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Unifying Concepts

Chronic Adaptations to Physical Training (PT)

Long-term responses that develop over a period of time (usually a minimum of 6 weeks) when training is repeated regularly are referred to as chronic adaptations to training. The combined effect of all chronic adaptations is known as the training effect.
Chronic adaptations to training may occur in the cardiovascular, respiratory and muscular systems. The result of these physiological adaptations is an improvement in performance.

Chronic adaptations to training vary greatly and are dependent upon the type and method of training undertaken, whether it be aerobic, anaerobic or resistance training

Chronic aerobic adaptations to training

Cardiovascular

  • Increased left ventricle size and volume (increased stroke volume): Aerobic training results in cardiac hypertrophy. An increase in the size and volume of the left ventricle, in particular, occurs. This increases stroke volume and cardiac output, allowing a greater volume of blood to be ejected from the heart, thus providing more oxygen for the athlete to use.
  • Increased capillarisation of the heart muscle: Cardiac hypertrophy also leads to an increase in the capillarisation of the heart muscle itself. The increased supply of blood and oxygen allows the heart to beat more strongly and efficiently during both exercise and rest.
  • Faster heart rate recovery rates increased heart rate recovery rates mean that the heart rate will return to resting levels in a much shorter time than that of an untrained individual. This is due to the greater efficiency of the cardiovascular system to produce energy aerobically.
  • Increased blood volume and haemoglobin levels: Red blood cells may increase in number and the haemoglobin content and oxygen-carrying capacity of the blood may also rise. There is also an increased ratio of plasma in the blood cells, which reduces the viscosity of the blood allowing it to flow smoothly through the blood vessels. This allows a greater amount of oxygen to be delivered to the muscles and used by the athlete.
  • Increased capillarisation of skeletal muscle: Aerobic training leads to increased capillarisation of skeletal muscle. Greater capillary supply means increased blood flow and greater surface area for gas diffusion to take place. Increasing the oxygen and nutrients into the muscles allows for more removal of by-products
  • Decreased heart rate at rest and during submaximal workloads: A greater stroke volume results in the heart not having to beat as often to supply the required blood flow (and oxygen). Aerobic training also results in a slower increase in heart rate during exercise and also a lower steady state that is reached sooner.

Respiratory

    • Increased alveolar surface area (increased pulmonary diffusion): Aerobic training increases the surface area of the alveoli, which in turn increases the pulmonary diffusion, allowing more oxygen to be extracted and transported to the working muscles for use.
    • Increased tidal volume: Aerobic training increases the amount of air inspired and expired by the lungs per breath. This allows for a greater amount of oxygen to be diffused into the surrounding alveoli capillaries and delivered to the working muscles.
    • Increased ventilation during maximal exercise: Aerobic training results in more efficient lung ventilation. Ventilation may be reduced slightly at rest and during submaximal exercise due to improved oxygen utilisation. At maximal workloads, ventilation is increased due to an increase in tidal volume and respiratory frequency. This allows for greater oxygen delivery to working muscles at maximum exercise intensities.



Muscular

  • Increased size and number of mitochondria: Mitochondria are the sites of aerobic ATP resynthesis and where glycogen and triglyceride stores are oxidised. The greater the number and size of the mitochondria located within the muscle, the greater the ability to resynthesise ATP aerobically.
  • Increased myoglobin stores: Myoglobin is responsible for extracting oxygen from the red blood cells and delivering it to the mitochondria in the muscle cell. An increase in the number of myoglobin stores increases the amount of oxygen delivered to the mitochondria for energy production.
  • Increased fuel storage and oxidative enzymes: Aerobic training increases the muscular storage of glycogen and triglycerides in the slowtwitch muscle fibres and there is also an increase in the oxidative enzymes that are responsible for metabolising these fuel stores to produce ATP aerobically. This means that there is less reliance upon the anaerobic glycolysis system until higher intensities. In addition to this, due to increased levels of the enzymes associated with fat metabolism, an aerobically trained athlete is able to ‘glycogen spare’ more effectively and therefore work at higher intensities for longer.
  • Increased muscle oxygen utilisation (a-VO2 difference): All of the above listed factors contribute to the body’s ability to attract oxygen into the muscle cells and then use it to produce adenosine triphosphate (ATP) for muscle contraction. A measure of this is the difference in the amount of oxygen in the arterioles in comparison to the venules.
  • Increased muscle fibre adaptation: Some research has indicated that skeletal muscle fast-twitch type 2A can take on some of the characteristics of slow-twitch as an adaptation of aerobic training. This would allow for a greater ability to generate ATP aerobically with fewer fatiguing factors.

