Samenvatting
Samenvatting Uitbreiding Mc Ardle
- Instelling
- Maastricht University (UM)
Uitbreiding Mc Ardle
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Voorbeeld 2 van de 8 pagina's
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Voorbeeld van de inhoud
Uitbreiding Mc ArdleBlz 136
Some energy for ATP resynthesis also comes directly from the anaerobic splitting of a phosphate from
phosphocreatine (PCr), another intracellular high-energy phoshphate compound.
Because PCr has a larger free energy of hydrolysis than ATP, its hydrolysis catalysed by the enzyme
creatine kinase drives ADP phosphorylation to ATP. Cells store approximately 4-6x more PCr than ATP.
Transient increases in ADP within the muscle’s contraction unit during exercise shift the creatine
kinase reaction toward PCr hydrolysis and ATP production; the reaction does not require oxygen and
reaches a maximum energy yield in about 10 seconds. Thus, PCr serves as a ‘reservoir’ of high-energy
phosphate bonds. The rapidity of ADP phosphorylation considerably exceeds energy transfer from
stored muscle glycogen because of the high activity rate of creatine kinase. If maximal effort
continues beyond 10 seconds, energy for continual ATP resynthesis must originate from less-rapid
catabolism of the stored macronutrients.
Intense physical activity of short duration requires immediate energy. This energy comes almost
exclusively from the intramuscular ATP en PCr. Each kilogram of skeletal muscle contains 3-8 mmol of
ATP and 4-5x more PCr. The quantity of these high-energy compounds probably becomes fully
depleted within 20-30 seconds of all-out exercise. The maximum rate of energy transfer from the
high-energy phosphates exceeds by 4-8x the maximal energy transfer from aerobic metabolism.
Blz 228
When movement begins at either fast or slow speed, intramuscular high-energy phosphates ATP and
PCr provide immediate energy to power muscle action. Following the first few seconds of movement,
glycolytic pathways generate an increasingly greater percentage of total energy required for
continuous ATP resynthesis. Continued activity places progressively greater demands on the long-
term aerobic system.
Oxygen consumption during exercise blz. 163
Oxygen consumption rises exponentially during the first minutes of physical activity, called the fast
component of exercise oxygen consumption, to attain a plateau between the third and fourth
minutes. It then remains stable for the duration of effort.
Steady state/rate describes the flat portion or plateau of the oxygen consumption curve. This means
that there is a balance between energy required by the working muscles, and ATP production in
aerobic metabolism. Within the steady-rate region, no appreciable blood lactate accumulates. The
steady-rate aerobic metabolism determines the capacity to sustain steady-rate exercise. Fluid loss and
electrolyte depletion during exercise often pose limiting factors, especially in hot weather.
At activity onset the oxygen consumption curve does not increase instantaneously to steady rate,
even though the exercise energy requirement remains unchanged throughout exercise. In the
beginning, the energy for muscle function comes directly from the immediate anaerobic breakdown
of ATP. Oxygen consumption increases rapidly in subsequent energy transfer reactions under 3
conditions: when oxygen combines with the hydrogens liberated in: 1. Glycolysis, 2. Beta oxidation of
fatty acids, or 3. Citric acid cycle reactions. After several minutes of submaximal physical activity,
hydrogen production and subsequent oxidation and ATP production become proportional to the
exercise-energy requirement. At this stage, oxygen consumption attains a balance, indicating a
relative steady rate between energy requirement and aerobic energy transfer.
The oxygen deficit quantitatively expresses the difference between the total oxygen consumption
, during activity and the total that would be consumed had steady-rate oxygen consumption been
achieved at the onset. This represents the immediate anaerobic energy transfer from the hydrolysis
of intramuscular high-energy phosphates and rapid glycolysis until steady-rate transfer matches the
energy requirements.
Maximal oxygen consumption
In the beginning, with each successive hill, during the first several hills, oxygen consumption increases
rapidly, with each new steady-rate value in direct proportion to exercise intensity. The last hills, the
oxygen consumption fails to increase as rapidly or to the same extent as in the precious hills:
eventually the VO2 max is reached. Energy transfer via anaerobic glycolysis allows performance of
more-intense physical activity with resulting lactate accumulation.
The VO2max is a quantitative measure of a person’s capacity for aerobic ATP resynthesis.
Ventilation-perfusion ratio blz. 264
Approximately 4.2 L of air normally ventilates the alveoli each minute at rest, and an average of 5.0 L
of blood flows through the pulmonary capillaries. In this case the ventilation-perfusion ratio is 0,84.
This ratio means that alveolar ventilation of 0.84 L matches each liter of pulmonary blood flow. In
light activity, the ventilation-perfusion ratio is about 0,8. In contrast, intense physical activity
produces a disproportionate increase in alveolar ventilation the ratio may exceed 5.0. In most
instances, this response ensures adequate aeration of venous blood. The mismatching of alveolar
ventilation to perfusion accounts for many of the gas exchange problems occurring in pulmonary
disease and possibly during intense activity.
The ventilation perfusion ratio depends largely on the region of the lung because of gravitational
effects, and because the base (lower region) of the lung positions below the heart, and its apex lies
above the heart, the ratio of the apex of the lung exceeds 1.0 (underperfusion/overventilation).
Despite these regional variations in ventilation in relation to blood flow, ventilation-perfusion ratios
that exceed 0.50 are sufficient to meet gas exchange demands at rest.
Regulation of ventilation during physical activity
• Chemical control: Neither chemical stimulation nor any other single mechanism entirely accounts
for the increase in ventilation: hyperpnea, during physical activity. Maximum changes in plasma
acidity and inspired PO2 and PCO2 does not increase minute ventilation to values during vigorous
exertion. As intensity increases, alveolar (arterial) PO2 does not decrease to an extent that increases
ventilation through chemoreceptor stimulation. The large ventilator volumes during intense physical
activity cause alveolar PO2 to rise above the average resting value of 100 mm Hg.
Pulmonary ventilation during light and moderate activity closely couples with metabolism
proportional to oxygen consumption an CO2 production. Under these conditions, alveolar and arterial
PCO2 generally averages 40 mm Hg.
During strenuous activity with its relatively large anaerobic component, increased CO2 and
subsequent H+ concentrations provide an additional ventilator stimulus. The resulting
hyperventilation reduces alveolar and PCO2 till sometimes 25 mm Hg. This decreases the ventilator
drive.
• Non - Chemical control:
- Neurogenic factors:
Cortical influence: Neural outflow from regions of the motor cortex and cortical activation in
anticipation of activity stimulate respiratory neurons in the medulla to initiate the abrupt increase in
exercise ventilation.
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