The Physiology of Training: Effects of aerobic and anaerobic training (part 2) Flashcards
Endurance training results in numerous adaptations in muscle fibres that assist in maintaining homeostasis, what are these?
- Shift in muscle fibre type (fast-to-slow) and increased number of capillaries.
- Increased mitochondrial volume.
- Training-induced changes in fuel utilization.
- Increased antioxidant capacity.
- Improved acid-base regulation.
Endurance training promotes a shift of fibre types in which direction?
fast-to-slow shift + increased capillarisation
What is the magnitude in muscle fibre type change determined by?
Duration of training, type of training, and genetics.
There is an increased number of capillaries surrounding muscle fibres as a result of endurance training. What does this cause?
*Enhanced diffusion of oxygen.
* Improved removal of wastes.
What is the significance of increased mitochondrial volume and turnover in skeletal muscle?
- Increased mitochondrial volume = greater capacity for oxidative phosphorylation
- Decreased cytosolic [ADP] due to increased ADP transporters in mitochondrial memb.
What does more ADP transporters in mitochondrial membrane result in?
- Less lactate and H+ formation.
- Less PC depletion.
What is the influence of mitochondrial volume on cytosolic ADP concentration during submaximal exercise?
- Increases in the number of ADP transporters in mitochondrial membrane
= faster ADP uptake into mitochondria and lower cytosolic [ADP] - Endurance exercise training-reduces the O2 deficit at the onset of work
Faster rise in O2 uptake = less lactate formation, less PC depletion
What changes in fuel utilization does endurance training cause?
- Increased utilization of fat and sparing of plasma glucose and muscle glycogen.
- Plasma glucose vital fuel source for CNS
- Intramuscular fat provides ~50% of lipid oxidized during exercise, plasma FFA provides the remainder.
Endurance training adaptations improve plasma FFA transport and oxidation, how?
- Increased transport of FFA into the muscle (from plasma)
- Transport of FFA from cytoplasm to mitochondria
- Mitochondria oxidation of FFA
Contracting skeletal muscles produce free radicals. What do these do?
- Radicals chemical species/molecule that contain unpaired electron, making them highly reactive and can damage proteins, membrane and DNA.
- Radicals promote oxidative damage and muscle fatigue
Endurance Training Improves the Antioxidant Capacity of Muscle
How does Endurance Training Improve the Antioxidant Capacity of Muscle?
Training increases endogenous antioxidant enzymes.
- Improves the fibres ability to remove radicals.
- Protects against exercise-induced oxidative damage and muscle fatigue
How does endurance training improve acid-base balance during exercise?
Training adaptations.
- Increased mitochondrial number. (Less carbohydrate utilization = less pyruvate formed.)
- Increased NADH shuttles (via ETC)
(Less NADH available for lactic acid formation.)
- Change in LDH isoform.
(M4 → M3H → M2H2 → MH3 → H4)
(Heart form (H4) has lower affinity for pyruvate = less lactic acid formation.)
What is the relationship between endurance/resistance training and protein synthesis?
Endurance and resistance exercise training promotes protein synthesis in fibres.
- Exercise “stress” activates gene transcription
What is the process of training-induced muscle adaptation?
- Muscle contraction activates primary and secondary messengers.
- Results in expression of genes and synthesis of new proteins.
- mRNA levels typically peak in 4 to 8 hours, back to baseline within 24 hours.
- Daily exercise required for training-induced adaptation.
Primary and Secondary Signalling Pathways Interact to Promote Exercise-Induced Adaptations. Name 4 primary signals.
- Mechanical stretch (resistance training).
- Calcium (endurance training).
- AMP / ATP (endurance training).
- Free radicals (endurance training)
Primary and Secondary Signalling Pathways Interact to Promote Exercise-Induced Adaptations. Name 7 secondary signals.
AMP kinase (AMPK).
Mitogen-activated kinase (p38).
PGC-1α.
Calmodulin-dependent kinases (CaMK).
Calcineurin (phosphatase).
Nuclear factor kappa B (NFκB).
mTOR (key in resistance training adaptation)
(detail of each of lecture slides)
What are training-induced reductions in HR and ventilation due to?
- Training results in improved muscle homeostasis during exercise and reduced “feedback” from muscle chemoreceptors to CV control center.
- Less feedback to CV control center from group 3 and group 4 nerve fibers (responsive to temperature and
biochemical changes). - Reduced number of motor units recruited.
What physiological effects does detraining have?
- Rapid decrease in VO2max.
↓ SV max (loss of plasma volume)
↓ Maximal a-v O2 difference (decrease mitochondria, oxidative muscle capacity, type 2a fibres) - Initial decrease in VO2 max due to ↓ SV max.
- Later decrease due to ↓ a-v O2 max.
What are detraining and submax performance primarily due to?
changes in mitochondria
- Muscle mitochondria adapt quickly to training.
- Mitochondrial adaptations lost quickly with detraining.
Requires 3 to 4 weeks of retraining to regain mitochondrial adaptations.
What does anaerobic exercise refer to?
Refers to short-duration (10-30s) all-out exercise (sprint training)
- recruits both type1 and 2 muscle fibres
- during exercise <10 seconds (energy primarily supplied by ATP-PC system)
- during exercise lasting 20-30 secs, 80% of energy needed is provided anaerobically
4-10 weeks of sprint training can increase peak anaerobic power by?%
3-28% across individuals
What effect can sprint training have on performance (anaerobic training)?
- Sprint training improves muscle buffering capacity by increasing both intracellular buffers and hydrogen ion transporters.
- Sprint training also results in hypertrophy of type 2 muscle fibres and elevates enzymes involved in both the ATP-PC system and glycolysis.
- High intensity interval training >30 seconds (at near or above VO2 max) promotes mitochondrial biogenesis.
