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Key points Adenosine triphosphate (ATP) is the principal high-energy phosphate molecule that enables muscle contraction. Energy supplies to muscle are initially provided from the immediate energy sources of ATP and phosphocreatine before other aspects of metabolism are activated. Muscle fibres are classified as type I, type IIa and type IIb fibres.

Pulmonary ventilation increases because of a rise in tidal volume and respiratory rate to meet increased oxygen demands. Oxygen delivery during strenuous exercise is limited by cardiovascular function. Immediate energy sources Adenosine triphosphate. Respiratory system During exercise, ventilation might increase from resting values of around 5–6 litre min −1 to 100 litre min −1. Ventilation increases linearly with increases in work rate at submaximal exercise intensities. Prema desam telugu mp3 free download. Oxygen consumption also increases linearly with increasing work rate at submaximal intensities. In an average young male, resting oxygen consumption is about 250 ml min −1 and in an endurance athlete oxygen consumption during very high intensity exercise might reach 5000 ml min −1.

The increase in pulmonary ventilation is attributable to a combination of increases in tidal volume and respiratory rate and closely matches the increase in oxygen uptake and carbon dioxide output. Breathing capacity, however, does not reach its maximum even during strenuous exercise and it is not responsible for the limitation in oxygen delivery to muscles seen during high intensity activity. Haemoglobin continues to be fully saturated with oxygen throughout exercise in people with normal respiratory function. Changes in arterial blood gases The changes which occur in arterial pH, P o 2 and P co 2 values during exercise are usually small.

Arterial P o 2 often rises slightly because of hyperventilation although it may eventually fall at high work rates. During vigorous exercise, when sufficient oxygen for flux through the Krebs cycle is not available, the increased reliance on glycolysis results in increased accumulation of lactic acid, which initially leads to an increase in Pa co 2. However, this is counteracted by the stimulation of ventilation and as a result Pa co 2 is decreased. This provides some respiratory compensation for further lactic acid production and prevents a decline in blood pH, which remains nearly constant during moderate exercise.

Changes in ventilation Ventilation increases abruptly in the initial stages of exercise and is then followed by a more gradual increase. The rapid rise in ventilation at the onset of exercise is thought to be attributable to motor centre activity and afferent impulses from proprioceptors of the limbs, joints and muscles. The mechanism of stimulation following this first stage is not completely understood. Arterial oxygen and carbon dioxide tensions are not sufficiently abnormal to stimulate respiration during exercise. Suggestions have been made that the sensitivity of peripheral chemoreceptors to oscillations in Pa o 2 and Pa co 2 is responsible for increasing ventilation, even though the absolute values remain stable.

Central chemoreceptors may be readjusted to increase ventilation to maintain carbon dioxide concentrations. Other theories are that the rise in body temperature may play a role, or that collateral branches of neurogenic impulses from the motor cortex to active muscles and joints may stimulate the brain stem and respiratory centre leading to hyperpnoea. Overall, a number of factors have been suggested for the increase in ventilation, which occurs with exercise. The respiratory rate might remain elevated after heavy exercise for up to 1–2 h. Cardiovascular system Substrate and oxygen requirements of working skeletal muscles are dramatically elevated above resting requirements. Resting blood flow to muscle is usually 2–4 ml100 g muscle −1 min −1, but might increase to nearly 100 ml100 g muscle −1 min −1 during maximal exercise.

This occurs in part because of vasodilatory metabolites such as AMP, adenosine, H +, K + and. Heart rate and stroke volume increase to about 90% of their maximum values during strenuous exercise and cardiovascular function is the limiting factor for oxygen delivery to the tissues. Oxygen utilization by the body can never be more than the rate at which the cardiovascular system can transport oxygen to the tissues.

There is only a moderate increase in blood pressure secondary to the rise in cardiac output. This is caused by stretching of the walls of the arterioles and vasodilatation, which in combination reduce overall peripheral vascular resistance. There is a large increase in venous return as a consequence of muscular contraction, blood diversion from the viscera and vasoconstriction. Maximum oxygen consumption As work rate is increased, oxygen uptake increases linearly. However, there is an upper limit to oxygen uptake and, therefore, above a certain work rate oxygen consumption reaches a plateau. This is termed the maximal oxygen uptake (.