PED Ch14 - Chronic Adaptations

Economy

The quantity of oxygen (mL/kg/min) required to generate movement at any given speed or intensity

Respiratory chronic adaptations to aerobic training (4)

• Increased pulmonary ventilation during maximal exercise

• Increased tidal volume

• Decreased resting and submaximal respiratory frequency

• Increased pulmonary diffusion

How do respiratory chronic adaptations improve performance?

Respiratory chronic adaptations usually increase the uptake of oxygen. Increased oxygen uptake increases the capacity of the aerobic energy system to resynthesise ATP, allowing the athlete to work at a higher aerobic intensity

Ventilation

The amount of air inspired or expired per minute by the lungs

Ventilation equation

Ventilation = Tidal volume x Respiratory frequency

V = TV x RF

Tidal volume

The amount of air that is inspired and expired with each breath

Respiratory frequency

The amount of breaths in and out per minute

Pulmonary diffusion

The exchange of oxygen and carbon dioxide between the alveoli and surrounding capillaries from an area of high concentration to low concentration

Cardiovascular chronic adaptations to aerobic training (9)

• Increased left ventricle size and volume

• Increased stroke volume

• Decreased resting and submaximal heart rate

• Faster heart rate recovery rates

• Increased cardiac output during maximal exercise

• Decreased blood pressure

• Increased capillarisation of the heart muscle

• Increased capillarisation of skeletal muscle

• Increased blood volume

How do cardiovascular chronic adaptations improve performance?

Cardiovascular chronic adaptations increase the delivery of oxygen to the muscles, allowing for greater aerobic ATP resynthesis, allowing the athlete to work at a higher aerobic intensity

Cardiac hypertrophy

The enlargement of the heart muscle as a result of training

Stroke volume

The amount of blood ejected from the left ventricle with each beat of the heart

Cardiac output

The amount of blood ejected from the left ventricle of the heart per minute (L/min)

Cardiac output equation

Cardiac output = Stroke volume x Heart rate

Q = SV x HR

Systolic blood pressure

The blood pressure recorded as blood is ejected during the contraction phase

Diastolic blood pressure

The blood pressure recorded during the relaxation phase of the heart cycle

Healthy blood pressure

120/80mm/Hg (systolic/diastolic)

Capillarisation

An increase in capillary density, increasing blood supply to the muscles and heart and increasing the exchange of gases and nutrients

Muscular chronic adaptations to aerobic training (6)

• Increased size and number of mitochondria

• Increased myoglobin stores

• Increased arteriovenous oxygen difference

• Increased muscular fuel stores and oxidative enzymes

• Increased oxidation of glucose and triglycerides

• Adaptation of muscle fibre type

Mitochondria

The site of aerobic ATP resynthesis, responsible for breaking down glycogen and triglycerides for energy

Myoglobin

Responsible for extracting oxygen from the blood and bringing it into the muscles

Arteriovenous oxygen difference

The difference in oxygen concentration between arterial and venous blood. Increased a-VO2 diff indicates a greater uptake and utilisation of oxygen by the muscles.

Increased muscular fuel stores and oxidative enzymes

• Increases the storage of glycogen and triglycerides in slow-twitch fibres

• Increases oxidative enzymes that break down these fuels, leading to faster aerobic ATP resynthesis and less reliance on the anaerobic glycolysis system

Adaptations to oxidation of glycogen and triglycerides

• Oxidation of glycogen decreases at submaximal intensity and increases at maximal intensity

• Oxidation of triglycerides increases at rest and submaximal intensity

Glycogen sparing

The process whereby glycogen stores are not used as early during exercise due to the increased ability to use triglycerides for energy production. This delays glycogen depletion, allowing the athlete to sustain higher intensities for longer, improving performance in endurance events.

Adaptation of muscle fibre type as a result of aerobic training (2)

• Type 2A fast-twitch oxidative fibres can take on the characteristics of slow-twitch fibres

• Slow-twitch fibres increase in cross sectional area

Maximum oxygen uptake (VO2 max)

The maximum amount of oxygen per minute that can be taken in, transported and utilised by the body for energy production

VO2 max equation

VO2 max = Cardiac output x a-VO2 diff

Relative VO2 max

A measurement that takes into account body weight and is given in mL/kg/min, allowing for comparison between athletes

Absolute VO2 max

A measurement of the total amount of oxygen consumed, irrespective of body weight, measured in L/min

Lactate inflection point (LIP)

The highest intensity point at which lactate production equals removal. It represents a person’s highest steady state intensity.

How does increased LIP improve performance?

Increased LIP allows the athlete to produce ATP aerobically at higher intensities so there in less reliance on the anaerobic glycolysis system. This means the athlete can work at higher intensities for longer without fatiguing from the accumulation of H+

How does exercising at intensities beyond LIP cause fatigue?

Above LIP, blood lactate concentration increases rapidly, causing rapid onset of fatigue. The athlete experiences increased muscle acidity, surges of adrenaline, increased recruitment of fast-twitch fibres and a decline in oxidative enzyme rate.

Muscular chronic adaptations to anaerobic training (6)

• Muscular hypertrophy

• Increased fuel stores and enzymes

• Increased glycolytic capacity

• Increased motor unit recruitment

• Cardiac hypertrophy

• Increased lactate tolerance

Muscular hypertrophy

The increase in the cross sectional area of a muscle caused by increased size and number of myofibrils per muscle fibre and increased amounts of myosin and actin

Myofibrils

Small fibres that run through each muscle fibre

Increased fuel stores and enzymes (anaerobic)

• Increased stores of ATP and CP, increasing the capacity of the ATP-CP system

• Increased ATP-ase and creatine kinase enzymes, allowing for faster ATP resynthesis

Increased glycolytic capacity

Increased muscle glycogen stores and increased glycolytic enzymes

Glycogen synthase

Promotes the conversion of glucose to glycogen to be stored in the muscles

Increased motor unit recruitment

Increases the number of motor units recruited for muscular contractions, increasing strength and power production

Motor unit

Consists of one motor neuron and all of the muscle fibres it innervates

Cardiac hypertrophy (anaerobic)

The thickening of the ventricular walls, which increases the force of heart contractions, causing blood to be ejected with greater force

Increased lactate tolerance

Occurs when the body increases its buffering capacity to tolerate the accumulation of H+ during anaerobic exercise, delaying the onset of fatigue, allowing the athlete to continue working at a high intensity

Buffering capacity

The ability of the muscle cell buffers to resist change in pH (acidity). Buffers such as bicarbonates and muscle phosphates combine with H+ to neutralise the increase in acidity.

Neuromuscular chronic adaptations to resistance training (5)

• Increased muscle size and change in muscle structure

• Muscle fibre adaptations

• Increased synchronisation of motor units

• Increased firing rate of motor units

• Decreased inhibitory signals

Size principle

Motor units are recruited in order of their size from smallest to largest, suggesting that all motor units are recruited to lift heavy loads

Increased firing rate (rate coding) of motor units

An increase in rate coding (the frequency of impulses sent to a muscle) increases the speed of muscle contractions

Decreased inhibitory signals (3 points)

• Inhibitory mechanisms provide a protective reflex that limits the excessive generation of force in a muscle

• Training can reduce these inhibitory mechanisms to allow the muscles to exert greater force

• Improved coordination of the agonists, antagonists and synergists allow for a reduced inhibitory effect