EP Ch. 13
Maximal oxygen uptake (aka maximal aerobic power/ VO2 max)
The measure of the maximal capacity of the body to transport and use oxygen during dynamic exercise using large muscle groups (ex/ legs)
VO2 Max training
The programs typically cause an increase between 15%-20%, the improvement can be as low as 2% to 3% for those who start with high VO2max values. -50% for individuals with low initial VO2 valuesbefore training can expierence improvements with fairly low training intensities (40%-50% VO max) -Those with high VO2 max may need training over 70%
Endurance training programs that increase VO2 max
They involve a large musle mass in dynamic activity for 20 to 60 minutes per session, three or more times per week, with an intensity of 50% to 85% VO2 max
Genetic predisposition
This accounts for about 50% of one's VO2 max value. Very strenuous and/or prolonged endurance training can increase VO2 max in normal sedentary individuals by up to 50%.
High-intensity endurance training
This can increase VO2 max by as much as 50% in individuals with the genetic potential to respond favorably to endurance training. -A much larger inrease in VO2 max with a certain 10-week training was due to a -higher intensity -higher frequency -higher duration
Endurance Exercise Training Improving VO2
This improves VO2 by increasing both maximal Q and the a-VO2 difference. -In this regard, endurance training studies using young sedentary subjects suggest that approximately HALF THE GAIN of VO2 max is due to SV INCREASES and half to increased OXYGEN extraction
Endurance Training
*refer to pick slide 41
Secondary Messengers in Skeletal Muscle
-AMPK -Glucose uptake, fatty acid oxidation, and mitochondrial biogenesis -PGC-1α (Μaster regulator of mitochondrial biogenesis) -Increases in capillaries, mitochondria, antioxidant enzymes -Activated by p38 and CaMK -Calcineurin -Fiber growth, fast-to-slow fiber type change -IGF-1 / Akt / mTOR -Muscle growth from resistance training -NFκB -Antioxidant enzymes
Links Between Muscle and Systemic Physiology
-Biochemical adaptations to training influence the physiological response to exercise -Due to: -Reduction in "feedback" from muscle chemoreceptors -Reduced number of motor units recruited -Demonstrated in one-leg training studies
The training-induced increase in the a-vo2 difference is due to:
-Due to an increase in the capillary density of the trained muscles, which is needed to accept the increase in maximal muscle blood flow. -The greater capillary density allows for a slow red blood cell transit time through the muscle, providing enough time for oxygen diffusion, which is facilitated by the increased number of mitochondria.
Effect of Mitochondria and Capillaries on Free-Fatty Acid and Glucose Utilization
-Endruance exercise training leads to -Increase Capillary dnesity -Slower blood flow in muscle and increased FFA transporters -Increased uptake of FFA -Increased FFA utilization -Spares plasma glucose -Increase Mitochondria number -Increased Beta oxidation enzymes and carnitine transferase
Training Adaptation- Big picture
-Endurance and resistance exercise increases specific muscle proteins -Process of training- induced muscle adaptation
Endurance Training improves Muscle Antioxidant Capacity
-Free radicals are produced by contractin g muscles -Training increases endogenous antioxidants
Peripheral Control of Heart Rate, Ventilation, and Blood Flow
-Increase temperature, tension and local factors- Group III fibers and Group IV fibers- leads to Spinal Cord- leads to Cardiorespiratory control centers-- leads to increase work rate, and with liver and kidney blood flow leads do decreased work rate
Changes in Muscle Fuel Utilization
-Increased utilization of fat and sparing of plasma glucose and muscle glycogen -Transport of FFA into the muscle -FABP and fatty acid translocase -Transport of FFA from the cytoplasm to the mitochondria -Increased mito number -CAT I and CAT II -Mitochondrial oxidation of FFA
Exercise Training Improves Acid-Base Balance During Exercise
-Lactate production during exercise -pyruvate and NADH- LDH yields- Lactate and NAD -Training adaptations -Increased mitochondrial number -Increased NADH shuttles -Change in LDH type -Heart form (h4) has lower affinity for pyruvate= less lactic acid formation
Intracellular Signaling and Inhibition of Protein Synthesis
-Look at slide
Endurance Training Increases Mitochondrial Content in Skeletal Muscle Fibers
-Mitochondria in the muscle -Subsarcolemmal are located below sarcolemma -Intermyofibrillar are located around contractile proteins -Mitochondrial content increases quickly -Results in increased endurance performance
Effects of Endurance Training on Maintenance of Homeostasis
-More rapid transition from rest to steady-state -Reduced reliance on glycogen stores -Cardiovascular and thermoregulatory adaptations -Due to neural and hormonal adaptations -Also due to structural and biochemical changes in muscle
Retraining and VO2 max
-Muscle mitochondria adapt quickly to training -Mitochondrial adaptations lost quickly with detraining -Requires 3-4 weeks of retraining to regain mitochondrial adaptations
