1. Molecular Exercise Physiology Endurance training Presentation 2 Henning Wackerhage

2. At the end of this presentation you should be able to: Explain how a maximal oxygen uptake test and lactate threshold test are carried out and how the data are interpreted. Describe the major cardiovascular and muscular adaptations to endurance training. List the major forms of endurance training. Learning outcomes

3. Adaptation to endurance training Part 1 How to test for endurance capacity?

4. What makes a good endurance athlete? Endurance athletes need to have a large heart (athlete’s heart syndrome) and a high maximal cardiac output (CO max ) to pump oxygenated blood to their working muscles. The blood should have a high haematocrit (i.e oxygen transport capacity). Their exercising muscles need to have a high percentage of slow fibres (also known as type I fibres) surrounded by many capillaries. Trained muscle fibres contain more mitochondria, enzymes for fat metabolism and have a higher glycogen concentration when rested than untrained muscle fibres. In addition, good endurance athletes need a high economy (i.e. energy for given work) for the sport they engage in. How can we test the performance of an endurance athlete? There are two major tests: 1) Determination of maximal oxygen uptake; 2) Determination of the lactate “threshold”.

5. Rowell (1993) Determination of maximal oxygen uptake Subjects perform a graded exercise test (i.e. the work is increased stepwise). Oxygen uptake is measured until the athlete fatigues. The maximal oxygen uptake is usually related to the body weight of a subject. Task: Interpret the figure on the left.

6. Lactate threshold The rate of glycolysis increases with exercise intensity. Endurance athletes have many mitochondria and can thus combust more pyruvate by oxidative phosphorylation. That is why lactate is lower in endurance athletes at any given intensity than in untrained subjects. Glucose, glycogen Pyruvate Oxidative phosphorylation Lactate Determining the maximal oxygen uptake give a good indication about the talent of an individual for endurance sports. A second test is to determine the “lactate threshold”. The power output at the lactate threshold is usually better correlated with actual endurance performance than the maximal oxygen uptake. Lactate is generated from pyruvate by lactate dehydrogenase. Its concentration depends on the rate of glycolysis (which is the rate of pyruvate production) minus the rate of pyruvate oxidation by oxidative phosphorylation.

7. 8642086420 100 200 300 Power (W) Athletes reach 4 mM lactate at higher workloads [Lacate] mM Athletes again perform a graded exercise test. Small blood samples are obtained from the earlobe or fingers. The relationship between power and [lactate] is plotted and the power at 4 mM lactate determined. The higher the power at 4 mM the more endurance trained the subject. Task: Interpret the figure on the left: Which subject is more endurance- trained?

8. Determinants of endurance performance Task: Interpret the schematical drawing below. What do the abbreviations mean?

9. Endurance training Part 2 Adaptation to endurance training

10. Homo sapiens: did we evolve as endurance runners? Bramble DM and Lieberman DE. Endurance running and the evolution of Homo. Nature 432, 345-352, 2004. In this landmark paper, Bramble and Lieberman argue that the anatomy of human beings has been selected for endurance running. The compare human beings and argue that human beings are actually very good at covering long distances when compared to numerous other species. Many skeletal features are advantageous for endurance running especially when compared to close species. They hypothesize that endurance running helped hominids to exploit protein-rich resources such as meat, marrow and brain. HumanChimpanzeeA. afarensis If the evolutionary pressure was favouring an endurance running human then our anatomy, biochemistry and muscle function may have all been selected for endurance running.

11. No comment

12. Adaptation is the key mechanism of training Evolution is one mechanism by which a species adapts to its environment (i.e. natural selection of genotypes; survival of the fittest; Darwin 1809-1882). A second mechanism is the functional adaptation of organs. Roux (1881) suggested that the functional adaptation of cells is regulated locally, governed by stimuli, in a self-organisational process. He explains that cells can adapt to signals with specific adaptations. Functional adaptation is the key mechanism by which training induces specific changes in the structure or size of our organs. It is responsible regulating the growth of the athlete’s heart, of increases in muscle “fitness” and size and strength of bones in response to exercise. W. Roux Task: Describe 3 functional adaptations of tissues to stimuli other than exercise.

13. How does adaptation work? There has been much speculation about how adaptation to training may work. One example is the “supercompensation” theory that has been proposed by Yakovlev (1967). It is an important model but fails to explain the underlying mechanisms. In addition, it does not apply to all systems (for examples, a heart always “trains” but still hypertrophies in response to exercise). Molecular exercise physiology has dramatically changed our knowledge about how adaptations occur: Molecular exercise physiologists have discovered several signals, the communication of these signals and their link to adaptive responses. Training Supercompensation Compensation Return to normal Time System status Yakovlev (1967)

14. Specific adaptations to endurance training Endurance training induces performance-enhancing adaptations mainly in the cardiovascular system and in the exercising muscles. However, other tissues such as bones, tendons, the immune system, liver and brain adapt as well. The following slides show some examples for adaptations. Cardiovascular systemMuscle Cardiac hypertrophy (athlete’s heart) facilitating greater stroke volume and maximal cardiac output More mitochondria (mitochondrial biogenesis) More capillaries (angiogenesis) Higher rate of fat metabolism Slower motor proteins Increased fatigue resistance Better glucose uptake and higher glycogen concentration Lower rate of maximal ATP hydrolysis Better antioxidant defence

