lecture 11 (physiology of trainning)
TRANSCRIPT
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Chapter 13:
The Physiology of TrainingEffect on VO2 MAX, Performance,
Homeostasis and Strength
EXERCISE PHYSIOLOGY
Theory and Application to Fitness and Performance, 5thedition
Scott K. Powers & Edward T. Howley
Presentation revised and updated by
TK Koesterer, Ph.D., ATC
Humboldt State University
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Objectives
Explain the basic principles of training: overload andspecificity
Contrast cross-sectional with longitudinal research
studies
Indicate the typical change in VO2 MAXwith endurancetraining programs, and the effect of the initial
(pretraining) value on the magnitude of the increase
State the VO2 MAXvalues for various sedentary, active
and athletic populations
State the formula VO2 MAXusing HR, SV and a-v O2
difference; indicate which of the variables is most
important in explaining the wide range of VO2 MAX
values in the population
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Objectives
Discuss, using the variables identified in objective 5,
how the increase in VO2 MAXcomes about for the
sedentary subject who participates in an endurance
training program
Define preload, afterload, and contractility, anddiscuss the role of each in the increase in the
maximal SV that occurs with endurance training
Describe the changes in muscle structure that are
responsible for the increase in the maximal a-v O2difference with endurance training
Describe the underlying causes for the decrease in
VO2 MAX that occurs with cessation of endurance
training
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Objectives
Describe how the capillary and mitochondrial changes
that occur in muscle as a result of an endurance training
program are related to the following: a lower O2deficit,
and increased utilization of FFA and a sparing of blood
glucose and muscle glycogen, a reduction in lactate andH+formation, and an increase in lactate removal
Discuss how changes in central command and
peripheral feedback following an endurance training
program can lower the HR, ventilation, andcatecholamine responses to a submaximal exercise bout
Contrast the role of neural adaptation with hypertorphy in
the increase in strength that occurs with resistance
training
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Exercise
A Challenge to Homeostasis
Fig 13.1
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Principles of Training
Overload
Training effect occurs when a system isexercised at a level beyond which it is
normally accustomed Specificity
Training effect is specific to the musclefibers involved
Type of exercise
Reversibility
Gains are lost when overload is removed
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Research Designs to
Study Training
Cross-sectional
studies
Examine groups ofdiffering physical
activity at one time
Record differences
between groups
Longitudinal studies
Examine groups
before and aftertraining
Record changes
over time in the
groups
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Stroke Volume
and Increased VO2max
Increased SVmax
Preload (EDV)
Plasma volume
Venous return
Ventricular volume
Afterload (TPR)
Arterial constriction
Maximal muscle blood flow with nochange in mean arterial pressure
Contractility
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Factors Increasing Stroke Volume
Fig 13.2
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a-vO2Difference and
Increased VO2max Improved ability of the muscle to extract
oxygen from the blood
Muscle blood flowCapillary density
Mitochondial number
Increased a-vO2difference accounts for 50%of increased VO2max
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Factors Causing Increased VO2max
Fig 13.3
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Detraining and VO2max
Decrease in VO2max
with cessation of
trainingSVmax
maximal a-vO2difference
Opposite of training
effect
Fig 13.4
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Endurance Training
Effects on Performance Improved performance following endurance
training
Structural and biochemical changes inmuscle
Mitochondrial number
Enzyme activity
Capillary density
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Structural and Biochemical
Adaptations to Endurance Training
Mitochondrial number
Oxidative enzymes
Krebs cycle (citrate synthase) Fatty acid (-oxidation) cycle
Electron transport chain
NADH shuttling system Change in type of LDH
Adaptations quickly lost with detraining
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Detraining
Changes in Mitochondria
About 50% of the increase in mitochondrialcontent was lost after one week of detraining
All of the adaptations were lost after fiveweeks of detraining
It took four weeks of retraining to regain theadaptations lost in the first week of detraining
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Mitochondrial Number and
ADP Concentration on VO2
[ADP] stimulates mitochondrial ATP
production
Increased mitochondrial number followingtraining
Lower [ADP] needed to increase ATP
production and VO2
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MitochondrialNumber and
ADP
Concentrationon VO2
Fig 13.7
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Eff t f E d T i i
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Effects of Endurance Training
on O2Deficit
Fig 13.8
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Biochemical Changes
and FFA Oxidation
Increased mitochondrial number and capillary
density
Increased capacity to transport FFA fromplasma to cytoplasm to mitochondria
Increased enzymes of -oxidation
Increased rate of acetyl CoA formation
Increased FFA oxidation
Spares muscle glycogen and blood
glucose
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FFA Oxidation and
Glucose-Sparing
Fig 13.9
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Blood Lactate Concentration
Balance between lactate production andremoval
Lactate production during exercise
NADH, pyruvate, and LDH in thecytoplasm
Blood pH affected by blood lactateconcentration
pyruvate + NADH lactate + NADLDH
Mit h d i l d Bi h i l
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Mitochondrial and Biochemical
Adaptations and Blood pH
Fig 13.10
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Blood Lactate Concentration
Fig 13.11
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Biochemical Adaptations
and Lactate Removal
Fig 13.13
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Links Between Muscle and
Systemic Physiology Biochemical adaptations to training influence
the physiological response to exercise
Sympathetic nervous system (E/NE)
Cardiorespiratory system (HR, ventilation)
Due to:
Reduction in feedback from musclechemoreceptors
Reduced number of motor units recruited
Demonstrated in one leg training studies
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C f
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PeripheralControl of
Cardiorespiratory Responses
Fig 13.15
C t l C t l f
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CentralControl of
Cardiorespiratory Responses
Fig 13.16
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Physiological Effects of
Strength Training Strength training results in increased muscle
size and strength
Neural factors Increased ability to activate motor units
Strength gains in initial 8-20 weeks
Muscular enlargement Mainly due enlargement of fibers
(hypertrophy)
Long-term strength training
N l d M l Ad t ti
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Neural and Muscular Adaptations
to Resistance Training
Fig 13.17