Chronic Training Adaptations
Chronic Training Adaptations
Exercise or training regularly over an extended period of time (3 times per week for 6-8 weeks) leads to the development of long-term or chronic adaptations to training. Evidence of these adaptations can occur at various stages
Once achieved, these adaptations are retrained unless training ceases. Upon cessation, the body will gradually revert to its pre-training condition (de-training).
Unlike acute responses to exercises, chronic adaptations to training vary greatly and are dependant upon: • Type and method of training undertaken – aerobic vs anaerobic training. Chronic responses are very specific to the type of training performed. • The frequency, duration and intensity of the training …show more content…
undertaken – the greater these things, the more pronounced the adaptations • The individual’s capacities and hereditary factors (genetic make-up)
Chronic Adaptations to Aerobic (endurance) Training: • Minimum period is 6 weeks • More evident over 12 weeks • Adaptations occur at both tissue and system levels.
Cardiorespiratory Adaptations to Aerobic (endurance) Training
• Chronic cardio-respiratory adaptations are primarily designed for more efficient delivery of larger quantities of oxygen to working muscles.
• They decrease cardiovascular disease (CVD)and other health-related illnesses. • Cardio-respiratory adaptations are best developed through continuous, fartlek and longer interval type training.
Cardiovascular Adaptations:
Cardiac hypertrophy (increased ventricular volume): • Enlargement of the heart muscle itself • Increase in size and volume of the ventricular chambers, particularly the left ventricle occurs. • Significantly increases stroke volume
Increased capillarisation of the heart muscle:
• Increase in capillarisation of the heart muscle itself (Increase in capillary density and blood flow to the heart muscle) • Increased supply of blood and oxygen allows the heart to beat more strongly and efficiently during rest and exercise • Coronary protective benefit (therefore decreased risk of heart attack)
Increased stroke volume of the heart:
Heart ejects a greater volume of blood with each beat
Stroke volume is greater at rest, during sub-max and max workloads for a trained athlete compared to an untrained …show more content…
person
Eg. Average stroke volume at rest: • Untrained male - 70-80millilitres/beat, • Trained male endurance athlete - 100millilitres/beat or more.
During maximal exercise: • Untrained person – 110 millilitres/beat • Trained person – 130 millilitres/beat • Elite endurance athletes – 190 millilitres/beat
Trained and untrained females have lower stroke volumes than their male counterparts under all exercise conditions, mainly due to a smaller heart size
Lower resting heart rate:
The amount of oxygen required by an individual at rest does not alter as a result of their training status.
At rest, it takes about 5 litres of blood per minute (cardiac output) to circulate around the body to supply the required amount of oxygen to the body cells
Cardiac output (Q) is equal to stroke volume (SV) multiplied by heart rate (HR).
Q = SV x HR
However, if an individual has developed a greater stroke volume, the heart does not have to beat as frequently to supply the required blood flow
Eg.
Before training:
Q = SV x HR
5L/min = 70 mL/beat x 71 beats/min
After training:
Q = SV x HR
5L/min = 100 mL/beat x 50 beats/min
This is why resting heart rate is a useful indicator of aerobic fitness.
Lower resting heart rate – greater level of aerobic fitness • Elite – 35bpm (marathon runners, triathletes, distance swimmers) • Average adult male – 70bpm
Lower heart rate during sub-maximal workloads:
Mainly a result of increased stroke volume.
The heart works more efficiently - (More blood is pumped with each beat, and therefore the heart doesn’t have to work as hard to supply the required blood flow and oxygen supply)
Slower increase in heart rate during exercise and a lower and faster attainment of steady state during exercise
Improved heart-rate recovery rates:
Heart rate of a trained athlete will return to pre-exercise levels (resting rate) in a much shorter time than that of an untrained individual.
Increased cardiac output at maximum workloads:
Cardiac output – unchanged at rest and even during sub-maximal exercise regardless of training status. Does increase during maximal exercise.
Maximal exercise – may increase to values of: • 20-22 litres per minute for untrained male • 15-16 litres per minute for untrained females • 30 litres per minute or more – highly trained athletes
Lower blood pressure:
May lower blood pressure, especially among people who suffer from hypertension (high blood pressure)
Systolic and diastolic pressure levels may decrease during both rest and exercise
Helps to reduce resistance to blood flow and reduces strain on the heart, thereby decreasing the risk of heart attack and other cardiovascular conditions
Increased arterio-venous oxygen difference (a-VO2 diff):
Trained individuals are able to absorb more oxygen from their bloodstream into their muscles during exercise performance compared to untrained subjects.
