Exercise Physiology Flashcards
Describe the homeostatic challenges during exercise
- Increase blood flow to muscle whilst maintaining MAP
- Increased VO2
- Increased PaCO2
- Increased metabolic waste (H+ ions / ketone / lactate)
- Increased CHO use - maintain euglycaemia
- Normothermia in the context of increase heat production
Differentiate dynamic and static exercise
Dynamic (isotonic)
- Muscles moving rhytmically, moving joints (running)
Static (isometric)
- Muscles contract against resistance but dont lengthen and shorten (weights)
Describe the different effects of dynamic and static exercise on DBP, HR and SVR
Dynamic
- Vasodilatation (aerobic metabolic activity) –> reduced SVR –> reduced DBP –> baroreceptor reflex –> tachycardia
Static
- Muscle capillary compression by muscle contraction –> increase anaerobic metabolic activity. Vessel compression increases SVR which increases DBP. In addition there is SNS stimulation –> increase heart rate but to a lesser extent than with dynamic exercise
Classify and describe the different muscle fibre types
Type 1
- Slow twitch and fatigue resistant
- Aerobic metabolism
- Rich in myoglobin
- Postural muscles (sustained contraction)
- contract slowly but resistant to fatigue
Type 2
Type 2a
- Fast twitch with moderate fatigue resistance
- Aerobic and anaerobic metabolism
- contract more slowly but are more resistant to fatigue than type 2 b fibres
Type 2b
- Fast twitch with fast fatigue
- Anaerobic metabolism
- Sprinting muscles
Describe the timeline with regards to the source of ATP at the onset of strenuous exercise
1 - 2 seconds of stored ATP depleted
15 - 30 seconds of rapid conversion of phosphocreatine to ATP
30 - 90 seconds: glycolysis
> 60 seconds oxidative phosphorylation
When glycogen is depleted –> fat metabolism ensues –> ‘hitting a wall’
What is muscle fatigue
The decline in the ability of muscle to generate force
Why does muscle fatigue occur
Protective mechanism –> stops the muscle from contracting to a point where it runs out of ATP –> which would result in ‘rigor mortis’ or worse, apoptosis
How does muscle fatigue occur
Exact mechanism unknown
- ADP and Pi accumulation
ADP + Pi accumulation –> reduced Ca uptake into SR
ADP + Pi accumulation –> open ATP sensitive K channels –> hyperpolarization
- K+ accumulation
- arterial K during exercise –> 8mmol/L (exercising heart protected??)
- interstitial K in muscle is 12 mmol/L
- High K postulated to be cause of muscle fatigue - Accumulation of lactate within muscle
- Exhaustion of glycogen stores
What does the anticipation of exercise cause
Increased SNS and decreased PSNS
- Venoconstriction (increase preload)
- Increased chronotropy and inotropy
- VD skeletal muscle vascular beds (prevent high BP)
- VC in GIT and skin
What are the effects of exercise on skeletal muscle
- Increase flow from 2 to 100 ml/100g of muscle/min
(50 times increase)
- Beta 2 adrenergic effects
- local VD metabolites (H+, AMP, K, PO4) in proportion to VO2 –> open pre-capillary sphincters.
What are the effects of exercise on the Cardiovascular system
- CO: 5L/min –> 25 L/minute
Preload - Increased. Venoconstriction
Afterload - Reduced. SVR falls (VD metabolites muscle)
Heart Rate - Increased. Increased SNS vs PSNS
Contractility - Increased. SNS + Bowditch
- BP: Little change SBP may go up d/t increased contractility. But increased CO matched by reduced SVR from arteriolar VD in skeletal muscle.
Dynamic exercise - SVR may increase leading to reduced DBP. SBP increases more than DBP falls. MAP may steadily increase with exercise intensity or duration
- Regional blood flow
Coronary - increase x 5
Skin - increases –> heat dissipation
Splanchnic - falls substantially
Renal - falls to lesser extent than splanchnic due to stronger autoregulation
Cerebral blood flow does not alter at any exercise intensity
What is the Bowditch effect
Tachycardia induces an increase in cardiac contractility
Describe how exercise affects the regional blood flow to the following:
Coronary Skin Splanchnic Renal Cerebral
Coronary - increase x 5
Skin - increases –> heat dissipation
Splanchnic - falls substantially
Renal - falls to lesser extent than splanchnic due to stronger autoregulation
Cerebral blood flow does not alter at any exercise intensity
How does exercise effect O2 consumption and CO2 production and how can minute ventilation compensate
Basal 250 ml / min –> Strenuous exercise: 5000 ml/minute (20 fold)
CO2 production increases proportionately
Ve can increase 20 fold to match increases in VO2 from 5L/min to 100L/min
Which is the limiting factor with regard to exercise performance CVS or RSP
VO2 can increase 20 fold (250 –> 5000 ml/min)
Ve can increase 20 fold (5 –> 100 L/minute)
CO can increase 5 fold (5 –> 25 L/minute)
Therefore the CVS is the limiting system on exercise performance
How is ventilation increased at the beginning of exercise?
