Seminar in Advanced Physiology of Exercise

1
Seminar in Advanced Physiology of Exercise

• Fred W. Kolkhorst, Ph.D.
• ENS 311, 594-1924
• fred.kolkhorst_at_sdsu.edu
• MWF 930-1100

2
Course information

• Textbook ACSMs Advanced Exercise Physiology.
  Lippincott Williams Wilkins, 2006.
• Course website http//www-rohan.sdsu.edu/ens661
• Southwest Chapter of American College of Sports
  Medicine Annual Meeting (http//www.swacsm.org)
• November 9-10, 2006, Marriott Mission Valley
  Resort Hotel, San Diego
• Abstract submission deadline is Sep 14 (500 pm
  PST)
• ACSM annual meeting (http//www.acsm.org)
• May 28-31, 2008, Indianapolis, IN
• Abstract submission deadline is Nov 1
• University Student Symposium
• February 29-March 1, 2008, Aztec Center
• Abstract submission deadline is Jan 15

3
Course Grading

• Two exams (100 points each)
• Participation
• Come to class prepared to discuss perspectives of
  assigned readings
• Group presentation

4
Measurement of Energy Expenditure

• Metabolism anabolism catabolism
• Muscles are chemotransducers of energy
• Food O2 ? CO2 H2O ATP heat
• Heat measured in units of calorie (generally in
  kilocalories)
• We use indirect calorimetry in our labs

5
Measuring VO2

• VO2 measured by indirect calorimetry that
  typically uses a
• mixing chamber, or
• breath-by-breath

6
Effect of smoothing data on VO2 noise
7
Descriptions of Exercise IntensitiesExercise
Domains
CP critical power LT lactate threshold
8
Critical Power

• A hyperbolic relationship between power
  output/running velocity and endurance.
• Strong predictor of endurance performance

9
Determining Critical Power

1. Perform gt3 tests to exhaustion (4-10 min)
2. Plot inverse exhaustion time against power
3. Use linear regression to determine power
   intercept, which equals CP

Coates et al., J Appl Physiol, 2003
10
Reading Assignmentfor Thursday

• Coats, EM, et al., Intensity-dependent tolerance
  to exercise after attaining VO2max in humans. J
  Appl Physiol 95 483-490, 2003.

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Critical Power (CP)

• Theoretically, how long could one exercise at an
  intensity above CP?
• At an intensity above CP, what would happen to
  VO2?
• At an intensity at or below CP, what would happen
  to VO2?

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Oxygen Uptake KineticsWhat does it mean and
what does it measure?
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What is VO2 and what is VO2 kinetics?

• VO2 is rate of O2 uptake determined from
  pulmonary measurements
• VO2 kinetics describes rate of VO2 change at
  exercise onset

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VO2 response to heavy exercise
? 5-s averages
? nonlinear regression modeling
Residuals
Kolkhorst et al., MSSE, 2004
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Three-component model of VO2 kinetics(for supra
LT intensity)

• Phase 1 (cardiodynamic component)
• due to rapid increase of HR and pulmonary blood
  flow
• occurs during first 15-25 s
• Phase 2 (rapid component)
• begins 20 s
• thought to reflect mitochondrial VO2
• Phase 3 (slow component)
• only occurs at intensities gt LT
• primary cause is recruitment of additional motor
  units due to fatigue

Phase I
Phase II
Phase III
?3
A'3
?2
VO2
A'2
?1
A'1
VO2base
TD2
TD3
Time
Initiation of exercise
VO2(t) VO2base A1 (1-e-(t-TD1)/?1) A2
(1-e-(t-TD2/?2) A3 (1-e-(t-TD3)/?3)
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What does time constant (?) represent?

• time constant (?) time for amplitude to ? 63
• 2? 86 of amplitude
• 3? 95
• 4? 98

17
Effect of tau on VO2 kinetics
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Why study VO2 kinetics?
Grassi et al., JAP, 1996
19
pVO2 (closed circles) and intramuscular PCr
responses to moderate- and high-intensity
exercise and recovery
Rossiter et al., J Physiol (2002)
20
Creatine Shuttle Stimulator of Mitochondria?
PCr is ? w/ exercise, which stimulates
mitochondria to synthesize ATP to replenish PCr
Walsh, MSSE, 2002
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What limits mitochondrial respiration at exercise
onset?