This is due to: • Increased muscle myoglobin stores • Increased number and size of mitochondria within their muscles
As a result of this, the concentration of oxygen within the venous blood is lower
Subsequently the arterio-venous oxygen difference is increased during both sub-max and maximal exercise
Therefore, and increased arterio-venous oxygen difference (a-VO2 diff) indicates a greater uptake of oxygen by the muscles with trained individuals
Increased blood volume and haemoglobin levels:
Total blood volume may rise by up to 25% (from 5.25L to 6.6L) for an average adult male with regular and sustained aerobic training.
Red blood cells may increase in number and the haemoglobin content and oxygen-carrying capacity of the blood may also rise.
Increased capillarisation of skeletal muscle:
The average number of capillaries supplying each muscle fibres is: • 5.9 for trained athletes • 4.4 for untrained athletes
Changes to blood cholesterol, triglycerides, low- and high-density lipoprotein levels:
Results may include a decrease in blood cholesterol levels, triglycerides and low-density lipoprotein (LDL).
These substances are associated with the development of coronary heart disease.
Aerobic training increases the ratio of high-density lipo-protein (HDL) to low-density lipoprotein.
High-density lipoprotein is thought to provide a coronary protective effect, lessening the risk of developing coronary heart disease.
Respiratory Adaptations
Increased lung ventilation:
More efficient and improved lung ventilation
At rest and during sub-maximal exercise, ventilation may be reduced due to improved oxygen extraction
However, during maximal workloads, ventilation is increased because of increased tidal volume (amount of air breathed in and out in one breath) and respiratory frequency (the number of breaths taken per minute).
Pulmonary diffusion (the ability of the blood to extract oxygen from the alveoli) is also enhanced.
Increased maximum oxygen uptake (VO2 max)
Increase in the maximum oxygen uptake (VO2 max) during maximal exercise
Improvement can be between 5–30% following a regular and sustained training program
This occurs because of adaptations such as: • Increased cardiac output • Increased red blood cell numbers • Increased a-VO2 difference • Increased muscle capillarisation • Greater oxygen extraction by the muscles
Increased anaerobic or lactate threshold
As a result of the adaptations that improve oxygen delivery and utilisation in the muscles, a higher lactate threshold (the point at which oxygen supply cannot keep up with oxygen demand) is developed.
Advantage:
• The anaerobic glycolysis (lactic acid) system is not utilised as much until higher exercise intensities are reached.
Consequently, lactic acid and hydrogen ion accumulation will be delayed until these higher work-load intensities are attained
The athlete can “work harder and for longer periods”
Muscle Tissue Adaptations to Aerobic (Endurance) Training:
Chronic aerobic training adaptations within muscular tissue are best produced through continuous training or high-repetition resistance training
The following tissue-level changes can be observed within skeletal muscles following extensive endurance training:
Increased oxygen utilisation:
Aerobic training enhances the body’s ability to attract oxygen into the muscle cells and then utilise it to produce adenosine triphosphate (ATP) for muscle contraction
This process occurs in the following ways: • Increased size and number of mitochondria – Mitochondria are the site of ATP synthesis and where glycogen and triglyceride stores are oxidised (Greater oxidisation of fuels to produce ATP) • Increased myoglobin stores – Myoglobin is the substance in the muscle cell that attracts oxygen from the bloodstream into the muscle.
(Increase ability to extract oxygen)
Increased muscular fuel stores:
Increase in the muscular storage of glycogen, free fatty acids and triglycerides, along with the oxidative enzymes required to metabolise these fuel stores and produce ATP.
Increased oxidation of glucose and fats:
The muscular adaptations result in an increase in the capacity of muscle fibres to oxidate both glucose and
fats
The capacity of the aerobic system to metabolise these fuels is increased
Increased oxidation of fats as a fuel source; due to: • Increased storage of triglycerides and free fatty acids • Increased levels of enzymes associated with fat metabolism
Means that:
At any given exercise intensity, a trained individual has to rely less on glycogen, thereby “sparing” glycogen stores (Glycogen sparing)
Therefore delaying the time to exhaustion due to glycogen depletion.
