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 Ca 2+, from the SR, parallel mechanism

Hormonally mediated cAMP  amplifies the local Ca 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 VO 2 consumed/VCO 2 produced  RQ: at the cell level  RER: at the mouth

RQ = RER, except at the onset and offset of exercise, due to body CO 2 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 “O 2 debt”  lactic acid is a “dead-end” metabolite, only formed, not removed during exercise  elevation of lactic acid levels during exercise represents anaerobiosis (O 2 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 (R a ) and Rate of disappearance (R d ) of lactate, glucose, etc. Mild to moderate intensity exercise, lot of lactate is formedMild to moderate intensity exercise, lot of lactate is formed High intensity exercise, more lactate is produced and appears in the bloodHigh intensity exercise, more lactate is produced and appears in the blood Muscle is a consumer of lactateMuscle is a consumer of lactate

Misconception #1) O 2 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 O 2 consumed during recovery, above resting O 2 was the O 2 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 14 C and 3 H 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 (HCO 3 - )- carbonic acid (H 2 CO 3 ) system  HLA→ H - + LA -  H + + HCO 3 - → H 2 CO 3  H 2 CO 3 →H 2 O + CO 2

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 T vent and T lact 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 non- steady rate exercise  if exercise > 55-60% of max, HLA accumulation  fatigue  HLA removal from blood is accelerated by active recovery  29-45% VO 2 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 VO 2 max  40 min 65% of VO 2 max  40 min combination: 7 65%, 33 35%  40 min passive  which is best? why?

 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