Seminar in Advanced Physiology of Exercise

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

2. Course information • Textbook:ACSM’s 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 (5:00 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 • Perform >3 tests to exhaustion (~4-10 min) • Plot inverse exhaustion time against power • 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.

11. 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?

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

13. 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

14. VO2 response to heavy exercise  5-s averages  nonlinear regression modeling Residuals Kolkhorst et al., MSSE, 2004

15. Three-component model of VO2 kinetics(for supra LT intensity) Phase I Phase II Phase III 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 > LT • primary cause is recruitment of additional motor units due to fatigue 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)

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 VO2 kinetics

18. Why study VO2 kinetics? Grassi et al., JAP, 1996

19. 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

20. 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)

21. 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)

22. 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?

23. 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)

24. 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, BiochemischeZeitschrift, 1934, 1935) • role of lactacid and alactacid contributed to O2D • resynthesis of PCr during rapid component of EPOC and lactate clearance during slow component

25. O2 Deficit and Excess Post-Exercise Oxygen Consumption (EPOC) exercise recovery O2D VO2 EPOC Resting energy requirements Time

26. Excess post-exercise oxygen consumption (EPOC)

27. 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)

28. Determining supramaximal intensities 120% 100% VO2max % of VO2max Exercise Intensity

29. Oxygen deficit affected by exercise intensity

30. Effect of time constant () on O2 deficit

31. 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

32. 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”

33. 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.

34. For Thu, Sep 13, read: • Wagner, PD. The oxygen transport system: integration of functions (chapter 11), ACSM’s Advanced Exercise Physiology. pp 300-308, 311-312.