Exercise-induced arterial hypoxaemia

Arterial blood gases taken during maximal exercise at sea level in highly trained athletes can show PaO₂<9.0 kPa, pH<6.8 and percentage saturation of haemoglobin <90%. These measurements were made in healthy, normal athletes without pulmonary disease. The mechanisms responsible for this desaturation have been a source of investigation for over 30 years; relative hypoventilation, V/Q mismatch, diffusion limitation secondary to rapid red cell transit time or transient pulmonary oedema and possible right-to-left or intrapulmonary shunt have all been proposed as explanations for exercise-induced arterial hypoxaemia (EIAH).1 8 EIAH only occurs in ∼50% of highly trained male athletes, and there appears to be a higher prevalence in women with EIAH occurring at a lower exercise intensity.10 11

A reduction in exercise performance is linked to the development of EIAH. In highly trained subjects who were exposed to mild and moderate hypoxaemia, there was a significant decrease in cycle performance tests and a linear relationship was reported between the change in the saturation of oxygen on haemoglobin and the decrease in work capacity.12

Vocal cord dysfunction

Upper airway extrathoracic obstruction can occur in athletes during high-intensity exercise when the flow rates are high. Paradoxical narrowing of the glottic aperture develops suddenly and immediately affects flow rates and minute ventilation.5 This results in dyspnoea, an audible inspiratory stridor, hypoxaemia, CO₂ retention and often affects performance. Many of these athletes receive the diagnosis of exercise-induced bronchoconstriction, merely on the basis of dyspnoea during exercise. They are often treated with inhaled asthma medications, which do not benefit this condition.

These athletes deserve to be seen by an ear, nose and throat specialist to rule out other causes of upper airway obstruction. To induce this condition in an exercise laboratory, it is necessary to use high-intensity exercise that requires high-flow rates. With the onset of vocal cord dysfunction, flow rates, minute ventilation and SaO₂ drop quickly, and there is a rapid rise in end-tidal CO₂. Examination of the breath-by-breath flow-volume curves during exercise will show a decrease and blunting of the inspiratory loop.5 The condition is self-limiting and recovery is rapid once the exercise is stopped and the flow rates decrease. Regretfully, this is a difficult clinical condition to treat effectively and a percentage of these athletes will also have exercise-induced bronchoconstriction.13

Expiratory flow limitation

Figure 1 shows the flow-volume curves from an untrained and trained athlete. Many endurance athletes show significant expiratory flow limitation (EFL) during heavy exercise. This results in hyperinflation of their end-expiratory lung volume which leads to reduced dynamic lung compliance and an increased work of breathing.5 14 15 The normal hyperventilatory response to heavy work is limited, which results in dyspnoea, EIAH and consequentially poor performance. Positive expiratory pleural pressures, which can exceed the critical closing pressure of the airway, lead to increased afterload on the left ventricle. This results in compromised stroke volume and cardiac output, further influencing performance.14 Tidal volume plateaus at a lower minute ventilation and increases breathing frequency. Finally, with EFL, inspiratory muscle fatigue ensues because the muscles are working at shorter than their optimal length and with a greater velocity of shortening.5

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Figure 1

On the left is the flow-volume (V-V) envelope of an untrained subject with a large ventilatory reserve given the size of the maximal tidal breath relative to this maximum flow-volume loop (MFVL). The graph on the right depicts the V-V loop of an endurance-trained athlete. The MFVL is identical but there are much higher ventilatory requirements to meet the increased metabolic demands. The figure shows the consequences of training. The inspiratory reserve volume is much smaller, the athlete is expiratory flow limited and end-expiratory lung volume (EELV) is creeping back towards resting values.

Relative to men, women have smaller lung volumes and narrower airway diameters for a given lung volume.16 This makes them more prone to EFL and its sequelae. The masters athlete, capable of heavy exercise, is also compromised, as with normal ageing there is a loss of elastic recoil leading to a reduction in the maximal flow-volume loop and higher proportions of dead space ventilation at rest and during exercise.5

Respiratory muscle fatigue/training

It is clear from the animal and human literature that RM will respond to an appropriate training stimulus. The average man has about 4 kg of skeletal muscle that can be recruited for respiration in heavy work. While the diaphragm has its own metabolic features and is resistant to fatigue, the remaining skeletal muscle can be trained either by ‘volume’, via voluntary isocapnic hyperpnoea or ‘resistance’, using breathing against a resistive load.17 With volume loading, there are significant increases in maximal sustainable voluntary capacity and maximum voluntary ventilation.18 Studies using resistive training have reported increases in maximum inspiratory pressure in the range of 8% to 45%.19

To the competitive athlete, whether RM training will improve performance remains a controversial issue. Some sport scientists report an improvement in time to exhaustion at submaximal workloads following RM training.20 21 However, most report no response to RM training in the parameters, assessed during maximal exercise, that would most likely be associated with a change in performance – for example, maximal minute ventilation, maximal aerobic capacity, heart rate, stroke volume, blood gas concentrations or % saturation of haemoglobin with oxygen.18 21

The RMs can fatigue with sustained exercise, and there is experimental evidence that RM resistive loading or RM unloading will significantly influence performance time in highly trained cyclists.22 There are improvements in ventilatory efficiency following RM training, and a reduction in minute ventilation for a given workload would influence the oxygen consumed by the RM, perhaps changing the blood flow distribution during exercise. Training these muscles to delay the onset of fatigue and ‘steal’ blood flow from the trained RM to locomotor muscles to improve performance is an attractive hypothesis that requires experimental evidence.6 23