Chapter 13: Physiology of Training: Effects of Aerobic and Anaerobic Training Flashcards
Overload
training effect occurs when a physiological system is exercised at a level beyond which it is normally accustomed
Specificity
Training effect is specific to:
- Muscle fibers recruited during exercise
- Energy system involved (aerobic vs anaerobic)
- Velocity of contraction
- Type of contraction (eccentric, concentric, isometric)
Reversibility
Gains are lost when overload is removed
Training to increase VO2 max
- large muscle groups
- dynamic activity
- 20-60 min
- more or equal to 3 times per week
- greater than or equal to 50% VO2 max
What is the average expected increase in VO2 max after 2-3 months of endurance training?
15-20%
Those with high initial VO2 max will have how much of an increase?
as low as 2-3%
requires higher intensity training (>70% VO2 max)
Those with low initial VO2 max will have how much of an increase?
as high as 50%
requires relatively low intensity training (40-50% VO2 max)
How much of VO2 max is determined by genetics in sedentary adults?
50% of VO2 max
Genetics play a key role in determining…
the training response
Large variations in training adaptations reveal that heritability of training adaptations is approximately
47%
Fick equation
defines VO2
VO2= maximal cardiac output x a-vO2 difference
Differences in VO2 max between individuals is primarily due to
differences in SV max
What is the dominant factor in increasing VO2 max during short duration training?
Increase in stroke volume
how long is short duration training?
approximately 4 months
how long is longer duration training?
approximately 28 months
Research reveals that in untrained subjects, relatively short durations of endurance training increases both ____ and _____, but does not significantly increase the ______
VO2 max; Maximal Cardiac Output; Maximal a-vO2 difference
Following short duration training, all of the training induced improvement in VO2 max is due to
increases in maximal cardiac output
Longer duration of training increases VO2 max by
increasing both maximal cardiac output and the maximal a-vO2 difference
Following both long term and short term duration endurance training, the exercise-induced increase in maximal cardiac output is entirely due to
stroke volume
– maximal HR either remains constant or slightly decreases
Stroke volume
SV= EDV- ESV
how much blood was ejected= how much blood is in the ventricle when filled - how much blood is in the ventricle after contraction
What increases maximal stroke volume?
- an increase in end diastolic volume (preload)
- an increase in contractility
- a decrease in total peripheral resistance (afterload)
Contractility
The strength of contraction
Total peripheral resistance
“afterload”
- The resistance of blood flow
- the pressure which the ventricle pushes against as it tries to push blood into the aorta
What increases Preload (EDV)?
- increase in plasma volume
- increase filling time and venous return
- increase in ventricular volume
What decreases Afterload (total peripheral resistance)?
- decrease in sympathetic vasoconstriction
- increase in maximal muscle blood flow
6 day training program (2hr/day at 65% VO2 max) resulted in…
7% increase in VO2 max due to:
- 11% increase in plasma volume
- 10% increase in stroke volume
Increase in a-vO2 difference in response to endurance training is due to
increased O2 extraction from the blood
Improved ability of the muscle to extract oxygen from the blood is due to
- increased capillary density
- increased mitochondrial number
Increased Capillary density
- slows rate of blood flow to allow time for O2 diffusion to take place (aka increases muscle blood flow)
- improves ability of the muscle to extract oxygen from the blood
- decreases diffusion distance to the mitochondria
The ability to continue prolonged, submaximal work is dependent on the
maintenance of homeostasis during the activity
Maintenance of homeostasis in response to endurance training is reached by:
- more rapid transition from rest to steady-state
- reduced reliance on liver and muscle glycogen stores
- cardiovascular and thermoregulatory adaptations
Endurance training result in a fast-to-slow shift in muscle fiber type… what does this mean?
- reduction in fast myosin and increase in slow myosin
- this means you can perform more work with less ATP use (aka increased mechanical efficiency, which can improve endurance performances)
The extent of the shift from fast to slow muscle fibers is determined by
intensity and duration of training sessions and number of years of endurance training
Extremely high aerobic capacity in elite athletes is likely due to
genetics
Endurance training results in increased number of capillaries… what does this mean?
- enhanced diffusion of oxygen and substrate delivery to muscle fibers
- increased removal of metabolic waste
Endurance training increases the volume of both _______ and ______ in muscle fibers
subsarcolemmal mitochondria
intermyofibrillial mitochondria
Increased mitochondrial content in skeletal muscles results in
improved oxidative capacity and ability to use fat as fuel
Mitochondrial turnover
– increased by training
breakdown of damaged mitochondria and replacement with healthy mitochondria
How quickly can muscle mitochondrial volume increase?
- can increase quickly (within the first 5 days of training)
- can increase 50-100% within first 6 weeks
- depends on intensity and duration of training
How does endurance training reduce the oxygen deficit? what does it result in (on a chemical level)?
The energy requirement can be met by oxidative ATP production at the onset of exercise
- faster rise in VO2 curve, and steady state is reached earlier
Following training, oxygen deficit is
lower
The faster rise in oxygen uptake results in:
- less lactate and H+ formation
- less PC depletion
- less disruption in homeostasis
What is the primary fuel of the nervous system?
Plasma glucose
Endurance training helps maintain blood glucose during prolonged submaximal exercise by
increasing fat utilization and sparing of plasma glucose and muscle glycogen
Endurance training increases _______ and decreases _______ during prolonged submaximal exercise.
fat metabolism; glucose utilization
How is increased transport of FFA into the muscle facilitated?
an increase in capillary density, which slows the blood flow in the muscle and increases FFA transporters; fatty acid binding protein and fatty acid translocase. Ultimately that increases the uptake of FFA which increases FFA utilization and spares plasma glucose.