All Three Systems – Cardiovascular, Respiratory and Muscular

  • Increased VO2 max: An increase in the maximum oxygen uptake (VO2 max) allows for a greater amount of oxygen that can be taken in by the respiratory system, transported by the cardiovascular system and utilised by the muscular system to produce ATP, improving the economy of the athlete.
  • Increased lactate inflection point (LIP): LIP represents the highest intensity point where there is a balance between lactate production and removal from the blood. The advantage of having a higher LIP is that the anaerobic glycolysis system isn’t contributing as much until higher exercise intensities are reached. This means that the athlete can work at higher intensities for longer periods without the fatiguing hydrogen ion accumulation.




Chronic anaerobic adaptations to training

Muscular

  • Muscular hypertrophy: An increase in muscle fibre size due to an increase in the size and number of myofibrils and the protein filaments actin and myosin. This increase in muscle size allows for a greater production of strength and power.
  • Increased muscular stores of ATP and CP: Increased muscular stores of ATP and creatine phosphate (CP) increases the capacity of the ATP-CP system, allowing for faster resynthesis of ATP for high intensity activities.
  • Increase in ATPase and creatine kinase enzymes: ATPase is responsible for breaking down ATP to form ADP and release energy for muscular contraction. Creatine kinase initiates the breakdown of CP, which provides the energy to resynthesise ATP at a fast rate.
  • Increased glycolytic capacity: Increased muscular storage of glycogen and consequently the increased levels of glycolytic enzymes, enhances the capacity of the anaerobic glycolysis system to produce energy.
  • Increase in the number of motor units recruited: An increase in the number of nerve axons and their corresponding muscle fibres increases the power and strength of muscular contractions.
  • Increased lactate tolerance: An increase in the ability of the muscles to buffer (neutralise) the acid that accumulates from the production of hydrogen ions during an exercise bout. The increase in lactate tolerance prevents the onset of fatigue and allows an athlete to continue to generate ATP anaerobically, which is at a faster rate, and allows them to work at a higher intensity, producing high lactate levels at the end of performance.




Chronic adaptations to resistance training

Neuromuscular

  • Increase in the cross-sectional area of a muscle (muscle hypertrophy): An increase in the total quantity of actin and myosin protein filaments, the size and number of myofibrils and also in the amount of connective tissue that surrounds the muscle. This allows the muscle to create a greater amount of strength and power with each contraction.
  • Increased synchronisation of motor units: An increase in the ability for a number of different motor units to fire at the same time and an improved ability to recruit larger motor units that require a larger stimulus to activate. The ability to recruit more motor units at the same time and to stimulate larger motor units creates a more powerful muscular contraction.
  • Increase in the firing rate (rate coding) of motor units: An increase in the frequency of stimulation of a given motor unit (rate coding) increases the rate of force development or how quickly a muscle can contract maximally. This is beneficial for rapid ballistic movements where maximal force is required in a very short period of time.
  • A reduction in inhibitory signals: The improved coordination of the agonists, antagonists and synergists is thought to allow for the reduced inhibitory effect. The reduction in the inhibitory mechanisms allow for a greater force production within a muscle group.




Summary of cardiovascular and metabolic adaptations with endurance training

Physiological
Parameter
Rest Submaximal
Exercise
Maximal
Exercise
Stroke volume  ↑
Heart rate ↓ or –
Cardiac output  ↑
a-vO2 difference  ↑  ↑
VO2  ↑
Systolic blood pressure
Diastolic blood pressure
Blood volume  ↑
Capillary density  ↑
Mitochondrial density  ↑

↑ = increase; ↓ = decrease; – = no change; a-vO2 = (CaO2– CVO2); VO2 = oxygen consumption.

 

 

References:

  1. Rivera-Brown AM, Frontera WR. Principles of exercise physiology: responses to acute exercise and long-term adaptations to training. PM R. 2012 Nov;4(11):797-804. [Medline]
  2. Gabriel BM, Zierath JR. The Limits of Exercise Physiology: From Performance to Health. Cell Metab. 2017 May 2;25(5):1000-1011. [Medline]
  3. Hellsten Y, Nyberg M. Cardiovascular Adaptations to Exercise Training. Compr Physiol. 2015 Dec 15;6(1):1-32. [Medline]

 

Created Nov 08, 2018.

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