The Physiology of Training Performance Effect on VO 2max and Strength Chapter 13.
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Transcript of The Physiology of Training Performance Effect on VO 2max and Strength Chapter 13.
![Page 1: The Physiology of Training Performance Effect on VO 2max and Strength Chapter 13.](https://reader034.fdocuments.us/reader034/viewer/2022051416/56649f145503460f94c28c05/html5/thumbnails/1.jpg)
The Physiology of Training
Performance Effect on VO2max and Strength
Chapter 13
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Principles of Training
Overload– Training effect occurs when a system is
exercised at a level beyond which it is normally accustomed
Specificity– Training effect is specific to the muscle
fibers involved– Type of exercise
Reversibility– Gains are lost when overload is removed
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Moffit’s corollary to Principles of Training Consistency
– Once in a while is better than nothing….. but just barely
– Even if just a little overload, as long as there is consistency there will be positive changes
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Result of Endurance Training
Structural and biochemical changes in muscle Mitochondrial number
Enzyme activity
Capillary density
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Result of Endurance Training
Ability to perform repeated sub maximal muscle contractions
Ability to support aerobic energy production– For longer periods (duration)– At higher intensities (work capacity)
Higher maximal oxygen consumption (VO2max).
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What is VO2max?
Maximum capacity to use oxygen in the recycling of ATP
Factors Affecting:– Delivery of oxygen
• Blood circulation
– Extraction of oxygen• Unloading
– Use in metabolism• Mitochondria
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Calculation of VO2max
Product of maximal cardiac output (Q) and arteriovenous difference (a-vO2)
a-vO2 difference
– Represents amount of oxygen taken into muscle tissue
– Known from PO2 in arterial and venous blood
– Greater difference = more O2 extracted
VO2max = HRmax x SVmax x (a-vO2)max
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Questions:
Can VO2max be improved?
How much can it be improved?
What change influences it the most?
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Answers:
Yes, it can be improved It can be increased by up to 15% Improvements in VO2max from:
– 50% due to a-vO2 difference
– 50% due to SV
Differences in VO2max in untrained
– Due to differences in SVmax
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a-vO2 Difference and Increased VO2max
Improved ability of the muscle to extract oxygen from the blood:– 1. Muscle blood flow (delivery)
Capillary density (delivery)
– 2. Mitochondial number
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Stroke Volume and Increased VO2max
Increased SVmax
Preload (EDV) Plasma volume Venous return Ventricular volume
Afterload (TPR) Arterial constriction Maximal muscle blood flow with no change in
mean arterial pressure
Contractility
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Structural and Biochemical Adaptations to Endurance Training Mitochondrial number Oxidative enzymes
– Krebs cycle (citrate synthase)– Fatty acid availability (-oxidation)– Electron transport chain (cytochromes)
NADH (shuttling system) Change in type of LDH (pyruvate unchanged) Adaptations quickly lost with detraining
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Influence of Mitochondrial Number on ADP Concentration and VO2
[ADP] stimulates mitochondrial ATP production
Increased mitochondrial number following training– Lower [ADP] needed to increase ATP production
and VO2
– More ATP available sooner when trained
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Effect of Exercise Intensity and Duration on Mitochondrial Enzymes Citrate synthase (CS)
– Marker of mitochondrial oxidative capacity
Light to moderate endurance training– Increased CS in high oxidative fibers (Type I and IIa)
Strenuous endurance training– Increased CS in low oxidative fibers (Type IIb)
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Biochemical Changes and FFA Oxidation
Increased mitochondrial number and capillary density– Increased capacity to transport FFA from plasma
to cytoplasm to mitochondria Increased enzymes of -oxidation
– Increased rate of acetyl CoA formation Increased FFA oxidation
– Spares muscle glycogen and blood glucose
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Blood *Lactate Concentration
Lactate production during exercise
Endurance training production – FFA use instead of glycolysis– H isoform of LDH = low affinity for pyruvate
removal– Malate-aspartate shuttle = NADH to mitochondria
pyruvate + NADH lactate + NADLDH
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Detraining and VO2max
Decrease in VO2max with cessation of training SVmax
maximal a-vO2 difference
(Opposite of training effect)
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Detraining: Time Course of Changes in Mitochondrial Number: Study Results
About 50% of the increase in mitochondrial content was lost after one week of detraining
All of the adaptations were lost after five weeks of detraining
It took four weeks of retraining to regain the adaptations lost in the first week of detraining
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Time-course of Training/Detraining Mitochondrial Changes
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Time Course of Changes Associated With Detraining
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Physiological Effects of Strength Training Neural factors
– Increased ability to activate motor units - recruitment– Strength gains in initial 8-20 weeks
Muscular enlargement– Mainly due enlargement of fibers (hypertrophy)
• More sarcomeres in parallel• More fluid within the cell
– Long-term strength training
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Neural and Muscular Adaptations to Resistance Training
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Questions?
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End