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rest to exercise transition to energy demand
we define energy utilization when its constant and standard
difference from rest to requirement during running
not a smooth transition in metabolic demand
muscle must increase ATP production from that required for standing to running
increase in HR and RR as we being ot exercise
increase in temp. slowly
not during initial transition
increase in BP
increase in SV → causes an increase in Q (cardiac output)
increasing ATP synthesis
energy system changers are supported by
respiratory changes increasing ventilation
increase O2
cardiovascular changes
increased Q
increased devilry of O2
vasodilation to working muscle
muscle changes
increased a release/uptake by SR
increase myoglobin shuttling
facilities O2 transfer to mm
mm protein structure
metabolic transition from rest to exercise
systemic response increases how we function until reaching steady state
utilization of free ATP - only takes a few secs
anaerobic lactate and aladctatic
PCr [] during prolonged exercise
does drop to 0 as another system sicks in
As PCr [] decreases ATP production through PCr hydrolysis decreases
Glycolysis steps up to pick pu the slack
ventilation increases as we continue to use glycolytic system
ATP produced through glycolytic origin
may be rate liming of not only using glycolysis
steady state occurs within 1-4mins
how does glycolysis know to start working
stimulated by products of PCr system
ATP, creatine kinase
all stimulates glycolysis
O2 defecit
amount of O2 produced via non aerobic sources
stead state - reached within 1-4mins
no fueling
ATP production aerobically
difference between O2 uptake in 1st few minutes of exercise and an equal time period after steady state has been obtained
lag in oxygen uptake at the beginning of exercise
oxygen deficit and EPOC
light ot moderate intensity exercise
metabolic rate remains constant up to 5mins post exercise even at moderate acitvity
oxygen uptake above the level needed to meet demands of standing following exercise
non steady state high intensity exercise
maintained for only 6mins before exhaustion
intensity that exceeds VO2max
could not meet oxygen requirement for task shown by increased oxygen deficit and VO2 above resting level 14mins after exercise
at plateau anaerobic production occurs
EPOC
Excess post-exercise oxygen copumotion
elevated O2 uptake (above resting VO2 following exercise
only 20% of elevated O2 consumption used to “repay” O2 defects and
convert lactate to glucose
gluconeogensis
convert lactate to pyruvate to engage with CAC and ETC in
Skeletal muscle
heart
brain
rapid portion of O2 EPOC
resynthesis of stored PC and ATP / lactate to pyruvate
replenishing muscle myoglobin and blood O2 stores (20% of EPOC)
resaturation of muscle
slow portion of O2 EPOC
elevated heart rate nad breathing
energy need
elevated blood temperature
metabolic rate
elevated epinephrine and norepinephrine
metabolic rate
conversion of lattice acid to glucose
CV and RR responses
heart and respiratory muscles maintain O2
increased sympathetic system
increased epinephrine and norepinephrine
increases réponse
gluconeogensis
glucose from non-carbohydrate sources generated in liver
why is O2 consumption so high if it is not exclusively used ot covert lactate ot glucose
summary of factors thought ot contribute to excess post exercise metabolism
glycolysis producing most of the ATP
elevated hormones
post-exercise elevation of HR and breathing
elevated body temperature
restoration of muscle and blood oxygen stores
lactate conversion to glucose
resynthesis of PC in muscle
removal of lactic acid following exercise
faster return to resting VO2 following cooldown
light exercise at 35% VO2 max
lactate removal is more rapid if continuous light exercise is performed as compared to resting recovery
light exercise increases oxidation of lactate by the working muscle
removal of lactic acid theories
classical theory
majority of lactic acid converted to glucose in liver
revent evidence
70% of lactic acid is oxidized by cells
used as a substrate by heart, brain and skeletal muscle
muscle using glucose producing lactate producing amino acids to structurally support the muscle
ability to utilize glucose depends on glucose stores in liver
20% converted to glucose
10% converted to amino acids
lactic acid is removed more rapidly from the blood if light exercise is performed during recovery
optimal intensity is ~30-40% VO2 max
bioenergetics during exercise: intensity and duration
Wingate sprint exercise
ATP turnover rate still not from most powerful tissues at beginning
30s all out sprints based on relative resistance
%7kg of bodyweight
ration shows more CHO than fasts even during sprint
Fats vs CHO
sustained steady state
more bonds takes time ot breakdown
once moving energy system takes off
plasma glucose is not that high even during 85% of VO2 max
requires medullas to be fuelled
may be beneficial to increase glycogen stores
use more glycogen to produce more glycogen
upward VO2 drift
hot and humid
drift upward of oxygen uptake
steady state is not maintained in this type of exercise even though work rate is constant
>75% VO2 max
slow rise in oxygen uptake across time
estimation of fuel utilization during exercise
respiratory exchange ration (RER or R)
R = VCO2/VO2
R for carbohydrate (glucose)
C6H12O6 + 6 O2 → 6 CO2 + 6 H2)
R = VCO2/VO2 = 6 CO2/6 O2 = 1.00
R for fat (palmitic acid)
C16H32O2 + 23 O2 → 16 CO2 + 16 H20
R = VCO2/VO2 = 16 CO2/23 O2 = 0.70
incremental exercise test
VO2 max
maximal capacity ot transport and utilize O2 during exercise
O2 uptake increases systematically with work rate until VO2 max is reached
at max an increase in power output does not result in an increase in oxygen uptake
physiological ceiling for the ability of the oxygen transport system to deliver O2 to contracting muscles
criteria for VO2 max
age predicted HR max
blood lactate of 8 mm or higher
RER above 1.15