• Oxygen utilization? (Grassi et al.)
• infers metabolic inertia
• Oxygen delivery? (Hughson Morrisey, JAP, 1982)
• infers that PmitO2 is not saturating in all
  active muscle fibers at all time points

22
VO2 response to electrical stimulation in
isolated canine muscleNo differences in VO2
time constant between three conditions. RSR13
is a drug that shifts O2-Hb dissociation curve to
the right, i.e., causes Hb to give off more
O2(Grassi et al., JAP 1998)
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Does O2 delivery limit mVO2 kinetics?Blood flow
enhanced with adenosine and VO2 kinetics was
compared to control. Moderate intensityAt 60
of VO2peak, enhancing blood flow had no effect on
?. Maximal intensityAt 100 of VO2peak,
enhanced ? was faster than control ? (18.5 vs.
24.9 s, respectively)(Grassi et al., 1998, 2000)
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Effect of bicarbonate on VO2 kinetics during
heavy exerciseMethods

• 10 active subjects (28 ? 9 yr 82.4 ? 11.2 kg)
• On separate days, performed two 6-min bouts at 25
  W greater than VT
• ingested 0.3 g?kg-1 body weight of sodium
  bicarbonate with 1 L of water or water only
• Measured pre-exercise blood pH and bicarbonate

Kolkhorst et al., MSSE, 2004
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VO2 kinetics from heavy exercise
Control Bicarbonate
A'2 (mL?min-1) 1444 ? 177 1597 ? 198
TD2 (s) 27.3 ? 3.5 27.2 ? 3.7
?2 (s) 20.8 ? 2.4 27.9 ? 3.5
A'3 (mL?min-1) 649 ? 53 463 ? 43
TD3 (s) 98.9 ? 11.9 127.5 ? 14.1
?3 (s) 244.8 ? 50.5 132.1 ? 21.5
?VO2(6-3) (mL?min-1) 302 ? 36 253 ? 40
P lt 0.05
Kolkhorst et al., MSSE, 2004
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• Why did bicarbonate affect rapid component?
• alkalosis decreased vasodilation and caused
  leftward shift of O2-Hb dissociation curve
• effects of prior heavy exercise on rapid
  component are equivocal
• ? ?2 and MRT (MacDonald et al., 1997 Rossiter et
  al., 2001 Tordi et al., 2003)
• n/c in ?2, but ? A'2 and ? A'3 (Burnley et al.,
  2001 Fukuba et al., 2002)
• Why did bicarbonate affect slow component?
• bicarbonate attenuates decreases in muscle pH
  (Nielsen et al., 2002 Stephens et al., 2002)
• Does ?pH cause fatigue?
• Westerblad et al. (2002) suggested Pi
  accumulation primary cause
• bicarbonate ingestion ? performance

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Effect of blood pH on VO2 kinetics during heavy
exercise

• Subjects completed two 6 min bouts of heavy
  cycling
• Recovered between bouts with moderate cycling for
  either 6 min or until blood pH returned to
  resting levels
• For the 6-min recovery trial, MRT of the two
  bouts decreased from 59.6 9.3 s to 46.1 8.0 s
  (P 0.002)
• For the long-recovery trial, MRT also decreased
  from 57.6 10.0 s to 49.5 5.6 s (P 0.002).
• no difference in MRT between the second bouts
• Conclusion blood pH does not influence MRT,
  rather faster second bout was result of
  mitochondrial adaptation

Wooten et al., unpublished data
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What is primary regulator of mitochondrial
respiration at exercise onset?

• Oxygen utilization?
• Oxygen delivery?

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Pulmonary VO2 kinetics are known to be

• faster in trained than untrained
• faster during exercise with predominantly ST
  fibers than FT fibers
• slower after deconditioning
• slower in aged population
• slower in patients with respiratory/CV diseases
  as well as in heart and heart/lung transplant
  recipients

VO2 kinetics appears to be more sensitive than
VO2max or LT to perturbations such as exercise
training
30
Measuring Anaerobic Work Capacity

• Wingate test most commonly used
• Measurement of blood La as a surrogate for
  muscle La
• Measurement of EPOC
• Measurement of O2D
• must accurately know energy expenditure
• what is the cause of exhaustion?

