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MacNutt, Meaghan J. and A. William Sheel. Performance of evacuated blood collection tubes at high altitude. High Alt. Med. Biol. 9:235–237, 2008—Researchers and clinicians may not be aware that the performance of evacuated blood collection systems is impaired at high altitude. We tested four sizes of Vacutainer® tubes at altitudes ranging from sea level to 5341 m to and determined that draw volumes are reduced by approximately 0.5 mL for every 1000 m gain in terrestrial elevation. Insufficient blood volume can limit possibilities for testing, inappropriate blood to additive ratios can skew test results and with smaller tubes at higher altitudes there is a possibility of air embolism. With foresight and proper planning, these problems can be avoided, and evacuated blood collection tubes can still be used safely and effectively at high altitude.

Women have smaller airways and lung volumes and lower resting maximal expiratory flow rates relative to men. Female athletes develop expiratory flow limitation more frequently than male athletes, and they have greater increases in end-expiratory and end-inspiratory lung volume at maximal exercise. Women use a greater fraction of their ventilatory reserve and have a higher metabolic cost of breathing.

The present study was designed to examine the dose-response relationship of inhaled salbutamol and its concentration in the urine while resting at various times after inhalation, and to compare these values against the current World Anti-Doping Code limits.An interventional, repeated-measures design.Sport Medicine Clinic, University of British Columbia (Vancouver, Canada).Eight healthy, nonasthmatic males participated in this study (age = 28 +/- 6 years, height = 179.4 +/- 5.1 cm, and weight = 77.4 +/- 5.4 kg).Administration of three different doses of inhaled salbutamol (800, 400, and 200 microg) in a randomized fashion separated by at least 72 hours.Urine concentration of nonsulphated salbutamolUrine concentrations were highly variable between subjects and increased as dose increased, with a significant difference noted between 800 and 200 microg at 30, 60, and 120 minutes after inhalation. Urine concentrations of salbutamol peaked at 60 minutes for all doses. No samples exceeded the doping criterion of 1000 ng/mL, and the maximum value observed was 904 ng/mL.These results indicate that after inhalation of doses up to 800 microg, urinary concentrations of salbutamol are well below the limits used in doping control.

Exposure to chronic or intermittent hypoxia produces alterations in the ventilatory response to hypoxia. These adaptations can differ depending on the severity of the hypoxic stimulus, its duration, its pattern, and the presence or absence of other chemical stimuli. As such, there are significant differences between the responses to intermittent versus continuous hypoxia. Intermittent hypoxia (IH) has been shown to elicit significant changes in the peripheral chemoresponse, but the functional implications of these changes for resting and exercise ventilation are not clear. We summarize the impact of IH on resting chemosensitivity and discuss the use of IH to better understand ventilatory control during exercise. We also suggest future directions for this relatively young field, including potential clinical applications of IH research.

We tested the hypothesis that following an acute bout of exercise cardiovascular and cerebrovascular responses to lower-body negative pressure (LBNP) would be altered due to post-exercise hypotension (PEH). Ten healthy, male, endurance-trained athletes (mean age ± SD = 29.6 ± 5) were assessed for cardiovascular and cerebrovascular responses to LBNP following acute bouts of interval and continuous exercise. Mean arterial pressure (MAP), cardiac output, total peripheral resistance, heart rate variability, and total cerebral oxygen index were determined during a baseline LBNP session. These indices were also determined during two other LBNP sessions: following an acute bout of interval exercise, and following an acute bout of continuous exercise. Compared with baseline, MAP was reduced after both exercise conditions, similar to values previously reported (10 mmHg; p < 0.05 vs. pre-exercise). Total peripheral resistance was significantly reduced following both exercise bouts, and heart rate was significantly increased post-exercise (rest: 59.6 ± 11.2; interval: 77.8 ± 12.8; continuous: 80.3 ± 15.2 beats·min–1). Both cardiac output and stroke volume responses to LBNP following exercise were not altered when compared with baseline measurements. Tissue oxygenation during –40 mmHg (interval: 74.31% ± 7.82% vs. continuous: 69.13% ± 5.23%) was significantly lower than during normobaric pressure (interval: 77.14% ± 1.30% vs. continuous: 74.41% ± 0.94%). It appears from these observations that although young, endurance-trained males experience PEH following acute bouts of interval or continuous exercise, this hypotension does not alter the cardiovascular and cerebrovascular responses to a moderate orthostatic stress.

