Week 3 (1) - Carbohydrate and fat

Question 1

Diet and exercise: Historical perspective:

Answer 1

• Low blood glucose at the end of a marathon was associated with fatigue and an inability to concentrate (Levine et al 1924).
• A high-CHO diet (83% CHO) for 3 to 7 days enabled subjects to exercise for 210min, but a high-fat diet (94% fat) reduced performance to 88min (Christensen and Hansen 1939). Reduced performance ~50%

Question 2

Energy for muscular effort: exercise intensity:

Answer 2

• As exercise intensity increases, energy cost increases and the contribution from muscle glycogen increases (predominant fuel at high intensity = muscle glycogen)
• Increase in blood glucose as intensity increases
• Low intensity, more fat contribution
• 2 factors to maintain blood glucose – liver and exogenous sources contribute to maintaining blood glucose

Question 3

Exercise for muscular effort: exercise duration

Answer 3

• As duration increases, we reduce our ability to rely on blood glucose and muscle glycogen
• As duration increases we rely more on fat

Question 4

Sources of carbohydrate

Answer 4

• Monosaccharides (single molecules): glucose, fructose, galactose (milk)
• Disaccharides (2 monosaccharides together): sucrose, maltose, lactose
• Oligosaccharides (8-12 monosaccharides): maltodextrin (maltodextrin (has a high GI) and fructose are used in sports drinks)
• Polysaccharides (longer chains – 10-12): amylopectin (starch), amylose

Question 5

Glucose metabolism in the fasted state:

Answer 5

In the fasted state nothing comes in from the small intestine
Most stores come from the liver in the fasted sate (liver glycogen converted back to glucose)
In the fasted state glucose is the predominant fuel of the brain
Muscle: Although muscles use stored glycogen for energy, they can also absorb glucose from the bloodstream when available.
Adipocytes (Fat Cells): Adipocytes can release fatty acids for energy; however, glucose may still be used in limited amounts.

Question 6

Glucose metabolism in the fed state - CHO enters from the small intestine

Answer 6

1) Pancreas and Insulin:
After eating, the pancreas releases insulin in response to elevated blood glucose levels.
Insulin acts as a signal for tissues to take up glucose from the blood, into the liver, muscle and adipocytes. This also decreases production from glycogen to glucose in the liver.

2) Glucose Distribution:
Liver: Insulin promotes glucose uptake by the liver for glycogen storage and metabolic use.
Adipocytes (Fat Cells): Insulin encourages glucose storage as fat within adipocytes.
Muscle: Insulin facilitates glucose uptake by muscle cells for energy or glycogen storage.
Brain: The brain takes up glucose independently of insulin as it relies heavily on glucose for energy.

3) Small Intestine:
Absorbs glucose from digested food, which enters the bloodstream and raises blood glucose levels, prompting insulin release.

This system demonstrates how, in the fed state, insulin regulates blood glucose by promoting glucose uptake and storage in the liver, adipocytes, and muscle, ensuring efficient energy use and storage after meals.

Question 7

GLUT4 translocation

Answer 7

In the muscle insulin increases GLUT4 translocation – by moving the GLUT4 proteins to the surface of the muscle cell, we can uptake more from the blood into the muscle.

Question 8

Fats (Lipids):

Answer 8

• Fats, oils, phospholipids and sterols
• Occur naturally in wide variety of foods
• Animal adipose tissue
• Milk and milk products
• Seeds, nuts and oils (cashews and walnuts = 45-60% fat)
• Eggs, fish oils
• 95% dietary fat intake is from triacylglycerols (TAG)

Question 9

Triacylglycerol (TAG)

Answer 9

• 3 FA chains which is linked to a glycerol backbone by an ester link
• Want to break them down into FFAs so we can transport them from adipose sites into the blood and the into the muscle to be used for beta oxidation

Question 10

Classification of FAs

Answer 10

• Classification is based on 2 factors: Number of carbon atoms in the chain and the Number and position of double bonds in the chain
• Saturated (0 C=C) – Palmitic acid 16:0 – no double bonds (16 carbons / no double bonds)
• Monounsaturated (1 C=C) – Oleic acid (18: 1n-9) – (classified based on the location of the double bond- the first carbon with the double bond is position 9)
• Polyunsaturated (2+ C=C) – Linoleic acid (18:2n-6) – 2 or more double carbon bonds – naming based on the location of the 1st e.g., position 6)

*Omega 3 and omega 6 can’t be produced from triglycerides (need to be consumed in the diet)