15. Rost (1997) This study shows the increase in heart volume over time in competitive swimmers. Note the decrease in heart volume in swimmers that end their swimming career. Athlete’s heart

16. Hollmann (1965) The volume of a normal heart is 750-800 ml whereas endurance- trained athletes reach 900-1200 ml. The figure shows the largest healthy heart reported in literature. It was 1700 ml and belonged to a world champion in professional cycling. Athlete’s heart

17. Ekblom (1969) uptake correlate (see figure). It seems likely that the size of the heart (or its maximal stroke volume) is a key determinator of maximal oxgygen uptake. The larger the heart of the athlete, the larger the stroke volume of the heart. Because maximal heart rate does not change much with training, the stroke volume largely determines the cardiac output during maximal exercise. Maximal cardiac output and maximal oxygen Athlete’s heart

18. Mitochondrial biogenesis Control Salmons, Jarvis, Higginson, Manolopoulos, Woods, Wackerhage, unpublished data (2001) Increased mitochondrial density after chronic electrical stimulation Exercise also increases the number of mitochondria in muscle fibres. The figures shows a large increase in mitochondria (stained dark) in a muscle that was electrically stimulated for several weeks. Such stimulation may be viewed as an extreme exercise stimulus.

19. Endurance training increases fat metabolism Hurley et al. (1986) After a period of endurance training, total energy expenditure is unchanged (because the exercise still requires the same amount of energy). Fat combustion, however, is increased whereas carbohydrates or glycogen are saved.

20. Jaschinski et al. (1998) Fast-to-slow exchange of motor proteins Chronic electrical stimulation also exchanges faster with slower motor proteins. The fast myosin heavy chain IId/x (MHCIId/x;  ) and MHCIIb (  ) motor proteins decrease and the intermediate MHC IIa (  ) motor protein increases. Exercise usually only leads to a small decrease of the fast MHC IIx and a small increase in the MHC IIa motor proteins. It is unclear whether exercise is just a lower “contraction” dose than chronic electrical stimulation or whether different mechanisms are involved.

21. Brodal et al. (1977) Another adaptation of endurance training is the increase in the number of capillaries that nourish a muscle fibre. The capillary-to- fibre ratio correlates with the maximal oxygen uptake and increases with training. Angiogenesis Task: Critically examine the figure above. Does it proof the effect of training on capillary growth? Does it proof that more capillaries per fibre increases maximal oxygen uptake?

22. Endurance training Part 3 Endurance training methods

23. Endurance training Today’s endurance training methods have not been scientifically developed. They are the result of subjective interpretations of trial and error “experiments”. Things that usually work well have been kept while training regimes that did not work have been abandoned. Endurance athletes usually train at various intensities with a focus on low to medium intensities. The total training volume depends on the sport. Swimmers and cyclists often train up to 6 hours a day whereas runners can run little more than 2 h probably because of the eccentric form of exercise. Athletes also periodise their training. The usual strategy is to train high volume first and then to reduce volume and to increase training intensity. Here, I will restrict myself to explain some major endurance training forms.

24. Long slow distance (LSD) A key endurance training method is long slow distance training. It is used especially by Marathon runners, cyclists, triathletes, cross country skiers and athletes competing in similar sports. Duration: 30 min-6 h Intensity: 50-60% of VO 2 max or HR reserve (some recommend higher intensities). Examples: 20 mile run, 100 mile cycle ride. Effects: Decrease in muscle and liver glycogen (which stimulates supercompensation), high energy turnover and fat combustion.

25. Medium and high intensity continuous training LSD training is the major training form but alone is insufficient. Medium and high intensity continuous training prepares athletes for maintaining a high pace. Duration: 20 min-70 min Intensity:60-85% of VO 2 max or HR reserve. Examples: 60 min run at 75% of HR reserve. Effects: Higher rates of fat and carbohydrate combustion than LSD; train motor units that are not normally activated during LSD; exercising closer to race pace (depends on race distance).

26. Interval and fartlek training A small percentage of the total training load; especially used closer to competitions. Duration: up to 60 min (exercise training) or 90 min (runner’s fartlek). Intensity: >85% of VO 2 max or HR reserve. Examples: 10 X 1000 m running; 70 min fartlek (running all uphill sections at high intensity). Effects: Close to 100% carbohydrate oxidation; medium to high lactate concentrations reached; innervation of intermediate and fast motor units; race pace or above.

27. Adaptation is the key mechanism of training Task: 1) A popular but unproven assumption is that a system adapts more if it is used more. Assuming this assumption was true, explain whether long slow distance or high-intensity endurance training is best to: a) increase mitochondrial biogenesis; b) increase angiogenesis; c) increase heart volume; d) increase fat oxidation. 2) We now know that adaptations are regulated by signals/stimuli that occur within an exercising muscle. Name 5 signals/stimuli that change with exercise in muscle.

28. The End