L32. Cardiovascular Response to Exercise Flashcards
(25 cards)
Cardiovascular response to exercise?
Heart rate (beat per minute)
- Increases from resting rate (~60bpm)
- Max HR is age dependent = 220 - age
- Increases by 3-4 times
Stroke volume (mL per beat)
- Increases from resting volume (~70mL)
- Increases by 1.5-2 times
Cardiac output (volume per min)
= HR x SV
- Increases from resting ~5 L/min
- Max ~40 L/min in elite athletes
- Increases by up to 8 times
Blood flow redistribution during exercise?
Global vasoconstriction or local vasodilation
Blood flow during exercise?
During exercise cardiac output increases and is redistributed
- Skeletal muscle: largest increase in blood flow; to provide O2 and nutrients, and remove CO2 and waste products
- Skin: increase in blood flow for heat loss
- Heart and brain: increased blood flow for the heart to meet increased demands due to exercise
- Abdominal organs: decrease in blood flow, as they are less active during exercise (opposite of ‘rest and digest’)
Global vasoconstriction?
Increased activity of sympathetic vasoconstrictor nerves causes global vasoconstriction
- Exercise stimulates sympathetic nervous system
- Noradrenaline (NA) is released from sympathetic nerve terminals and binds to a1 and a2 receptors
- NA causes vasoconstriction (narrowed radius) of arterioles
- Vasoconstriction reduces blood flow
- Great for abdominal organs during exercise as they don’t need a high blood flow supply
Local vasodilation?
Local vasodilation of skeletal muscle overrides the vasoconstriction from sympathetic vasoconstrictor nerves: functional sympatholysis
- Metabolites from working muscle act on the smooth muscle of skeletal muscle arterioles causing vasodilation: metabolic regulation/active hyperaemia
- Muscle contraction creates mechanical compression on the outside of the blood vessels which cause reflexive vasodilation: mechanical feed-forward vasodilation
- Adrenaline binds to B2 adrenergic receptors on smooth muscle of skeletal muscle arterioles and causes vasodilation
- These vasodilation mechanisms override sympathetic vasoconstriction: functional sympatholysis
- Blood flow is increased to working muscle during exercise
CVS changes during exercise?
- Increased cardiac output
- Blood flow redistribution
- Increased blood flow to exercising muscle
- Decreased blood flow to viscera
- Overall decrease in TPR
Blood pressure during exercise?
MABP = CO x TPR
Moderate, steady-state exercise:
- CO increase = TPR decrease
- MABP is relatively constant
High intensity exercise:
- CO increase > TPR decrease
- MABP increases
* Mostly due to increase in systolic pressure
Normal baroreflex (at rest)?
Normally, stimulating the baroreceptors causes decreased sympathetic nervous activity
- Baroreceptors detect increase MABP and increase their rate of AP firing
- Activation of barosensitive neurons in the medulla
- Barosensitive neurons inhibit sympathetic nervous system (SNS) central command
- Reduced sympathetic output to the heart and blood vessels
- MABP decreases to return to normal set point
Baroreflex during exercise?
The MABP set point is increased for exercise
- Mechano- and chemo-receptors in exercising muscle send information to the exercise ‘central command’
- MABP set point is increased via the exercise ‘central command’:
* Overriding the inhibition of the SNS which normally occurs when MABP increased
* Directly stimulating the SNS to increase MABP
= Exercise pressor response
Exercise pressor response?
- Exercise ‘central command’ activates neurons which inhibit the barosensitive neurons in the medulla
- This means that even though MABP has increased there is no inhibition of the SNS central command; allowing increased sympathetic output to the heart and blood vessels
- Exercise ‘central command’ also directly stimulates the SNS central command to increase SNS output
- MABP increases to exercise set-point
Muscle fibre types?
Muscle fibre type is not fixed and can be changed by activity or training
Anaerobic training:
- Type IIa; fast oxidative glycolytic
- Type IIx; fast glycolytic
Aerobic training:
- Type I; slow oxidative
Anaerobic (strength) training effects?
- High intensity, low rep training
- Anaerobic (anaerobic glycolytic system)
- Adaptations occur within 3 weeks
Goals of anaerobic training:
- Increase strength; due to muscle hypertrophy
- Increase anaerobic capacity; due to sarcoplasmic hypertrophy and increased lactate threshold
Muscle hypertrophy - anaerobic strength training effects?
Muscle hypertrophy = increase in size and strength of skeletal muscle
- Within a whole muscle (e.g. biceps brachii) each muscle cell/fibre gets bigger because each muscle fibril within the muscle cell gets bigger
- Increased contractile strength comes from increasing the SIZE of muscle cells/fibres (rather than adding more muscle fibres)
Increased protein synthesis:
- More actin and myosin (more sarcomeres) added to each muscle fibril: more contractile strength
Satellite cell (myogenic stem cells) activity:
- Proliferate and fuse to existing fibres to make each muscle cell/fibre bigger
Sarcoplasmic hypertrophy:
- Increased volume of the sarcoplasm and therefore sarcoplasmic components
Micro-trauma theory?
