FAQ’s: Exercise Physiology 1. Clarification on the difference between lactate threshold, anaerobic threshold & OBLA. See VCAA Clarification 2. Clarification of OBLA, LT and AnT - lots of book contradict each other. See VCAA Clarification 3. What training methods would bring about biggest increases in LT and clear up terms LT & OBLA. In terms of chronic adaptations, how would an increase in LT be classified. In answering this question, it is important to keep in mind the plethora of terms and definitions used across this very contested area. Different studies have investigated the impact of training on various indices of the Lactate Inflection Point (LIP) using a range of population groups. Some reviews have also integrated all of the data irrespective of the definition of LIP used. It is generally acknowledged that an increase in a given LIP is best achieved by training at an intensity greater than the specific LIP (Henritze et al., 1985). This can be achieved using continuous or interval training. Londeree (1997) reviewed 29 studies with 69 study groups and concluded endurance training at an intensity near the ventilatory threshold (and probably lactate threshold) is necessary to produce a training effect (increase VO2max). Training at higher intensities has minimal benefit over the minimum intensity in sedentary subjects, but is be beneficial in conditioned subjects. Most changes that occur take place in the first 8-12 weeks of training, but small changes may accrue beyond this period. A specific study conducted by Keith et al (1992) provided more detailed evidence about the intensity of training needed to achieve an improvement in Individual Anaerobic Threshold. They concluded that it is the mean intensity during training that determines the extent of the adaptation in IAT regardless of whether the exercise is performed intermittently or continuously. Henritze, J., A. Weltman, R.L. Schurrer and R.T. Barlow. (1985). Effects of training at and above the lactate threshold on the lactate threshold and maximal oxygen uptake. European Journal of Applied Physiology, 54:84-88. Keith, S.P., I. Jacobs and T.M. McLellan. (1992). Adaptations to training at the individual anaerobic threshold. European Journal of Applied Physiology, 65: 316-323. Londeree, B.R. (1997). Effect of training on lacate/ventilatory thresholds: a meta-analysis. Medicine and Science in Sports and Exercise, 29(6): 837-843. 4. Latest recovery strategies. There are a range of strategies that are used to optimise recovery from athletic events. These strategies include a range of nutritional strategies, exercise regimens and various ergogenic aids. Two recovery strategies about which there are ongoing debates as to their efficacy are massage and ice-water immersion. In a recent review on the effect of massage on performance, Weerapong et al. (2005) concluded that the effects of massage on performance are inconclusive. It is also unknown whether massage has a demonstrable effect upon injury prevention or can enhance the recovery from injury. Much of the literature on the ability of water immersion as a means to improve athletic recovery appears to be based on anecdotal information, with limited research on actual performance change (Wilcock et al., 2006). Water immersion may cause physiological changes within the body that could improve recovery from exercise. These physiological changes include intracellular- intravascular fluid shifts, reduction of muscle oedema and increased cardiac output (without increasing energy expenditure), which increases blood flow and possible nutrient and waste transportation through the body. Also, there may be a psychological benefit to athletes with a reduced cessation of fatigue during immersion. Water temperature alters the physiological response to immersion and cool to thermoneutral temperatures may provide the best range for recovery. Further performance-orientated research is required to determine whether water immersion is beneficial to athletes. Wilcock, I., J. Cronin and W. Hing. (2006). Physiological response to water immersion: A method for sport recovery? Sports Medicine, 36(9):747-765. Weerapong, P., P.A. Hume and G.S. Kolt. (2005). The mechanisms of massage and effects on performance, muscle recovery and injury prevention. Sports Medicine, 35(3):235-256. 