VO₂ max

[image]

point at which lactate entry into blood exceeds its removal

that point during incremental exercise where lactate begins to accumulate in the blood

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the classic "AT" model

(need whiteboard)

low muscle oxygen

*accelerated glycolysis

*recruitment of FT muscle fibers

*reduced rate of lactate removal

type of LDH enzyme

*may not be related to low levels of muscle O₂ and are therefore evidence against AT

why lactate accumulation may be independent of oxygen availability

INCREASED RATE OF GLYCOLYSIS

when rate of NADH production exceeds shuttle into mitochondria PA accepts some hydrogens and LA is formed

this can occur during exercise due to INC levels of E and NE

rate of NADH production can exceed shuttle rate causing pyruvic acid to accept unshuttled hydrogens

this can occur even when sufficient O₂ is present

[image]

when lactate accumulation may be independent of oxygen availability

LDH (lactate dehydrogenase) isozymes

LDH in FT fibers favor formation of LA from PA, whereas LDH in ST fibers favor conversion of LA to PA

this can occur when FT fibers are recruited even though oxygen is present in muscle

why lactate accumulation may be independent of oxygen availability

reduced rate of LA removal

blood LA concentration is determined by rate of LA entry into and rate of LA removal from the blood

shunting of blood flow from viscera (eg. liver) during intense exercise reduces rate of removal of LA

↑L_acc = P - R↓

  ↔

• LA rapidly dissociates into lactate and H⁺

• lactate accumulates in the blood, NOT LA

• lactate is formed and utilized continuously during exercise via lactate shuttles
• b/w FT and ST fibers
• b/w skeletal muscle and heart muscle
• b/w muscle and liver
• 70% oxidized, rest converted to glucose

• working skeletal muscle is both the site of lactate production and the major site its removal

• it is now known that lactate is oxidized in the mitochondria
• a H⁺ is removed from lactate forming NADH and pyruvate
• pyruvate goes to Krebs

1.) excretion in urine and sweat negligible

2.) conversion to glucose/glycogen (~20%)

3.) conversion to protein (~10%) small amount during immediate recovery

4.) oxidation/conversion to CO₂ and H₂O (~70%)

LA to PA: PA into Kreb's and ETC

this is the primary fate of LA after exercise

trained subjects have higher lactate metabolic clearance rate (clearance),

lower rate of appearance of lactate in the blood (appearance),

and lower lactate concentration

[image]

glucose released into the blood from the digestion of CHO bypasses the liver and is taken up by skeletal tissue

the muscle can either synthesize glycogen or produce LA

the LA then recirculates to the liver and stimulates glucose and glycogen formation

LA formed in active, FT fibers can reach adjacent ST fibers where it is a preferred fuel and can be combusted to CO₂

alternatively, lactate that comes from FT fibers can reach muscle capillaries and then go into the general circulation

the cori cycle: lactate as a fuel source

(need whiteboard)

*change LA at bottom to lactate*

[image]

the time it takes for 1/2 of the total accumulated LA to be removed during rest-recovery is 2x as long as that during exercise-recovery

b/w ST fibers (ones ones that better utilize LA) are the ones that contribute to light exercise

[image]

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-a break in V_E/VO₂ w/out a break in V_E/VCO₂

-ventilation INC w/ VCO₂

-when VCO₂ INC fater than VO₂, the ventilation (V_E) will follow VCO₂

- V_E will INC linerally with VCO₂, but NOT VO₂

-using measures at the mouth, VCO₂, VO₂, and V_E, a break poitn in ventilatory responses can be determined

-this disproportionate INC in VCO₂ is due to the non-metabolic production of CO₂ due to the buffering of LA

-since VCO₂ relates to both INC in LA buffering and ventilatory drive (V_E), then break in V_E must be due to INC in lactate production, ie AT or LT

V_E/VCO₂

(since relationship is linear throughout exercise intensities up to max, V_E/VCO₂ is a straight line relative to exercise intensity)

V_E/VO₂

(since V_E INC disproportionally to VO₂ as exercise intensity INC, V_E/VO₂ curves upward relavite to INC in exercise intensity)

[image]

McArdle syndrome results from a defect in a gene that makes glycogen phosphorylase

w/out glycogen phosphorylase, the body cannot break down glycogen during exercise and skeletal muscle cannot produce LA

w/out buffering of LA, ther should be no non-metabolic production and no VT during incremental exercise

-there shouldn't be a VT in McArdle's patients b/c they supposedly can't make non-metabolic CO₂

there is no lactate threshold in McArdle's patients, however there is a ventilatory threshold

[image]

1.) a good predictor of endurance performance is % utilization of VO₂max at LT or VT

2.) LT and VT are INC by training, i.e. occur at higher % of VO₂max after training

3.) LT and VT serve as markers separating moderate from high intensity exercise

determining exercise intensity using HRR (heart rate reserve)

(need whiteboard)

*the only reason we use HR as the basis of rx is because we can measure it*

1.)if HR max not available, 200-age

(220-22= 198)

2.) HRR = HRmax - HRrest

(198-68= 130)

3.) Multiply HRR by desired %age

(60-8%, 130x0.6= 78, 130x0.8= 104)

4.) THR (training heart rate)= step #3 + RHR

(78+68= 146, 104+68= 172)

*estimated THR range: 146-172 bpm*

as exercise intensity INC,

[image] 

greatest difference on curve between HR and LA

see slide 29, 30

exercise domains as described by blood lactate and oxygen kinetics

"MODERATE"

all work rates which can be done below the LT

VO₂ rises to reach a sustained steady state value within about 3 min

exercise domains as described by blood lactate and oxygen kinetics 

"HEAVY"

begins at LT

upper limit is work rate where blood lactate can be stabilized (MLSS or W_cp)

a steady state VO₂ is achieved above that predicted from intensities in the moderate domain due to slow component O₂ kinetics

*W_cp is max WR you can sustain aerobically*

exercise domains as described by blood lactate and oxygen kinetics

"SEVERE"

begins at W_cp

 upper limit is WR that elicits fatigue before slow component can drive VO₂ to a maximal value

lactate and VO₂ never stabilize

1.) exercise intensities below LT can be accomplished with steady state blood lactate and VO₂ responses

2.) exercise intensities above LT but below W_cp can be done with blood lactate levels that level off at an elevated value. 

VO₂ responses also level off but at a point above that predicted by the submax VO₂-WR relationship

3.) Prescribing exercise intensity within the heavy and severe domains as a % VO₂max is flawed since above W_cp and the VO₂ (ie. metabolic demand) is a f(x) of both WR and time

4.) be cautious when applying data obtained from non-steady state lab tests to steady rate situations