Transcript Anaerobic Threshold

Anaerobic Threshold
Does it exist?
How is it determined?
Anaerobic Threshold
 How is anaerobic threshold defined?
– power just before onset of metabolic acidosis & 
RER (Wasserman et al., 1973)
 What was/is theoretical basis for anaerobic
threshold?
– effects on R (RER), lactate formation, VCO2, blood
[bicarbonate]
 How is anaerobic threshold determined?
– changes in blood [lactate]
– ventilatory measures
• RER, VCO2, VE, PETO2 and PETCO2, VE/VO2 and VE/VCO2
Anaerobic threshold: does it exist
Comments by GA Brooks (1985)
 Key component of AnT hypothesis is that muscle
becomes hypoxic during submaximal exercise
– femoral PvO2 did not fall <10 Torr when at 50% of
VO2max (Pirnay et al., JAP, 1972)
– muscle produced La at 10% of VO2max; La production
linearly related to work rate;  blood flow did not affect
La production (Connett et al., Am J Physiol, 1984)
– muscle produces La before blood LT or VT (Green et al.,
JAP, 1983)
Anaerobic threshold: does it exist
Comments by GA Brooks
 VT and AnT occur at same point  AnT causes
VT
– this relationship does not always hold, therefore must
be considered invalid
– disassociation of AnT and VT in glycogen-depleted
subjects (Segal & Brooks, JAP, 1979)
– McArdles patients cannot produce La, but still exhibit
VT (Hagberg et al., JAP, 1982)
– measuring LT is cheaper (and more accurate) than
VT
Control of Ventilation
 Ventilatory control is by:
– feedback (central and carotid chemoreceptors)
– feed forward (central command, muscle feedback)
 Redundancy mechanisms control VE
 VE responds more closely to demands for CO2
clearance than O2 uptake
– ventilation below lactate threshold regulates PaCO2
keeping it at resting levels
Buffering of blood pH
 Primary blood buffer is bicarbonate
H+ + lactate- + Na+ + HCO3-  Na+ + lactate- + H2CO3  H2O + CO2
Wasserman et al., JAP, 1973
New method for detecting AnT by gas exchange
(Beaver, Wasserman & Whipp, JAP, 1986)
V-slope method criteria
 break in linearity of VCO2–VO2
 break in linearity of VE–VO2
 VE/VO2 breaks with linearity while VE/VCO2 remains
constant
 PETO2–VO2 begins to rise while PETCO2–VO2 is
slowly rising or constant
 RER–VO2 having been flat or rising slowly changes to
more positive slope
VE vs VO2
200
180
Respiratory compensation point
stimulated by pH
160
VE (L/min)
140
120
100
80
60
Ventilatory threshold
stimulated by CO2 production
40
20
0
0
1
2
3
4
VO2 (L/min)
5
6
7
AnT points detected by six
investigators (multiple
vertical lines).
Most difficult subject. AnT
was detected by only two
investigators.
Beaver, Wasserman, & Whipp, JAP, 1986)
Blood Lactate Accumulation and
Removal
Effects on Blood Lactate Concentration
Lactate Response to Prolonged Exercise
(70% of VO2max)
Lactate (mM)
3.0
2.5
2.0
1.5
1.0
0.5
0.0
0
30
60
90
120
150
180
Time (min)
(Kolkhorst & Buono, Virtual Exercise Physiology Lab, 2004)
Lactate Response to Prolonged Exercise
Lactate Response to Incremental Exercise
(endurance-trained athlete)
Lactate (mM)
12
10
8
6
4
2
0
0
10
20
30
40
50
60
70
80
90
100
% of VO2max
(Kolkhorst & Buono, Virtual Exercise Physiology Lab, 2004)
Mitochondrial PO2 during exercise
Relationship between mitochondrial
VO2 and PO2. Critical mitochondrial
PO2 is around 1.0 torr. (Rumsey et al.,
1990)
Muscle intracellular PO2 and net
lactate release. Note that PO2
remains above critical
mitochondrial O2 tension (1 torr).
(Richardson et al., 1998)
Why does blood lactate increase during
heavy exercise?
 lactate appearance exceeds
lactate removal
 evidence does not point to
muscle hypoxia
 FT recruitment
– FT fibers have M-LDH
– ST fibers have H-LDH
 epinephrine release
Effects of epinephrine (EPI) on
metabolism
  glycogenolysis
  glycolysis
 inhibits lipolysis
La and EPI Response to Exercise
La
EPI
Effect of Altitude on La Response
At altitude:
 LT occurs at same relative intensity
 blood [La] higher at same absolute workloads
 muscle blood flow similar at same absolute workloads
 EPI threshold occurs earlier at altitude
 Lactate paradox – peak [La] is less under hypoxic
conditions than at normoxia
Metabolic Fate of Lactate
Reading Assignment
for Tue, Oct 9
Holden, S-MacRae, SC Dennis, AN Bosch, and TD
Noakes. Effects of training on lactate production and
removal during progressive exercise in humans. J Appl
Physiol 72: 1649-1656, 1992.
-- or -Stanley, WC, EW Gertz, JA Wisneski, DL Morris, R Neese,
and GA Brooks. Systemic lactate turnover during graded
exercise in man. Am J Physiol 249 (Endocrinol Metab
12): E595-E602, 1985.
Energetic Value of Lactate
Glycolysis/
oxidation
Kreb's Cycle
Electron
Transport Chain
Total
Muscle
glycogen (C6)
2
Palmitic acid
(C16)
--
2
8
32-34
121
36-38
129
Lactate Shuttle
Cori Cycle
Metabolic Fate of Lactate
 During exercise:
– ~75% oxidized by heart, liver, and ST fibers
 During recovery:
–
–
–
–
oxidized by heart, ST fibers, and liver (1 fate)
converted to glycogen
incorporated into amino acids
La metabolism depends on metabolic state
Fate of lactate 4
hr after injection
under three
recovery
conditions. Note
that oxidation is
1 pathway of
removal.
Determining lactate turnover during
exercise: tracer methodology
 use naturally occurring isotopes
–
13C
and 2H isotopes most commonly used
 pulse injection tracer technique
– labeled La added to blood in single bolus
– concentration measurements taken over time
– rate of concentration decline represents turnover rate
 continuous-infusion technique
– labeled La added at increasing rate until equilibrium
point is reached, i.e., La appearance = La removal
Pulse injection tracer technique
Continuous infusion tracer technique
WHEN YOU ARE IN DEEP TROUBLE,
LOOK STRAIGHT AHEAD, KEEP YOUR
MOUTH SHUT and SAY NOTHING.
Primed continuous-infusion technique
(used by Stanley et al. and MacRae et al.)
 turnover rate = appearance - disappearance
 Ra dependent on:
– volume of distribution
– arterial [La]
 Rd = Ra minus arterial [La]
 metabolic clearance rate (MCR) = Rd / [La]
– calculates La clearance rate relative to arterial [La]
– increasing MCR indicates Rd is dependent on arterial [La]
Lactate response to graded exercise
(Stanley et al., JAP, 1985)




