabolism
Does carbohydrate assist with anabolism?
Insulin release, increases perfusion to the muscle (amino acid amount getting delivery to the cell and into the cell),
Depends if they are rate dependent steps
However in reality they don’t help, the already modest insulin response from protein is enough to stimulate maximal muscle protein synthesis
Does fat assist with anabolism?
No, it just slows down the digestion and absorption of amino acids
4 factors that will allow for an anabolic response to dietary protein?
Postprandial insulin response (carbs isn’t need to make it valid)
Bioavailability
Digestion and absorption kinetics
Amino acid composition
Does protein timing and distribution influence daily muscle protein synthetic rates?
Looked at 12h recovery from resistance exercise
80g fed to all volunteers as
1) 8 x 10g every 1.5h (pulse)
2) 4 x 20g every 3h (intermediate)
3) 2 x 40g every 6 (bolus)
Intermediate resulted in most protein synthesis
Dietary recommendations of protein for athletic populations?
Maximal anabolic response with 25-30g protein
5-6 meals per day
1.6-2.2g per kg body mass / day
Summary on protein diet advice?
Exercise sensitises the muscle tissue to the anabolic properties of nutrition during each and every meal for at least a 24h period
20-30g per post exercise meal will induce an optimal anabolic response
We can look at the types of protein that would be most effective, select optimal sources or fortify those sub optimal sources
Ideally each protein meal would be rapidly digestible, rich in essential amino acids, and leucine in particular (2.5-3 g of leucine)
Protein is the only fundamentally anabolic nutrient, as such additional energy from other macronutrients from an anabolism perspective, but clearly being part of real food has benefits
Protein meals should be adequately spaced apart to gain the most anabolism from each meal
Presleep protein ingestion offers a unique timing opportunity to improve overnight muscle protein accretion
Functions of gut microbiome? (Amon and Sanderson, 2017)
Protection against pathogens
Synthesis of vitamins
Immune system
Promotion of intestinal angiogenesis
Adipocyte function
Short Chain Fatty Acid production by fermentation of dietary fibre
Modulation of central nervous system
Healthy gut micrombime relies on?
Increase in diversity and SCFAs+, and decrease in gut permeability
If these are all reversed bad things happen:
Dysbiosis - reduction in protection against autoimmunity
Increased cytokine production eg. IFN-y, meaning a reduction in Tree cell production
Increase in inflammation
A good microbiome supports homeostasis in what ways?
Immune function
Appetite regulation
Mood
Metabolism
Vascular function
Factors that affect the gut microbiome?
Birthing process - c section or not
Infant feeding method
Stress (exercise, metabolic, psychological)
Diet
Pharmaceuticals
geography
Lifecycle stages
How does exercise performance and gut microbiota help each other?
Exercise performance results in:
Higher microbial resistance
Higher abundance of beneficial Akkermansia, Veillonelaa, Prevotella
Selection advantage for lactate utilising bacteria
Benefits of a good microbiota for the athlete:
Production of bioactive metabolites (SCFA and neurotransmitters)
Maintenance of intestinal barrier function
Modulation of immune system
Improved energy harvest and utilisation
Regulation of muscle metabolism
Stimulant definition?
Stimulate the central nervous system with a marked effect on:
Mental function and behaviour
Producing excitement and euphoria
Reduced sensation of fatigue
Increase in motor activity
What is caffeine?
1,3,7 - trimethlyxanthine
Takes an hour to have maximal ergogenic effect
Half life of 5 hours
Metabolism affected by:
Hepatic dysfunction
Habituation
Removed from banned list in 2004
Caffeine mechanisms?
