Biomedical subjects

Glen E Foster

Publications and source records attributed to Glen E Foster.

11 recordsLinked to original sources

PubMed2007

Effects of continuous positive airway pressure on cerebral vascular response to hypoxia in patients with obstructive sleep apnea.

RATIONALE: The mechanism leading to increased risk of stroke in patients with obstructive sleep apnea (OSA) is unknown. It may occur through alteration in the regulation of cerebral blood flow, reflected in part by the response of the cerebral vasculature to hypoxia. We hypothesized that the cerebrovascular response to hypoxia is reduced in patients with OSA. OBJECTIVE: To determine the cerebral blood flow response to hypoxia in patients with OSA. METHODS: The cerebral blood flow response to 20 minutes of isocapnic hypoxia was measured in eight male patients with OSA before and after 4 to 6 weeks of continuous positive airway pressure (CPAP) therapy and in 10 matched healthy control subjects. MEASUREMENTS AND MAIN RESULTS: The cerebral blood flow response to hypoxia was significantly lower in patients with OSA compared with control subjects (0.56 +/- 0.10 vs. 0.97 +/- 0.09% [mean +/- SE] change in blood flow velocity per % desaturation; p=0.007). After CPAP therapy, the cerebral blood flow response to hypoxia was similar between patients with OSA and control subjects (1.08 +/- 0.15 vs. 0.92 +/- 0.13% change in blood flow velocity per % desaturation; p=0.4). Moderately strong correlations were found between the cerebral blood flow response to hypoxia and the apnea-hypopnea index (r=-0.57; p=0.04) and nocturnal oxyhemoglobin saturation (r=0.48; p=0.01). CONCLUSIONS: The cerebral blood flow response to hypoxia is significantly reduced in patients with OSA. Treatment of OSA with CPAP increases the cerebral blood flow response to hypoxia to normal levels. An attenuated cerebrovascular response to hypoxia in patients with OSA may contribute to their elevated risk of stroke.

Adult↗

PubMed2006

Intermittent hypoxia and vascular function: implications for obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) has been implicated as a risk factor for the development of hypertension, stroke and myocardial infarction. The main cause of cardiovascular and cerebrovascular disease in OSA is thought to be exposure to intermittent hypoxia, which can lead to oxidative stress, inflammation, atherosclerosis, endothelial dysfunction and hypertension. These proposed mechanisms have been drawn from basic research in animal and human models of intermittent hypoxia in addition to clinical investigation of patients with OSA. This review outlines the association between OSA and vascular disease, describes basic mechanisms that may be responsible for this association and compares the results from studies of OSA subjects with those in experimental models of intermittent hypoxia.

Animals↗

PubMed2006

Effects of acetazolamide on ventilatory, cerebrovascular, and pulmonary vascular responses to hypoxia.

RATIONALE: Acute mountain sickness (AMS) may affect individuals who (rapidly) ascend to altitudes higher than 2,000-3,000 m. A more serious consequence of rapid ascent may be high-altitude pulmonary edema, a hydrostatic edema associated with increased pulmonary capillary pressures. Acetazolamide is effective against AMS, possibly by increasing ventilation and cerebral blood flow (CBF). In animals, it inhibits hypoxic pulmonary vasoconstriction. OBJECTIVES: We examined the influence of acetazolamide on the response to hypoxia of ventilation, CBF, and pulmonary vascular resistance (PVR). METHODS: In this double-blind, placebo-controlled, randomized study, nine subjects ingested 250 mg acetazolamide every 8 h for 3 d. On the fourth test day, we measured the responses of ventilation, PVR, and CBF to acute isocapnic hypoxia (20 min) and sustained poikilocapnic hypoxia (4 h). Ventilation was measured with pneumotachography. Hypoxia was achieved with dynamic end-tidal forcing. The maximum pressure difference across the tricuspid valve (DeltaPmax, a good index of PVR) was measured with Doppler echocardiography. CBF was measured by transcranial Doppler ultrasound. RESULTS: In normoxia, acetazolamide increased ventilation and reduced DeltaPmax, but did not influence CBF. The ventilatory and CBF responses to acute isocapnic hypoxia were unaltered, but the rise in DeltaPmax was reduced by 57%. The increase in DeltaPmax by sustained poikilocapnic hypoxia observed after placebo was reduced by 34% after acetazolamide, the ventilatory response was increased, but the CBF response remained unaltered. CONCLUSIONS: Acetazolamide has complex effects on ventilation, PVR, and CBF that converge to optimize brain oxygenation and may be a valuable means to prevent/treat high-altitude pulmonary edema.

