Download Physiology of Training #1

Physiology of Training
Homeostatic Variables
Purpose of Training
• Exercise disrupts homeostasis
• Training reduces the disruption
• Reduced disruption of homeostasis results
in improved performance
Principles
• Overload
• Specificity
• Reversibility
Overload and Reversibility
• a system or tissue must be stressed with a
workload which it is unaccustomed
– can be intensity, duration or frequency
• this stress results in adaptation
• Reversibility is the converse
– once the overload stimulus is removed, the
adaptation is lost
Specificity
• the training effect is specific to the
– tissue or system stressed (eg. Arms do not adapt
to cycling stimulus)
– the mode of stress imposed (eg. Strength
training does not result in endurance
adaptations)
– eg. Run training vs. Cycle training and LT
(58% & 20% vs. 39% alone)
Research Designs
• Cross-sectional
– take samples of populations ie. Cardiac
patients, normal sedentary & elite athletes
– disadvantage - black box
• Longitudinal
– changes over time ie. VO2max improvements
in cardiac patients after 1 year of endurance
training
– advantage - can find mechanisms for
differences between groups, but expensive
VO2max
• ability of the cardiovascular system to
deliver blood (oxygen) to a large muscle
mass involved in dynamic work and the
ability of the muscle mass to utilize the
oxygen
• how does training affect VO2max?
Improvements in VO2max
• training must involve
–
–
–
–
large muscle groups in dynamic exercise
20 - 60 minutes in duration
3-5 times per week
50 - 85% VO2max
Law of Initial Values
• training programs of 3 months duration can
increase VO2max ~15 % on average
• values may be as low as 2-3 % or as high as
50 %
• persons with low initial values will realize
greatest improvements
• persons with high initial values will realize
smallest improvements
Genetics and VO2max
• genetics are thought to account for 40 -66 %
of one’s VO2max
• you can blame your parents for not being
able to win the Olympic marathon, but you
can’t blame them for not being able to run
one
Contributions to Improved
VO2max
• VO2max = HRmax x SVmax x (a-vO2
diff)max
• We know that max HR cannot be changed
significantly
• What will be the most important contributor
to improved VO2max?
Insert Table 13.2 & 13.3
Factors Increasing Stroke Volume
End Diastolic Volume
• endurance training increases left ventricle
size with no increase in wall thickness
(volume overload vs. pressure overload)
• plasma volume increases contribute to
increased filling volume
• bradychardia increases filling time
• Frank-Starling says increased stretch means
increased stroke volume
Cardiac Contractility
• strength of the cardiac muscle (ventricle)
contraction
• contractility does increase in response to
sympathetic stimulation
• not a large contributor to adaptation as
sedentary individuals already have high
ejection fraction
Afterload
• amount of resistance offered as ventricle
forces blood into the aorta
• if force of contraction does not change, but
peripheral resistance (afterload) decreases,
stroke volume will increase
• trained muscles offer less resistance to
blood flow than untrained during
maximal work
Afterload cont’d
• MAP = Q x TPR
• decrease in peripheral resistance balances
the increase in cardiac output to maintain
homeostatic blood pressure
• vasoconstriction is decreased in the trained
exercising muscles
• this is possible due to the increased cardiac
output (two legged exercise)
– willy nilly vasodilation is dangerous
Arteriovenous Difference
• comprises 50% of improvement in VO2max
during extended training programs
• not due to increases in Hb content
• not due to increases in PO2 saturation
• must be due to decrease in mixed venous
O2 content
– increased O2 extraction due to capillary density
Increased Capillary Density
• accommodates increased muscle blood flow
due to cardiac output
• decreases diffusion distance to individual
cells and hence mitochondria
• slows rate of blood flow to allow more time
for diffusion (transit time)
Factors Contributing to Improved VO2max
insert fig 13.4
Detraining
• decreased VO2max after detraining is result
of
– first decreased stroke volume
– second decreased oxygen extraction
Time-course of changes with detraining
Changes in Citrate Synthase Activity
Endurance Training Effects
Maintenance of Homeostasis
• more rapid transition from rest to steady
state
• reduced reliance on limited liver and
glycogen stores
• cardiovascular adaptations that are more
capable of maintaining homeostatic
conditions
Adaptations
• neural – Central Command
– Respiratory and Circulatory Control centers
• neural-hormone - reduced catecholamines
(sympathetic) response to submaximal workload
• biochemical - mitochondrial enzymes (citrate
synthase)
• structural - contractile proteins
Note:
• performance improvements - the ability to
sustain submaximal work is reliant more on
adaptations (biochemical and structural) in
skeletal muscle; as opposed to small
increases in VO2max
Skeletal Muscle Adaptations
• increased number of mitochondria (up to 4
times in type II)
• increased capillary density
– increased Krebs cycle enzymes
– increased ß-oxidation enzymes
– increased electron transport chain (ETC) enzymes
Cont’d
• improved shuttle which moves NADH from
glycolysis to mitochondria
• change in LDH which converts lactate to
pyruvate and vice versa
Training/Detraining Adaptations in
Mitochondial Content
Biochemical Adaptations and O2
Deficit
• ATP > ADP + Pi by muscle contraction (crossbridges) is stimulus for ATP producing systems
– 1st - ATP-PC
– 2nd - glycolysis
– 3rd - Krebs oxidative
• oxidative metabolism primary system during
steady state
• increased mitochondria due to training adaptation
means…...
Mitochondrial Number and Changes in [ADP]
During Steady State...
• O2 consumption shared between
mitochondria as opposed to only 1
• it takes a smaller change in [ADP] to
stimulate mitochondria to take-up O2
• oxidative metabolism will be activated
earlier, reducing the O2 deficit
• therefore - less PC depletion, less glycogen
depletion, less lactate production
Endurance Training Reduces O2 Deficit
Biochemical Adaptations and Blood
Glucose
• increased FFA transport into muscle
– at same [FFA] transport into cell is
increased post-training
• increased movement of FFA from
cytoplasm to mitochondria
– carnitine transports FFA and carnitine
transferase facilitates the transport
– more mitochondria results in more surface area
which exposes more carnitine transferase
– FFA can be transported at a greater rate across
the mitochondrial membrane
• increased FFA oxidation
– increased mitochondrial number means
increased enzymes involved in ßoxidation
– results in more acetyl-coA (breakdown
product of FFA) and formation of citrate
(first compound in Krebs cycle)
– increased citrate inhibits glycolysis
Increased Mitochondrial Number, Increased
FFA Utilization, Spared Gycogen
Biochemical Adaptations and
Blood pH
• [pyruvate] + [NADH] <=LDH=> [lactate]
+ [NAD+]
• ^ mitochondrial number lowers pyruvate
formation (reduced glycolysis)
• ^ likelihood pyruvate will be oxidized
(^ mitochondria)
• ^ shuttling of NADH into mitochondria
(less for lactate production)
• change in LDH (5 isoforms
– change to low affinity for pyruvate (like the
heart)
Increased Mitochondria and Maintenance of
Blood pH
Biochemical Adaptations and
Lactate
• lactate accumulation is balance between formation
and removal
– lactate can rise either by increased production
or decreased clearance
• due to increaed a-vo2difference less blood need to
go to working muscles at given workload
• more blood can go to liver for Cori cycle (less
sympathetic stimulation as well)
• also, the LDH change results in less production