Gycogenolysis
 catabolism of glycogen molecule
 glycogen is polymer of glucose units
 form a pin-wheel-like structure around a
foundation protein, P-glycogenin
 linkages at C1-C4 or some C1-C6
Approx. 80% of carbon for
Glycolysis from glycogen, not
glucose
Breakdown is dependant on
activity of enzyme
phosphorylase, hydrolyzes the
C1-C4 linkages
Other enzyme, de-branching
enzyme hydrolyzes the C1-C6
or side linkages
Phosphorylase is controlled by
two mechanisms:
 hormonally mediated: extracellular action of
epi on intracellular action of cAMP
(intracellular hormone)
 too slow during the onset of heavy exercise
 mechanism mediated by Ca2+, from the SR,
parallel mechanism
Hormonally mediated cAMP
 amplifies the local Ca2+ -- mediated process
in active muscle
 mobilizes glycogen in inactive muscle to
provide lactate as glycogenic precursor
Phosphorylase is converted
from phosphorylase b
(inactive) to phosphorylase a
(active)
During exercise, AMP
increases, helping to minimize
the conversion from
phosphorylase a to b
RQ vs RER
 both are VO2 consumed/VCO2 produced
 RQ: at the cell level
 RER: at the mouth
RQ = RER, except at the
onset and offset of exercise,
due to body CO2 storage
changes
Protein RQ = 0.83
CHO RQ = 1.00
Fat RQ = 0.70
Anaerobic metabolism is not
well understood compared to
aerobic metabolism
Anaerobic: three misconceptions
 anaerobic metabolism during exercise
results in “O2 debt”
 lactic acid is a “dead-end” metabolite, only
formed, not removed during exercise
 elevation of lactic acid levels during exercise
represents anaerobiosis (O2 insufficiency)
Two assumptions about indirect
calorimetry
 ATP-PC stores are maintained, ATP comes
from respiration
 protein catabolism is insignificant during
exercise
– invalid, but necessary
Steady state/steady rate:
 oxygen consumption is relatively constant,
directly proportional to the constant submax
work load
Rate of appearance (Ra) and
Rate of disappearance (Rd) of
lactate, glucose, etc.
•Mild to moderate intensity exercise, lot of
lactate is formed
•High intensity exercise, more lactate is
produced and appears in the blood
•Muscle is a consumer of lactate
Misconception #1) O2
consumption during exercise
is insufficient to meet the
demands of exercise; creating
a debt
 body “borrows” from energy reserves or
credits
 after exercise, pay back credits
 the extra O2 consumed during recovery,
above resting O2 was the O2 debt
 Cease exercise: HR, breathing, etc. still
elevated
 B/c oxygen cost is still higher after
exercise compared to rest, originally
why thought is was “debt”
Excess Postexercise Oxygen
Consumption (EPOC)
 better descriptor of oxygen consumption
during recovery
EPOC due to




Temperature
Hormones
increased energy cost of ventilation
increased energy cost of HR
Two phases of recovery: fast
and slow
Much of work is based on
tracer methodology: infuse
radio-labeled 14C and 3H
tracers
Misconception #2) Lactate levels
lower in trained for both easy and
hard exercise
 lower lactate in TR concealed fact that LA
production was same in TR and UNTR
 TR improve lactate clearance
Anaerobic Threshold:
 increase in intensity
 oxygen consumption increases linearly
 but lactate levels not change until 60% of
max
marked inflection point, often
termed “anaerobic threshold” AT,
or “lactate threshold” LT
 Linkages between insufficient oxygen
(anaerobiosis)
 lactate production
 pulmonary ventilation
Lactic acid, HLA is strong acid:
 can readily dissociate a proton (H+ ion)
 HLA must be buffered:
 in blood, bicarbonate (HCO3-)- carbonic acid
(H2CO3) system
 HLA→ H- + LA H+ + HCO3-→ H2CO3
 H2CO3→H2O + CO2
McArdle’s Syndrome:
 lack enzyme phosphorylase
 still demonstrate ventilatory or “anaerobic
threshold”
Healthy young men: normally fed
and glycogen-depleted
 after depletion: ventilatory threshold at lower
power output and blood lactate threshold at
a higher power output
 dissociation of Tvent and Tlact in young men
after endurance training
Recovery
 active: cool down or tapering, submaximal
exercise
 passive: no exercise, lie down
Optimal recovery from steady
rate exercise
 if ex. <55-60% of max, little build up of HLA
 recovery: resynthesis of high energy
phosphates, replenish oxygen in blood,
body fluids, myoglobin, increased ventilation
 recovery is more rapid with passive
recovery, exercise elevate metabolism and
delay return to resting
Optimal recovery from nonsteady rate exercise
 if exercise > 55-60% of max, HLA
accumulation
 fatigue
 HLA removal from blood is accelerated by
active recovery
 29-45% VO2 max is optimal for bike
exercise
 55-60% is optimal for TM exercise
 difference is probably due to localized
nature of bike exercise, lower HLA
accumulation
Active Recovery
 40 min 35% of VO2 max
 40 min 65% of VO2 max
 40 min combination: 7 min @ 65%, 33 min
@ 35%
 40 min passive
 which is best? why?
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
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active recovery:
increases blood flow to active muscles
increases oxidation of LA
brings it to heart and liver, which have
increased perfusion
Intermittent Exercise
 decrease the LA buildup, contribution from
anaerobic metabolism
 can increase the capacity of aerobic system
to sustain exercise at a high rate of aerobic
energy transfer
 if exhaustion would ensue 3-5 minutes if
performed continuously, interval training
would benefit
 work to rest cycles, supramaximal
exercise to overload the desired energy
system
 if exercise < 8 sec, intramuscular
phosphates “worked”
 this form of exercise has a rapid
recovery, why?
 will discuss this more when discuss
training aerobic and anaerobic energy
systems