Decreased utilisation of the anaerobic glycolysis (lactic acid) system:
The enhanced capacity of the muscles to aerobically metabolise glucose and fats and other muscular level adaptations also means that there is less reliance upon the anaerobic glycolysis system to produce energy for ATP resynthesis until higher exercise intensities are reached. • Allows athletes to work at higher intensities without exceeding lactate threshold. OR • Aerobic training results in an increase in the lactate threshold
Eg. An athlete must run at a faster pace in order to accumulate the same amount of blood lactic acid as before training
Muscle-fibre type adaptation:
Some research has shown evidence that skeletal muscle switches fibre types from fast twitch to slow twitch as a result of endurance training.
Skeletal muscle fibres are classified into three types:
Type 1 – Slow-twitch oxidative fibres: • Contain large amounts of myoglobin, and large numbers of mitochondria and blood capillaries. • Red • Split ATP at a slow rate • Slow contraction velocity • Very resistant to fatigue • High capacity to generate ATP by oxidative metabolic processes.
Type 2A – Fast-twitch oxidative fibres: • Contain an extremely large amount of myoglobin, and huge numbers of mitochondria and blood capillaries. • Red • Very high capacity for generating ATP by oxidative metabolic processes • Split ATP at a very rapid rate • Fast contraction velocity • Resistant to fatigue
Type 2B – Fast-twitch glycolytic fibres:
• Contain low myoglobin content, relatively few mitochondria and blood capillaries, and large amounts of glycogen • White • Geared to generate ATP by anaerobic metabolic processes • Fatigue easily • Split ATP at a fast rate • Fast contraction velocity
Individual muscles are a mixture of the three types of muscle fibres, but their proportions vary depending on the action of the muscle and the genetic make-up of the individual
Summary of muscle tissue adaptations to aerobic (endurance) training:
|Before Training |After Training |
|Mitochondria (size and number) |Increased |
|Glycogen Stores |Increased |
|Myoglobin |Increased |
|Triglyceride Stores |Increased |
|Oxidation (both glucose and fats) |Increased |
|Anaerobic Glycolysis (lactic acid system) |Decreased |
|Muscle Type Adaptation (number and type) |Increased |
| | |
| |Some conversion of: |
| |Type 2B fibres to |
| |Type 2A fibres |
Chronic Adaptations to Anaerobic Training
Anaerobic training effects are best developed through sprint training, shorter and faster interval training, plyometric training, circuit training, and resistance (strength and power) training.
The greatest adaptations occur at the muscle-tissue level. They include:
Muscle hypertrophy:
Significant enlargement of muscle fibres (mainly Type 2B fast-twitch fibres) resulting in muscular hypertrophy (an increase in the cross-sectional size of the muscle) and subsequently, greater strength
Hypertrophy occurs as a result of an increased size and number of myofibrils per muscle fibre and increased amounts of myosin and actin myofilaments
Muscular hypertrophy is more pronounced in males than females due to greater levels of testosterone.
Increased muscular stores of ATP and PC: • Muscular hypertrophy is accompanied by increased muscular stores of ATP and PC, as well as enzymes required to break down and resynthesise ATP • Increased capacity of the ATP-PC system – greater energy release and faster restoration of ATP • Benefits athletes in activities that require speed, strength and power
Increased glycolytic capacity: • Enhanced muscular storage of glycogen and increases in the levels of glycolytic enzymes. • Capacity of the anaerobic glycolysis system to produce energy is enhanced
Cardiac hypertrophy: • Most significant circulatory system adaptation resulting from anaerobic training • Increase in heart muscle size • Anaerobic training produces an increase in the thickness of the ventricular walls • No change in stroke volume, however there is a more forceful contraction.
