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Biomedical subjects

C M St Croix

Publications and source records attributed to C M St Croix.

7 recordsLinked to original sources
PubMed1999

Assessment of nitric oxide formation during exercise.

We measured the end-tidal plateau in exhaled NO concentration (CETNO) by chemiluminescence and calculated the product of V E and CETNO (V NO) in nine healthy subjects at rest and during three intensities of cycling exercise (30%, 60%, and 90% V O2max), two levels of hyperventilation (V E = 42.8 +/- 9.1 L/min and 84.2 +/- 6. 6 L/min), and during breathing of hypoxic gas mixtures (five subjects, FIO2 = 14%) at rest and during exercise at 90% V O2max. Immediately after each trial we also measured exhaled [NO] at constant expiratory flow rates ([NO]CF) of 46 ml/s and 950 ml/s, utilizing added expiratory resistance to increase mouth pressure and close the velum (Silkoff and colleagues, Am. J. Respir. Crit. Care Med. 1997;155:260). CETNO decreased and V NO increased above resting levels with increasing exercise intensity during hyperventilation and during hypoxic exercise (p < 0.05). [NO]CF, measured at either 46 ml/s or 950 ml/s, did not increase under any of the conditions investigated (exercise, hyperventilation, or hypoxia). Venous blood from seven of the subjects was sampled for the measurement of plasma [NO3-]. Resting plasma [NO3-] averaged 42.5 +/- 14.7 micromol/L, with no change during exercise, hyperventilation, or hypoxia. On the basis of these results we conclude that reported increases in V NO do not reflect an exercise-induced augmentation of systemic and/or airway NO production. Rather, the increases in V NO during exercise or hyperventilation are a function of high airflow rates, which reduce the luminal [NO]. This decreases the concentration gradient for NO between the alveolar space and pulmonary capillary blood, which results in a decrease in the fraction of NO taken up by the blood and an increase in the volume of NO recovered in the exhaled air (V NO).

Adult↗
PubMed1998

Effects of prior exercise on exercise-induced arterial hypoxemia in young women.

Twenty-eight healthy women (ages 27.2 +/- 6.4 yr) with widely varying fitness levels [maximal O2 consumption (VO2 max), 31-70 ml . kg-1 . min-1] first completed a progressive incremental treadmill test to VO2 max (total duration, 13.3 +/- 1.4 min; 97 +/- 37 s at maximal workload), rested for 20 min, and then completed a constant-load treadmill test at maximal workload (total duration, 143 +/- 31 s). At the termination of the progressive test, 6 subjects had maintained arterial PO2 (PaO2) near resting levels, whereas 22 subjects showed a >10 Torr decrease in PaO2 [78.0 +/- 7.2 Torr, arterial O2 saturation (SaO2), 91.6 +/- 2.4%], and alveolar-arterial O2 difference (A-aDO2, 39.2 +/- 7.4 Torr). During the subsequent constant-load test, all subjects, regardless of their degree of exercise-induced arterial hypoxemia (EIAH) during the progressive test, showed a nearly identical effect of a narrowed A-aDO2 (-4.8 +/- 3.8 Torr) and an increase in PaO2 (+5.9 +/- 4.3 Torr) and SaO2 (+1.6 +/- 1.7%) compared with at the end point of the progressive test. Therefore, EIAH during maximal exercise was lessened, not enhanced, by prior exercise, consistent with the hypothesis that EIAH is not caused by a mechanism which persists after the initial exercise period and is aggravated by subsequent exercise, as might be expected of exercise-induced structural alterations at the alveolar-capillary interface. Rather, these findings in habitually active young women point to a functionally based mechanism for EIAH that is present only during the exercise period.

Adolescent↗
PubMed1997

A model of oxygen transport capacity changes for independently living older men and women.

The purpose of the present investigation was to describe, for a subset of a large random survey of men and women, restricted to the ages of 55 to 85 years, the physiological decay pattern for aerobic fitness and contributing factors of cardiovascular and pulmonary function. The time course of the age-related changes in maximal oxygen uptake (VO2max), ventilatory threshold (TVE), maximal ventilation (VEmax), maximal heart rate (HRmax), and O2 pulse (VO2max/HRmax) were examined by fitting the data to a decaying exponential model by use of a least-squares parameter estimation technique. The time constant (tau) was used to describe the rate of decline. The women showed a much slower decline in VO2max (tau = 47.4 years) and TVE (tau = 83.3 years) than the men (tau = 20.8 and 15.4 years, respectively). There was a significant age-related decrease in body weight (0.45 kg.yr-1) in the men, whereas the women showed no change. Pulmonary function did not limit performance based on the very slow decline in VEmax and the normal FEV1.0. The decay in HRmax was better described by a linear model, resulting in an extremely slow tau. Maximal O2 pulse clearly exhibited an exponential decay, with a shorter tau (tau men = 13.5 years; tau women = 28.5 years) than any other variable.