The purpose of this study was to determine which upper-limb muscle exhibits the greatest change in muscle deoxygenation during arm-cranking exercise (ACE). We hypothesized that the biceps brachii (BB) would show the greatest change in muscle deoxygenation during progressive ACE to exhaustion relative to triceps brachii (TR), brachioradialis (BR), and anterior deltoid (AD). Healthy young men (n = 11; age = 27 ± 1 y; mean ± SEM) performed an incremental ACE test to exhaustion. Near-infrared spectroscopy (NIRS) was used to monitor the relative concentration changes in oxy- (O2Hb), deoxy- (HHb), and total hemoglobin (Hbtot), as well as tissue oxygenation index (TOI) in each of the 4 muscles. During submaximal arm exercise, we found that changes to NIRS-derived measurements were not different between the 4 muscles studied (p > 0.05). At maximal exercise HHb was significantly higher in the BB compared with AD (p < 0.05). Relative to the other 3 muscles, BB exhibited the greatest decrease in O2Hb and TOI (p < 0.05). Our investigation provides two new and important findings: (i) during submaximal ACE the BB, TR, BR, and AD exhibit similar changes in muscle deoxygenation and (ii) during maximal ACE the BB exhibits the greatest change in intramuscular O2 status.

To provide a systematic review of the studies assessing exercise training and inspiratory muscle training (IMT) in individuals for the improved respiratory function of patients with spinal cord injury (SCI).Thirteen studies (5 exercise training, 8 IMT) were identified. Articles were scored for their methodological quality using the Physiotherapy Evidence Database scores and Downs and Black tools for randomized and nonrandomized studies, respectively. Conclusions were based on the most rigorously executed studies using Sackett's levels of evidence.Study comparison was compromised by diverse research designs; small sample sizes; and heterogeneity of studied populations, protocols, and outcome measures. Based on current literature, there is level 2 evidence supporting exercise training as an intervention to improve respiratory strength and endurance and level 4 evidence to support exercise training as an intervention that might improve resting and exercising respiratory function in people with SCI. There is level 4 evidence to support IMT as an intervention that might decrease dyspnea and improve respiratory function in people with SCI.There are insufficient data to strongly support the use of exercise training or IMT for improved respiratory function in people with SCI. There is some evidence of efficacy of both regimens; however, the evidence is not of the best possible quality.

Intermittent hypoxia (IH) consists of bouts of hypoxic exposure interspersed with normoxic intervals. The optimal IH regime for increasing the ventilatory response in humans is unknown, although in animals there is evidence that multiple short duration bouts of intermittent hypoxia (SDIH) provoke larger changes in chemosensitivity than longer duration bouts of intermittent hypoxia (LDIH). The purpose of this study was to compare responses to both hypercapnia and hypoxia between the two protocols. Methods: In a randomised crossover design, 10 healthy males underwent two 7-day poikilocapnic IH protocols. The LDIH protocol consisted of daily 60-minute exposures to normobaric 12% Ο 2 (balance N2). The SDIH protocol comprised twelve 5-minute bouts of normobaric 12% Ο 2 , separated by 5-minute bouts of room air daily. We measured the isocapnic acute hypoxic ventilatory response (HVR), hypercapnic ventilatory response (HCVR) and CO 2 threshold and sensitivity by the modified Read rebreathing technique. Pre-testing was performed immediately prior to intermittent hypoxic training. Follow-up testing occurred on the first day following IH and at 7 days after completion of IH. HVR testing was also performed on every day of the IH protocol prior to the hypoxic exposure. Results: Following each 7-day IH protocol, mean HVR was significantly (p < 0.05) increased by 67% and 49% (for LDIH and SDIH, respectively). One week post IH, HVR values were not different from pre-values. HCVR was increased significantly by the LDIH protocol by 44.1% (p < 0.01) and remained elevated by 41.5% at 7 days post (p < 0.01). The changes following the SDIH protocol were smaller (20.7% and 13.5%, at 1 and 7 days post IH, respectively) and not significant. The HCVR remained elevated 7 days following IH (26.7%, p < 0.01). In both the hyperoxic and hypoxic modified rebreathing tests, the CO 2 sensitivity was unchanged by either intervention. In hypoxia, the CO 2 threshold was significantly reduced following both protocols (p < 0.05). LDIH reduced the threshold by 1.60mmHg, whereas following SDIH it was reduced by 1.98mmHg. Under hyperoxic conditions, LDIH reduced the CO 2 threshold by 2.06 mmHg, and SDIH caused a reduction of 2.53 mmHg. There were no significant differences between the two IH protocols for any of the above measures. A 7-day intermittent hypoxic protocol consisting of daily 60-minute exposures to normobaric poikilocapnic hypoxia caused increases in HVR and HCVR. This protocol caused a left-shift in the CO 2 threshold but no change in CO 2 sensitivity by the modified rebreathing protocol. Neither protocol proved superior in effecting these changes in the resting control of breathing.