Question 11

Fat metabolism (aim: need to get FAs into mitochondria to be used for b-oxidation)

Answer 11

• TG are stored in the adipose tissue – we use HSL to break FAs down into FFAs and glycerol. Using a fatty acid binding protein can take that into the blood where it binds with albumin and then transfers into the muscle fibre. Here it combines with CoA to formulate fatty acyl CoA. Fatty acyl CoA cannot transfer across into the mitochondrial membrane without carnitine.
• Need carnitine in the muscle to produce fatty acyl Carnitine which can go across the mitochondrial membrane. Then it transfers back to fatty acyl CoA ad is eventually taken into the Krebs cycle to produce ATP
• 2 factors that are important = insulin, epinephrine (adrenaline)
• Insulin inhibits the 1st process – exercise or CHO ingestion increases insulin which reduces the breakdown of triglycerides into FFA.
• Epinephrine increases the process – stimulates breakdown

Question 12

Carbohydrate stores (Values assume a body mass of 80kg and a 15% body fat%)

Answer 12

Plasma Glucose:
Mass: 0.02 kg
Energy: 328 KJ (78 kcal)

Liver Glycogen:
Mass: 0.1 kg
Energy: 1630 KJ (388 kcal)

Muscle Glycogen:
Mass: 0.4 kg
Energy: 6510 KJ (1550 kcal)

Total Carbohydrate (CHO) Stores:
Total Mass: 0.52 kg
Total Energy: 8400 KJ (2000 kcal)

The data indicates that muscle glycogen is the largest CHO store, contributing the majority of available energy, while plasma glucose is minimal, serving as a readily accessible but limited energy source.

Question 13

Fat stores:

Answer 13

Plasma Free Fatty Acids (FFA):
Mass: 0.0004 kg
Energy: 17 KJ (4 kcal)

Plasma Triglycerides (TAG):
Mass: 0.004 kg
Energy: 164 KJ (39 kcal)

Muscle Triglycerides (TAG):
Mass: 0.3 kg
Energy: 11,100 KJ (2616 kcal)

Adipose Tissue:
Mass: 12.0 kg
Energy: 420,000 KJ (100,000 kcal)

Total Fat Stores:
Total Mass: 12.3 kg
Total Energy: 447,300 KJ (106,500 kcal)

Adipose tissue is by far the largest fat store, containing the majority of the body’s fat-derived energy, making it a critical long-term energy reserve. Plasma FFA and TAG provide minimal, readily accessible energy, while muscle TAG offers an intermediate reserve.

Question 14

Diet, muscle and exercise performance:

Answer 14

• High fat diets may shift us towards fat oxidation
• Gave 3 different types of diet to 6 subjects
• Measured pre-exercise muscle glycogen content against exercise capacity
• After low CHO diet there was low muscle glycogen content and low exercise capacity at ~60-70% vo2 max
• Medium muscle glycogen – medium exercise capacity
• After high CHO diet muscle glycogen content was highest and exercise capacity was highest
• Linear relationship between muscle glycogen content and exercise capacity

Question 15

Low CHO training diets:

Answer 15

Low CHO diets result in a gradual decline in muscle glycogen content

Question 16

Carbohydrate Intake Targets by Training Load

Answer 16

Light Training Load:
Activities: Low-intensity or skill-based.
CHO Intake: 3-5 g/kg/day.

Moderate Training Load:
Activities: Moderate exercise, about 1 hour per day.
CHO Intake: 5-7 g/kg/day.

High Training Load:
Activities: Endurance programs, 1-3 hours per day of moderate-to-high intensity.
CHO Intake: 6-10 g/kg/day.

Very High Training Load:
Activities: Extreme commitment, 4-5 hours per day of moderate-to-high intensity.
CHO Intake: 8-12 g/kg/day.

