A/Prof Chin Moi Chow
Discipline of Exercise and Sport Science
The University of Sydney
Outline
• Endurance training defined
1
• Endurance training and adaptations
o Genetic variation in cardiorespiratory fitness
o The Fick equation
o Central (cardiorespiratory)
2
adaptations
o Peripheral (muscle) adaptations 3
o Intracellular signaling for metabolic
responses
• Mode of endurance training
4
o Continuous, SIT, HIIT
o Applications (performance, health and
rehabilitation)
• Is there best practice?
5
VO2max is
not ‘endurance’
McArdle Katch&
Katch 8th Ed
Peripheral adaptations to ET
Muscle blood flow
During exercise:
• Blood flow to active muscles ↑ up to nearly 100x
from rest due to ↑ CO and local muscle vasodilation
Exercise training:
• ↑ skeletal muscle blood flow capacity
o Structural vascular remodeling
- Capillary bed and arterial tree
- altered vasomotor reactivity of arterioles
Peripheral adaptations to ET
Mitochondrial biogenesis
The most important adaptations:
• ↑ size and number of mitochondria in
trained skeletal muscles
 matching between ATP requirements and
production via oxidative metabolism
• ↑ in capillary density
• ↑ enzyme activities in main metabolic pathways
• ↑ Glut 4 transporters
Myoplasticity
• Skeletal muscle's capacity for adaptive changes
through changes in gene expression
 alteration in structural, contractile and
enzymatic proteins
Factors influencing skeletal muscle protein
expressions:
• Physical training (volume, intensity,frequency)
• Nutrition
• Genetic variability
Mitochondrial Biogenesis
• ↑ number, size of mitochondria
including capillarity (angiogenesis)
(‘local CV system’)
 optimize diffusion distances
Relationship
between
VO2max and
capillary to
fibre ratio
Mitochondrial Enzymes
Cross-sectional:
UT-untrained, MT-mod trained,
HT-highly trained
SDH = enzyme in TCA cycle
Longitudinal:
D.L. Costill et al., 1979, "Lipid
metabolism in skeletal muscle of
endurance-trained males and
females," Journal of Applied
Physiology 28: 251-25
Peripheral adaptations to ET
Substrates/ fuel supply
1 CHO
• ↓ in CHO utilisation with a parallel ↑ in lipid oxidation
in trained muscles
 glucose sparing and ↑ glycogen storage
What are the benefits of increased muscle and liver
glycogen storage?
Mechanisms
• ↓ glycogenolysis due to ↓ in phosphorylase activity in
response to ↓ ADP, AMP, Pi content
• ↑ gluconeogenesis
Peripheral adaptations to ET
Substrates/ fuel supply
2 Fat
Training ↑ capacity of muscle to oxidise lipids
Increase rate of free FA oxidation depends on:
• ↑ mobilisation of FFA from adipose tissue
• ↑ level of plasma FFA at submax exercise
• ↑ fat storage adjacent to mitochondria within
muscles
• ↑ capacity to utilise fat at any given plasma
concentration
Peripheral adaptations to ET
Glut 4 transporters
• ↑ GLUT-4 transporters
Rest: ↑ muscle glucose uptake
 ↑ whole body glucose clearance (70-90%) at any
resting Insulin level
Exercise: ↑ GLUT 4 do not increase muscle glucose
uptake because of decreased Glut 4 translocation to
the sarcolemma
 ↓ glucose transport from blood into muscles
 consistent with ↓ CHO utilisation
Skeletal muscle adaptations to ET
Fibre type transition
• Type I appears to be genetically determined
o Endurance athletes have high proportion of
type I
o Some hypertrophy of type I fibers
o The capacity of type I and II fibers to
interconvert:
o Conflicting findings
Wilson et al. J Strength & Conditioning Research 2012:26(6): 1724–1729
Functional significance of skeletal muscle
adaptive responses
• When ATP supply from Ox Phos can match ATP demand:
delay accumulation of products of metabolism (ADP,
AMP, Pi, H+)  Delay fatigue
• Smaller O2 deficit at exercise onset  less PCr depletion
• ↓ stimulation of PFK (glycolysis)
• ↑ capacity to oxidize FFA, other fuels
 Glycogen sparing
• Max blood flow ↑ in active motor units
• Submax blood flow not altered or ↓
• Capillarity ↑ by 5-10% ↓ RBC transit time
 ↑ greater nutrient extraction
 Supports
↑oxidative
capacity
Endurance adaptations and gene expressions
Flueck and Eilers, 2010
Gene expressions
Upregulation of genes
• Mitochondrial number, size and capillarity
• Contractile protein expression
Endurance
• Metabolic proteins
phenotype
o Enzymes (e.g., succinate DH,
lipoprotein lipase)
o Transporters (Glut 4 expression)
• Upregulation peaks in the initial hours of recovery
• Return to resting level within 24h
• Cumulative effect with repeated bouts of exercise
Muscle contractile activity
•
•
•
•
•
Mechanical stretch
Rapid ↑ in cytosolic and mitochondrial [Ca2+]
Reactive oxygen species (ROS)
Nitric oxide (NO) production
Metabolic changes that are exercise
intensity-dependent:
‐ ↑ in ADP, AMP, ↓ATP
‐ ↓ in glycogen
Signaling network
•
•
•
•
•
•
Cellular
Ca2+-dependent pathways
reactive oxygen species (ROS)
nitric oxide (NO)
AMP-dependent protein kinase (AMPK)
p38 MAPK
peroxisome proliferatoractivated receptor-γ
co-activator-1α (PGC-1α)
 contractile protein
expression, angiogenesis,
mitochondrial biogenesis,
other adaptations
signaling
Lira et al, 2010
Exercise signalling for mitochondrial biogenesis