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Seminar in Advanced Physiology of Exercise Fred W. Kolkhorst, Ph.D. ENS 311, 594-1924 MWF 9:30-11:00.

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Presentation on theme: "Seminar in Advanced Physiology of Exercise Fred W. Kolkhorst, Ph.D. ENS 311, 594-1924 MWF 9:30-11:00."— Presentation transcript:

1 Seminar in Advanced Physiology of Exercise Fred W. Kolkhorst, Ph.D. ENS 311, MWF 9:30-11:00

2 Course information  Textbook: ACSM’s Advanced Exercise Physiology. Lippincott Williams & Wilkins,  Course website:  Southwest Chapter of American College of Sports Medicine Annual Meeting (http://www.swacsm.org)http://www.swacsm.org –November 9-10, 2006, Marriott Mission Valley Resort Hotel, San Diego –Abstract submission deadline is Sep 14 (5:00 pm PST)  ACSM annual meeting (http://www.acsm.org )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 + O 2  CO 2 + H 2 O + ATP + heat  Heat measured in units of calorie (generally in kilocalories)  We use indirect calorimetry in our labs

5 Measuring VO 2  VO 2 measured by indirect calorimetry that typically uses a –mixing chamber, or –breath-by-breath

6 Effect of smoothing data on VO 2 noise

7 CP = critical power LT = lactate threshold Descriptions of Exercise Intensities Exercise Domains

8 Critical Power  A hyperbolic relationship between power output/running velocity and endurance.  Strong predictor of endurance performance

9 Determining Critical Power 1.Perform >3 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 Assignment for Thursday  Coats, EM, et al., Intensity-dependent tolerance to exercise after attaining VO 2max in humans. J Appl Physiol 95: , 2003.

11 Critical Power (CP)  Theoretically, how long could one exercise at an intensity above CP?  At an intensity above CP, what would happen to VO 2 ?  At an intensity at or below CP, what would happen to VO 2 ?

12 Oxygen Uptake Kinetics: What does it mean and what does it measure?

13 What is VO 2 and what is VO 2 kinetics?  VO 2 is rate of O 2 uptake determined from pulmonary measurements  VO 2 kinetics describes rate of VO 2 change at exercise onset

14 VO 2 response to heavy exercise Kolkhorst et al., MSSE, 2004  5-s averages  nonlinear regression modeling Residuals

15 Three-component model of VO 2 kinetics (for supra LT intensity) Phase 1 (cardiodynamic component)  due to rapid increase of HR and pulmonary blood flow  occurs during first s Phase 2 (rapid component)  begins ~20 s  thought to reflect mitochondrial VO 2 Phase 3 (slow component)  only occurs at intensities > LT  primary cause is recruitment of additional motor units due to fatigue 22 33 11 TD 2 A' 3 A' 2 A' 1 VO 2base Phase IPhase II Time VO 2 Initiation of exercise TD 3 Phase III VO 2(t) = VO 2base + A 1 (1-e -(t-TD1)/  1 ) + A 2 (1-e -(t-TD2/  2 ) + A 3 (1-e -(t-TD3)/  3 )

16 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 VO 2 kinetics

18 Why study VO 2 kinetics? Grassi et al., JAP, 1996

19 pVO 2 (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? Walsh, MSSE, 2002 PCr is  w/ exercise, which stimulates mitochondria to synthesize ATP to replenish PCr

21 What limits mitochondrial respiration at exercise onset?  Oxygen utilization? (Grassi et al.) –infers metabolic inertia  Oxygen delivery? (Hughson & Morrisey, JAP, 1982) –infers that P mit O 2 is not saturating in all active muscle fibers at all time points

22 VO 2 response to electrical stimulation in isolated canine muscle No differences in VO 2 time constant between three conditions. RSR13 is a drug that shifts O 2 -Hb dissociation curve to the right, i.e., causes Hb to give off more O 2 (Grassi et al., JAP 1998)