Aged↗
PubMed1996

Nature of the interaction between central and peripheral chemoreceptor drives in human subjects.

The purpose of the current study was to investigate the nature of the interaction between the central and peripheral chemoreflex loops in humans, using the different speeds of response of the central and peripheral chemoreceptors to enable a temporal separation of their chemical stimulation. Subjects were exposed to an end-tidal Pco2 of 8-10 torr (1 torr = 1 mmHg = 133.3 Pa) above resting Pco2, with end-tidal Po2 = 100 torr, for 8 min. Thirty seconds after the hypercapnic stimulus was withdrawn, a 5-min hypoxic stimulus (end-tidal Po2 = 50 torr) was introduced. The 30-s interval was believed to be sufficient time for the peripheral chemoreceptors to adapt to the new level of carbon dioxide. Over the subsequent 5 min of hypoxia, however, the central chemoreceptors were exposed to diminishing hypercapnia. The response to the hypoxic step was compared with the effect of the same hypoxic step without the preceding period of hypercapnia. In 4 of the 5 subjects studied, the ventilatory response to hypoxia was unaffected by relative hypercapnia at the central chemoreceptor, suggesting that the central and peripheral chemoreflexes were independent of each other.

Adult↗
PubMed1996

Peripheral chemoreflex drive in moderate-intensity exercise.

The purpose of this study was to measure the contribution of the peripheral chemoreceptor (pR) to VE during the steady-state of moderate-intensity cycle ergometer exercise using continuous hyperoxic suppression of pRc drive, while stabilizing the drive from the central chemoreceptor by clamping end-tidal PCO2 (PETCO2) at the peak level attained during the hyperoxic period of a poikilocapnic ride. In the isocapnic protocol, the PETCO2 was maintained at a constant level by a negative feedback, open loop system. Five subjects completed four repetitions of each of the poikilocapnic and isocapnic protocols. In the poikilocapnic protocol, VE declines following the step into hyperoxia and then began to increase, whereas the decline in VE was maintained in the isocapnic protocol. However, the mean decrease in VE was not significantly different between the poikilocapnic (16.1 +/- 5.0%) and isocapnic (14.9 +/- 4.4%) protocols. These results suggest that the declining phase of VE is fully complete before the secondary central stimulating actions of hyperoxia on VE and that the pRc contributes about 15% of the drive to breathe in moderate intensity exercise.

Adult↗
PubMed1995

Estimation of arterial PCO2 in the elderly.

Arterial PCO2 (PaCO2), determined directly in the radial artery, was compared with indirect estimates of PCO2 in six elderly men (mean age 73.8 yr). Estimates of PaCO2 included arterialized venous PCO2 (PavCO2); end-tidal PCO2; mean alveolar PCO2, calculated by using a reconstruction of the alveolar oscillation in PCO2 and accounting for the presence of dead space (time-weighted mean for PCO2 throughout the respiratory cycle); and values calculated by using the empirical formula developed by Jones et al. (N. L. Jones, D. G. Robertson, and J. W. Kane. J. Appl. Physiol. 47: 954-960, 1979), which incorporates end-tidal PCO2 and tidal volume (PaCO2 derived from end-tidal PCO2 and VT). Measurements were made at rest and during cycle ergometry at 25 and 50 W while the subjects breathed various gas mixtures (euoxic-eucapnic, hypoxic-eucapnic, hyperoxic-eucapnic, and hyperoxic-hypercapnic). The mean differences between the estimates and the actual PaCO2 at rest and in 25- and 50-W exercise were as follows: PavCO2, 0.3 +/- 0.7 (SD), -0.1 +/- 0.7, and 1.8 +/- 1.2 Torr; end-tidal PCO2, 2.9 +/- 1.7, 4.0 +/- 3.1, and 3.7 +/- 3.2 Torr; time-weighted mean of alveolar PCO2, 2.6 +/- 1.9, 3.3 +/- 3.1, and 3.6 +/- 3.8 Torr; and PaCO2 derived from end-tidal PCO2 and VT, 2.4 +/- 1.3, 1.3 +/- 3.0, and 0.6 +/- 2.9 Torr. It is concluded that mean PavCO2 agreed most closely with mean PaCO2 both at rest and in exercise. All methods of deriving PaCO2 using measurements from the respired gases overestimated arterial values at rest. Of the noninvasive techniques, mean estimates calculated using the regression equation developed by Jones et al. corresponded most closely with PaCO2 in exercise.

Adult↗