FAQ s fatigue

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					                                 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

   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.,

   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

   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):

   Nielsen B & Nybo L (2003). Cerebral changes during exercise in the heat. Sports Medicine

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

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