Transcript Aerobic Training

Aerobic Conditioning
 Muscle
Adaptations
Key Points
 1.
Muscle adapts to become a more
effective energy provider.
 An improved capacity for oxygen
extraction from the blood supply.
 An altered cellular control of energy
metabolism.
Key Points
 Improvements
in maximal cardiac
output and other adaptations not
related to biochemical changes in the
muscles.
Key Points
 2.
Training adaptations are induced
specifically in the muscles actively used
in the exercise.
 These adaptations are sustained by
continued activity and lost following
inactivity.
Key Points
 Intensity
and duration are important
factors influencing muscle adaptations.
Key Points
 3.
Muscle adaptations enhances
performance in competitive sport.
 Adaptations developed in non-athletic
populations by routine activity are
important in promoting healthier living.
Aerobic Conditioning
 The
ability to sustain an exercise task
such as running or cycling requires that
the energy utilization within the active
muscle (i.e., the rate of ATP
breakdown) is fully matched by energy
supply processes (i.e., ATP resynthesis).
Aerobic Conditioning
 If
the energy demand is not met, muscle
fatigue ensues.
Aerobic Conditioning
 Extended
duration activity is driven by
aerobic metabolism, i.e., the
consumption of oxygen to drive the
oxidation of CHO and fatty acids.
Aerobic Conditioning
 The
mitochondria within the muscle
fibers respond to chemical signals
produced during the contractions by
using the energy derived through
oxygen consumption to resynthesize
ATP from ADP + P (the products of
ATP breakdown).
Aerobic Conditioning
 This
process requires a sufficient
delivery of oxygen to the active muscle
fibers and an adequate fuel supply
within the cell to support oxygen
consumption.
Aerobic Conditioning
 These
fuels include CHO and fatty
acids supplied from within the cell or
from the circulation.
Aerobic Conditioning
 Oxygen
must be derived from an
adequate blood flow and must defuse
from the red blood cells in the
capillaries to the mitochondria in the
muscle fibers.
Aerobic Conditioning
 Thus,
disruption in energy provision
could occur if fuel supplies within the
muscle fibers are exhausted and/or if
the circulation does not provide an
adequate supply of fuels or oxygen.
Aerobic Conditioning
 Participation
in endurance types of
exercise training causes muscular
adaptations that influence these
processes controlling energy provision.
Aerobic Conditioning
 Such
training adaptations serve to
redesign muscle and lead to an
improved capacity for oxygen exchange
between capillary and tissue, and to an
improved control of metabolism within
the muscle fibers.
Aerobic Conditioning
 Both
factors provide a better foundation
for improved physical performance.
Muscle Design
Muscle Fiber Type:
 Type I = SLO
 Type IIa = FTO
 Type IIb = FTG
Classification of Muscle
Fibers
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Characteristic
Type I
Oxidative capacity High
Glycolytic capacity Low
Contractile speed Slow
Fatigue resistant High
Motor unit strength Low
Type IIa
Mod. High
High
Fast
Moderate
High
TypeIIb
Low
Highest
Fast
Low
High
Characteristics of Muscle
Fiber Types
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Characteristic
ST
Fibers per motor neuron 10-180
Motor neuron size
Small
Nerve conduction velocity Slow
Contraction speed (ms)
110
Type of myosin ATPase Slow
Sarcoplasmic Ret. Dev.
Low
FTa
300-800
Large
Fast
50
Fast
High
FTb
300-800
Large
Fast
50
Fast
High
Muscle Fibers
 While
there are meaningful adaptations
in skeletal muscle fibers induced by
exercise training, training does not
seem to cause marked shifts between
slow and fast fiber type distributions.
Muscle Fibers
 Thus
the very high proportion of type I
fibers (e.g., 70-90%) observed in the
muscles of elite endurance athletes is
probably a genetic endowment rather
than an adaptation to training.
Mitochondria
 One
fundamental biochemical
adaptation induced by exercise is an
increase in the mitochondrial content
throughout the trained muscle fibers.
Mitochondria
 This
greater mitochondrial content
increases the capacity for aerobic
energy provision from both fatty acid
and CHO oxidation and can be found in
both slow and fast twitch fibers when
they are prompted to adapt by the
exercise program.
Mitochondria
 It
is also likely that the increase in
mitochondrial content improves the
control of energy metabolism,
influences the muscle fibers to oxidize
more fatty acids and less glycogen, and
improves muscle performance.
Muscle Capillary Density
 Exercise
training increases the number
of capillaries surrounding individual
muscle fibers.
Muscle Capillary Density
Increased capillary density improves the O2
exchange between capillary and fiber by:
 presenting a greater surface area for the
diffusion of oxygen,
 by shortening the average distance required
for oxygen to diffuse into the muscle,
 and/or by increasing the length of time for
diffusion to occur.
Muscle Capillary Density
 Increased
capillary density contributes
to the increased O2 extraction.
 This accounts, in part, for the increase
in VO2max that is observed in endurance
trained individuals.
Blood Flow Capacity
 The
blood flow capacity of normal
skeletal muscle is exceptionally high.
 Cardiac output could not increase
sufficiently to perfuse all the blood
vessels in our muscle mass, if they were
to maximally dilate.
Blood Flow Capacity
 Even
during intense exercise requiring
VO2max , this limitation of cardiac
output means that only a fraction of an
individual’s entire muscle mass can be
active, and then it functions only at a
fraction of its blood flow capacity.
