Metabolic training adaptations

1
Metabolic training adaptations
2
Adaptations to Endurance Training
3
Endurance training

• Endurance training results in a number of
  adaptations that lead to improved endurance
  performance
• Adaptations include
• Higher maximal oxygen uptake
• Increased fat metabolism
• Lower blood and muscle lactate concentrations at
  given submaximal work load
• Improved glycogen preservation

4
Endurance training - effects on intramuscular
fuel stores

• Endurance training increases muscle
  triacylglycerol and glycogen stores
• Mechanism for triacylglycerol increase not known
• Muscle glycogen content can increase by 2.5 times
• Increased GLUT 4 transporter protein content
• Increased glycogen synthase activity

5
Endurance training - effects on extramuscular
fuel stores

• Endurance training increases
• Gluconeogenic capacity of liver and kidney
• Fatty acid availability for oxidation, due to
  increased
• lipoprotein lipase activity
• Increased uptake of fatty acids by skeletal
  muscle
• Acyl CoA synthetase activity
• Increases activation of fatty acids for transport
  into mitochondria
• Carnitine transporter activity

6
Endurance training - effects on cytosolic enzymes

• Most studies report no change or slight decrease
  in activity of glycolytic enzymes
• Only adaptations of note are
• Increase in Hexokinase
• Occurs after single bout of exercise
• decrease in total LDH activity
• Increase in LDH-H (low Km for lactate)
• Decrease in LDH-M (low Km for pyruvate)
• Overall effect is decreased reduction of pyruvate
  to lactate when pyruvate and NADH elevated in
  cytosol

From Summerlin LR (1981) Chemistry for the Life
Sciences. New York Random House p 543.
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Endurance training - effects on cytosolic enzymes

• NADH formed in cytosol during glycolysis
  transported into mitochondria via
• glycerol-phosphate shuttle
• Not affected by endurance training
• Predominant in fast-twitch fibres
• Malate-aspartate shuttle
• Increased as result of endurance training
• Predominant in slow-twitch fibres
• Increased activity of MA shuttle facilitates
• Increased yield of ATP per glycolytic NADH
• More rapid removal of NADH from cytosol
• Reduces lactate production

8
Endurance training - effects on cytosolic enzymes

• Alanine aminotransferase (formerly alanine
  transaminase) activity is increased with
  endurance training
• AAT transaminates pyruvate to alanine
• Would increase competition with LDH for pyruvate
• Would reduce availability of pyruvate for LDH
  reaction
• Reduced lactate production

9
Endurance training - effects on cytosolic enzymes

• Pyruvate dehydrogenase activity increased through
  endurance training
• Increases competition with LDH for pyruvate
• Reduced lactate production

10
Endurance training - effects on mitochondrial
enzymes

• Endurance training induces an increase in both
  the size and number of mitochondria
• Occurs in both slow-twitch and fast-twitch fibres
• Enhances oxidative capacity due to increases in
  enzymes of
• ?-oxidation
• Krebs cycle
• Electron transport chain

From Keissling et al. (1971) Effect of physical
training on ultrastructural features in human
skeletal muscle. In Muscle metabolism during
exercise (ed. B Pernow and B Saltin). New
YorkPlenum Press Pp.97-101.
11
Endurance training - effects on mitochondrial
enzymes

• Mitochondrial bound creatine kinase (MBCK)
  activity increased through training
• Facilitates rephosphorylation of creatine to PCr
  in mitochondria
• PCr then used to rephosphorylate ATP at
  contraction site via creatine phosphate shuttle
• Increased MBCK activity facilitates
• more rapid removal of ADP from cytosol
• Improved maintenance of cytosolic ATP
• Both would lead to reduced PFK activity
• Reduced lactate production?