Anticipation of exercise
- Increase SNS vs PSNS –> increase Ve
- Voluntary motor cortex –> increase Ve
- Proprioception from limb joints –> increase Ve
How is ventilation increased after prolonged exercise
Ve increased in proportion to PaCO2
(sensed predominantly by central but also peripheral chemoreceptors)
As CO2 is a byproduct of skeletal muscle metabolism, Ve increases in proportion to the intensity of exercise
When does Ve increase disproportionately to VO2 and why does this occur
At the anaerobic threshold.
Anaerobic threshold –> DO2 cannot match VO2 –> anaerobic metabolism and acidosis –> reduced pH –> sensed by the carotid bodies –> further stimulation of the respiratory center
What are the effects of exercise on pulmonary blood flow
CO increased 5 fold –> delivered to lungs
Pulmonary vasculature responds by recruitment and distention to prevent MPAP increasing substantially.
Increase in MPAP NB to diminish the effect of gravity on the lung and to move regional V:Q to 1.0 (rest 0.8)
Gas exchange becomes more efficient and physiological shunt is reduced
How does the PaO2 change with moderate and strenuous exercise
It remains constant
OHDC P50 shifts to the right –> easier release of O2 to muscle
How efficient is skeletal muscle at converting energy into mechanical energy
25 % of chemical energy is converted into mechanical energy
75% dissipated as heat energy
Describe the process of thermoregulation during exercise
Intense exercise –> transient fall in Tcore as venous return increases from the limbs
Ongoing exercise –> net heat generation: sweating and peripheral vasodilation commence (also increase Ve contributes to heat loss through latent heat of evaporation as dry inhaled gases are humidified)
Controller - hypothalamus
Sensor - peripheral and central thermoreceptors
Effectors - Eccrine sweat glands + Cutaneous VD
How does heat stroke occur
Hot environment
- impaired heat loss via radiation and conduction
Humid environment
- impaired evaporative heat loss
Thermoregulation fails leading to heat stroke
At what Tcore does heat stroke occur
Tcore > 40,6 deg C
confusion
syncope
Rapid external cooling is required
Define VO2 max
VO2 increases linearly with exercise but reaches a plateau at VO2 max.
VO2 max is the maximum capacity of a person’s body to transport and use O2 during incremental exercise and is used as a measure of a person’s physical fitness
Unit: mLO2/kg/min
How is VO2 max determined
- O2 carrying capacity
- anaemia reduces VO2 max
- capillary density in muscles themselves
(altitude training increases vascular endothelial growth factor and EPO secretion) - CVS disease / beta blockers
- reduce VO2 max - Mild to moderate lung disease
- does not reduce VO2 max because Ve can increase 20 fold (vs CO 5 x) it is rarely the limiting factor
- Severe lung disease will reduce VO2 max
What are the two most important measurements acquired during cardiopulmonary exercise testing (CPET)
VO2 max (the maximum capacity of a persons body to transport and use O2 during incremental exercise)
Anaerobic threshold (the point at which O2 demand exceeds O2 delivery and anaerobic metabolism is commenced)
What are typical VO2 max values in normal, elite athletes, high risk postop complications, very high mortality
Units: mL/kg.min
Normal 25 - 40
Highest: 97.5 (elite cyclist)
High post op risk < 15
High post op mortality < 10 (consider conservative Rx)
What is 1 MET.
Give examples of activities requiring higher METs
The BMR of a fasted (8hr) and rested patient which has a VO2 of 3.5 ml/kg.min
3 METs - 1 flight stairs (VO2 ± 10 ml/kg.min) high periop mortality
4 METs - 2 flights of stairs (VO2 14 ml/kg.min) lower mortality risk
8 METs - 8 flights of stairs (VO2 > 20ml/kg.min) minimal perioperative mortality
What happens to VO2 after patient stops exercising
Excess post-exercise O2 consumption (EPOC) = O2 debt.
Phase 1 - alactacid phase - rapid
- ATP and phosphocreatine replenishment
- O2 replenishment to myoglobin
- Glycogen replenishment muscle/liver
Phase 2 - Lactacid phase - takes much longer
- Lactate converted back to pyruvate
What happens to metabolism in the longer term after exercise?
High catecholamine levels + raised temperature cause a global increase in metabolic rate
Anabolic processes (muscle repair and hypertrophy) occur over days to weeks of repeated exercise.
How does the CVS Elite athletes differ from the normal population
SV - Up to 40% increase
HR - Max HR unchanged. Resting HR low: increased Vagal tone. CO remains same due to increased SV
CO - Increased SV means that maximal CO is increased in atheletes
VOc max - Increase by 25% with training
(Increased O2 delivery due to increased muscle vascularization)
How do the RSP , MSK systems differ in elite athletes
RSP
- Max RR increases
- Increase lung volume
- Increase # pulm. capillaries
- -> Overall: Ve may increase by up to 15L/minute with training
MSK
- Hypertrophy
- Endurance: wider diameter of type 1 muscle fibers + increase activity of anaerobic metabolic enzymes
- Repetitive intense exercise:
