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