Other anaerobic training adaptations: • Increase in the strength and size of connective tissues such as tendons and ligaments • Increase in the number of motor units recruited for maximum contractions • Increase in the speed of nerve-impulse transmission to the muscle cells and increase in the speed of muscular contraction
Summary of Chronic Adaptations to Training:
|Tissue of System Level |Specific Adaptation to Types of Training |Rest |Sub-maximal |Maximal Exercise |
| | | |exercise | |
|Circulatory System |Aerobic Training | | | |
| |Cardiac Hypertrophy – increase in size of ventricular | | | |
| |cavities | | | |
| |Increased capillarisation of the heart muscle | | | |
| |Increased stroke volume | | | |
| |Lower resting heart rate | | | |
| |Lower heart rate during sub-maximal workloads | | | |
| |Improved heart-rate recovery rates | | | |
| |Increased cardiac output at maximum workloads | | | |
| |Lower blood pressure | | | |
| |Increased a-VO2 difference | | | |
| |Increased capillarisation of skeletal muscle | | | |
| |Changes to blood cholesterol, triglycerides, low and | | | |
| |high-density lipoprotein levels | | | |
| |Anaerobic Training | | | |
| |Cardiac hypertrophy – increase in thickness of | | | |
| |ventricular walls | | | |
| | | | | |
|Respiratory System |Aerobic Training | | | |
| |Increased lung ventilation | | | |
| |Increased VO2 max | | | |
| |Increased lactate threshold | | | |
| | | | | |
|Muscle Tissue |Aerobic Training | | | |
| |Increased oxygen utilisation | | | |
| |Increased size of mitochondria | | | |
| |Increased myoglobin stores | | | |
| |Increased muscular fuel stores | | | |
| |Glycogen | | | |
| |Triglycerides | | | |
| |Free Fatty Acids | | | |
| |Oxidative Enzymes | | | |
| |Increased oxidation of fats | | | |
| |Decreased utilisation of the anaerobic glycolysis | | | |
| |system | | | |
| |Muscle-fibre type adaptations | | | |
| | | | | |
| |Anaerobic Training | | | |
| |Muscle hypertrophy | | | |
| |Increased number of myofibrils | | | |
| |Increased size of myofibrils | | | |
| |Increased amounts of myosin and actin filaments | | | |
| |Increased capacity of the ATP-PC system | | | |
| |Increased stores of ATP | | | |
| |Increased stores of PC | | | |
| |Increased glycolytic capacity | | | |
| |Increased storage of glycogen | | | |
| |Increased levels of glycolytic enzymes | | | |
| |Increased speed and force of contraction | | | |
Exercise or training regularly over an extended period of time (3 times per week for 6-8 weeks) leads to the development of long-term or chronic adaptations to training. Evidence of these adaptations can occur at various stages
Once achieved, these adaptations are retrained unless training ceases. Upon cessation, the body will gradually revert to its pre-training condition (de-training).
Unlike acute responses to exercises, chronic adaptations to training vary greatly and are dependant upon: • Type and method of training undertaken – aerobic vs anaerobic training. Chronic responses are very specific to the type of training performed. • The frequency, duration and intensity of the training …show more content…
undertaken – the greater these things, the more pronounced the adaptations • The individual’s capacities and hereditary factors (genetic make-up)
Chronic Adaptations to Aerobic (endurance) Training: • Minimum period is 6 weeks • More evident over 12 weeks • Adaptations occur at both tissue and system levels.
Cardiorespiratory Adaptations to Aerobic (endurance) Training
• Chronic cardio-respiratory adaptations are primarily designed for more efficient delivery of larger quantities of oxygen to working muscles.
• They decrease cardiovascular disease (CVD)and other health-related illnesses. • Cardio-respiratory adaptations are best developed through continuous, fartlek and longer interval type training.
Cardiovascular Adaptations:
Cardiac hypertrophy (increased ventricular volume): • Enlargement of the heart muscle itself • Increase in size and volume of the ventricular chambers, particularly the left ventricle occurs. • Significantly increases stroke volume
Increased capillarisation of the heart muscle:
• Increase in capillarisation of the heart muscle itself (Increase in capillary density and blood flow to the heart muscle) • Increased supply of blood and oxygen allows the heart to beat more strongly and efficiently during rest and exercise • Coronary protective benefit (therefore decreased risk of heart attack)
Increased stroke volume of the heart:
Heart ejects a greater volume of blood with each beat
Stroke volume is greater at rest, during sub-max and max workloads for a trained athlete compared to an untrained …show more content…
person
Eg. Average stroke volume at rest: • Untrained male - 70-80millilitres/beat, • Trained male endurance athlete - 100millilitres/beat or more.