Blood Flow Capacity
 Nevertheless,
there is evidence that the
peak flow capacity of muscle is
increased by endurance training, but
the value of this adaptation in muscles
in unclear.
Blood Flow Capacity
Important adaptations to training:
 Optimal utilization of the flow
delivered to the muscle.
 Exchange of nutrients between
capillaries and fibers.
Blood Flow Capacity
 This
places importance on the
vasomotor control of the arterial
supply/resistance vessels and on
diffusion exchange properties of vessels
surrounding the muscle fibers.
Metabolism
 The
increase in mitochondrial content
of trained muscles should have a
number of metabolic effects that serve
to improve performance, at least during
prolonged exercise.
Metabolism
 First,
the increase in mitochondria
should make it possible for a greater
rate of fatty acid oxidation after
training, even when the circulating fatty
acid concentration available to the
muscle is not elevated.
Metabolism
 Second,
an increase in mitochondrial
content of a muscle fiber alters the
biochemical signals controlling energy
metabolism during submaximal
exercise.
Metabolism
 In
effect, when compared to the
untrained state, the signals within
trained muscle fibers that accelerate
metabolism during exercise are
attenuated, thereby reducing the rate of
CHO breakdown and probably
contributing to the sparing of muscle
glycogen observed in trained subjects.
Metabolism
 Thus,
the biochemical adaptations in
muscle help provide the foundation for
metabolic changes favorable to
endurance performance in trained
subjects.
Training Stimulus
 At
present, the underlying mechanisms
responsible for inducing the training
adaptations in muscle are not known.
Training Stimulus
 However,
it is clear that the muscles
must be recruited during the exercise
task in order to adapt to the training
program.
Training Stimulus
 Those
muscles (or fibers within a
muscle) not involved in the exercise
task do not adapt.
Training Stimulus
 Thus,
the critical stimulus for
adaptation is something very specific to
the active fibers and not likely to be
some generalized factor circulating in
the blood that influences all muscles.
Training Stimulus
 Further,
for a given exercise program,
training must be performed for a
sufficient duration of days or weeks to
allow the muscle-specific biochemical
adaptations to reach steady-state.
Training Stimulus
 For
example, muscle mitochondrial
content appears to reach a steady-state
after approximately 4-5 weeks of
training.
Training Stimulus
 The
magnitude of the training-induced
increase in mitochondrial content is also
influenced by the duration of the daily
exercise bout.
Training Stimulus
 Longer
exercise bouts generally
produce greater increases in
mitochondrial content.
Training Stimulus
 Further,
exercise intensity interacts with
the duration of the exercise bout to
make the initial minutes of exercise
even more effective in establishing a
stimulus for adaptation.
Training Stimulus
 The
peak adaptation in mitochondrial
content seems to occur with shorter
durations of exercise as the intensity of
each training bout is increased.
Training Stimulus
 The
benefit of very prolonged training
sessions in enhancing performance may
be related to adaptations in
cardiovascular function, fluid balance,
substrate availability, or other factors
not directly related to muscle-specific
adaptations.
Training Stimulus
 At
least part of the beneficial effect of
increasing exercise intensity on
training-induced adaptations in
muscles can be attributed to the effect of
intensity on muscle recruitment.
Training Stimulus
 Once
peak performance (e.g., force
development and/or power output) is
obtained from an involved set of muscle
fibers, a greater power output is
achieved by recruitment of additional
muscle fibers.
Training Stimulus
 This
is illustrated by the marked
adaptation that becomes apparent in
the low-oxidative fibers as they are
recruited to meet the demands of the
more intense exercise task.
Short-term Training
 Not
all of the improvement in exercise
performance that accompanies training
can be accounted for by long-term
biochemical adaptations.
Short-term Training
 For
example, even within days of
beginning an exercise program, there is
evidence for an improvement in the
performance of muscle and in
metabolism.
Short-term Training
 The
brief training time causes an initial
shift in neuromuscular and/or
cardiovascular control that improves
muscle fiber utilization, metabolism,
and blood flow distribution.
Short-term Training
 This
is an example of the complexity of
changes and the variety of training
durations required to achieve particular
adaptations that occur in the transition
from a relatively inactive condition to
an optimally trained state.
Short-term Training
 All
the improvement in exercise
performance after training cannot be
attributed solely to the muscle
adaptations developed in this
summary.
Short-term Training
 Other
changes (e.g., neuromuscular,
cardiovascular, and endocrine) can be
instrumental in contributing to
enhanced exercise performance after
training for many weeks or months.
Detraining
 Just
as meaningful adaptations are
induced by physical activity, they are
gradually lost in persons who become
inactive.
Detraining
 The
extent and time course of
regression are not known for many
variables and are likely related to the
exact process under consideration.
Detraining
 For
example, roughly 50% of the
increased muscle mitochondrial content
induced by training can be lost within 1
week of detraining.
Detraining
A
return to training will recover the
muscle adaptations; however, the time
required to reestablish the steady-state
trained condition can take longer than
the detraining interval.
Summary
 While
the adaptations to an endurance
type of training are very complex and
multifaceted, change within the active
muscles are probably fundamental to
the metabolic and functional alterations
that support the enhanced endurance
performance observed after training.
Summary
 The
adaptations that involve
remodeling of the muscle (e.g.,
enhanced mitochondrial content and
increased capillary density) are
influenced by the duration and
intensity of daily exercise, require an
extended training period to achieve a
steady-state adaptations, and are lost
with inactivity.