Acetazolamide↗

PubMed2006

Entrainment of breathing in cyclists and non-cyclists during arm and leg exercise.

The purpose of this study was to compare the incidence of entrainment of breathing (ENT) between cyclists (C; n=8) and non-cyclists (NC; n=8) during leg cycling (LC) and arm cycling (AC). No subjects were training regularly in upper body endurance exercise. Day 1 consisted of spirometry and a VO2max test on both an arm and leg ergometer in random order separated by at least 60 min. On Day 2, subjects performed both AC and LC exercise with each session consisting of 5 min of warm-up at 20% and three consecutive 6 min loads at 40%, 60%, and 80% of task specific peak power output (WL1, WL2, WL3, respectively). Sessions were separated by at least 45 min. The final 3 min of each load were analyzed for entrainment of pedal and breathing frequencies using integer and half-integer ratios. A total of six subjects were unable to complete at least one exercise session at WL3 and therefore this load was excluded from analysis. Mean % VO2max during exercise was not different between cyclists and controls with respect to intensity and mode (AC= approximately 50% and 70%; LC= approximately 55% and 75% at WL1 and WL2, respectively). A repeated measures ANOVA revealed no effect on incidence of entrainment (%ENT) by group, mode of exercise, or exercise intensity (p=0.12, 0.24, and 0.88, respectively). %ENT was highest in cyclists during leg exercise (cyclists: LC=32%; AC=19%; controls: LC=18%; AC=21%) however this difference was not significant (p=0.07). In all situations that would be considered unfamiliar for both groups %ENT was similar. These results suggest that during cycling exercise at intensities of 75% VO2max or less, regular training may result in higher %ENT and that ENT is not transferable to an unfamiliar mode of exercise using different muscle groups.

Adult↗

PubMed2006

Human ventilatory responsiveness to hypoxia is unrelated to maximal aerobic capacity.

Ventilatory responsiveness to hypoxia (HVR) has been reported to be different between highly trained endurance athletes and healthy sedentary controls. However, a linkage between aerobic capacity and HVR has not been a universal finding. The purpose of this study was to examine the relationship between HVR and maximal oxygen consumption (VO2 max) in healthy men with a wide range of aerobic capacities. Subjects performed a HVR test followed by an incremental cycle test to exhaustion. Participants were classified according to their maximal aerobic capacity. Those with a VO2 max of >or=60 ml x kg(-1) x min(-1) were considered highly trained (n = 13); those with a VO2 max of 50-60 ml x kg(-1) x min(-1) were considered moderately-trained (n = 18); and those with a VO2 max of <50 ml x kg(-1) x min(-1) were considered untrained (n = 24). No statistical differences were detected between the three groups for HVR (P > 0.05), and the HVR values were variable within each group (range: untrained = 0.28-1.61, moderately trained = 0.23-2.39, and highly trained = 0.08-1.73 l x min.%arterial O2 saturation(-1)). The relationship between HVR and VO2 max was not statistically significant (r = -0.1723; P > 0.05). HVR was also unrelated to maximal minute ventilation and ventilatory equivalents for O2 and CO2. We found that a spectrum of hypoxic ventilatory control is present in well-trained endurance athletes and moderately and untrained men. We interpret these observations to mean that other factors are more important in determining hypoxic ventilatory control than physical conditioning per se.

Adult↗

PubMed2006

Variable effects of respiratory muscle training on cycle exercise performance in men and women.