During maximal exercise: • Untrained person – 110 millilitres/beat • Trained person – 130 millilitres/beat • Elite endurance athletes – 190 millilitres/beat
Trained and untrained females have lower stroke volumes than their male counterparts under all exercise conditions, mainly due to a smaller heart size
Lower resting heart rate:
The amount of oxygen required by an individual at rest does not alter as a result of their training status.
At rest, it takes about 5 litres of blood per minute (cardiac output) to circulate around the body to supply the required amount of oxygen to the body cells
Cardiac output (Q) is equal to stroke volume (SV) multiplied by heart rate (HR).
Q = SV x HR
However, if an individual has developed a greater stroke volume, the heart does not have to beat as frequently to supply the required blood flow
Eg.
Before training:
Q = SV x HR
5L/min = 70 mL/beat x 71 beats/min
After training:
Q = SV x HR
5L/min = 100 mL/beat x 50 beats/min
This is why resting heart rate is a useful indicator of aerobic fitness.
Lower resting heart rate – greater level of aerobic fitness • Elite – 35bpm (marathon runners, triathletes, distance swimmers) • Average adult male – 70bpm
Lower heart rate during sub-maximal workloads:
Mainly a result of increased stroke volume.
The heart works more efficiently - (More blood is pumped with each beat, and therefore the heart doesn’t have to work as hard to supply the required blood flow and oxygen supply)
Slower increase in heart rate during exercise and a lower and faster attainment of steady state during exercise
Improved heart-rate recovery rates:
Heart rate of a trained athlete will return to pre-exercise levels (resting rate) in a much shorter time than that of an untrained individual.
Increased cardiac output at maximum workloads:
Cardiac output – unchanged at rest and even during sub-maximal exercise regardless of training status. Does increase during maximal exercise.
Maximal exercise – may increase to values of: • 20-22 litres per minute for untrained male • 15-16 litres per minute for untrained females • 30 litres per minute or more – highly trained athletes
Lower blood pressure:
May lower blood pressure, especially among people who suffer from hypertension (high blood pressure)
Systolic and diastolic pressure levels may decrease during both rest and exercise
Helps to reduce resistance to blood flow and reduces strain on the heart, thereby decreasing the risk of heart attack and other cardiovascular conditions
Increased arterio-venous oxygen difference (a-VO2 diff):
Trained individuals are able to absorb more oxygen from their bloodstream into their muscles during exercise performance compared to untrained subjects.
This is due to: • Increased muscle myoglobin stores • Increased number and size of mitochondria within their muscles
As a result of this, the concentration of oxygen within the venous blood is lower
Subsequently the arterio-venous oxygen difference is increased during both sub-max and maximal exercise
Therefore, and increased arterio-venous oxygen difference (a-VO2 diff) indicates a greater uptake of oxygen by the muscles with trained individuals
Increased blood volume and haemoglobin levels:
Total blood volume may rise by up to 25% (from 5.25L to 6.6L) for an average adult male with regular and sustained aerobic training.
Red blood cells may increase in number and the haemoglobin content and oxygen-carrying capacity of the blood may also rise.
Increased capillarisation of skeletal muscle:
The average number of capillaries supplying each muscle fibres is: • 5.9 for trained athletes • 4.4 for untrained athletes
Changes to blood cholesterol, triglycerides, low- and high-density lipoprotein levels:
Results may include a decrease in blood cholesterol levels, triglycerides and low-density lipoprotein (LDL).
These substances are associated with the development of coronary heart disease.
Aerobic training increases the ratio of high-density lipo-protein (HDL) to low-density lipoprotein.
High-density lipoprotein is thought to provide a coronary protective effect, lessening the risk of developing coronary heart disease.
Respiratory Adaptations
Increased lung ventilation:
More efficient and improved lung ventilation
At rest and during sub-maximal exercise, ventilation may be reduced due to improved oxygen extraction
However, during maximal workloads, ventilation is increased because of increased tidal volume (amount of air breathed in and out in one breath) and respiratory frequency (the number of breaths taken per minute).
Pulmonary diffusion (the ability of the blood to extract oxygen from the alveoli) is also enhanced.
