Effects of deconditioning on slow twitch / type 1 fibres

• Effects of deconditioning on slow twitch / type 1 fibres:

  • Fibre atrophy (↓ muscle mass = ↓ VO2 max)
  • Poor ability to extract oxygen
  • Poor ability to utilise oxygen for the synthesis of ATP
  • Increased reliance on glucose as prime energy source
  • If generalised - “Unfit” heart - poor ability to provide oxygenated blood to skeletal muscle via the systemic circulation
• Fibre atrophy:

  • Imbalance between contractile protein synthesis & degradation with a reduced production leads to a net loss of mass
  • leads to a decrease in VO2 max
  • VO2 = the amount of O2 consumed by tissues for metabolic purposes per unit of time (usually 1 minute) & can be standardised for body weight
• Poor ability to extract O2:

  • Ideally each type 1 fibre is associated with 3-6 capillaries which leads to efficient O2 diffusion i.e efficient O2 delivery / extraction
  • whereas in Deconditioning = paucity (decrease in number) of capillaries
  • Possible reduction in myoglobin
• Poor ability to utilise O2:

  • low volume of mitochondria
  • low quantities of aerobic enzymes
  • both leading to low aerobic ATP production
• Reliance on glucose metabolism:

  • Relatively poor ability to utilise available lipids / free fatty acids for ATP purposes
  • Shame because lipid stores are 60 x greater than glucose stores
  • Glucose stores need to be safe-guarded as prime energy substrate for neurological tissue
• “Unfit” heart

  • An unfit heart is a substandard pump
  • Unable to adequately supply skeletal muscle
  • The more unfit the heart is and the poorer skeletal muscle’s ability to extract and utilise O2 to synthesise ATP the harder the heart has to work in terms of:
  • higher heart rate
  • stronger force of contraction (larger stroke volume)
• One way to maintain VO2 max is to adhere the exercise guidelines – i.e to present skeletal muscle with an appropriate physiological challenge.