Respiratory muscle training (RMT) has been proposed as an effective means to increase the strength of the inspiratory muscles and improve exercise performance. The purpose of this study was to examine the effect of RMT on cycling time to exhaustion (TTE) and to determine any potential sex effect. We hypothesized that RMT would improve maximal inspiratory pressure (MIP) and TTE to a similar degree in men and women. Males (n = 7; mean (+/- SD) age, 22.1 +/- 1.5 y) and females (n = 8; mean (+/- SD) 24.5 +/- 4.9 y) performed an incremental cycle test to determine maximal oxygen consumption ((.)VO(2) (max)) (day 1), followed by a familiarization TTE (day 2) and baseline TTE (day 3) at 80% maximal work achieved during the ((.)VO(2) (max)) test. Subjects then completed 5 weeks of respiratory muscle training (RMT) (5 d/week, 2 sets of 30 inspirations against 50% MIP). Four training sessions per week were performed at home and the 5th was supervised, during which the threshold load was increased if necessary. Following RMT, subjects completed 2 TTE tests (days 4 and 5). MIP increased in each subject (37% +/- 18%, P < 0.05). There was no difference between men (pre = -100 +/- 20 vs. post = -140 +/- 29 cmH(2)O) and women (pre = -90 +/- 28 vs. post = -117 +/- 28 cmH(2)O). Baseline TTE (male = 301 +/- 122 s; female = 338 +/- 98 s) was shorter in comparison with the best of the 2 TTE-post tests (male = 353 +/- 68 s; female = 416 +/- 116 s; P < 0.01), but not when compared with days 4 or 5 (P > 0.05). RMT increases MIP and may improve exercise performance; however, improvements are variable with no differences between men and women.

Adult↗

PubMed2005

Effects of enhanced human chemosensitivity on ventilatory responses to exercise.

It is not clear what the effects of different types of intermittent hypoxia have on human exercise ventilation. The purpose of this study was to determine whether short-duration intermittent hypoxia, and the subsequent augmentation of the hypoxic ventilatory response (HVR), would lead to an increase in ventilatory responses during exercise at sea level. It was hypothesized that subjects exposed to short-duration intermittent hypoxia would have a greater increase in the ventilatory response to exercise compared to those exposed to long-duration intermittent hypoxia. Subjects (n = 17, male) were randomly assigned to short-duration intermittent hypoxia (SDIH: 5 min of 12% O2 separated by 5 min of normoxia for 1 h) or long-duration intermittent hypoxia (LDIH: 30 min of 12% O2). Both groups had 10 exposures over a 12 day period. The HVR was measured on days 1 and 12. Maximal oxygen consumption (VO2max) was determined using a ramped cycle exercise test. Maximal exercise data were not different (P > 0.05) between SDIH and LDIH groups or following intermittent hypoxia. Minute ventilation, tidal volume and respiratory frequency were compared at 20, 40, 60, 80 and 100% of VO2max . There was no difference in the ventilatory responses at any intensity of exercise following the intermittent hypoxia period. The HVR was significantly increased following the intermittent hypoxia intervention (P < 0.05) but was not different between SDIH and LDIH (P > 0.05). The relationships between HVR and VO2max were non-significant on day 1 (r = 0.30) and day 12 (r = 0.47; P > 0.05). Our findings point to a lack of functional significance of increasing HVR via intermittent hypoxia on ventilatory responses to exercise at sea level.

Atmospheric Pressure↗

PubMed2005

Effects of two protocols of intermittent hypoxia on human ventilatory, cardiovascular and cerebral responses to hypoxia.

We determined the ventilatory, cardiovascular and cerebral tissue oxygen response to two protocols of normobaric, isocapnic, intermittent hypoxia. Subjects (n = 18, male) were randomly assigned to short-duration intermittent hypoxia (SDIH, 12% O2 separated by 5 min of normoxia for 1 h) or long-duration intermittent hypoxia (LDIH, 30 min of 12% O2). Both groups had 10 exposures over a 12 day period. The hypoxic ventilatory response (HVR) was measured before each daily intermittent hypoxia exposure on days 1, 3, 5, 8, 10 and 12. The HVR was measured again 3 and 5 days after the end of intermittent hypoxia. During all procedures, ventilation, blood pressure, heart rate, arterial oxyhaemoglobin saturation and cerebral tissue oxygen saturation were measured. The HVR increased throughout intermittent hypoxia exposure regardless of protocol, and returned to baseline by day 17 (day 1, 0.84 +/- 0.50; day 12, 1.20 +/- 1.01; day 17, 0.95 +/- 0.58 l min(-1) %S(aO2)(-1); P < 0.01). The change in systolic blood pressure sensitivity (r = +0.68; P < 0.05) and the change in diastolic blood pressure sensitivity (r = +0.73; P < 0.05) were related to the change in HVR, while the change in heart rate sensitivity was not (r = +0.32; NS). The change in cerebral tissue oxygen saturation sensitivity to hypoxia was less on day 12, and returned to baseline by day 17 (day 1, -0.51 +/- 0.13; day 12, -0.64 +/- 0.18; day 17, -0.51 +/- 0.13; P < 0.001). Acute exposure to SDIH increased mean arterial pressure (+5 mmHg; P < 0.01), but LDIH did not (P > 0.05). SDIH and LDIH had similar effects on the ventilatory and cardiovascular response to acute progressive hypoxia and hindered cerebral oxygenation. Our findings indicate that the vascular processes required to control blood flow and oxygen supply to cerebral tissue in a healthy human are hindered following exposure to 12 days of isocapnic intermittent hypoxia.

