Metabolic Response to Exercise

1
Metabolic Response to Exercise

• Foss ch. 3
• Brooks - Exercise Phys. Ch. 10
• selected sections - Brooks Ch. 5-7
• Outline
• Fuel utilization - crossover concept
• Recovery
• Glycogen re-synthesis
• lactate
• performance
• Lactate shuttles
• Endurance Training effects
• lactate, Glycolysis, mitochondria
• Anaerobic Threshold??

2
Measurement of Metabolic Response

• Evaluation provides info about absolute and
  relative intensity of exercise bout (fig 10.1a)
• absolute VO2 (L/min or ml/Kg/min)
• of VO2 max
• of HR max
• multiples of Metabolic Rate (METs)
• 1kcal/Kg/hour at rest
• determination of metabolic response allows
  estimation of
• Total energy cost
• Nutritional requirements
• Efficiency calculations
• Estimation of workload indicates metabolic system
  utilization, and the potential for fatigue

3
Substrate Utilization

• Brooks p 133
• Power output is the most important factor
  determining fuel utilization
• Crossover concept
• post absorptive and resting
• lipid used predominantly
• with increasing intensity
• fuel mix switches from lipid to CHO
• Fig 7-12
• training - displaces absolute intensity at which
  crossover occurs
• epinephrine suppression
• inc lactate clearance
• inc mitochondria
• prolong onset of glycogen breakdown, depletion
  and fatigue

4
Fuel Utilization

• Fig 7-11
• Glucose - fatty acid cycle
• FFA breakdown inhibits glycolysis
• PDH is inhibited by Acetyl-CoA from Beta
  oxidation
• PFK is inhibited by inc citrate from Beta
  oxidation and ATP
• in highly trained and glycogen depleted this is
  accentuated
• Fig 7-10 - higher FFA utilization with higher
  mitochondrial enzyme activity following training
• Hexokinase is inhibited by its product G6P, which
  builds up if glycolysis is not active.

5
Recovery from Exercise

• Ch. 3 - Foss
• process of recovery from exercise involves
  transition from catabolic to anabolic state
• breakdown of glycogen and fats to replenishment
  of stores
• breakdown of protein to protein synthesis for
  muscle growth and repair
• Our discussion of recovery will include
• oxygen consumption post exercise
• Replenishment of energy stores
• Lactate metabolism(energy or glycogen)
• Replenishment of oxygen stores
• intensity and activity specific recovery
• guidelines for recovery

6
Recovery Oxygen

• Recovery O2 - Net amount of oxygen consumed
  during recovery from exercise
• excess above rest in Litres of O2
• Fast and Slow components
• Based on slope of O2 curve
• first 2-3 min of recovery - O2 consumption
  declines fast
• then declines slowly to resting
• Fig 3.1
• Fast Component - first 2-3 minutes
• restore myoglobin and blood oxygen
• energy cost of elevated ventilation
• energy cost of elevate heart activity
• replenishment of phosphagen
• volume of O2 for fast component area under
  curve
• related to intensity not duration

7
Recovery Oxygen

• Slow Component
• elevated body temperature
• Q10 effect - inc metabolic activity
• cost of ventilation and heart activity
• ion redistribution Na/K pump
• glycogen re-synthesis
• effect of catecholamines and thyroid hormone
• oxidation of lactate serves as fuel for many of
  these processes
• duration and intensity do not modify slow
  component until threshold of combined duration
  and intensity
• After 20 min and 80
• We observe a 5 fold increase in the volume of the
  slow component

8
Energy Stores

• Both phosphagens (ATP, CP) and glycogen are
  depleted with exercise
• ATP/CP - recover in fast component
• measured by sterile biopsy, MRS
• rate of PC recovery indicative of net oxidative
  ATP synthesis (VO2)
• study of ATP production
• 20-25 mmol/L/min glycogen and all fuels
• during exercise
• CP can drop to 20, ATP to 70
• CP lowest at fatigue, rises immediately with
  recovery
• Fig 3.2 - very rapid recovery of CP
• 30 sec 70, 3-5 min 100 recovery

9
Phosphagen Recovery(cont.)

• Fig 3.3
• occlusion of blood flow - no phosphogen recovery
• requires aerobic metabolism
• estimate 1.5 L of oxygen for ATP-PC recovery
• Energetics of Recovery
• Fig 3.4
• breakdown carbs, fats some lactate
• produce ATP which reforms CP
• high degree of correlation between phosphagen
  depletion and volume of fast component oxygen
• Fig. 3.5
• Strong correlation between phosphagen depletion
  and volume of the fast component of recovery
  oxygen - sea level and altitude
• anaerobic power in an athlete related to
  phosphagen potential - Wingate test

10
Glycogen Re-synthesis

• Requires 1-2 days and depends on
• type of exercise and amount of dietary
  carbohydrates consumed
• Two types of exercise investigated
• continuous endurance (low intensity)
• intermittent exhaustive (high intensity)
• Continuous - (low- moderate intensity)
• Fig 3.6 - diet effect
• minor recovery in 1-2 hours, does not continue
  with fasting
• complete re-synthesis requires high carbohydrate
  diet 2 days
• Recovery does not occur without high carbohydrate
  diet
• depletion of glycogen related to fatigue
• Fig 3.7 - heavy training

11
Glycogen Re-synthesis

• Intermittent (high intensity) exercise
• Fig 3.8
• significant re-synthesis in 30 min-2 hrs
• does not require food intake
• complete re-synthesis does not require high
  carbohydrate intake
• only 24 hrs for 100 recovery
• rapid recovery in first few hours
• Continuous vs. intermittent
• amount of glycogen depleted
• Much higher with long duration
• precursor availability
• lactate, pyruvate and glucose available after
  high intensity exercise
• Muscle fiber type involved in activity
• re-synthesis is faster in type II fibers which
  are utilized with higher intensity activity

12
Lactate Recovery

• Blood lactate levels are fairly constant with
  rising intensity until a threshold of intensity
  is reached(10.1b)
• After threshold, you observe a sharp rise in
  lactate along with intensity
• Lactate is influenced by the duration of
  exercise and rest interval between repeated bouts
  
• Fig 10-2 - lactate turnover
• fig 3.10 - exhaustive exercise
• 25 min for 1/2 recovery (passive)
• passive recovery - minimal activity
• Fig 3-11 active vs passive recovery
• Fig 3-12 intensity of active recovery
• untrained 30- 45 VO2 Max
• trained up to 50-60 - in some studies
• glycogen re-synthesis is slowed with higher
  intensity active recovery

13
Recovery

• fig. 3.13(fate of lactate)
• Fig 3.14 (lactate vs slow component)
• close association between the slow component of
  O2 recovery and the removal of lactate - but not
  exact
• restoration of O2 stores
• fast component - 10-80 seconds
• Ion concentrations
• pH - rapid return after light exercise
• heavy exercise dec. From 7-6.4
• 20 min for recovery
• close correlation to lactate and fatigue
• Recovery of Maximum Voluntary Contraction
  correlates with Pi (both factors are restored in
  5 min)

14
Performance Recovery

• How quickly do we regain performance? - force,
  power, MVC
• Guidelines Table 3.2
• Dependant on
• energy system utilized
• Intensity of exercise and type of recovery
• Aerobic fitness (VO2 max) is an important
  influence as well
• good correlation between fast recovery of muscle
  function and VO2 max
• why?
• Fast component requires O2

15
Lactate Shuttles

• Intracellular lactate shuttle (Brooks p 69)
• Within one cell
• evidence of LDH in mitochondria of muscle, liver
  and other cells
• evidence that mito in liver and heart oxidize
  lactate more than pyruvate
• lactate- more than pyruvate - is link between
  glycolytic and oxidative met
• Fig 5-13, 14 (Brooks)
• rapid glycolysis -creates a rise in cytosolic
  lactate
• lactate enters mitochondria via MCT
  pyruvate/lactate carrier (Brooks p79)
• oxidized to pyruvate in mito
• continues through TCA (Krebs)
• NADH formed inside mitochondria, as well as
  recycled in cytosol

16
Intercellular Lactate Shuttle

• Between different cells (Brooks p 78)
• Lactate actively oxidized - preferred fuel in
  heart and slow twitch muscle
• produced in Type IIb fibers
• transported directly between cells in same muscle
• or through blood circulation to type I fibers or
  heart muscle cells
• Fig 5-20 (Brooks)

17
Muscle as Consumer of Lactate

• P 202 - 209 (Brooks)
• Similar to discussions in Foss
• EPOC - Excess post-exercise oxygen consumption-
  instead of Recovery Oxygen
• Causes for excess oxygen used in recovery
• 13 increase in BMR / degree Celsius
• similar to Q10 effect
• Fig 10-11 - uncoupling of mitochondria - inc ATP
  needs
• Calcium- accumulates with contraction -
  mitochondria may sequester Ca- ATP required to
  remove it, which may alter net oxidative
  phosphorylation

18
Endurance Training

• Table 6-1, 6-2
• With endurance training, we observe
• a doubling of enzyme activity
• TCA and ETC - in all muscle fiber types
• a doubling of mitochondrial content
• Table 6-3
• improvements in oxidative capacity correlate well
  with running endurance
• 90 percent correlation
• Correlation between oxidative capacity and VO2
  max is not as strong
• 70 percent correlation
• 10- 15 increase in VO2 max with training vs.
  100 for oxidative capacity
• With an increased mitochondrial content
• The given rate of O2 consumption can occur at a
  much higher ATP/ADP ratio
• Fig 6-13
• This reduces carbohydrate breakdown in favor of
  lipid metabolism

19
Anaerobic Threshold??

• Brooks p 215
• Historically, the non linear rise in blood
  lactate at 60 VO2 Max was termed the anaerobic
  threshold
• does not however provide info about anaerobic
  metabolism
• reflects balance between lactate entry and
  removal from blood (turnover)
• Lactate inflection point is now the preferred
  term
• Inflection often corresponds to ventilatory
  threshold
• (non linear rise in ventilation) (talk test)
• However Fig 10-17
• Patients with McArdles syndrome
• lack of phospohorylase - unable to breakdown
  glycogen
• Have normal ventilatory threshold
• Association, therefore, is not causal

20
Lactate Inflection Point

• Many factors may influence either the production
  or removal of lactate
• Type II b fiber recruitment - increases with
  intensity - results in higher lactate production
• Sympathetic NS activity increases with intensity
  of exercise
• vasoconstriction (many tissues)
• Leads to reduced oxidation of circulating lactate
  - ie. less removal
• local factors (paracrines) in muscle
• Stimulate vasodilation
• raising of Cardiac Output to muscle
• Epinephrine and glucagon
• stimulate glycogenolysis and glycolysis
• higher lactate production
• increased Calcium with contraction - activates
  glycogenolysis - (Fig 10-18)

21
Learning Objectives

• Understanding of metabolic influences in glucose
  fatty acid cycle
• Distinction between fast and slow components of
  recovery oxygen
• What contributes to the volume of each component
• Pathways for recovery of energy stores -
• Phosphagens, glycogen
• Recovery of resting lactate concentrations
• Active vs passive recovery
• Performance recovery
• Force, power, MVC
• Lactate shuttles
• Oxidative use of lactate - intra vs inter
  cellular
• Training impacts on fuel use and recovery
• Influences on lactate inflection point