Central effects - stimulant:
Binds to adenosine receptors in the brain, displacing adenosine which has a stimulant effect
Increased lipolysis (sympathetic activation): Increased availability of fatty acids through the sympathetic system being activated, so more carb sparing so improved performance:
Reduced extracellular potassium Sarcoplasmic Reticulum Ca2+ release:
Improving calcium handling (binds to troponin, allowing myosin to be bound and cross bridge cycling can occur - release and uptake of calcium into the sarcoplasmic reticulum, improving contractility, faster time to peak force
Caffeine preserves the resting membrane potential of the nerve impulse in the muscle, meaning even after being stimulated a lot from exercise can still generate action potentials
What did Bowtell and colleagues 2018 find through “Caffeine supplementation and fatigue during repeated maximal contractions?
Received 6 mg caffeine . kg^-1 or placebo 1 hour prior to performing exercise
5 bouts of single leg knee extensor exercises to fatigue
Time to fatigue was recorded and they had 5 mins each time to recover
Caffeine made exercise capacity far better, but you also see an increase in blood lactate (from doing more work)
Muscle metabolites:
Sets 2-5 is Per conc is far lower in caffeine condition,
Muscle pH goes more acidic in caffeine condition, showing they are doing more work
Overall benefit was from an increased voluntary activation
This is from: Increased contractility Increased relaxation rate Increased excitability Increased wave amplitude
Conclusions: Increases in exercise capacity Delays fatigue Inceazed contractility? Increased voluntary activation Helpful where central fatigue is a key cause of poor performance
Metabolic effects of caffeine (Graham et al, 2000) features of the study?
10 healthy untrained subjects
Caffeine (6 mg.kg^-1) vs placebo
Complete1h at 70% VO2max, 1h after ingestion of supplement
Arterial fatty acid conc higher in caffeine, especially at the beginning of exercise
Increased adrenaline due to caffeine
Reduced extracellular potassium Sarcoplasmic Reticulum Ca2+ release:
RER is the same, so no difference in fat and carbo oxidation
Conclusions:
Caffeine stimulates lipolysis at rest
Appears to stimulate sympathetic nervous system activity
No metabolic effects
Lowers plasma potassium
Endurance performance (Hulston and Jeukendrup, 2008) what did they do and find?
10 subjects 3 trials
105 min @ 60%VO2max + time trial (calculated what work would have been done at 70% VO2max over 45 mins, then had to complete it as fast as possible)
Placebo
Cho (0.7g/min)
Cho + caff (5mg/kg)
No carb sparing shown, as affects of caffeine overwhelmed by carb dosing
Caffeine + CHO = better performance (4.6% better performance)
Conclusions on 2019 caffeine meta analysis? (Shen et al)
3% increase in performance
Magnitude of effects not influenced by Sex, age, VO2max, event, or timing prior to competition
Performance benefits are greater for longer duration events
Not effective for 800m performance and impaired subsequent sleep quality (Ramos-Campo et al, 2019.). (one study)
Schneiker et al 2006, caffeine improves intermittent sprint performance?
10 male amateur team sport players
Repeated cyclic sprints to mimic team sports
2 x 36min halves - 18 x 4 sprints
5 mg.kg^-1 caffeine or placebo
Caffeine showed increased world done and power output
Faster reaction time
Team sport performance saline et al 2019 showed that caffeine did what?
Increased small benefit to repeated and single jumping
Same in single and repeated sprint
Bit larger improvement to agility
Improved running distance
All these factors are cumulative
Sex differences in ergogenic effects of caffeine for endurance performance (skinner et al 2019)?
Endurance trained participants:
11 female on oral contraception
16 male
Randomised, double blind, placebo-controlled crossover trial
Incremental test, 2 x familiarisation, 2 x performance trials (test were how fast can you do your 75% vo2max distance for an hour )
3mg.kg^-1 90 min per exercise
No sex differences found
Does caffeine work the same even at different points in the menstural cycle (Lara et al 2019)?
13 well trained eumenorrheic triathletes no on oral contraception
Randomised, double blind, crossover trial
Placebo and caffeine (3mg.kg^-1) trials in:
Early follicular
Pre-ovulation
Mid-luteal
Found to have no effect
Good Important roles of ROS and RNS?