End Diastolic Volume (EDV)
-One of the key factors responsible for training-induced increases in maximal SV is an increase in EDV -An increase in EDV results in stretch of the left ventricle and a corresponding increase in cardiac contractility via Frank-Starling mechanism
Peripheral and Central Control of Cardiorespiratory Responses
-Peripheral feedback from working muscles -Group III and group IV nerve fibers -Central Command -Motor cortex, cerebellum, basal ganglia
The increase of EDV in enduranc-trained heart is a result of several training-induced changes
-Primary mechanism is that plasma volume increases with endurance training, and this contributes to augmented venous return and increased EDV -A training-induced increase in stroke volume is likeley due to an increase in EDV -Prolonged endurance training (months to years) increases the size of the left ventricle with little change in ventricular wall thickness. THe increase in ventricular size will accommodate a larger EDV and there could be a factor in contributing to the training-induced increase in SV -Endurance training not only increases SV during maximal exercise, but also increases SV at rest -Bradycardia- slower resting heart rate- occurs following endurance training
Primary Signal Transduction Pathways Skeletal Muscle
-Primary signals for muscle adaptation 1. Mechanical stretch 2. Calcium -Via calmodulin-dependent kinase 3. Free radicals 4. Phosphate/ muscle energy levels -AMP/ATP ratio activates AMPK -Primary signals lead to adaptations -Effect depends on exercise stimulus
Afterload
-Refers to the peripheral resistance against which the ventricle is contracting as it tries to push blood into the aorta. -It's important bc when the heart contracts against a high peripheral resistance, SV will be reduced -Following an endurance training program, trained muscles offer less resistance to blood flow during maximal exercise due to a reduction in the sympathetic vasoconstrictor activity to the arterioles of the trained muscles. -The decrease in resistance parallels the increase in maximal cardiac output so that mean arterial blood pressure during exercise is unchanged
Cardiac Contractility
-The strength of the cardiac muscle contraction when: -the fiber length (EDV) -afterload (peripheral resistance) -Heart rate all remain constant -It is difficult to determine if the inherent contractility of the human heart changes with endurance training (this is bc tthe factors that affect contractility (EDV, HR, and afterload) are affected by endurance training). -Finidings though, indicate that eendurance exercise training improves ventricular contractility
Arteriovenous O2 Difference
-The trainind-induced increase in the a-VO2 difference is due to increased O2 extraction from the blood. -The increased capacity of the muscle to extract O2 following training is mostly due to the increase in capillary density, with an increase in mitochondrial number being of secondary importance. -Increased capillary density in trained muscle accomadates: 1. Increase in muscle blood flow during maximal exercise 2. Decreases the diffusion distance to the mitochondria 3. Slows the rate of blood flow to allow more time for oxygen diffusion from the capillary to the muscle fiber to occur -Mitochondria is not the key factor limiting VO2 max
Relative VO2 max can vary
-VO2 max can be less than 20ml*kg^-1*min^-1 in patients with severe cardiovascular and pulmonary disease -It can be more than 80ml*kg^-1*min^-1 in world-class distance runners and cross -country skiers- super high VO2 max can be due to
Factors Causing Increased VO2 Max
-^ Maximal CO -^ SV -^ Preload -Decreased Afterload -^ A-VO2 difference -^ Muscle Blood Flow -Decrease Sympathetic N.S. activity to working muscle -^ capillaries mitochondria
mRNA and Protein Changes in Response to Exercise
-look at text
Reasons training induced improvements in VO2 max occur
-occur due to both increases in maximal cardiac output (ex/ SV increases) and an increase in a-VO2 difference
Mechanisms to Explain the Lactate Threshold**
1. Low Muscle Oxygen 2. Accelerated glycolysis 3. Recruitment of fast-twitch fibers 4. Reduced rate of lactate removal
The trainining- induced increase in maximal SV is due to both an INCREASE in preload and a DECREASE in afterload
A. Increased preload is primarily due to an increase in EDVentricular Volume and the associated increase in plasma volume B. The decreased afterload is due to a decrease in the arteriolar constriction in the trained muscles, increasing maximal muscle blood flow with no change in the mean arterial blood pressure
Increased Mitochondrial number and Blood PH
An increase in mitochondria leads to- Increased FFA oxidation and decreased PFK activity- which leads to decreased pyruvate formation- which and Increased H4 form of LDH occurs- and leads to Decreased lactate and Hydrogen formation- which is ALSO caused by increased mitochondrial uptake of pyruvate and NADH--- and all leads to blood PH being maintained--- refer to chart
Why Does Exercise Training Improve VO2 Max?
