Progressive Effect Of Endurance Training On Metabolic Adaptations In Working Skeletal MusclePresentation 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.
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.
7 healthy males (untrained).
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.
Small sample size
So many biopsies?
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.