Intermittent hypoxia (IH) consists of bouts of hypoxic exposure interspersed with normoxic intervals. The optimal IH regime for increasing the ventilatory response in humans is unknown, although in animals there is evidence that multiple short duration bouts of intermittent hypoxia (SDIH) provoke larger changes in chemosensitivity than longer duration bouts of intermittent hypoxia (LDIH). The purpose of this study was to compare responses to both hypercapnia and hypoxia between the two protocols.In a randomised crossover design, 10 healthy males underwent two 7-day poikilocapnic IH protocols. The LDIH protocol consisted of daily 60-minute exposures to normobaric 12% O2 (balance N2). The SDIH protocol comprised twelve 5-minute bouts of normobaric 12% O2, separated by 5-minute bouts of room air daily. We measured the isocapnic acute hypoxic ventilatory response (HVR), hypercapnic ventilatory response (HCVR) and CO2 threshold and sensitivity by the modified Read rebreathing technique. Pre-testing was performed immediately prior to intermittent hypoxic training. Follow-up testing occurred on the first day following IH and at 7 days after completion of IH. HVR testing was also performed on every day of the IH protocol prior to the hypoxic exposure.Following each 7-day IH protocol, mean HVR was significantly (p0.05) increased by 67% and 49% (for LDIH and SDIH, respectively). One week post IH, HVR values were not different from pre-values. HCVR was increased significantly by the LDIH protocol by 44.1% (p0.01) and remained elevated by 41.5% at 7 days post (p0.01). The changes following the SDIH protocol were smaller (20.7% and 13.5%, at 1 and 7 days post IH, respectively) and not significant. The HCVR remained elevated 7 days following IH (26.7%, p0.01). In both the hyperoxic and hypoxic modified rebreathing tests, the CO2 sensitivity was unchanged by either intervention. In hypoxia, the CO2 threshold was significantly reduced following both protocols (p0.05). LDIH reduced the threshold by 1.60mmHg, whereas following SDIH it was reduced by 1.98mmHg. Under hyperoxic conditions, LDIH reduced the CO2 threshold by 2.06 mmHg, and SDIH caused a reduction of 2.53 mmHg. There were no significant differences between the two IH protocols for any of the above measures. A 7-day intermittent hypoxic protocol consisting of daily 60-minute exposures to normobaric poikilocapnic hypoxia caused increases in HVR and HCVR. This protocol caused a left-shift in the CO2 threshold but no change in CO2 sensitivity by the modified rebreathing protocol. Neither protocol proved superior in effecting these changes in the resting control of breathing.

Studies examining pulmonary gas exchange during exercise have primarily focused on young healthy men, whereas the female response to exercise has received limited attention. Evidence is accumulating that the response of the lungs, airways, and (or) respiratory muscles to exercise is less than ideal and this may significantly compromise oxygen transport in certain groups of otherwise healthy, fit, active, male subjects. Women may be even more susceptible to exercise-induced pulmonary limitations than height-matched men, by virtue of their smaller lung volumes, lower maximal expiratory flow rates, and smaller diffusion surface areas. We have recently shown that exercise-induced arterial hypoxaemia (EIAH) is more prevalent and occurs at relatively lower fitness levels in females than in males. Despite this finding, few physiologically based mechanisms have been identified to explain why women may be more susceptible to EIAH than men. Potential mechanisms of EIAH include relative alveolar hypoventilation, ventilation–perfusion inequality, and diffusion limitation. Whether these mechanisms are different between sexes remains controversial. The primary purpose of this review is to summarize the available data on EIAH in women and to discuss potential sex-based mechanisms for gas exchange impairment. Furthermore, we discuss unresolved questions dealing with pulmonary system limitations during exercise in women.