5. Advice on lactate inflection point & lactate threshold/OBLA. See VCAA Clarification 6. Fatigue mechanisms - metabolic by-products Muscular fatigue is defined as a decline in muscle performance. This decline could be a decrease in maximal force output, reduced contraction velocity and/or slower relaxation rate after contraction. The mechanism(s) initiating fatigue are complex and are specific to the athletes sport, training status, physical characteristics (e.g. fibre type), ambient competition environment and diet The origin of fatigue during exercise may occur in the parts of the brain regulating muscle contraction, along the nerves serving the muscle and/or within the muscle itself. Fatigue is evident within seconds of non paced anaerobic sprinting exercise until exhaustion. The transition of energy supply (adenosine tri-phosphate re-synthesis) from predominately the creatine phosphate system (whose stores are largely depleted within 10 seconds) to the lactic acid system (which is largely inhibited within 60 s) and then finally to the aerobic system causes a decline in force production. The decline in force output occurs as each succeeding energy system cannot re-synthesize adenosine tri-phosphate at the rate of the previous energy system (Spencer et al., 2005). Anaerobic exercise also may reduce the nerve’s ability to activate the muscle mass resulting in a reduction in a decline in muscle performance. In particular, elevated blood potassium levels appear to reduce a nerve’s excitability to stimulation (McKenna et al., 1996). Metabolite accumulation during anaerobic exercise such as the generation of phosphate ions from the breakdown of adenosine tri-phosphate may reduce the availability of calcium that is needed for muscle contraction (Hargreaves et al., 1998). Recent evidence suggests the traditional view of excessive lactic acid accumulation and subsequent decline in muscle pH causing fatigue within the muscle is unlikely (Allen and Westerbald 2004, Cairns 2006). An increase in lactic acid may actually increase force production in isolated muscle force output in vitro (test-tube). However, lactic acid may still play a role in initiating fatigue by reducing the brain’s capacity for muscle mass recruitment (Cairns 2006) In endurance exercise, the depletion of glycogen may prevent may reduce calcium availability or its ability to initiate muscle contraction, or even potentially trigger changes in brain neurotransmitter (serotonin to dopamine ratio) that decreases the athlete’s ability to recruit muscle mass (Meeusen et al., 2006). A rise in core temperature to 40°C is also associated with fatigue and changes in brain function (Nielsen & Nybo 2003). Cairns S.P (2006). Lactic acid and exercise performance : culprit or friend? Sports Medicine 36(4):279-91. Meeusen R, Watson P, Hasegawa H, Roelands B & Piacentini MF (2006). Central fatigue: the serotonin hypothesis and beyond. Sports Medicine. 36(10):881-909. Hargreaves M, McKenna MJ, Jenkins DG, Warmington SA, Li JL, Snow RJ & Febbraio MA. (1998). Muscle metabolites and performance durng high-intensity intermittent exercise. Journal of Applied Physiology, 84(5): 1687-1691. Westerblad H & Allen ,D. (2004). Physiology. Lactic acid- the latest performance enhancing drug. Science 30(5): 1112-1113. McKenna MJ, Heigenhauser GJ, McKelvie RS, MacDougall JD & Jones NL. (1997). Sprint training enhances ionic regulation during intense exercise in men. Journal of Physiology 15;501 ( Pt 3):687-702. Spencer M, Bishop D, Dawson B. & Goodman, C (2005). Physiological and metabolic responses of repeated-sprint activities specific to field-based team sports. Sports Medicine 35(12): 1025-1044. Nielsen B & Nybo L (2003). Cerebral changes during exercise in the heat. Sports Medicine 33(1):1-11. 7. What happens to both ST & FT fibres during aerobic and anaerobic training - do the fibres "tear" and then repair larger than before? The complex process of adaptation to training in skeletal muscle primarily involves the synthesis of new molecular proteins and their functional consequences to the adaptation response are determined by the training stimulus. Aerobic training elicits numerous changes in skeletal muscle including enhanced glycogen storage, fat oxidation and lactate kinetics (Hawley 2002). While these factors all contribute to enhance endurance improved aerobic capacity is most associated with an increase in mitochondrial density and enzyme activity, termed mitochondrial biogenesis (Adhihetty et al. 2003; Irrcher et al. 2003). Identifying the factors responsible for initiating increases in mitochondrial protein content remains elusive but candidates include phosphorylation state (ATP: AMP), calcium release and uptake and hypoxia. Regardless, it is clear that aerobic training can increase steady state mitochondrial