| Summary: | Factors Influencing Ventilation, Gas Exchange and Arterial Blood Oxygenation During Exercise in Man.
1. At rest and during sub anaerobic steady-state exercise, alveolar and arterial carbon dioxide and oxygen partial pressures are maintained relatively constant by a ventilation which is proportional to both carbon dioxide output and oxygen uptake. Hypoxemia occurs in highly trained athletes at high work intensities. The magnitude of the fall in arterial oxygen tension is related to the degree of relative hypoventilation. Hypoxemia has also been observed following the onset of exercise. To test whether this is similarly related to the degree of hypoventilation 12 normal subjects performed a series of runs, of varying duration, at near maximal intensity, on an electrically driven treadmill. Ventilation and gas exchange variables were computed on a breath-by-breath basis. Arterial blood samples were drawn from the radial artery at regular intervals. Ventilation, oxygen uptake and carbon dioxide output all exhibited a typical three phase response. The kinetics of oxygen uptake were significantly faster than that of carbon dioxide output. The kinetics of ventilation and carbon dioxide output were virtually identical. Occurring simultaneously with the onset of phase II was a fall in ventilator equivalent, end tidal oxygen partial pressure and arterial oxygen tension. In the first 2 minutes of exercise, there were significant correlations between these 3 variables. As exercise continued, arterial oxygen tension
remained depressed while ventilatory equivalent and end tidal oxygen partial pressure returned to resting levels. This data suggests that larger gas stores for carbon dioxide than oxygen causes a kinetic disparity between oxygen uptake and carbon dioxide output following the onset of exercise. As ventilation is proportional to carbon dioxide output hypoventilation occurs with respect to oxygen uptake. This causes a fall in end oxygen of end tidal oxygen partial tension. However, as exercise continues, an increasing dissociation of end tidal oxygen partial pressure and arterial oxygen tension occurs. This further suggests that factors other than hypoventilation also contribute to hypoxemia following the onset of exercise.
2. The degree of hypoventilation and hypoxemia occurring following the onset of exercise exhibits considerable individual variability. The extent to which this is related to the mode of exercise and the frequency of limb movement was studied in 12 normal subjects. Six cyclists each performed an incremental test to maximum on a bicycle ergometer and a series of 2 minute constant load trials using 4 different combinations of load and pedal frequency. Six runners each performed an incremental test to maximum on an electrically driven treadmill and a series of 2 minute constant load trials using 2 different combinations of grade and stride frequency. In all of the incremental tests, ventilation and gas exchange variables were determined from mixed expired samples collected during the last 30 seconds of each 3 minute increment. In all of the 2 minute constant load trials ventilation and gas exchange variables were computed on a breath-by-breath basis. The relationships of ventilation to oxygen uptake and ventilation to carbon dioxide output were constant and independent of pedal frequency during cycling in both the non steady-state and steady-state. However, these relationships were significantly different when both cycling and running on a grade were compared with running on the flat. This was true in both the non steady-state and the steady-state. While running on the flat there was slight hyperventilation with respect to both oxygen uptake and carbon dioxide output, with a slight increase in end tidal oxygen and a slight fall in end tidal carbon dioxide partial pressure. While cycling and running on a grade there was a marked hypoventilation with respect to both oxygen uptake and carbon dioxide output with a large increase in end tidal carbon dioxide and a large fall in end tidal oxygen partial pressure. Entrainment of breathing frequency to movement frequency occurred for varying amounts of time in all subjects. Entrainment interfered with the normal breathing frequency. During running on the flat, a ventilation appropriate to the carbon dioxide output was achieved by compensatory changes in tidal volume. During running up steep grades and cycling with high loads, ventilation was compromised by entrainment of breathing to a lower than normal movement frequency, at a time when tidal volume had attained maximal exercise values. This caused significantly lower than normal ventilatory equivalents for oxygen and carbon dioxide, significant increases in end tidal carbon dioxide partial pressure and significant falls in end tidal oxygen partial pressure. This data suggests that the entrainment of breathing frequency to slow movement frequencies, in certain exercise modes, can cause hypoventilation and a fall in end tidal oxygen partial pressure. It is hypothesised that this in turn will be reflected in the arterial oxygen tension.
3. Sensitivity to carbon dioxide at rest correlates with steady state exercise ventilation. Exercise ventilation increases in proportion to carbon dioxide output in both the non steady-state and the steady-state. It is therefore likely that sensitivity to carbon dioxide at rest will also correlate with exercise ventilation in the non steady-state. The relationship between the resting hypercapnic response and ventilation was studied in 12 normal subjects while running and cycling at near maximal
intensities. Sensitivity to carbon dioxide, expressed as the increase in ventilation per Torr increase in end tidal carbon dioxide partial was determined in all subjects at rest by rebreathing a gas pressure, mixture containing 5% carbon dioxide and 40% oxygen. To facilitate comparisons between individuals of different size, the relationship was expressed per 2 body surface area. Ventilation and gas exchange variables were computed on a breath-by-breath basis. Ventilation was expressed per litre output of carbon dioxide. Occlusion pressure was also measured at regular intervals throughout the 2 minute trial and the relationship to ventilation examined. There were significant correIations between exercise ventilation and the resting hypercapnic response throughout nearly all of the 2 minute trials.
No significant correlations were found between occlusion pressure and exercise ventilation. This data suggests that the individual variability in ventilation and the fall in end tidal oxygen partial pressure following the onset of exercise can, to some extent, be predicted from the resting hypercapnic response.
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