- Damage (‘tearing’) of muscle fibres
- ‘Micro’: tears in small areas of a muscle fibre (not the whole muscle)
Satellite cells are needed to repair the muscle fibres/cells
- Satellite cells are myogenic stem cells (can build muscle) and are quiescent (dormant) until activated
- Are activated and migrate to heal micro-tears
- They span micro-tear to prevent further damage, differentiate into myoblasts (immature muscle cell) and fuse with existing muscle cell/fibres adding new myofibrils and more nuclei:
* Increasing the size of cell/fibre
* More protein (actin and myosin) synthesis (nuclei)
* Increasing the contractile length
Sarcoplasmic hypertrophy?
- Increased volume of the cytoplasm
- No direct change in contractile strength BUT
- Increased capacity for anaerobic glycolysis
- Due to increased amount of enzymes and substrates for anaerobic metabolism
Increased anaerobic capacity:
- Increased ATP and substrate stores (creatine phosphate, glycogen)
- Increased enzymes for anaerobic glycolysis etc.
Muscle atrophy?
Muscle atrophy = decrease in size and strength of skeletal muscles due to inactivity or denervation
Myostatin:
- Increased with inactivity
- Causes atrophy
- Prevents excessive muscle growth
- Myogenesis regulator
Myostatin inhibitors:
- Prevent muscle atrophy
- Clinical trials for muscular dystrophy treatment
- Could be used as a performance enhancer
Increased lactate threshold?
Increase in exercise intensity before reaching lactate threshold
The type of training which increases lactate threshold:
- High volume, maximal steady-state, interval workouts (80-90% of VO2 max)
* Uses the anaerobic glycolysis energy system, producing lactate
Muscle modifications:
- Build-up of lactate/lactic acid triggers adaptations in the muscle cells
* Muscle fibres become better at tolerating lactate build up (buffering)
*Increased transport of lactate out of muscle cells + improved systems in the body to clear lactate from the blood and use it as a fuel source
- Lactate accumulation reduced
Benefits of this type of training:
- Improved performance for both endurance athletes and speed and power
Aerobic (cardio) training effects?
- Low intensity training, high rep, longer duration endurance training
- Aerobic (oxidative phosphorylation systems)
- Adaptations occur within 4-6 weeks
Goals of aerobic training:
- Increase aerobic capacity; aerobic threshold and VO2 max
Increased VO2 max?
Increased aerobic threshold:
- Sustain a higher level of exercise intensity for longer before needing to use anaerobic glycolysis and therefore increasing lactate production
Increased VO2 max:
- Increased physical fitness, greater performance during aerobic endurance exercise
VO2 (oxygen consumption):
- Increases with exercise intensity
- Until a maximal level = VO2 max
* Maximum oxygen consumption at max exercise level
VO2 max:
- Increases with aerobic training
- Limited by age
- Improved cardiovascular health
- Reduced risk of heart disease, diabetes, cancer, and stroke
Increase VO2 max by:
- Increasing oxygen supply to exercising muscle
* Cardiovascular adaptations
- Increasing the ability of exercising muscle to use oxygen to make ATP
* Muscle cell metabolic adaptations
Cardiovascular adaptations - increasing VO2 max?
Heart rate (HR)
- Max HR unchanged (determined by age)
- Resting HR decreased, higher output at lower HR
- Increase HR range during exercise
Stroke volume (SV)
- Increased stroke volume at rest and during exercise
- Remodelling of ventricular walls:
* Moderate hypertrophy, increased ventricular volume and increased contractility
Cardiac output
- Increase in maximum cardiac output due to increases in HR and SV
Muscle cell metabolic adaptations - increasing VO2 max?
Increased oxidative ATP synthesis capacity:
- Change in muscle cell/fibre type to more type I fibres (oxidative)
- Increased production of oxidative enzymes
- Mitochondria biogenesis (make more mitochondria)
* Increased oxidative phosphorylation
The baroreflex is modified in exercise permitting an increase in mean arterial blood pressure (MABP) BECAUSE during exercise the sensitivity of the baroreceptors decreases
A. If both statements are true, and the second causes the first
B. If both statements are true, but the second does not cause the first
C. If the first is true and the second is false
D. If the first is false and the second is true
E. Both statements are false
C
Which of the following does NOT contribute to the increase in cardiac output during exercise?
A. Increased cardiac contractility
B. Increased total peripheral resistance
C. Increased circulating adrenaline
D. Increase heart rate
B
Local release of metabolites by exercising skeletal muscles overrides the global vasoconstriction induced by noradrenaline
True or false?
True
