1. BS277 Biology of Muscle. The response of muscle to endurance training. Objectives. After this lecture and associated reading you should be able to; Describe the effects of endurance training on muscle structure, metabolism and function (phenotype). Discuss the relative contributions of genetics and environment to muscle fibre isotype.

2. There are two components to increasing the aerobic capacity. Oxygen delivery Cardiovascular Haematocrit Unloading kinetics? Oxygen utilisation (muscular adaptations) Switch to slow fibres? Adaptation of fibres (both ‘fast’ and slow become more aerobic)

3. Training increases oxygen consumption and oxygen extraction at the muscle.

4. The effect of endurance training on fibre type. Endurance exercise is similar to prolonged artificial stimulation in that the muscle is activated for long periods at low frequencies. But:- –artificial stimulation recruits all motor units –endurance exercise recruits slow motor units first (faster units when fatigued or at higher intensity). Adaptation to endurance training resembles fast-slow transformation in artificial stimulation. One year of artificial stimulation increases expression of 2a (90% of fibres). BUT no evidence for type 2 to type 1 switch in endurance training. Changes in the aerobic capacity of muscle are also mediated by other factors.

5. Changes induced by endurance training. Capillarity Metabolic effects –Increased aerobic enzymes –Increased number of mitochondria –Increased ability to metabolise fat –Increased glycogen storage Decreased volume of SR in fast fibres. Increased expression of type 1 and type 2a myosin Switch from type 2x to type 2a. Rapidly reversible by detraining

6. Time course of changes in endurance training? (Jones et al 2004). This doesn’t happen in fibres that are already slow!

7. Metabolic effects of endurance training. Relative contribution of fat metabolism . Exercise duration (min) 306090120

8. Muscle adaptations to endurance training. Note increase in aerobic enzymes, oxidative potential of FT fibres (x-a transition) Area of type 1 fibers (Jones says they become smaller).

9. Mechanisms for endurance training related changes in muscle. Capillary growth is stimulated by increased flow through existing capillaries and production of vascular epithelial growth factor (VEGF). Upstream regulation? Hypoxia induces HIF-1, VEGF and heat shock proteins (HSP). Could induce mitochondrial proliferation? Hypoxia does not change myosin expression (not a stimulus for x-a transition). Induced by low glucose, high lactate? (in mitochondrial defects lactate  and mitochondrial number increases. In McArdle’s disease, lactate is not produced, normal mitochondrial number). Chronic elevation of Ca ++ not responsible for any change in myosin isotype.

10. Coffey, V.G. and Hawley, J.A. (2007) The molecular bases of training adaptation. Sports Med. 37(9) 737-6 Gibala, M.J. and McGee, S.L. (2008) Metabolic adaptations to short term high intensity interval training: a little pain for a lot of gain. Exerc. Sport Sci. Rev. 36 (2) 58-63. Hakini, P. et al., (2007) Overexpression of the Cytosolic Form of Phosphoenolpyruvate Carboxykinase (GTP) in Skeletal Muscle Repatterns Energy Metabolism in the Mouse. J.Biol. Chem. 282, (45), 32844–32855. Narkar, V.A. et al. (2008) AMPK and PPAR  agonists are exercise mimetics. Cell 134 405-415.