Bioenergetics (Lec 7) Flashcards
Energy Supply at Rest
- 2/3 from fats
- 1/3 from carbohydrates
- VO2 = 0.3L/min
- Blood lactate ~1mmol/L
Determining Exercise Intensity
- Peak power (6s sprint)
- Anaerobic Capacity (30s wingate)
- % VO2 max
- Blood lactate concentration
- % Critical Power
Steady State
Characterised by a stable VO2
• It takes at least 2-3mins for O2 consumption to stabilize to new, higher level exercise demands
Limitations during Aerobic Exercise
Performance is limited by oxygen delivery and utilization
• VO2 = SV x a-vO2
Blood Lactate
Marker of Glycolytic energy production
• Allows Glycolysis to continue
Critical Power
CP is the power-asymptote
– i.e power that can be maintained ‘indefinitely’.
CP and W’
• The W’, (pronounced w prime) represents a finite work capacity (J) available to the athlete once he or she attempts a power output above CP
– Is the curvature constant
Above CP
Steady state is unable to be attained
– [PCr] decreases
– VO2 increases
– Muscle pH decreases
Carbohydrates
- Primary fuel source for short duration, incremental or high intensity exercise
- During prolonged work (>30 min) there is a gradual shift from carbohydrate metabolism towards an increasing reliance on fat as a fuel substrate.
Blood Glucose Homeostasis During Exercise: 4 Processes
- Mobilisation of glucose from liver glycogen
- Mobilisation of FFA (free fatty acids) from adipose tissue (Spares blood glucose)
- Gluconeogenesis from amino acids, lactic acid, and glycerol
- Blocking the entry of glucose into cells
Blood Glucose Homeostasis During Exercise: Hormonal
Fast-acting
• Insulin, glucagon epinephrine, norepinephrine,
Slow-acting
• Cortisol, growth hormone
Insulin and Glucose
Insulin increases cellular uptake of glucose
• Declines during exercise of increasing intensity and duration
Glucagon increases blood glucose
• Increased mobilisation of liver glycogen
• Increased liver glucose output
• Increased sensitivity of the liver to epinephrine
Fat Metabolism
- First fat (triglyceride) must be broken down via lipase into FFA
- Then metabolised via β-Oxidation into 2 carbon chains and oxidised in the krebs cycle
Regulation of Lipolysis
- Epinephrine, Norepinephrine and glucagon increase lipase activity promoting lipolysis
- During prolonged exercise insulin levels decline and epinephrine increases promoting higher level of fat metabolism
Inhibition of Lipolysis
Mobilisation of FFA is inhibited by
– Insulin: Inhibits lipase activity, Decline in insulin during longer duration exercise results in increased FFA and glycogen sparing
– Lactate: High levels promote recombination of FFA and glycerol to form fats thereby decreasing the available FFA as fuel