Ra and Rd exponentially related to VO2
“linear” relationship between Ra and arterial [La]
curvilinear relationship between Rd and arterial [La]
MCR decreased at higher work rates
– Rd was slowed as blood [La] increased
– Rd is dependent on blood [La]
– Rd is function of blood [La] and Ra
Rates of blood lactate appearance (Ra) and disappearance
(Rd) during graded exercise before and after training
Holden et al., JAP, 1992
Training adaptations to lactate kinetics
(Holden et al., JAP, 1992)







submaximal Ra  by training
peak Ra similar regardless of training status
at same relative intensities, Ra was  at <60% and similar at >60%
submaximal Rd  by training
peak Rd  regardless of training status
at same relative intensities, Rd was similar at <60% and  at >60%
at same relative intensities,  [La]
– at <60% was due primarily to  Ra ( EPI and CHO metabolism)
– at >60% was due primarily to  Rd (lactate shuttle)
65% pretraining
65% posttraining (same relative workload)
65% posttraining (same absolute workload as
45% pretraining)
45% pretraining
Effect of training on blood
lactate response
Bergman et al., Am. J. Physiol., 1999
Lactate clearance
Monocarboxylate transporters (MCTs)
Andrew Halestrap, University of Bristol
Monocarboxylate transporters
 facilitated diffusion transport of lactate and
pyruvate in and out of cells
– located on plasma and mitochondrial membrane
– reversible transporter
– involves H+ transport
 MCT1 and MCT4 are major MCT isoforms
– MCT1 found more in oxidative fibers
– MCT4 found more in glycolytic fibers
– at least 8 isoforms of MCTs known in humans
MCT1 in heart is
concentrated at the
intercalated disks
and t-tubules
Prevalence of MCT1
and MCT4 in
muscles of different
fiber type
composition
MCT1
MCT4
Semimembranosus
soleus
Monocarboxylate transporters
 La transport is essential for muscle pH
regulation
 MCT activity regulated mostly by La gradient
– pH gradients can also increase transport rate
 exercise training  MCT1, but not MCT4