23 Does O 2 delivery limit mVO 2 kinetics? Blood flow enhanced with adenosine and VO 2 kinetics was compared to control. Moderate intensity At 60% of VO 2peak, enhancing blood flow had no effect on . Maximal intensity At 100% of VO 2peak, enhanced  was faster than control  (18.5 vs s, respectively) (Grassi et al., 1998, 2000)

24 Effect of bicarbonate on VO 2 kinetics during heavy exercise Methods  10 active subjects (28  9 yr; 82.4  11.2 kg)  On separate days, performed two 6-min bouts at 25 W greater than V T –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

25 VO 2 kinetics from heavy exercise ControlBicarbonate A' 2 (mL  min -1 )1444   198 TD 2 (s) 27.3   3.7  2 (s)20.8   3.5* A' 3 (mL  min -1 )649   43* TD 3 (s) 98.9   14.1  3 (s)244.8   21.5 ΔVO 2 (6 -3) (mL  min -1 )302   40 * P < 0.05 Kolkhorst et al., MSSE, 2004

26 Why did bicarbonate affect rapid component? –alkalosis decreased vasodilation and caused leftward shift of O 2 -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

27 Effect of blood pH on VO 2 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

28 What is primary regulator of mitochondrial respiration at exercise onset?  Oxygen utilization?  Oxygen delivery?

29 Pulmonary VO 2 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 VO 2 kinetics appears to be more sensitive than VO 2max or L T 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 O 2 D –must accurately know energy expenditure –what is the cause of exhaustion?

31 Oxygen deficit  August Krogh and Johannes Lindhard (both Danish) reported the lag in O 2 uptake, which they quantified and defined as O 2 deficit, and its relation to O 2 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 VO 2 with exercise onset –quantified work and efficiency of frog muscle –pioneered physiological study of exercising humans including lactate production and interrelationship with O 2 debt (EPOC), and VO 2max –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 O 2 debt (now called O 2 deficit)

32 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 O 2 D –resynthesis of PCr during rapid component of EPOC and lactate clearance during slow component

33 O 2 Deficit and Excess Post-Exercise Oxygen Consumption (EPOC) VO 2 Time Resting energy requirements EPOC O2DO2D exerciserecovery

34 Excess post-exercise oxygen consumption (EPOC)

35 Oxygen deficit  O 2 D is a capacity, not a rate –MAOD achieved at ~2 min  Components of O 2 D –Glycolysis (Glucose  3ATP + 2HLa) (60-70%) –ATP and PCr stores (PCr + ADP  ATP + Cr) (22-30%) –adenylate kinase Rx (2ADP  ATP + AMP) (?) –stored O 2 in Hb and Mb (8-10%)  Anaerobic training will  maximal accumulated O 2 deficit (MAOD)

36 % of VO 2max Exercise Intensity VO 2max 100% 120% Determining supramaximal intensities

37 Oxygen deficit affected by exercise intensity

38 Effect of time constant (  ) on O 2 deficit

39 For Tue, Sep 5, read: Green, S, BT Dawson, C Goodman, and MR Carey. Anaerobic ATP production and accumulated O 2 deficit in cyclists. Med. Sci. Sport Exerc. 28(3): , 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): , identify the purpose of the study, 2.briefly, describe the exercise protocol and the primary physiological measurements taken, 3.identify primary results of the study, 4.identify conclusions of the study, and 5.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): , focus on pp , Creaking Edifices 1 - 3

41 Three “ugly and creaking edifices” (Noakes, 1997, pp ) 1.VO 2 plateaus at maximal effort O 2 limitation at maximal effort causes muscle hypoxia to terminate exercise what limits VO 2 ? 2.Progressive muscle hypoxia limits exercise performance hypoxia results from CO insufficiency to match muscle demands 3.Anaerobiosis explains onset of La production O 2 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): , OR Noakes, TD. Maximal oxygen uptake: "classical" versus "contemporary" viewpoints: a rebuttal. Med. Sci. Sports Exerc. 30(9): , 1998.

43 For Thu, Sep 13, read:  Wagner, PD. The oxygen transport system: integration of functions (chapter 11), ACSM’s Advanced Exercise Physiology. pp ,


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