Cell communication: SR Ca2+ release Glut 4 translocation Increased protein synthesis Metabolic regulation
Vasodilation
Immune function
Consequences if reactive species exposure exceeds antioxidant defences?
Oxidative damage:
Damaging lipids:
Peroxidation
Cells membranes damaged - dysfunctional cells
Reduced NO bioavailability - impaired blood vessel function
Damage to body proteins:
Oxidative modification - carbonisation, nitrosylation
Altered function - aging
DNA damage:
Aging
Cancer
Triggers inflammation
Direct antioxidant properties?
Radical scavengers
Only about 5-10% of dietary polyphenols go into circulation, rest are digested by microbiome which then can be used
Due to his poor bioavailability, they are converted to prooxidants such as Semiquinones and quinones
These then trigger increased synthesis of endogenous antioxidants by cells
Also the actual antioxidants can inhibit ROS production
Effect of exercise on ROS generation?
NADPH oxidase creates O2- radicals which with the product of the mitochondria produced H2O2 intracellularly
Extracellularly NADPH oxidase and XO form O2- radicals which forms H2O2
When exercise occurs both their concentrations increase
Process of fatigue?
Ioninc gradients E-C coupling Central drive Substrate depletion By-product accumulation Muscle perfusion
ROS and RNS can contribute to these processes, so does antioxidant supplementation improve performance
ROS expose can trigger what?
Increased production of antioxidant enzymes
For example ROS and RNS allows Nrf2 to unbind with Keap1, NRF2 then can fit into the cell and cause a antioxidant response element
So exercise training increases antioxidant defences
So does antioxidant supplementation block training adaptation
Antioxidant relevance to exercise recovery?
ROS and RNS can result in:
Damaged cell membranes - leaky- impaired permeability
Damaged proteins - altered function - transporters, enzymes, contractile proteins
Inflammation - soreness, pain
Can lead to injury which worsens inflammation and the immune response, which increases the ROS and RNS concs
So can antioxidant supplementation improve recovery
Effect of antioxidant vitamins on recovery from muscle damage?
38 active healthy mean
Randomised to 6 week nutritional supplementation, twice per day
Placebo or Vit C (400mg) and E (268mg a-tocopherol)
90 min intermittent shuttle running
Bloods and muscle function tests
Found no significant effects of antioxidant vitamin supplementation, some studies find it, some don’t but mostly likely doesn’t help recovery. Also they might stop adaptations to training
Conclusions on polyphenols?
Enhance functional recovery:
Reduced oxidative damae
Reduced inflammation
Consume 1000mg.d^-1 for 3 days minimum prior to exercise
Optimal mix, dose and timing still not known
Why is there fatigue in repeated sprints?
Glycogen depletion (can help with carb loading, but glycogen depletion isn’t that important)
Phosphocreatine depletion (can creatine load)
Muscle acidosis (Can increase buffering capacity loading) - delaying the effect of acidosis (pH below 7, caused by the hydrogen ions associated with lactate)
Products of glycolysis that causes glycolysis, and what transporters are there to get rid of the it?
Produces Hydrogen ions
Monocarboylase enzymes can remove H+ and Lactate from the muscle
Sodium hydrogen transporter, can take hydrogen out and put sodium into the muscle
Sodium bicarbonate takes sodium out, and puts in bicarbonate (alkali) in
The bicarbonate binds with hydrogen forming carbonic acid which can dissociate into carbon dioxide and water, which is better for the body to cope with
So the alkali is neutralising the hydrogen ions
Effects of extracellular potassium on peak force?
As extracellular potassium increases, peak force decreases
Same as extracellular potassium increases resting membrane potential increases
When the membrane increases past -65mv there is a critical drop in the peak power that can be generated
Alkalosis may attenuate the increase in potassium
Arteries (what’s going to the muscle):
Hydrogen ions dropped
Lactate stayed the same
K+ ions decreased
Veins (what’s leaving the muscle):
Lower hydrogen ions
Higher lactate concentration (they exercised longer due to the supplement so lactate was allowed to increase further)
Lower potassium concentration
Exercised 25% longer
Features of sodium bicarbonate?
