Andrew T. Thornton

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

Abstract A group of 15 competitive male cyclists [mean peak oxygen uptake, V˙O2peak 68.5 (SEM 1.5 ml · kg−1 · min−1)] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% V˙O2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (V˙O2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (PAO2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (PA−aO2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At V˙O2peakPaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both PAO2 and PA−aO2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and V˙O2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and PAO2 with the first exercise intensity and at V˙O2peak led to the conclusion that inadequatehyperventilation is a major contributor to exercise-induced hypoxaemia.

Arterial hypoxaemia in endurance athletes is greater during running than cycling.

The effect of both training discipline and exercise modality on exercise-induced hypoxaemia (EIH) was examined in seven runners and six cyclists during 5 min high intensity treadmill and cycle exercise. There were no significant interactions between training discipline, exercise modality and arterial P(O(2)) (Pa(O(2))) when subject groups were considered separately but when pooled there were significant differences between exercise modalities. After min 2 of exercise arterial hydrogen ion concentration, minute ventilation, alveolar P(O(2)) (PA(O(2))) and Pa(O(2)) were all lower with treadmill running with the largest differential for the latter occurring at min 5 (treadmill, 80.8+/-1.8; cycle, 90.2+/-2.5, mmHg, N=13, P< or = 0.05). At every min of exercise, the differences in Pa(O(2)) between the ergometers were strongly associated with similar differences in PA(O(2)) and alveolar to arterial P(O(2)) (PA(O(2))-Pa(O(2))). It is concluded that the greater EIH with treadmill running is a consequence of the combined effect of a reduced lactic acidosis-induced hyperventilation and greater ventilation-perfusion inequality with this exercise mode.

AASM criteria for scoring respiratory events: interaction between apnea sensor and hypopnea definition.

STUDY OBJECTIVES To examine the impact of using a nasal pressure sensor only vs the American Academy of Sleep Medicine (AASM) recommended combination of thermal and nasal pressure sensors on (1) the apnea index (AI), (2) the apnea-hypopnea index (AHI), where the AHI is calculated using both AASM definitions of hypopnea, and (3) the accuracy of a diagnosis of obstructive sleep apnea (OSA). DESIGN Retrospective review of previously scored in-laboratory polysomnography. SETTING A tertiary-hospital clinical sleep laboratory. PATIENTS OR PARTICIPANTS One hundred sixty-four consecutive adult patients with a potential diagnosis of OSA, who were examined during a 3-month period. INTERVENTIONS N/A. MEASUREMENTS AND RESULTS Studies were scored with and without the use of the oronasal thermal sensor. AIs and AHIs, using the nasal pressure sensor alone (AI(np) and AHI(np)), were compared with those using both a thermal sensor for the detection of apnea and a nasal pressure transducer for the detection of hypopnea (AI(th) and AHI(th)). Comparisons were repeated using the AASM recommended (AASM(rec)) and alternative (AASM(alt)) hypopnea definitions. AI was significantly different when measured from the different sensors, with AI(np) being 51% higher on average. Using the AASM(rec) hypopnea definition, the mean AHI(np) was 15% larger than the AHI(th); with large interindividual differences and an estimated 9.8% of patients having a false-positive OSA diagnosis at a cutpoint of 15 events and 4.3% at 30 events per hour. Using AASM(alt) hypopnea definition, the mean AHI(np) was 3% larger than the AHI(th), with estimated false-positive rates of 4.6% and 2.4%, respectively. The false-negative rate was negligible at 0.1% for both hypopnea definitions. CONCLUSIONS This study demonstrates that using only a nasal pressure sensor for the detection of apnea resulted in higher values of AI and AHI than when the AASM recommended thermal sensor was added to detect apnea. When the AASM(alt) hypopnea definition was used, the differences in AHI and subsequent OSA diagnosis were small and less than when the AASM(rec) hypopnea definition was used. In situations in which a thermal sensor cannot be used, for example, in limited-channel diagnostic devices, the AHI obtained with a nasal pressure sensor alone differs less from the AHI obtained from a polysomnogram that includes a thermal sensor when the AASM(alt) definition rather than the AASM(rec) definition of hypopnea is used. Thus, diagnostic accuracy is impacted both by the absence of the thermal sensor and by the rules used to analyze the polysomnography. Furthermore, where the thermal sensor is unreliable for sections of a study, it is likely that use of the nasal pressure signal to detect apnea will have modest impact.