Adaptation, Physiological↗

PubMed2005

Repeated measurement of hypoxic ventilatory response as an intermittent hypoxic stimulus.

Measurement of hypoxic ventilatory response (HVR) involves an exposure to hypoxia which, if repeated over several days might act as an intermittent hypoxic stimulus. The purpose of this study was to measure HVR repeatedly over 5 days to determine whether it was affected by repeated measurement. Nine healthy male subjects completed an isocapnic HVR test, on one occasion, followed 5 days later by one measurement each day for 5 days. Each test lasted approximately 5-8 min with inspired oxygen concentration declining to as a low as 5-6%. No systematic trend was observed in HVR over the 5-day period (p>0.05). There were no significant differences in HVR between any of the test days. Regression failed to show any trend in HVR over the five sequential days. The calculated mean coefficient of variation for HVR for each subject was 27%. There is no evidence that the short exposure to hypoxia as part of HVR measurement is a co-intervention when measured repeatedly over 5 days in physiological studies.

Adaptation, Physiological↗

PubMed2004

Acute hypoxic ventilatory response and exercise-induced arterial hypoxemia in men and women.

Recent studies claim a higher prevalence of exercise-induced arterial hypoxemia (EIAH) in women relative to men and that diminished peripheral chemosensitivity is related to the degree of arterial desaturation during exercise in male endurance athletes. The purpose of this study was to determine the relationship between the acute ventilatory response to hypoxia (AHVR) and EIAH and the potential influence of gender in trained endurance cyclists and untrained individuals. Healthy untrained males (n = 9) and females (n = 9) and trained male (n = 11) and female (n = 10) cyclists performed an isocapnic AHVR test followed by an incremental cycle test to exhaustion. Oxyhemoglobin saturation (Sa(O(2)) was lower in trained men (91.4 +/- 0.9%) and women (91.3 +/- 0.9%) compared to their untrained counterparts (94.4 +/- 0.8% versus 94.3 +/- 0.7%) (P < 0.05). AHVR and maximal O(2) consumption were related for all subjects (r = -0.46), men (r = -0.45) and women (r = -0.53) (P < 0.05) but AHVR was unrelated to Sa(O(2)) for any groups (P > 0.05). We conclude that resting AHVR does not have a significant role in maintaining Sa(O(2)) during sea-level maximal cycle exercise in men or women.

Adult↗

PubMed2004

Sex differences in respiratory exercise physiology.

Respiratory exercise physiology research has historically focused on male subjects. In the last 20 years, important physiological and functional differences have been noted between the male and female response to dynamic exercise where sex differences have been reported for most of the major determinants of exercise capacity. Female participation in competitive and recreational sport is growing worldwide and it is universally accepted that participation in regular physical activity is of health benefit for both sexes. Understanding sex differences is of potential importance to both the clinician-scientist and the exercise physiologist since differences could impact upon exercise rehabilitation programmes for patient populations, exercise prescription for disease prevention in healthy individuals and training strategies for competitive athletes. Sex differences have been shown in resting pulmonary function, which may impact on the respiratory response to exercise. Women typically have smaller lung volumes and maximal expiratory flow rates even when corrected for height relative to men. Differences in resting and exercising ventilation across the menstrual cycle and relative to men have also been reported, although the functional significance remains unclear. Expiratory flow limitation and a high work of breathing are seen in women. Pulmonary system limitations, in particular exercise-induced arterial hypoxia, have been reported in both men and women; however, the prevalence in women is not yet known. From the available literature, it appears that there are sex differences in some areas of respiratory exercise physiology. However, detailed sex comparisons are difficult because the number of subjects studied to date has been woefully small.

Canada↗