Saturday, 13 October 2012

Science of Oxygen Transport in Soccer

The oxygen transport system comprises an integrated involvement of lungs, heart, oxygen carriage in the blood and utilization in muscle cells. The take up at cellular level is influenced by the blood supply, the network of capillaries around muscle fibres, the mitochondrial number and content and the type of muscle fibres. Central factors, incorporating pulmonary and cardiac parameters as well as blood volume and content, determine the amount of oxygen that is delivered to the active tissues. Peripheral or local factors refer to the ability of skeletal muscles to use the oxygen that is offered to them by means of the circulation. These factors are influenced both by heredity and by training.



   The process by which ambient air is brought into the lungs and exchanged with air passing through them is known as pulmonary ventilation. At rest approximately 250 ml of oxygen leaves the alveoli and enters the blood for each breath, whereas about 200 ml of CO2 diffuses in the reverse direction to be exhaled during breathing. Over 20 times this amount of oxygen may be transferred across the alveolar membrane during heavy exercise and pulmonary ventilation may increase from 6 l.min 1 at rest to about 200 l.min 1 in top class athletes. The main purpose of ventilation during aerobic exercise is to maintain a constant and favorable  concentration of O2 and CO2 in the alveolar chambers. An effective exchange of gases is thereby ensured before the oxygenated blood leaves the lungs for transport throughout the body.

   The performance of aerobic exercise is not normally limited by lung capacity except under certain circumstances. Lung function may be restricted in asthmatic individuals. This restriction is usually indicated by a subnormal value for the forced expiratory volume (FEV1) which is measured in a single breath of forceful exhalation and reflects the power of the lungs. Values are reduced in players suffering from asthma or exercise-induced bronchospasm. Exercise induced asthma is generally triggered post-exercise and recovery may take 30–50 min unless bronchodilators are employed to ease breathing difficulties.



   Ventilatory responses to exercise may be altered as a consequence of aerobic training. As maximal oxygen uptake (V.O2 max) is elevated with training, there is an increase in the corresponding minute ventilation (V.Emax). There is a reduction in the ventilation equivalent of oxygen (V.E/V.O2) at sub-maximal exercise so that less air is inhaled at a given oxygen consumption. The expired air of trained athletes contains less oxygen than that of untrained individuals for a given V.O2 . This reduction reflects the capacity of trained muscle to extract more of the oxygen passing through the tissues in the local circulation. Endurance training also results in an elevation in the ventilation threshold (Tvent) which represents the exercise intensity at which V.E starts to rise disproportionately to V. O2 in response to a progressive exercise test. This effect may be related to metabolic alterations but is specific to the exercise modality used in training.



   The cardiac output, which indicates the amount of blood pumped from the heart, is a function of the stroke volume and the heart rate. Cardiac output may increase from 5 l.min 1 at rest to 30 l.min 1 at maximal oxygen consumption, depending on the capacity of the individual. The cardiac output of Olympic endurance athletes may exceed this upper level. With endurance training there is an increase in left ventricular chamber size and a consequent decrease in resting and sub-maximal heart rate, an increase in maximal cardiac output, a rise in maximal oxygen uptake and an increase in total blood volume. The maximal ability to consume oxygen tends to be limited by central factors (cardiac output) rather than peripheral factors (including oxidative capacity of skeletal muscle) in elite athletes who are adapted physiologically to endurance training. Both of these limitations may apply to soccer players.

   The improved endurance capacity of trained muscle is partly due to an increase in its capillary density. In athletes, values 20% greater than normal have been reported for the number of capillaries per muscle and in a given cross section. A corresponding difference in V.O2 max was observed between endurance athletes and an untrained group. There are also metabolic adaptations in muscle that enhance oxidative capacity. There is, for example, an increase in both number and size of the mitochondria with enhancement of enzymes of the Krebs cycle and electron transport system.

   Elite endurance athletes tend to be endowed with a muscle fibre type composition that is appropriate to the demands of the sport (Bergh et al., 1978). For example, whilst the twitch characteristics of muscle fibres seem to be unaffected by endurance training, their histochemical properties are altered. Endurance runners have a predominance of ST muscle fibres as do cross-country skiers. The abundance of myoglobin gives rise to the naming of these fibres as red and they also possess high levels of mitochondria. Furthermore with endurance training the so-called intermediate FTa (Type IIa) fibres assume more of the biochemical make-up of ST (Type I) fibres, showing increased oxidative enzymes and elevated myoglobin levels. Muscle biopsies from soccer players demonstrate a balanced combination of fibre types, variability within a team reflecting the specialized roles of different playing positions.
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