The purpose of this study was to compare chemoresponses following two different intermittent hypoxia (IH) protocols in humans. Ten men underwent two 7-day courses of poikilocapnic IH. The long-duration IH (LDIH) protocol consisted of daily 60-min exposures to normobaric 12% O2. The short-duration IH (SDIH) protocol comprised twelve 5-min bouts of 12% O2, separated by 5-min bouts of room air, daily. Isocapnic hypoxic ventilatory response (HVR) was measured daily during the protocol and 1 and 7 days following. Hypercapnic ventilatory response (HCVR) and CO2 threshold and sensitivity (by the modified Read rebreathing technique) were measured on days 1, 8, and 14. Following 7 days of IH, the mean HVR was significantly increased from 0.47 ± 0.07 and 0.47 ± 0.08 to 0.70 ± 0.06 and 0.79 ± 0.06 l·min−1·%SaO2−1 (LDIH and SDIH, respectively), where %SaO2 is percent arterial oxygen saturation. The increase in HVR reached a plateau after the third day. One week post-IH, HVR values were unchanged from baseline. HCVR increased from 3.0 ± 0.4 to 4.0 ± 0.5 l·min−1·mmHg−1. In both the hyperoxic and hypoxic modified Read rebreathing tests, the slope of the CO2/ventilation plot was unchanged by either intervention, but the CO2/ventilation curve shifted to the left following IH. There were no correlations between the changes in response to hypoxia and hypercapnia. There were no significant differences between the two IH protocols for any measures, indicating that comparable changes in chemoreflex control occur with either protocol. These results also suggest that the two methods of measuring CO2 response are not completely concordant and that the changes in CO2 control do not correlate with the increase in the HVR.

The purpose of this study was to use a hypoxic stress as a mean to disrupt the normal coordinative pattern during cycling. Seven male cyclists pedalled at three cadence (60, 80, 100 rpm) and three power output (150, 250, 350 W) conditions in normoxia and hypoxia (15% O2). Simultaneous measurements of pedal force, joint kinematics, % oxyhaemoglobin saturation, and minute ventilation were made for each riding condition. A conventional inverse dynamics approach was used to compute the joint moments of force at the hip, knee, and ankle. The relative contribution of the joint moments of force with respect to the total moment was computed for each subject and trial condition. Overall, the ankle contributed on average 21%, the knee 29% and the hip 50% of the total moment. This was not affected by the relative inspired oxygen concentration. Results showed that the relative ankle moment of force remained at 21% regardless of manipulation. The relative hip moment was reduced on average by 4% with increased cadence and increased on average by 4% with increased power output whereas the knee moment responded in the opposite direction. These results suggest that the coordinative pattern in cycling is a dominant characteristic of cycling biomechanics and remains robust even in the face of arterial hypoxemia.

Noninvasive imaging techniques have been used to assess pulmonary edema following exercise but results remain equivocal. Most studies examining this phenomenon have used male subjects while the female response has received little attention. Some suggest that women, by virtue of their smaller lungs, airways, and diffusion surface areas may be more susceptible to pulmonary limitations during exercise. Accordingly, the purpose of this study was to determine if intense normobaric hypoxic exercise could induce pulmonary edema in women. Baseline lung density was obtained in eight highly trained female cyclists (mean ± SD: age = 26 ± 7 yr; height = 172.2 ± 6.7 cm; mass = 64.1 ± 6.7 kg; V̇o2max = 52.2 ± 2.2 ml·kg−1·min−1) using computed tomography (CT). CT scans were obtained at the level of the aortic arch, the tracheal carina, and the superior end plate of the tenth thoracic vertebra. While breathing 15% O2, subjects then performed five 2.5-km cycling intervals [mean power = 212 ± 31 W; heart rate (HR) = 94.5 ± 2.2%HRmax] separated by 5 min of recovery. Throughout the intervals, subjects desaturated to 82 ± 4%, which was 13 ± 2% below resting hypoxic levels. Scans were repeated 44 ± 8 min following exercise. Mean lung density did not change from pre (0.138 ± 0.014 g/ml)- to postexercise (0.137 ± 0.011 g/ml). These findings suggest that pulmonary edema does not occur in highly trained females following intense normobaric hypoxic exercise.

The purpose of this study was to determine the changes in human cerebrovascular function associated with intermittent poikilocapnic hypoxia (IH). Healthy men (n=8; 24+/-1 years) were exposed to IH for 10 days (12% O(2) for 5min followed by 5min of normoxia for 1h). During the hypoxic exposures, oxyhemoglobin saturation (SaO(2)) was 85% and the end-tidal partial pressure of CO(2) was permitted to fall as a result of hypoxic hyperventilation. Pre- and post-IH intervention subjects underwent a progressive isocapnic hypoxic test where ventilation, blood pressure, heart rate, and cerebral blood flow velocity (middle cerebral artery, transcranial Doppler) were measured to determine the ventilatory, cardiovascular and cerebrovascular sensitivities to isocapnic hypoxia. When compared to the pre-IH trial, cerebrovascular sensitivity to hypoxia significantly decreased (pre-IH=0.28+/-0.15; post-IH=0.16+/-0.14cms(-1)%SaO(2)(-1); P0.05). No changes in ventilatory, blood pressure or heart rate sensitivity were observed (P0.05). We have previously shown that the ability to oxygenate cerebral tissue measured using spatially resolved near infrared spectroscopy is significantly reduced following IH in healthy humans. Our collective findings indicate that intermittent hypoxia can blunt cerebrovascular regulation. Thus, it appears that intermittent hypoxia has direct cerebrovascular effects that can occur in the absence of changes to the ventilatory and neurovascular control systems.