Because maximal oxygen uptake is the product of systemic blood flow (cardiac output) and systemic oxygen extraction (avo2), training-induced changes in VO2 max must be due to an increase in maximal cardiac output or an increase in the avo2 difference, or a combination.
Redistribution of Blood Flow and Lactate Removal
Cardiac output leads to- increased blood flow in the LIVER- which leads to increased lactate removal- which leads to decreased Blood lactate -And in the MUSCLE it (CO) leads to decreased blood flow and increased oxygen extraction- which leads to decreased lactate production- which leads to decreased blood lactate
Endurance Training-Induced Changes in Fiber Type and Capillarity
Endurance training results in a shift in fast to slow mucle fiber type. The exercise- induced shift in muscle fiber type involves a reduction in the amount of fast myosin in the muscle and an increase in slow myosin isoforms. -Slow myosin isoforms have LOWER myosin ATPase activity but are able to perform more work with less ATP utilization (more efficient) -The fast-to-slow shift in myosin isoforms- phsiologically important- it increases mechanical efficiency and can potentially improve endurance performance -number of type I (slow) fibers in leg muscles of distance runners is correlaed to the number of years of training
High Responders
Genetically gifted individuals that show large improvements (40%-50% increase) in VO2 max following endurance training. -Even though the average VO2 max increase is of about 15% to 20%
Specificity as a result of training
If a muscle is engaged in endurance types of exercise, the primary adaptations are increases in CAPILLARY and MITOCHONDRIA number, which INCREASE the capacity of the muscle to produce energy aerobically. If a muscle is engaged in heavy resistance training, the primary adaptation is an INCREASE in the quantity of the CONTRACTILE proteins, as the MITOCHONDRIAL and CAPILLARY densities may actually DECREASE.
Reversibility
Indicates that the fitness gains by exercising at an overload are quickly lost when training is stopped and the overload is removed.
Central Control of Cardiorespiratory Responses
Motor cortex, cerebellum and basal ganglia leads to- Motor unit recruitment- which leads to increased VO2 work rate -And also Cardiorespiratory control centers- that lead to increased workmate HR VE, and Liver and kidney blood flow that decrease work rate
Overload
Refers to an organ system (ex/ cardiovascular) or tissue (ex/ skeletal muscle) must be exercised at a level beyond which it is accustomed in order to achieve a training adaptation. -intensity -duration -frequency
Specificity
Refers to the effect that exercise training is specific to: 1. the muscles involved in that activity 2. the fiber types recruited 3. the principal energy system involved (aerobic vs anaerobic) 4. The velocity of contraction 5 The type of muscle contraction (eccentric, concentric, or isometric).
Stroke Volume
The amount of blood ejected from the heart with each beat and is equal to the difference between EDV and ESV. Exercise training does NOT increase maximal HR and months of training result in a small DECREASE in maximal HR. Therefore ALL training induced increases in maximal Q must come from increases in SV. Things that can increase SV: 1. Increase in EDV (preload) 2. Increased Cardiac Contractility 3. A decreased in total peripheral resistance (afterload)
Fick Equation
VO2max= Maximal Cardiac Output (Q) * (maximal a-VO2 difference) -Cardiac output- is determined by the product of HR * SV (amount of blood ejected per heart beat) -A-VO2 difference is a measure of how much oxygen is removed from arterial blood and used by the tissues.
The HERITAGE Family Study
Was designed "to study the role of the genotype in cardiovascular, metabolic, and hormonal responses to aerobic exercise training and the contribution of regular exercise to changes in several cardiovascular disease and diabetes risk factors" 1. 50% of VO2 max of untrained subjects can be explained by the genetic differences of individuals. 2. Genetics plays an important role in training-induced improvements in VO2 max. 3. The large variation in human adaptive capacity to endurance training is largely due to 21 different genes that play important roles in training adaptation.