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Oxygen deficit

• August Krogh and Johannes Lindhard (both Danish)
  reported the lag in O2 uptake, which they
  quantified and defined as O2 deficit, and its
  relation to O2 debt (EPOC) (J Physiol, 1919/1920)
• They were pioneers in study of gas exchange in
  lungs, contribution of fat and CHO oxidation
  during exercise, redistribution of blood flow,
  measurement of cardiorespiratory dynamics
• Krogh received Nobel prize in 1920 for discovery
  of mechanism in controlling capillary blood flow
• Archibald Vivian Hill, British physiologist,
  documented the exponential increase of VO2 with
  exercise onset
• quantified work and efficiency of frog muscle
• pioneered physiological study of exercising
  humans including lactate production and
  interrelationship with O2 debt (EPOC), and VO2max
• Hill received Nobel prize in 1921 for work in
  energy metabolism
• regarded as one who has made greatest
  contribution to exercise physiology
• Hill-Meyerhof proposed theory of O2 debt (now
  called O2 deficit)

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Oxygen deficit

• Lundsgaard (1930) demonstrated that muscle unable
  to produce lactic acid can still contract
  (Biochemische Zeitschrift, 1930)
• led to understanding of role of PCr and ATP
  (Lohmann, Biochemische Zeitschrift, 1934, 1935)
• role of lactacid and alactacid contributed to O2D
• resynthesis of PCr during rapid component of EPOC
  and lactate clearance during slow component

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O2 Deficit and Excess Post-Exercise Oxygen
Consumption (EPOC)
exercise recovery
O2D
VO2
EPOC
Resting energy requirements
Time
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Excess post-exercise oxygen consumption (EPOC)
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Oxygen deficit

• O2D is a capacity, not a rate
• MAOD achieved at 2 min
• Components of O2D
• Glycolysis (Glucose ? 3ATP 2HLa) (60-70)
• ATP and PCr stores (PCr ADP ? ATP Cr)
  (22-30)
• adenylate kinase Rx (2ADP? ATP AMP) (?)
• stored O2 in Hb and Mb (8-10)
• Anaerobic training will ? maximal accumulated O2
  deficit (MAOD)

36
Determining supramaximal intensities
120
100
VO2max
of VO2max
Exercise Intensity

37
Oxygen deficit affected by exercise intensity
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Effect of time constant (?) on O2 deficit
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For Tue, Sep 5, read

• Green, S, BT Dawson, C Goodman, and MR Carey. 
  Anaerobic ATP production and accumulated O2
  deficit in cyclists.  Med. Sci. Sport Exerc.
  28(3) 315-321, 1996.
• Scott, CB, FB Roby, TG Lohman, and JC Bunt.  The
  maximally accumulated oxygen deficit as an
  indicator of anaerobic capacity.  Med. Sci.
  Sports Exerc. 23(5) 618-624, 1991.
• identify the purpose of the study,
• briefly, describe the exercise protocol and the
  primary physiological measurements taken,
• identify primary results of the study,
• identify conclusions of the study, and
• respond to all other questions listed under the
  reading assignment.

40
For Thu, Sep 6, read

• Noakes, TD. Challenging beliefs ex Africa semper
  aliquid novi.  Med. Sci. Sports Exerc. 29(5)
  571-590, 1997.
• focus on pp 577-585, Creaking Edifices 1 - 3

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Three ugly and creaking edifices (Noakes,
1997, pp 577-585)

• VO2 plateaus at maximal effort
• O2 limitation at maximal effort causes muscle
  hypoxia to terminate exercise
• what limits VO2?
• Progressive muscle hypoxia limits exercise
  performance
• hypoxia results from CO insufficiency to match
  muscle demands
• Anaerobiosis explains onset of La production
• O2 delivery become inadequate at anaerobic
  threshold

42
For Tue, Sep 11, read

• Bassett, Jr., DR and ET Howley.  Maximal oxygen
  uptake "classical" versus "contemporary"
  viewpoints. Med. Sci. Sports Exerc. 29(5)
  591-603, 1997.
• OR
• Noakes, TD. Maximal oxygen uptake "classical"
  versus "contemporary" viewpoints a rebuttal. 
  Med. Sci. Sports Exerc. 30(9) 1381-1398, 1998.

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For Thu, Sep 13, read

• Wagner, PD. The oxygen transport system
  integration of functions (chapter 11), ACSMs
  Advanced Exercise Physiology. pp 300-308, 311-312.