Increased maximum oxygen uptake (VO2 max)
Increase in the maximum oxygen uptake (VO2 max) during maximal exercise
Improvement can be between 5–30% following a regular and sustained training program
This occurs because of adaptations such as: • Increased cardiac output • Increased red blood cell numbers • Increased a-VO2 difference • Increased muscle capillarisation • Greater oxygen extraction by the muscles
Increased anaerobic or lactate threshold
As a result of the adaptations that improve oxygen delivery and utilisation in the muscles, a higher lactate threshold (the point at which oxygen supply cannot keep up with oxygen demand) is developed.
Advantage:
• The anaerobic glycolysis (lactic acid) system is not utilised as much until higher exercise intensities are reached.
Consequently, lactic acid and hydrogen ion accumulation will be delayed until these higher work-load intensities are attained
The athlete can “work harder and for longer periods”
Muscle Tissue Adaptations to Aerobic (Endurance) Training:
Chronic aerobic training adaptations within muscular tissue are best produced through continuous training or high-repetition resistance training
The following tissue-level changes can be observed within skeletal muscles following extensive endurance training:
Increased oxygen utilisation:
Aerobic training enhances the body’s ability to attract oxygen into the muscle cells and then utilise it to produce adenosine triphosphate (ATP) for muscle contraction
This process occurs in the following ways: • Increased size and number of mitochondria – Mitochondria are the site of ATP synthesis and where glycogen and triglyceride stores are oxidised (Greater oxidisation of fuels to produce ATP) • Increased myoglobin stores – Myoglobin is the substance in the muscle cell that attracts oxygen from the bloodstream into the muscle.
(Increase ability to extract oxygen)
Increased muscular fuel stores:
Increase in the muscular storage of glycogen, free fatty acids and triglycerides, along with the oxidative enzymes required to metabolise these fuel stores and produce ATP.
Increased oxidation of glucose and fats:
The muscular adaptations result in an increase in the capacity of muscle fibres to oxidate both glucose and
fats
The capacity of the aerobic system to metabolise these fuels is increased
Increased oxidation of fats as a fuel source; due to: • Increased storage of triglycerides and free fatty acids • Increased levels of enzymes associated with fat metabolism
Means that:
At any given exercise intensity, a trained individual has to rely less on glycogen, thereby “sparing” glycogen stores (Glycogen sparing)
Therefore delaying the time to exhaustion due to glycogen depletion.
Decreased utilisation of the anaerobic glycolysis (lactic acid) system:
The enhanced capacity of the muscles to aerobically metabolise glucose and fats and other muscular level adaptations also means that there is less reliance upon the anaerobic glycolysis system to produce energy for ATP resynthesis until higher exercise intensities are reached. • Allows athletes to work at higher intensities without exceeding lactate threshold. OR • Aerobic training results in an increase in the lactate threshold
Eg. An athlete must run at a faster pace in order to accumulate the same amount of blood lactic acid as before training
Muscle-fibre type adaptation:
Some research has shown evidence that skeletal muscle switches fibre types from fast twitch to slow twitch as a result of endurance training.
Skeletal muscle fibres are classified into three types:
Type 1 – Slow-twitch oxidative fibres: • Contain large amounts of myoglobin, and large numbers of mitochondria and blood capillaries. • Red • Split ATP at a slow rate • Slow contraction velocity • Very resistant to fatigue • High capacity to generate ATP by oxidative metabolic processes.
Type 2A – Fast-twitch oxidative fibres: • Contain an extremely large amount of myoglobin, and huge numbers of mitochondria and blood capillaries. • Red • Very high capacity for generating ATP by oxidative metabolic processes • Split ATP at a very rapid rate • Fast contraction velocity • Resistant to fatigue
Type 2B – Fast-twitch glycolytic fibres:
• Contain low myoglobin content, relatively few mitochondria and blood capillaries, and large amounts of glycogen • White • Geared to generate ATP by anaerobic metabolic processes • Fatigue easily • Split ATP at a fast rate • Fast contraction velocity
Individual muscles are a mixture of the three types of muscle fibres, but their proportions vary depending on the action of the muscle and the genetic make-up of the individual
Summary of muscle tissue adaptations to aerobic (endurance) training:
|Before Training |After Training |
|Mitochondria (size and number) |Increased |
|Glycogen Stores |Increased |
|Myoglobin |Increased |
|Triglyceride Stores |Increased |
|Oxidation (both glucose and fats) |Increased |
|Anaerobic Glycolysis (lactic acid system) |Decreased |
|Muscle Type Adaptation (number and type) |Increased |
| | |
| |Some conversion of: |
| |Type 2B fibres to |
| |Type 2A fibres |
Chronic Adaptations to Anaerobic Training
Anaerobic training effects are best developed through sprint training, shorter and faster interval training, plyometric training, circuit training, and resistance (strength and power) training.