The purpose of this study was to examine the effects of exercise on extravascular lung water as it may relate to pulmonary gas exchange. Ten male humans underwent measures of maximal oxygen uptake (V̇o2 max) in two conditions: normoxia (N) and normobaric hypoxia of 15% O2 (H). Lung density was measured by quantified MRI before and 48.0 ± 7.4 and 100.7 ± 15.1 min following 60 min of cycling exercise in N (intensity = 61.6 ± 9.5% V̇o2 max) and 55.5 ± 9.8 and 104.3 ± 9.1 min following 60 min cycling exercise in H (intensity = 65.4 ± 7.1% hypoxic V̇o2 max), where V̇o2 max = 65.0 ± 7.5 ml·kg−1·min−1 (N) and 54.1 ± 7.0 ml·kg−1·min−1 (H). Two subjects demonstrated mild exercise-induced arterial hypoxemia (EIAH) [minimum arterial oxygen saturation (SaO2 min) = 94.5% and 93.8%], and seven subjects demonstrated moderate EIAH (SaO2 min = 91.4 ± 1.1%) as measured noninvasively during the V̇o2 max test in N. Mean lung densities, measured once preexercise and twice postexercise, were 0.177 ± 0.019, 0.181 ± 0.019, and 0.173 ± 0.019 g/ml (N) and 0.178 ± 0.021, 0.174 ± 0.022, and 0.176 ± 0.019 g/ml (H), respectively. No significant differences ( P > 0.05) were found in lung density following exercise in either condition or between conditions. Transient interstitial pulmonary edema did not occur following sustained steady-state cycling exercise in N or H, indicating that transient edema does not result from pulmonary capillary leakage during sustained submaximal exercise.

Although high-altitude exposure can lead to neurocognitive impairment, even upon return to sea level, it remains unclear the extent to which brain volume and regional cerebral vascular reactivity (CVR) are altered following high-altitude exposure. The purpose of this study was to simultaneously determine the effect of 3 weeks at 5050 m on: (1) structural brain alterations; and (2) regional CVR after returning to sea level for 1 week. Healthy human volunteers (n = 6) underwent baseline and follow-up structural and functional magnetic resonance imaging (MRI) at rest and during a CVR protocol (end-tidal PCO2 reduced by -10, -5 and increased by +5, +10, and +15 mmHg from baseline). CVR maps (% mmHg(-1)) were generated using BOLD MRI and brain volumes were estimated. Following return to sea level, whole-brain volume and gray matter volume was reduced by 0.4 ± 0.3% (P < 0.01) and 2.6 ± 1.0% (P < 0.001), respectively; white matter was unchanged. Global gray matter CVR and white matter CVR were unchanged following return to sea level, but CVR was selectively increased (P < 0.05) in the brainstem (+30 ± 12%), hippocampus (+12 ± 3%), and thalamus (+10 ± 3%). These changes were the result of improvement and/or reversal of negative CVR to positive CVR in these regions. Three weeks of high-altitude exposure is reflected in loss of gray matter volume and improvements in negative CVR.

We determined the effects of 10 daily exposures of intermittent hypoxia (IH; 1 h day(-1); oxyhaemoglobin saturation = 80%) on muscle sympathetic nerve activity (MSNA, peroneal nerve) and the hypoxic ventilatory response (HVR) before, during and after an acute 20 min isocapnic hypoxic exposure. We also assessed the potential parallel modulation of the ventilatory and sympathetic systems following IH. Healthy young men (n = 11; 25 +/- 1 years) served as subjects and pre- and post-IH measures of MSNA were obtained on six subjects. The IH intervention caused HVR to significantly increase (pre-IH = 0.30 +/- 0.03; post-IH = 0.61 +/- 0.12 l min(-1) %S(aO(2)) (-1)). During the 20 min hypoxic exposure sympathetic activity was significantly greater than baseline and remained above baseline after withdrawal of the hypoxic stimulus, even though oxyhaemoglobin saturation had normalized and ventilation and blood pressure had returned to baseline levels. When compared to the pre-IH trial, burst frequency increased (P0.01), total MSNA trended towards higher values (P = 0.06), and there was no effect on burst amplitude (P = 0.82) during the post-IH trial. Following IH the rise in MSNA burst frequency was strongly related to the change in HVR (r = 0.79, P0.05) suggesting that these sympathetic and ventilatory responses may have common central control.

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 (V̇o2 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 V̇o2 max of ≥60 ml·kg−1·min−1 were considered highly trained ( n = 13); those with a V̇o2 max of 50–60 ml·kg−1·min−1 were considered moderately-trained ( n = 18); and those with a V̇o2 max of −1·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·min·%arterial O2 saturation−1). The relationship between HVR and V̇o2 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.

Cardiovascular abnormalities and arrhythmias are common in individuals with spinal cord injury (SCI) who are undergoing vibrostimulation for sperm retrieval. The study aimed to examine cardiovascular control in men with SCI undergoing this procedure.Individuals with chronic cervical (n=8; age: 33.1 +/- 1.9 years) and upper thoracic SCI (n=5; age: 35.2 +/- 2.9 years) volunteered for vibrostimulation, with continuous blood pressure (Finometer) and electrocardiographic monitoring. Patients were characterized further by sympathetic skin responses (SSR) to assess descending autonomic spinal pathways and American Spinal Injury Association (ASIA) scores to assess motor and sensory pathways.All but one subject with cervical SCI were ASIA A or B and were negative for SSR in the hands and feet. All subjects with upper thoracic SCI were ASIA A or B and were positive for SSR in the hands. Systolic blood pressure was lower in men with cervical injury at rest. Vibrostimulation induced an increase in systolic blood pressure20 mmHg in all patients with cervical SCI (range = 125/65 - 280/152; median = 167/143 mmHg) and in 2 thoracic subjects (151/104 and 170/121 mmHg). During ejaculation, 6 cervical and 3 thoracic subjects developed arrhythmias (5 with bradycardia, 6 with premature atrial contractions, 4 with ventricular excitation, 1 with junctional rhythm, and 1 with heart block).The vibrostimulation procedure induced electrocardiographic abnormalities and autonomic dysreflexia in subjects with either cervical or high thoracic SCI.

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 (P0.05) 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 (P0.05) but was not different between SDIH and LDIH (P0.05). The relationships between HVR and VO2max were non-significant on day 1 (r = 0.30) and day 12 (r = 0.47; P0.05). Our findings point to a lack of functional significance of increasing HVR via intermittent hypoxia on ventilatory responses to exercise at sea level.

The purpose of this study was to evaluate the accuracy of a respiratory inductive plethysmograph (RIP) designed for ambulatory data collection during exercise by comparison to a pneumotachograph. Healthy young males (n=10) wore an elastic body garment embedded with inductance sensors encircling the rib cage and abdomen. Breathing frequency (f(R)), tidal volume (V(T)) and minute ventilation (V (I)) were monitored during 5min of rest, slow walking (3.7kmh(-1)), fast walking (6.1kmh(-1)) and slow running (8.9kmh(-1)) followed by an incremental treadmill test to exhaustion (14.4+/-2.7kmh(-1)). Mean f(R), V(T) and V (I) values were not statistically different between the two methods (P>0.05). Within each of the subjects at rest and different exercise intensities, the average coefficient of determination was high for f(R), V(T) and V (I) (R(2)=0.9233, 0.8743 and 0.9652, respectively) and the mean bias values were low (-0.102+/-2.91, 0.033+/-0.207 and -0.715+/-8.362, respectively). These data suggest that the ambulatory RIP provides reasonable estimates of ventilation during rest and exercise.

Exercise-induced arterial hypoxemia (EIAH) is reported to occur in approximately 50% of highly trained male endurance athletes. Few studies have examined EIAH in women and the prevalence remains unclear. It has been reported that some female subjects who develop EIAH possess maximal oxygen consumption (VO2max) values that are within 15% of their predicted value. This is unique to women, where EIAH has generally been reported in men who have a high VO2max. The primary objective of this investigation was to determine the prevalence of EIAH in a large female population with a wide range of VO2max values. It was hypothesized that EIAH would occur with a greater prevalence and at relatively lower predicted VO2max than that previously reported in males.Young women (N = 52; 26.5 +/- 4.9 yr) performed a cycle test to exhaustion to determine VO2max, and oxyhemoglobin saturation (SaO2) was monitored via pulse oximetry. All subjects were tested during the early follicular phase of their menstrual cycle. A/= 4% drop in SaO2 represented EIAH.Values for VO2max were variable (VO2max range: 28.0-61.3 mL x kg(-1) x min(-1)). EIAH was present in 67% of the women with N = 19 displaying mild EIAH (92-94%SaO2) and N = 16 displaying moderate EIAH (87-91%SaO2).It appears that the prevalence of EIAH in women is slightly greater than the 50% prevalence value that is typically reported for highly fit men.

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.

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.

