cardiorespiratory adjustments in exercise Flashcards
3 muscle types
slow twitch - type I
fast twitch - type IIa and IIb
slow twitch is carried out by what process
oxidative phosphorylation
fast twitch is carried out by what process
relies on creatine phosphate to regenerate ATP
physical characteristics of slow twitch muscles
– good blood supply
– lots of mitochondria & myoglobin
– mainly postural but also used in endurance events
physical characteristics of fast twitch muscles
– not so dependent on blood supply or mitochondria
– large amount of glycolytic enzymes
– used in sprinting and “explosive” events
ATP pool required for contraction is regenerated from three sources
– cellular respiration (requires O2)
– creatine phosphate (4 – 5x that of ATP)
– muscle glycogen
when is creatine phosphate used
for short bursts of energy can be used to replenish ATP from ADP
when is glycogen used?
– large stores of glycogen can be broken down to provide substrate for glycolysis
– yields 2 ATP and 2 lactic acid molecules, enough to function if O2
is insufficient
– however, it is limited and eventually muscle must depend on cellular respiration
exercise intensity is defined in terms of
oxygen uptake
how does oxygen consumption change with work during dynamic exercise
in a linear manner
maximal oxygen consumption
VO2 Max
how is maximal oxygen consumption measured
incremental increases in exercise intensity
cardiorespiratory adjustment
• To facilitate O2 consumption and prevent fatigue there needs to be
the continued delivery of O2
to the muscle
what can a lack of oxygen during respiration lead to
lack of O2 means anaerobic respiration and lactate acidosis
• O2 delivery depends on three aspects
- Getting O2
into the body and blood (respiration) - Getting O2 from the lungs to the tissues (cardiovascular delivery)
- Getting O2 from the blood to the respiring tissues (O2 extraction)
how does the oxygen consumption and carbon dioxide production change during exercise
In exercise both O2 consumption and CO2 production increase
how is oxygen delivery and CO2 removal facilitated during exercise
both respiratory rate and tidal
volume increase
– tachypnoea not hyperventilation
how is respiratory function controlled
“chemically” controlled
– via peripheral and central chemorecptors
how does peripheral receptor respond to adjustments and what does it respond to?
drive peripheral receptor due to increase in acidity
lead to hyperventilation
anaerobic threshold
The anaerobic threshold is when demand for O2 exceeds delivery
– tissues start to respire anaerobically
how can glycolysis continue
NADH must be recycled back to NAD+
– done by lactate dehydrogenase converting pyruvate to lactate
drops pH
increasing acidity
metabolic lactic acid acidosis
stimulates peripheral chemoreceptors and increased ventilation
what drives cardiovascular adaptation
SNS
How does SNS help adapt cardiovascular
Increase in cardiac output and the redistribution of blood flow
– SNS increase in heart rate and stroke volume as well as vasoconstriction
• Direct sympathetic action on heart rate and contractility
• Increased venous return and therefore stroke volume
– due to increased muscle pump, respiratory pump and venoconstriction
• Sympathetic vasoconstriction and metabolite vasodilatation alter
pattern of distribution
– away from GI, renal and to working muscle and heart
hyperaemia
dilate all capillary vessel when there is greater surface area for perfusion and decrease in perfusion distance to accommodate greater oxygen demand
greater concentration gradient
no change in solute diffusity
how does increased CO2 and H+ and temp affect oxygen delivery to tissue
reduce affinity for Hb - Bohr effect - shift dissociation curve to the right
promote oxygen delivery to tissue
how is oxygen debt repaid
– fast: re-phosphorylation of ATP/creatine
– slow: lactate conversion back to glucose/glycogen
– ultraslow: increased metabolic rate after exercise
oxygen debt
as the VO2
in excess of resting after exercise
3 stages in which oxygen debt is incurred
– depletion of ATP, depletion of creatine phosphate then the build up of lactic acid
why is there such thing as an oxygen debt
Adaptations aim to supply O2 to match demand during exercise - but when exercising is over the initial deficit will need to be repaid
how does training affect muscle
increase muscle strength and resistance to fatigue
muscle hypertrophy - larger muscle fibres not hyperplasia - getting more muscle fibres
increased glycolytic and oxidative capacity - increased glycogen, ATP , phospho-creatinine, mitochondrial enzymes
cardiorespiratory effects of training
Bradycardia and cardiac remodeling
reduced blood pressure - enhances endothelial function, inc. muscle capillary density
increased myoglobin and 2,3,BPG
reduced ventilation at same work rate - shift in anaerobic threshold
other effects of training
increase VO2 max and O2 debt and anaerobic threshold
during what time period can significant improvement be seen
8-10 weeks
30 min sessions, 2/3 times per week
60% max O2 consumption
what will training not improve
– VO2 or the cardiac output at rest
– diffusing capacity or the haemoglobin concentration
– maximum heart rate