From Bessman Geiger (1981) Transport of
energy in muacle The phosphorylcreatine shuttle.
Science 211448-452
12
Endurance training -myoglobin

• Animal studies have shown that endurance training
  can increase myoglobin by up to 80
• Would facilitate low PO2 in sarcoplasm
• Increased gradient for O2 diffusion from
  capillary
• No evidence of increase in myoglobin in humans
• May be a small decrease

13
Endurance training -maximal oxygen uptake

• Maximal oxygen uptake (VO2max) increases as a
  result of endurance training

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Endurance training -maximal oxygen uptake

• Excess glycolytic capacity in untrained
• Generates pyruvate and NADH in cytosol in excess
  of capacity for mitochondrial processing
• Capacity to deal with excess glycolytic capacity
  enhanced through training
• Leads to increased acetyl CoA production and NADH
  formation from glycolysis during maximal exercise
• Results from training induces increases in
• PDH - increases formation of acetyl CoA from
  pyruvate
• MA shuttle - increases transport of NADH into
  mitochondria

From Summerlin LR (1981) Chemistry for the Life
Sciences. New York Random House p 543.
15
Endurance training -maximal oxygen uptake

• Endurance training increases production of acetyl
  CoA and NADH from fatty acids due to increased
  activities of
• Lipoprotein lipase - hydrolysis of
  triacylglycerols
• Acyl CoA synthetase - activates fatty acids
• Carnitine transporter - transports fatty acyl CoA
  into mitochondria
• Enxymes of ?-oxidation

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Endurance training -maximal oxygen uptake

• Enzymes of Krebs Cycle increase through training
• Increased capacity to deal with extra acetyl CoA
  produced from glycolysis and ?-oxidation
• Leads to increased formation of NADH

17
Endurance training -maximal oxygen uptake

• Enzymes of Electron Transport Chain increase
  through training
• Increased capacity to deal with extra NADH (and
  FADH2) produced from glycolysis, ?-oxidation and
  Krebs Cycle
• Facilitates increased utilisation of O2 as final
  electron acceptor
• VO2max increases

18
Endurance training -reduced blood and muscle
lactate

• Blood and muscle lactate concentrations reduced
  at given submaximal absolute or relative exercise
  intensity
• May be due to
• Decreased lactate production
• Increased lactate clearance
• Blood and muscle lactate often increased at
  maximal exercise
• Improved buffer capacity?

19
Endurance training - decreased lactate production

• Long believed that lactate production during
  exercise reflected muscle hypoxia
• Therefore, lower blood lactate following training
  due to cardiovascular adaptations which increase
  oxygen delivery and reduce hypoxia
• Blood lactate lower following training despite no
  change (or small decrease) in VO2
• Therefore, reduced blood lactate not due to
  reduction in hypoxia
• Muscle not hypoxic during exercise

20
Endurance training - decreased lactate production

• VO2 not changed at given workload after training
  but mitochondrial content increased
• Rate of electron transport and VO2 per
  mitochondria must be less
• Respiratory stimulus per mitochondrion must be
  less
• Results from tighter control over cytoplasmic
  phosphorylation potential ATP / ADP x Pi
• MBCK increase facilitates translocation of ADP
  and ATP
• Reduces stimulation of GPHOS and PFK and reduces
  potential for lactate production

21
Endurance training - decreased lactate production

• Increased activity of MA shuttle would facilitate
  removal of NADH from cytosol
• Less NADH available for LDH
• Increased alanine aminotransferase would compete
  with LDH for pyruvate
• Increased LDH-H would reduce formation of lactate
  from pyruvate
• Combined effect of these changes
• Less pyruvate and NADH available in cytosol for
  LDH which has less affinity for pyruvate
• Less lactate production

22
Endurance training - decreased lactate production

• Most important adaptation to endurance training
  which reduces lactate production is increased
  fatty acid oxidation
• Leads to inhibition of glycolysis via
  glucose-fatty acid cycle during submaximal
  exercise

23
Endurance training - increased lactate clearance

• No evidence of increased lactate clearance by
  trained skeletal muscle
• Some evidence of
• increased gluconeogenesis from lactate in liver
  and kidneys
• Increased lactate utilisation by heart

From Buckley et al (2001) No difference in net
uptake or disposal of lactate by trained and
untrained forearms during incremental lactate
infusion. European Journal of Applied
Physiology. 85(5)412-419, 2001
24
Endurance training - hormonal adaptations

• Secretion of most hormones reduced at given
  submaximal exercise intensity after training,
  leads to reduced fuel mobilisation
• Adrenaline - stimulates glycolysis, lipolysis
• ACTH - stimulates cortisol secretion by adrenal
  cortex
• Cortisol - stimulates gluconeogenesis, lipolysis
• glucagon - increases glycogenolysis and
  gluconeogenesis
• HgH - increases lipolysis and glycogenolysis
• Insulin secretion increased - inhibits lipolysis,
  glycogenolysis, gluconeogenesis
• Reduced mobilisation of fuels, but muscle better
  able to extract fuel molecules (particularly fat)
  that are available
• More efficient control of metabolism

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Time course of endurance training adaptations

• Peak adaptations in mitochondrial content occur
  with shorter duration-higher intensity exercise
• eg interval training
• Prolonged training sessions result in lesser
  adaptation in muscle oxidative capacity, but
  adaptation in
• Cardiovascular function
• Blood volume
• Fluid balance (sweating etc)

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Time course of endurance training adaptations

• Time course of alterations in substrate
  utilisation parallel increases in mitochondrial
  enzyme activity
• Initial 5-7 day change in substrate utilisation
  more closely follows reduced sympathetic hormone
  response
• 50 of increased mitochondrial content can be
  lost within 1 month of detraining

From Maughan R., Gleeson M, Greenhaff P (1997)
Biocehmistry of Exercise and Training. Oxford
Oxford University Press pp.195
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Mechanisms of muscular adaptation

• Expression of proteins (including enzymes)
  regulated by genes
• Most genes switched on and off by actions of
  signal molecules such as hormones and/or growth
  factors
• Muscular training adaptations specific to muscle
  fibres recruited
• Signal(s) for adaptations in enzymes in response
  to endurance training believed to be
• Increased cAMP
• Rate of metabolic flux
• Possibly related to free radicals?

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Adaptations to Anaerobic Training
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Anaerobic training

• Anaerobic training (i.e. training for strength,
  power, speed)
• increases anaerobic capacity
• Phosphagens
• Glycolysis
• but has little effect on
• Oxidative capacity
• Cardiovascular adaptation

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Effects on fuel availability

• Anaerobic training increases resting
  intramuscular concentrations of
• ATP
• PCr
• Glycogen

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Effects on glycolytic capacity

• Anaerobic training increases glycolytic capacity
  via increases in
• PFK activity
• LDH activity
• Relative aerobic capacity of muscle fibres
  reduced due to mitochondrial dilution

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Effects on buffer capacity

• Higher muscle and blood lactate concentrations
  can be achieved during maximal exercise following
  anaerobic training
• Increased buffer capacity
• Due to greater growth of fast-twitch relative to
  slow-twitch muscle fibres
• Increase in lactate transporters
• Number and activity of lactate transporters in
  sarcolemma increased

From Brinkworth, GD, JD Buckley, PC Bourdon, JP
Gulbin and AZ David. (2002) Oral bovine colostrum
supplementation enhances buffer capacity but not
rowing performance in elite female rowers.
International Journal of Sports Nutrition, In
press
33
Effects on hypertrophy

• Anaerobic training can lead to muscle hypertrophy
• Passive stretch can also induce hypertrophy
• Hypertrophy result of increase in contractile
  protein content
• Actin and myosin added to periphery of fibre
• Some evidence of hyperplasia

From Kreider, RB (2000) High intensity training
1 set vs 3 sets. Muscular Development Sports
Fitness Magazine 37(8) 104-121
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Mechanisms of muscular adaptation

• Expression of proteins (including enzymes)
  regulated by genes
• Most genes switched on and off by actions of
  signal molecules such as hormones and/or growth
  factors
• Muscular training adaptations specific to muscle
  fibres recruited
• Muscle genes regulated largely by mechanical and
  or metabolic stimuli
• Transduction of mechanical forces to nuclei may
  occur
• directly - via cytoskeleton
• Indirectly - via stretch activated ion channels
  in membrane
• Exercise induced muscle damage causes
• release of autocrine growth factors
• Loss of contact inhibition between satellite
  cells and muscle fibres (leads to fusion and
  hypertrophy)