Extracellular anion
Biocarbonate loading results in increases in blood bicarbonate pools
Muscles become buffered
Helps in events in which a low pH is a limiting factor (banned in horse racing)
Acidosis following sprints (Bishop et al 2004)?
5 x 65 sprint
No difference in placebo compared to sodium bicarbonate in muscle H+ concentration
But post workout increased muscle lactate concentration in sodium bicarbonate compared to placebo (so you have worked longer, so more lactate but your hydrogen ions haven’t increased as they have been buffered)
Performance improved in sodium bicarbonate condition
Why is there a far larger increase in sodium bicarbonate supplementation improving performance in untrained compared to trained?
Trained already have adaptations that increase monocarboxylase transporters so already have an improved buffering capacity
This effect is less in longer duration, quite similar
Features of the intracellular buffer carnosine?
Dipeptide present in animal flesh
L-histidie (EAA)
Beta alanine (AA)
Buffers hydrogen ions, when you exercise there is an increase in lactic acid which dissociates into lactate and hydrogen ions, carnosine prevents this accumulation
Carnosine also acts as a antioxidant protecting against oxygen radicals
Glycation and carbonisation prevention - stop glucose and protein sticking
Carnitine is made in the body, but beta alanine is rate limiting in it’s production
15% of our muscle buffering ability comes from carnosine
More carnosine in type 2 muscles, this makes sense as explosive contractions are more likely to result in increased lactate concentration
Aging decreases carnosine
Males have more
If you eat more beta alanine, you will have more carnosine
Carnosine synthesis?
You can’t absorb it whole
You eat it and splits into L-histidie and beta alanine
Dietary carnosine is absorbed into hepatic portal veins and splits into its parts
Beta-alanine shares transport with taurine so need to make sure don’t have too much in which taurine uptake is decreased
Carnosine synthesase puts them back together
Supplementation does just with Beta alanine supplementation
Meta analysis looking at different times on carnosine effect?
Under 60 secs = no improvement
50-240 secs = biggest impact
Over 240 secs = some impact
Why is BA more important than sodium bicarbonate?
It is in the muscle, while sodium biacrobate is extracellular so its in the blood, so has to go into the muscle to work
So the beta alanine is in the muscle already so can buffer straight away
2 phases of muscle glycogen resynthesis?
During exercise muscle glycogen drops
During exercise GLUT4 is at membrane to take up glucose thanks to calcium and adrenaline
Once exercise stops consume CHO which means the pancreas releases insulin
GLUT4 to cell membrane which takes up more glucose, so there is a large amount of GLUT4 at the membrane at this point
So there is a rapid rise in glycogen resynthesis (first phase, which slows down after this initial rise (second phase)
How does glycogen synthesis actually occur and exercises influence?
Glycogen synthase goes to it’s active form when there is increase Insulin, Glucose, and Glucose-6-phosphate which makes Protein phosphatase which activates glycogen synthase
However exercise increases the amount of calcium ions, glucagon, and adrenaline which increases protein kinase A, which converts glycogen synthase into it’s inactive form
Bowtell 1999 showed what about glutamine?
Glutamine alone doesn’t really increase insulin
But greatest rise came from glutamine with glucose polymer
Glutamine alone provide the smallest muscle glycogen concentration
Glutamine and glucose polymer provided medium response
Glucose polymer alone provided largest muscle glycogen concentration
Glutamine + glucose also resulted in largest non oxidative CHO disposal, so wasn’t being used, but also wasn’t being stored in the muscle, but the liver
Caffeine mechanism on adenosine?