The greatest adaptations occur at the muscle-tissue level. They include:
Muscle hypertrophy:
Significant enlargement of muscle fibres (mainly Type 2B fast-twitch fibres) resulting in muscular hypertrophy (an increase in the cross-sectional size of the muscle) and subsequently, greater strength
Hypertrophy occurs as a result of an increased size and number of myofibrils per muscle fibre and increased amounts of myosin and actin myofilaments
Muscular hypertrophy is more pronounced in males than females due to greater levels of testosterone.
Increased muscular stores of ATP and PC: • Muscular hypertrophy is accompanied by increased muscular stores of ATP and PC, as well as enzymes required to break down and resynthesise ATP • Increased capacity of the ATP-PC system – greater energy release and faster restoration of ATP • Benefits athletes in activities that require speed, strength and power
Increased glycolytic capacity: • Enhanced muscular storage of glycogen and increases in the levels of glycolytic enzymes. • Capacity of the anaerobic glycolysis system to produce energy is enhanced
Cardiac hypertrophy: • Most significant circulatory system adaptation resulting from anaerobic training • Increase in heart muscle size • Anaerobic training produces an increase in the thickness of the ventricular walls • No change in stroke volume, however there is a more forceful contraction.
Other anaerobic training adaptations: • Increase in the strength and size of connective tissues such as tendons and ligaments • Increase in the number of motor units recruited for maximum contractions • Increase in the speed of nerve-impulse transmission to the muscle cells and increase in the speed of muscular contraction
Summary of Chronic Adaptations to Training:
|Tissue of System Level |Specific Adaptation to Types of Training |Rest |Sub-maximal |Maximal Exercise |
| | | |exercise | |
|Circulatory System |Aerobic Training | | | |
| |Cardiac Hypertrophy – increase in size of ventricular | | | |
| |cavities | | | |
| |Increased capillarisation of the heart muscle | | | |
| |Increased stroke volume | | | |
| |Lower resting heart rate | | | |
| |Lower heart rate during sub-maximal workloads | | | |
| |Improved heart-rate recovery rates | | | |
| |Increased cardiac output at maximum workloads | | | |
| |Lower blood pressure | | | |
| |Increased a-VO2 difference | | | |
| |Increased capillarisation of skeletal muscle | | | |
| |Changes to blood cholesterol, triglycerides, low and | | | |
| |high-density lipoprotein levels | | | |
| |Anaerobic Training | | | |
| |Cardiac hypertrophy – increase in thickness of | | | |
| |ventricular walls | | | |
| | | | | |
|Respiratory System |Aerobic Training | | | |
| |Increased lung ventilation | | | |
| |Increased VO2 max | | | |
| |Increased lactate threshold | | | |
| | | | | |
|Muscle Tissue |Aerobic Training | | | |
| |Increased oxygen utilisation | | | |
| |Increased size of mitochondria | | | |
| |Increased myoglobin stores | | | |
| |Increased muscular fuel stores | | | |
| |Glycogen | | | |
| |Triglycerides | | | |
| |Free Fatty Acids | | | |
| |Oxidative Enzymes | | | |
| |Increased oxidation of fats | | | |
| |Decreased utilisation of the anaerobic glycolysis | | | |
| |system | | | |
| |Muscle-fibre type adaptations | | | |
| | | | | |
| |Anaerobic Training | | | |
| |Muscle hypertrophy | | | |
| |Increased number of myofibrils | | | |
| |Increased size of myofibrils | | | |
| |Increased amounts of myosin and actin filaments | | | |
| |Increased capacity of the ATP-PC system | | | |
| |Increased stores of ATP | | | |
| |Increased stores of PC | | | |
| |Increased glycolytic capacity | | | |
| |Increased storage of glycogen | | | |
| |Increased levels of glycolytic enzymes | | | |
| |Increased speed and force of contraction | | | |