Question 17

Typical marathon runner diet (Kenyan)

Answer 17

• 76.5% CHO (10.4 g/kg), 10.1% PRO, 13.4% Fat
• Fluid intake from water and sugary milky tea
• Typically eat lots of Ugali (very high carb)
• Very high CHO diets
• Estimated energy intake was less than estimated energy expenditure

Question 18

Short term ‘fat loading’

Answer 18

• 3 day high fat (65% fat; 9% CHO) or high carbohydrate (82% CHO; 9% fat) diet
• 70% vo2 max to fatigue in 10 and 30 degrees C
• Impaired performance with short term high fat diet (in 10 degrees the fatigue was substrate dependent- at 30 degrees other factors in place e.g., dehydration, effect of increased heat storage)
• Decreased muscle glycogen stores
• Short term high fat diet of 3 days impaired performance (only decreased muscle glycogen stores)

Question 19

Longer ‘fat loading’ (Goedecke et al 1999):

Answer 19

• Normal (30±8%) or high (69±1%) fat diet for 15 days
• By day 5 there was increased fat oxidation during exercise
• We need at least 5 days of fat ingestion to adjust effectively
• Increased fat oxidation during submaximal exercise
• Increased fat oxidation will lead to Decreased carbohydrate oxidation during submaximal exercise (less reliant on CHO, and have less CHO available as you don’t have the muscle/ liver glycogen stores) – same time process of 5 days
• No difference in performance in 40 km cycling time trial

Question 20

Dietary periodisation (Burke et al 2000):

Answer 20

• 5 days high fat diet decreased muscle glycogen
• 1 d high CHO restored muscle glycogen
• High fat diet decreased rate of muscle glycogen use
• When both groups returned to original baseline, the 5 day fat adaptation diet group were low in muscle glycogen. The high CHO were similar to baseline. After 1 day of refeeding they both super compensated
• Increased fat oxidation even with CHO loading – but can’t tell if this is because of increased FFA release, uptake or oxidation, or increased reliance on IMTG
• After post exercise the amount used in the 120mins was much greater in the high CHO group. After 5 days of adaption, the body almost ignored the increased muscle glycogen stores and continued to rely on the fat oxidation again
• No significant difference in time trial performance

Question 21

High fat diet and race performance (Havemann et al 2006):

Answer 21

• 100 km TT including 1 km and 4 km efforts periodically included (increase intensity at different aspects)
• Ingestion of CHO drink during exercise
• No difference in performance time – consistent results (during the prolonged effort)
• Reduced 1km performance (High intensity work) with high fat diet but high CHO diet maintained performance
• During high intensity exercise we need high CHO

Question 22

Low CHO, high fat diet – elite race walkers (Burke et al 2017):

Answer 22

For low carb high fat, oxygen cost was increased – inefficient (vo2 increased). In other groups (with CHO in diet) % of vo2 peak decreased (dipping int reserves less which is beneficial).
- In a 10km performance: high CHO and periodised performance increased but low CHO/high fat, performance did not improve
- In terms of elite race walkers, high CHO are needed and high fat diets have a negative performance effect.

Question 23

Oxygen cost of CHO and FAT

Answer 23

The oxygen cost of carbohydrate is about 5-5.5% more efficient than fat – need less oxygen to produce the same amount of energy- therefore the preferred substrate when working at HI.

Question 24

Why periodise CHO intake?

Answer 24

• Periodise allows for molecular adaptions – low CHO availability switches on a cascade of events which increases concentrations of PGC1-a and ultimately increases mitochondrial biogenesis (more and bigger mitochondria) – this creates a greater capacity for HI exercise
• Trade off – we need fuel to perform but if we can do something without the CHO we get molecular benefits

Question 25

Different methods to training at low carbohydrate availability:

Answer 25

1) Low carb diet
2) Training after an overnight fast
3) No carb during recovery
4) sleep low (training before sleep and not consuming CHO until the next morning)
5) long training without CHO intake
6) Training twice a day

Training with low CHO availability allows for molecular adaptions

Question 26

Low CHO knee extension study

Answer 26

looked at knee extensor exercise (1 leg had a rest day and 1 didn’t) - in low CHO group, time to exhaustion was increased to a greater extent than high CHO due to:
1) Increased Citrate synthase activity
2) Increased HAD activity
- Molecular adaptations aided training

Question 27

Training with low CHO availability:

Answer 27

• Potential to increase molecular adaptions
• Increase in AMPK and PCG1-α leading to increased mitochondrial biogenesis
• Reduced self-regulated training volume – pick the right session/ method (groups were doing less training, but receiving the same performance benefits)
• Decreased CHO in diet has been suggested to Increase risk of injury/ illness?

Question 28

Lecture summary:

Answer 28

• High carbohydrate diets are preretinal for high intensity activity
• High fat diets are unlikely to enhance performance but may benefit a very small group (e.g., ultra-endurance)
• High fat diets increase fat use during exercise and spare muscle glycogen
• Low carbohydrate availability can increase molecular adaptions but may compromise training intensity
• Athletes are likely to benefit from fuelling with carbohydrate to meet the demands of the exercise