protein content 50-100% within ~6 wk promoting resistance to fatigue with repeated moderate intensity contractions (Hood 2001). On the other hand, adaptation to anaerobic (resistance) training includes increased muscle cross- sectional area i.e. hypertrophy (Rennie et al. 2004). Fundamentally, a threshold tension created by concentric, isometric and eccentric contractions promotes functional and structural protein synthesis in existing muscle fibres and also the production of new muscle cells that are added to existing muscle fibres (Sartorelli and Fulco 2004). The specific contribution of each mechanism to training-induced muscle growth has yet to be established but altered protein synthesis appears to be regulated by anabolic signals (e.g. hormones such as testosterone, growth hormone, insulin and insulin-like growth factor) while activation of new muscle cells principally occurs in response to muscle damage (Rathbone et al. 2003; Rennie et al. 2004). Both adaptive responses provide additional contractile machinery resulting in a greater capacity to generate force. Adhihetty, P.J., Irrcher, I., Joseph, A.M., Ljubicic, V., and Hood, D.A. 2003. Plasticity of skeletal muscle mitochondria in response to contractile activity. Exp Physiol 88: 99-107. Hawley, J.A. 2002. Adaptations of skeletal muscle to prolonged, intense endurance training. Clin Exp Pharmacol Physiol 29: 218-222. Hood, D.A. 2001. Plasticity in Skeletal, Cardiac, and Smooth Muscle Invited Review: Contractile activity-induced mitochondrial biogenesis in skeletal muscle. J Appl Physiol 90: 1137-1157. Irrcher, I., Adhihetty, P.J., Joseph, A.M., Ljubicic, V., and Hood, D.A. 2003. Regulation of mitochondrial biogenesis in muscle by endurance exercise. Sports Med 33: 783-793. Rathbone, C.R., Wenke, J.C., Warren, G.L., and Armstrong, R.B. 2003. Importance of satellite cells in the strength recovery after eccentric contraction-induced muscle injury. Am J Physiol Regul Integr Comp Physiol 285: R1490-1495. Rennie, M.J., Wackerhage, H., Spangenburg, E.E., and Booth, F.W. 2004. Control of the size of the human muscle mass. Annu Rev Physiol 66: 799-828. Sartorelli, V., and Fulco, M. 2004. Molecular and Cellular Determinants of Skeletal Muscle Atrophy and Hypertrophy. Science's STKE 2004: re11-. 8. Clarification of lactate at rest It is apparent that the various energy systems are in constant operation, with a given energy system being involved in the release of a majority of the energy needed to sustain life or for exercise depending upon the characteristics of the particular activity. At rest, the dominant energy system is the aerobic system but there is still some contribution from the anaerobic systems that results in the production of limited amounts of lactic acid. Some of the lactic acid and the resultant lactate is released into the blood stream and transported to the liver. The lactate transported to the liver via the blood is subsequently converted into glucose via the Cori cycle (Brooks GA, pg 62 2000). Brooks GA, Fahey TD, White TP & Baldwin KM. (2000). Exercise Physiology Human Bioenergetics and its applications (3rd Ed). Mayfield Publishing Company, London. 9. Lactate threshold/OBLA clarification See VCAA Clarification 10. Where does the H+ come from in anaeorbic glycolysis? The Hydrogen ion comes from the dissociation of lactic acid into lactate and hydrogen ions 11. Energy system contribution during the MSFT test? The Multi-Stage Fitness Test (MSFT) is an incremental running test, the results of which are used to predict maximal aerobic power. No specific data appear to be available that quantify the energy system contribution to the MSFT. The MSFT begins at a very low velocity and the increments in exercise intensity (running speed) employed within the test are very small. Given that the test involves repeated runs over 20 m, it also requires the participants to decelerate and accelerate frequently after completing each 20 m run. Therefore, it is likely that the test will largely involve aerobic metabolic pathways (a small oxygen deficit at the start of each increment) and involve a limited amount of energy released as a result of anaerobic metabolic pathways. Towards the end of the test, the participant may exercise at a work load that exceeds his/her maximal aerobic power and thereby meet this energy requirement via the involvement of the anaerobic energy system – primarily the LA system. In addition, the need for repeated periods of rapid acceleration may increase the involvement of the anaerobic metabolic pathways to some extent.