Peripheral Fatigue - Submax Exercise

Question 1

Define submaximal exercise

Answer 1

• Duration30-180 minutes, below Vo2max
• Exercise intensity 60-80% Vo2max
• Rate of ATP resynthesis relatively slow; involves an interaction between PCr, CHO and fats oxidation

Question 2

Rate of fat oxidation and exercise performance - Van Loon et al (2001)

Answer 2

• Increased exercise intensity = decreased rate of fat oxidation
• Contribution of fats at moderate intensity exercise is 50% (60% Vo2max)
• With increased exercise intensity, CHO oxidation increased

Question 3

Why is fat oxidation limited at high intensity?

Answer 3

• IMTG stores increase with increased exercise intensity

- Therefore, no problem with the delivery of fat stores, has to be a problem with the oxidation

Question 4

Increased Glycolytic Flux limits fat oxidation rate - Coyle et al (1997)

Answer 4

High glucose vs fasted group

• Ability to utilise long-chain fatty acids impaired
• Long-chain FA are transported through the mitochondria by CPT1, medium chain aren’t
• Increased glycolytic flux inhibits CPT1

Question 5

What is CPT1 role during fat oxidation?

Answer 5

• CPT1 takes Acyle group and bonds with carnitine to form Acyle carnitine
• Acyle carnitine transports into the mitochondria
• This process is inhibited by Glycolytic Flux

Question 6

Free carnitine availability - Van Loon et al (2001)

Answer 6

• Free carnitine availability becomes limiting to CPT1 during high intensity exercise due to increased Acetyl Carnitine
• Increased Acetyl Carnitine due to increased Glycolytic Flux

Question 7

Why does Acetyl Carnitine increase during high intensity exercise?

Answer 7

• There becomes too much Acetyl CoA
• Free carnitine buffers Acetyl groups to allows CoA to be used for other processes
• Free carotene is used to buffer Acetyl groups to form Acetyl Carnitine, therefore free carnitine isn’t available for fat oxidation

Question 8

Carnitine - Wall et al (2011)

Answer 8

• 24 week feeding of muscle carnitine
• Increased carnitine didn’t increase fat oxidation
• Free carnitne was used to further buffer Acetyl CoA and improve efficiency of Glycolytic Flux
• Carnitine increase performance by 11%

Question 9

O2 deficit - Karlson and Saltin (1970)

Answer 9

• Increase in ATP demand at exercise onset, not initially met by O2 therefore creating O2 deficit
• During O2 deficit; decease in PCr and increase in lactate

Question 10

Armstong and Laughlin (1983)

Answer 10

• Increased the blood flow to the muscle
• Still saw O2 debt
• Meaning the O2 debt isn’t due to decrease oxygen supply to muscle, suggested to be delayed activation on PDC

Question 11

Campbell and O’Sullivan (2001)

Answer 11

• Prior exercise activates PDC
• Activating PDC buffers Acetyl CoA - accumulating Acetyl Carnitine
• This reduces O2 debt - therefore less PCr degradation and lactate accumulation at the start of exercise

Question 12

Does high fat diet improve performance? Burke et al (2017)

Answer 12

3 weeks of intense training - competitive 10km walking race before and after

• 3 groups:
  High CHO diet throughout the day
  High CHO diet at strategic points in the day
  High fat diet
• High fat diet significantly increased fat oxidation
• Hight fat diet did not increased performance - fat oxidation not limiting in performance

Question 13

Muscle glycogen determinant of fatigue - Bergstrom et al (1967)

Answer 13

• 70% Vo2max until exhaustion
• At fatigue glycogen is very low - glycogen depletion coincides with fatigue

Depleting glycogen following by a high CHO diet

• Methods for further elevating muscle glycogen
• Prolonges TTE