Tachykinins contribute to the acute airways response to allergen in sheep actively sensitized to Ascaris suum

Abstract Tachykinins, found in sensory nerves, have effects in the airways which suggest that they may contribute to the pathogenesis of asthma. We aimed to find evidence for tachykinin involvement in the immediate airway response to allergen in a sheep model of experimental asthma. Twenty‐four sheep were actively sensitized to Ascaris suum, then challenged with nebulized Ascaris extract in a dose‐response fashion. Change in lung resistance (RL) in response to challenge was measured. Responder sheep (those with an increase in RL of >100% over baseline) that had reproducible responses over three challenges were identified (n= 4 sheep) and a PC100 (number of breaths of extract required to induce a 100% increase in RL) was determined. The effect of the neutral endopeptidase inhibitor phosphoramidon, the NK‐1 receptor‐specific antagonist CP 96, 345 and capsaicin desensitization on the RL response to Ascaris challenge was then assessed. Administration of phosphoramidon before Ascaris decreased the PC100 to 31 ± 7% of the PC100 seen with Ascaris alone (P<0.05), whereas CP 96,345 and capsaicin desensitization increased the PC100 to 285 ± 41% and 555 ± 93% respectively (P<0.05 for both). These findings suggest that endogenous tachykinins are released in response to allergen challenge and that they contribute to the immediate increase in RL.

Rectal temperature correction overestimates the frequency of exercise-induced hypoxemia.

INTRODUCTION Exercise-induced hypoxemia (EIH) occurs in an uncertain proportion of endurance trained athletes. Whereas blood gas measurements must be corrected for core temperature at the time of sampling, the commonly used rectal temperature readings may not be the most appropriate. METHODS Ten males [mean peak oxygen uptake, (.-)VO(2peak), 65.4 +/- 7.0 mL x kg x min] performed incremental treadmill exercise from rest to exhaustion with radial artery blood samples collected at the end of each 2-min workload for gas analysis. The thermogenic effect of exercise was monitored with rectal, arterial blood, and esophageal temperature probes, and the values obtained at all three sites, simultaneous with blood sampling, were used to correct the standard blood gas measurements made at 37 +/- C. RESULTS The mean increase in rectal temperature across exercise (1.4 +/- 0.4 +/- C) was approximately half that recorded in radial arterial blood (2.3 +/- 0.5+/- C) and the esophagus (2.4 +/- 0.5 degrees C). In consequence, the uncorrected fall in PaO2 across exercise of 15.4 +/- 8.2 mm Hg was reduced to 8.4 +/- 7.7 mm Hg when corrected for rectal temperature, and to 2.9 +/- 7.4 and 2.1 +/- 8.8 mm Hg when corrected for arterial blood and esophageal temperatures. Using a fall of > or = 10 mm Hg as the index of EIH, the proportion in the 10 subjects in the present study fell from 80% (uncorrected) through 50% (rectal correction) to 20% (arterial blood and esophageal corrections). CONCLUSION When correcting arterial blood gas values for the thermogenic effects of exercise, the proportion of athletes meeting the definition of EIH depends on the site of core temperature measurement.

Spontaneous mode non-invasive ventilation fails to treat respiratory failure in a patient with Multi-mincore disease: a case report

The increased morbidity and mortality resulting from respiratory failure in patients with neuromuscular disorders and/or kyphoscoliosis can be reversed with non-invasive ventilation. Spontaneous mode bilevel pressure ventilation is preferred to other modes of ventilation, due to relative ease of use, but may not be suitable for all patients. We report a 27-year old woman with Multi-minicore disease whose respiratory failure was refractory to spontaneous mode bilevel pressure ventilation. When we altered settings and provided mandatory inspiratory rise time and respiratory rate, it augmented her respiratory efforts and improved ventilation. Our case report describes the benefit of individualising non-invasive ventilation in the management of respiratory failure due to neuromuscular weakness and kyphoscoliosis.

The impact of core temperature corrections on exercise-induced hypoxemia.

ered as an important limitation to physical performance with a prevalence of ~50 % in trained male athletes, but described in both sexes, across the range of both age and physical fitness in more in both arterial oxygen partial pressure (PaO2) and oxy-haemoglobin saturation 2 2 2 correction made for the change in body temperature during intense exercise. an offset of approximately 1.3oC, and were considered much more appropriate and relevant indicators of therm work active muscle temperature (vastus lateralis) was measured during the The primary purpose of this doctoral dissertation was to investigate the effect of body temperature responses at physiologically relevant sites during an incremental exercise test on the phenomenon of exercise-induced hypoxemia (EIH). This phenomenon has been consid recent literature. Previously this phenomenon has been described as a decrement (SaO or SpO ) with, particularly important for PaO , a lack of or inappropriate The initial study of this thesis determined the thermal response within the body at physiologically relevant sites measured simultaneously during an incremental exercise test. The results demonstrated the inadequacy of rectal temperature as an indicator of the acute temperature changes occurring during an incremental exercise test due to its slow response rate and relative thermal inertia. Radial arterial blood and oesophageal temperatures were shown to behave almost identically during the exercise test, albeit with al changes during exercise. As an extension of the initial