Progressive Effect Of Endurance Training On Metabolic Adaptations In Working Skeletal Muscle
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Progressive Effect Of Endurance Training On Metabolic Adaptations In Working Skeletal Muscle

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Progressive Effect Of Endurance Training On Metabolic Adaptations In Working Skeletal Muscle Progressive Effect Of Endurance Training On Metabolic Adaptations In Working Skeletal Muscle Presentation Transcript

  • S.M. Phillips, H.J. Green, M.A. Tarnopolsky, G.J.F. Heigehauser, and S.M. Grant American Journal of Physiology 1996 Question: Can metabolic and mitochondrial adaptations be “de-linked?”
    • What we know : both metabolic and mitochondrial adaptations occur with endurance exercise.
    • Metabolic/Biochemical Adaptation : increase in activity of enzymes involved in oxidative pathways such as the Krebs cycle, β-oxidation, and electron transport chain.
    Kang, Human Kinetics, 2008
    • Mitochondrial Adaptation : endurance training that consists of repeated bouts of sub-maximal exercise has been shown to increase the number and size of mitochondria within the muscles being conditioned.
    • This increase improves control of energy metabolism, causes fiber-types to oxidize more fatty acids and less glycogen, and improves muscle performance.
    Terjung, Sports Science Exchange, 1995
    • Gollnick, 1986 and Holloszy et al. 1984
      • Extensive metabolic and mitochondrial adaptations occur with endurance training.
      • Only measured changes after a prolonged period of time
        • no consideration to how short-term training fit in.
    • Green HJ, et al., 1985
      • Increases in mitochondrial potential do not occur until later in training.
      • This study’s short-term training program of 5 days was based off these results.
    • Next Step : authors of this paper intended to see what metabolic and mitochondrial adaptations occurred after a short-term training program of 5 days and after a prolonged program of 31 days.
    • Hypotheses:
      • Prolonged training (31 days) would result in metabolic adaptations on top of those seen during short-term training (5 days); i.e. a “progressive effect” would be seen.
    • Methods:
      • Subjects :
        • 7 healthy males (untrained).
      • Exercise tests
        • The “Training Test”: cycle test administered 3 times: 1-2 wks before training (PRE), 5 days, and 31 days into training.
        • The “Exercise Test”: 90-minute of cycling at 59% PRE VO2 peak 5-6 days a week.
      • Biopsies and Analysis
        • Biopsied vastus lateralis muscle (before, 30, and 90 minutes); analyzed for: muscle lactate concentration, phosphocreatine (PCr), and glycogen.
        • Measured muscle adenine nucleotides (ATP, ADP, and AMP), citrate, glycogen content and intramuscular triglycerides (IMTG).
        • Assessed muscle oxidative capacity by testing succinate dehydrogenase (SDH).
        • Also looked at markers of muscle metabolism like: hexokinase (HK), phosphorylase (PHOS), PFK and lactate dehydrogenase, and fructose-1, 6-bisphosphate.
    • Adenine nucleotides (ATP, ADP, and AMP) did not change with training or exercise.
    • Training and exercise duration did have an effect on muscle IMP concentrations.
    • During the pretraining exercise IMP concentrations increased 2X resting value by15 minutes of exercise and 4X by 90 minutes. During 5 days of training the accumulation was less than pretraining and by 31 days even more so.
    • In the pretraining exercise PCr decreased 42% from rest to 15 minutes, after 5 days 28.5%, after 31 days only 23%.
    • Cr and Phosphate levels increase with duration, (as a results of less PCr hydrolysis).
    • The concentrations of AMP and ADP did change during exercise and training.
    • Exercise caused a significant increase in ADP and AMP.
    • Training caused lower concentrations of both with increasing duration.
    • During the pretraining exercise Lactate concentration increased after 15 minutes and 90 minutes, but after 15 minutes the increase was smaller.
    • With training the muscle lactate concentration at 15 minutes duration was reduced 44% by 5 days and another 15% at 31.
    • Pyruvate concentration increased above resting at both 15 minutes and 90 minutes of exercise for all training states.
    • The lactate-to-pyruvate potential (L/P) (an indication of cellular redox potential) was elevated only at 15 minutes of exercise. Training caused a 40% reduction of the L/P.
    • Only in the pretraining exercise did the pH decrease after 15 minutes.
    • Exercise caused an increase in muscle glucose and G-6-P at all exercise time points.
    • Training duration only affected muscle glucose at 31 days. For G-6-P exercise resulted in an increased concentration at both 15 and 90 minutes.
    • Citrate concentrations were consistent in all training conditions, and were not significantly increased by 90 minutes.
    • At 31 days of training an increase in the concentration of IMTG stores was observed at rest and at 15 minutes of exercise.
    • In all training states IMTG concentrations were reduced by 90 minutes.
    • Glycogen concentration was progressively higher with training state and decreased with exercise duration.
    • Training increased the activity of HK at 5 days.
    • PHOS, PFK, and fructose-1, 6-bisphosphate activity did not change after 5 and 31 days of training.
    • Training did affect LH, which decreased over the training period.
    • Training had no effect on the maximal activity of SDH and MDH after 5 days, but did after 31.
    • After 5 days of training:
      • Results showed tighter metabolic control reflected in phosphate metabolism, glycolysis, and glycogen depletion.
      • However, at 5 days, muscle oxidative capacity was unchanged from pretraining.
    • After 31 days of training (26 days later):
      • Muscle oxidative potential was increased by 41% estimated from the maximal activity of SDH.
    • A period of short-term training results in many characteristic metabolic training adaptations, which occur before the increases in mitochondrial potential.
    • Further increases in metabolic potential with prolonged training are responsible for increases in mitochondrial-dependent oxidative potential.
    It seems you can’t get the mitochondrial changes without the short-term metabolic adaptations. These two adaptations to endurance training cannot be de-linked.
    • Limitations
      • Small sample size
      • Males only
      • So many biopsies?
    • Further research
      • Determine if mitochondrial changes occur earlier than the 31 day “prolonged training” period.
      • Many other non-muscular (neuromuscular, cardiovascular, and endocrine) changes to short-term training could be assessed and compared to the biochemical changes.
    • When do training-induced adaptations take place?
      • Many biochemical improvements take place with short-term training (5 days), and improve over time as the size and number of mitochondria increase.
    • Why does submaximal endurance increase with endurance exercise?
      • Because of a “progressive” enhancement in metabolic functioning which leads to mitochondrial adaptations and increased oxidative capacity.