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%) (P0.05). AHVR and maximal O(2) consumption were related for all subjects (r = -0.46), men (r = -0.45) and women (r = -0.53) (P0.05) but AHVR was unrelated to Sa(O(2)) for any groups (P0.05). 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.

We found that patients with transplants, regardless of transplant type, and sedentary control subjects experience significant increases in aerobic fitness after 10 weeks of Dragon boat training. However, the magnitude of improvement in aerobic fitness depends on the transplant type, with patients having cardiac transplant experiencing greater relative changes in response to training than patients with noncardiac transplant. It also appears that patients with cardiac and noncardiac transplants have an increased reliance on anaerobic energy systems during exercise conditions compared with healthy control subjects.

We have attempted to synthesize findings dealing with four types of respiratory system influences on sympathetic outflow in the human. First, a powerful lung volume-dependent modulation of muscle sympathetic nerve activity (MSNA) occurs within each respiratory cycle showing late-inspiratory inhibition and late-expiratory excitation. Secondly, in the intact human, neither reductions in spontaneous respiratory motor output nor voluntary near-maximum increases in central respiratory motor output and inspiratory effort, per sec, influence MSNA modulation within a breath, MSNA total activity or limb vascular conductance. Thirdly, carotid chemoreceptor stimuli markedly increase total MSNA; but most of the MSNA response to chemoreceptor activation appears to be mediated independently of increased central respiratory motor output. Fourthly, repeated fatiguing contractions of the diaphragm or expiratory muscles in the human show a metaboreflex mediated time-dependent increase in MSNA and reduced vascular conductance and blood flow in the resting limb. Recent evidence suggests that these respiratory influences contribute significantly to sympathetic vasomotor outflow and to the distribution of systemic vascular conductances and blood flow in the exercising human.

The respiratory system has traditionally been viewed to be capable of meeting the substantial demands for ventilation and gas exchange and the cardiopulmonary interactions imposed by short-term maximum exercise or long-term endurance exercise. Recent studies suggest that specific respiratory muscle (RM) training can improve the endurance and strength of the respiratory muscles in healthy humans. The effects of RM training on exercise performance remains controversial. When whole-body exercise performance is evaluated using submaximal fixed work-rate tests, significant improvements are seen and smaller, but significant improvements have also been reported in placebo-trained individuals. When performance is measured using time-trial type performance measures versus fixed workload tests, performance is increased to a much lesser extent with RM training. It appears that RM training influences relevant measures of physical performance to a limited extent at most. Interpretation of the collective literature is difficult because most studies have utilised relatively small sample sizes and very few studies have used appropriate control or placebo groups. Mechanisms to explain the purported improvements in exercise performance remain largely unknown. However, possible candidates include improved ratings of breathing perception, delay of respiratory muscle fatigue, ventilatory efficiency, or blood-flow competition between respiratory and locomotor muscles. This review summarises the current literature on the physiology of RM training in healthy individuals and critically evaluates the possible implications for exercise performance.

The purpose of this study was to determine whether the human diaphragm, like limb muscle, has a threshold of force output at which a metaboreflex is activated causing systemic vasoconstriction. We used Doppler ultrasound techniques to quantify leg blood flow (QL) and utilized the changes in mouth twitch pressure (ΔPMT) in response to bilateral phrenic nerve stimulation to quantify the onset of diaphragm fatigue. Six healthy male subjects performed four randomly assigned trials of identical duration (8 ± 2 min) and breathing pattern [20 breaths/min and time spent on inspiration during the duty cycle (time spent on inspiration/total time of one breathing cycle) was 0.4] during which they inspired primarily with the diaphragm. For trials 1- 3, inspiratory resistance and effort was gradually increased [30, 40, and 50% maximal inspiratory pressure (MIP)], diaphragm fatigue did not occur, and QL, limb vascular resistance (LVR), and mean arterial pressure remained unchanged from control ( P > 0.05). The fourth trial utilized the same breathing pattern with 60% MIP and caused diaphragm fatigue, as shown by a 30 ± 12% reduction in PMT with bilateral phrenic nerve stimulation. During the fatigue trial, QL and LVR were unchanged from baseline at minute 1, but LVR rose 36% and QL fell 25% at minute 2 and by 52% and 30%, respectively, during the final minutes of the trial. Both LVR and QL returned to control within 30 s of recovery. In summary, voluntary increases in inspiratory muscle effort, in the absence of fatigue, had no effect on LVR and QL, whereas fatiguing the diaphragm elicited time-dependent increases in LVR and decreases in QL. We attribute the limb vasoconstriction to a metaboreflex originating in the diaphragm, which reaches its threshold for activation during fatiguing contractions.