Adenosine normally binds to and adenosine receptor, and this makes you feel tired
Caffeine blocks this and binds to the receptor itself , pituarity gland sees this as an issue and increases adrenaline
Adrenaline stimulates hepatic glucose output, and promotes intestinal absorption
More glucose in blood
More glucose taken up by muscle
Greater muscle glycogen synthesis
Dosing for maximal glycogen resynthesis in muscle?
Small regular feeding better than few large doses
No difference if solid or liquid CHO
but liquid might help rehydrate, and easier to consume when appetite is reduce
You want glucose/sucrose as fructose increases it in the liver to be able to converted into glucose
Factors influencing hydration?
Gastric emptying - maximise
Depends on volume / energy content / osmolality / temperature / exercise / dehydration
Intestinal absorption - electrolyte content
Palatability - flavour / temp / electrolyte content
How can we favour hydration?
Fluid volume topped up (not too high) enhances gastric emptying
Energy content. not too high (6% CHO) - higher will slow gastric emptying
Same as above for osmolality
Temp - no effect on gastric emptying but tastes better
Dehydration - avoid below 2% weight loss - reduced splanchnic blood flow
Flavour - tasty - drink more
Electrolyte - tasty levels - maintains Na+ conc and thirst
Why would protein help recovery from eccentric training?
Following EE there is increased muscle protein synthesis, muscle damage and loss of contractile function
Protein increases muscle protein synthesis - inhibiting mTOR delays the recovery of muscle function
Protein shown to enhance recovery - but not through increasing muscle protein synthesis (Pavis et al., 2020) in the exam
Pavis et al 2020 showed?
Effect of protein with polyphenols after 300 eccentrics
Soreness reduced with protein, and function recovered quicker
Early on there are hue signalling changes driven by nutritional intervention - perhaps the real rational for protein being effective
Don’t forget polyphenols and antioxidant lecture and how they effect recovery
For adaptation do we want homeostasis?
For performance we want a nutritional intervention if we are going to be performing later that day, ie carbohydrate after an endurance bout to replenish glycogen stores
We want homeostasis to result in adaptation
Theory on exercising in the low glycogen state to disrupt homeostasis more to result in a larger adaptation
Pilegaard et al 2002 showed that there was more activation of PDK4 (means less PDC which means less glucose oxidation = harsher conditions) that result in adaptation in the low glycogen state compared to the normal following exercise, there was also more expression of UCP3 in low muscle glycogen indicating more mitochondrial expression
The low glycogen state was achieved by working out only 1 leg, and not providing CHO so glycogen not restored in that leg, but the other is fine as it didn’t do the workout
Same in LPL, so more efficient utilising lipids
Take home message is avoid carbs after training to drive larger adaptation as glycogen is not replenished
Different study looked also at PGC-1 which is believed to be main determinant on mitochondria biogenesis, and low carb diet enhances this
Skeletal muscle adaptation training twice every second day vs training once daily show about the low glycogen state?
In low state (Training twice every second day, so second session is in the glycogen depleted state) had higher muscle glycogen content by the end of the study, compared to training once every day (never in the glycogen depleted state and overall do the same amount of work)
Better muscle oxidative capacity seen as well, as well an improvement in exercise performance
But under tightly controlled laboratory conditions - not allowing for any alteration in training load dependent on nutritional status)
Best nutritionists working with runners, chose specific times of year (off season) to work in low carb state to get maximal adaptation
Practical approach to going low carb diet?
Chonric low CHO diet
Twice per day training
Train after overnight fast
Withhold CHO in early recovery
Sleep low/ train low
Issues:
Poor training quality
Immunosuppression
Muscle protein loss
Possible effects of creatine
Increased {PCr}
Increase capacity to perform high intensity contraction within a bout (anaerobic performance)
Increased rate of PCr resyntehsis
Increased capacity to perform multiple bouts of high intensity contractions
Increased training adaptations as result of training load
Glycogen resynthesis
Aerobic permanence?
H+ buffering
Improved diffusion of ATP through the muscle
Activation of glycolytic enzymes
Main way it works is that it allows you to do more reps