How is increased transport of FFA from the cytoplasm to the mitochondria facilitated?
an increase in mitochondrial number and size (or mitochondrial membrane surface area), results in increased beta oxidation enzymes and carnitine palmitoyltransferase I and fatty acid translocase.
Because beta oxidation occurs in the mitochondria
Increased capillary density enhances
the delivery of free fatty acids to the muscle
Fat metabolism occurs in
the mitochondria
called beta oxidation
beta oxidation
fat metabolism
converts FFA to acetyl-CoA for metabolism in the Krebs cycle
How is mitochondrial oxidation of FFA increased?
increased mitochondrial number increases the enzymes of beta oxidation. This increases the rate of acetyl-CoA formation and high citrate level inhibits PFK and glycolysis
Free radicals
- chemical molecules that contain an unpaired electron in their outer orbital, which makes them highly reactive
- can damage proteins, membranes, and DNA
free radicals are produced by
contracting muscles
Free radicals effect on muscles/during exercise
can disturb cellular homeostasis, damage muscle contractile proteins and contribute to muscle fatigue during prolonged endurance events
Antioxidants
molecules that neutralize free radicals
- endogenous and exogenous (from diet)
Endogenous antioxidants
- increased by training
- protects against oxidative damage and fatigue
How does endurance training-induced increases in mitochondria volume affect lactate and H+ formation?
They are decreased to maintain blood pH
Acid-Base balance during exercise
lots of words on this slide… main idea about lactate and H+
By increasing the mitochondrial volume, endurance training increases the number of shuttles available to transport electrons associated with NADH from the cytoplasm into the mitochondrion. If the NADH formed in glycolysis is more quickly transported to the mitochondria, there will be less lactate and H+ formation.
Endurance training causes a change in the type of LDH present in the muscle cell. The H form of LDH has a low affinity for the available pyruvate; therefore, the likelihood of lactate production is diminished. Endurance training shifts the LDH towards this form, making lactate formation less likely and the uptake of pyruvate by the mitochondrion more likely.
How do muscle biochemical adaptations to training influence the systemic response to exercise?
- reduction in “feedback” from muscle chemoreceptors
- reduced number of motor units recruited
How does the Sympathetic Nervous System respond to muscle biochemical adaptations to training?
decrease in epinephrine and norepinephrine
How does the Cardiorespiratory System respond to muscle biochemical adaptations to training?
decrease in heart rate and ventilation
Responses to prolonged submaximal exercise are determined by
the training state of the specific muscle groups, not by the specific adaptation of each organ system.
Is there a transfer of training effect from one muscle to another?
there is no transfer of training effect to the nervous, cardiovascular, and pulmonary systems
“Peripheral feedback” from muscle influences cardiopulmonary responses to exercise
The cardiorespiratory control center receives neural feedback from the working muscle, resulting in output from the cardiorespiratory control center that increases both HR and pulmonary ventilation.
The afferent signals to the cardiorespiratory control center result in decreased liver and kidney blood flow in order to increase the available blood flow to the working muscles.
How does endurance exercise training impact central command control of the cardiorespiratory response to exercise?
Endurance exercise training reduces the feedforward output from higher brain centers to the cardiovascular control center. This results in lower sympathetic system output, heart rate, and ventilation responses to exercise.
With endurance training, biochemical and structural adaptations in skeletal muscles make them more
efficient, needing less muscle to do the same amount of work
How rapidly does VO2 max decrease during detraining?
decreases about 8% within 12 days
decreases 20% after 84 days
The initial decrease of VO2 max is due to
(12 days of detraining)
decrease in stroke volume max
Sudden decrease in maximal stroke volume is due to
rapid loss of plasma volume with detraining
Later decrease of VO2 max with detraining is due to
(21-84 days)
decrease in a-vO2 max
Decrease in maximal a-vO2 difference is due to
a decrease in muscle mitochondria, but capillary density remains unchanged
decreased oxidative capacity of muscle
Detraining causes a fiber type shift
slow-to-fast fiber type switch
decrease in type IIa fibers
increase in type IIx fibers
Endurance training causes a fiber type shift
fast-to-slow fiber type shift
what occurs to mitochondria with 5 weeks of training?
mitochondria double
What occurs to mitochondria with detraining?
- about 50% of the increase in mitochondrial content is lost after 1 week of detraining
- majority of adapations are lost within 2 weeks
How many weeks of retraining are needed to regain the adaptations lost in the first week of detraining?
3 to 4 weeks
Anaerobic exercise refers to
short duration (10-30 seconds) all-out effort, which is also referred to as “sprint training”
Anaerobic exercise recap
(muscle fiber types, energy supply)
- recruits both type 1 and 2 muscle fibers to perform the exercise
- during exercise lasting 10 seconds or less, the energy is primarily supplied by ATP-PC system
- During exercise lasting 20-30 seconds, 80% of energy needed is provided anaerobically whereas the remaining 20% is provided aerobically
4-10 weeks of sprint training can increase peak anaerobic power by
3-25% across individuals
Sprint training improves muscle buffering capacity by
increasing both intracellular buffers and hydrogen ion transporters
Sprint training results in
hypertrophy of type 2 muscle fibers and elevates enzymes involved in both the ATP-PC system and glycolysis