to the editor: We agree with Drs. Debevec and Millet ([1][1]) that a study with either a longer duration (>6 h) or intermittent hypoxic exposures might detect differences in certain outcomes between hypobaric hypoxia (NH) and normobaric hypoxia (HH). Symptoms of acute mountain sickness (AMS) can

1. We recently showed that fatigue of the inspiratory muscles via voluntary efforts caused a time-dependent increase in limb muscle sympathetic nerve activity (MSNA) (St Croix et al. 2000). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow also accompany inspiratory muscle fatigue. 2. In six healthy human subjects at rest, we measured leg blood flow («Q L) in the femoral artery with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while subjects performed two types of fatiguing inspiratory work to the point of task failure (3–10 min). Subjects inspired primarily with their diaphragm through a resistor, generating (i) 60 % maximal inspiratory mouth pressure (P M) and a prolonged duty cycle (TI/TTOT = 0.7); and (ii) 60 % maximal PM and a TI/TTOT of 0.4. The first type of exercise caused prolonged ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of contraction. End-tidal P CO2 was maintained by increasing the inspired CO2 fraction (FI,CO2 ) as needed. Both trials caused a 25–40 % reduction in diaphragm force production in response to bilateral phrenic nerve stimulation. 3. «Q L and LVR were unchanged during the first minute of the fatigue trials in most subjects; however, «QL subsequently decreased (_30 %) and LVR increased (50–60 %) relative to control in a time-dependent manner. This effect was present by 2 min in all subjects. During recovery, the observed changes dissipated quickly (< 30 s). Mean arterial pressure (MAP; +4–13 mmHg) and heart rate (+16–20 beats min _1 ) increased during fatiguing diaphragm contractions. 4. When central inspiratory motor output was increased for 2 min without diaphragm fatigue by increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or inspiratory flow rate (5 w eupnoea), «Q L, MAP and LVR were unchanged; although continuing the high force output trials for 3 min did cause a relatively small but significant increase in LVR and a reduction in «Q L. 5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance, LVR was reduced and «Q L increased significantly; these changes were attributed to the negative feedback effects on MSNA from augmented tidal volume. 6. Voluntary increases in inspiratory effort, in the absence of diaphragm fatigue, had no effect on «Q L and LVR, whereas the two types of diaphragm-fatiguing trials elicited decreases in «QL and increases in LVR. We attribute these changes to a metaboreflex originating in the diaphragm. Diaphragm and forearm muscle fatigue showed very similar time-dependent effects on LVR and «Q L.

The purpose of this study was to determine the effects of repeated heavy exercise on postexercise pulmonary diffusing capacity (DL) and the development of exercise induced arterial hypoxemia (EIH).13 endurance-trained, male athletes (age = 27+/-3 yr, height = 179.6+/-5.0 cm, weight = 71.8+/-6.9 kg, VO2max = 67.0+/-3.6 mL x kg(-1) x min(-1) performed two consecutive, continuous exercise tests on a cycle ergometer to VO2max, separated by 60 min of recovery. Arterial oxygen saturation (%SaO2) was measured via ear oximetry, and resting DL was measured and partitioned by the single-breath method, before exercise and 60 min after each exercise bout.No significant differences resulted in VO2max, VE, peak heart rate (HR), or breathing frequency between exercise bouts (P0.05). There was a small but significant decrease (454-446 W; P0.05) in peak power output in the second test. %SaO2 decreased from resting values during both exercise tasks, but there was no difference between the minimum saturation achieved in test 1 (91.4) or test 2 (91.6; P0.05). After the initial exercise bout, significant decreases (P0.05) occurred in DL (11%), membrane diffusing capacity (DM) (11%) and pulmonary capillary volume (VC) (10%). Further decreases occurred in DL (6%; P0.05), DM (2%; P0.05), and VC (10%; P0.05) after the second exercise bout.These observations question the meaning of post exercise measurements of pulmonary diffusion capacity, and its components, relative to pulmonary gas exchange and pulmonary fluid accumulation during exercise. The fact that there was no further change in %SaO2 after the second test suggests that if any interstitial edema developed, it was of no clinical significance; alternatively, the changes in DL(CO) may be related more to redistribution of blood than the development of pulmonary edema.

We investigated the time course of changes in post-exercise pulmonary diffusing capacity for carbon monoxide (DLCO), membrane diffusing capacity (DM), and pulmonary capillary blood volume (VC) in highly trained (HT), moderately trained (MT) and untrained (UT) male subjects (n = 8/group). Subjects were assigned to groups based on their aerobic capacity from a preliminary VO2max test (HT > or = 65, MT = 50-60, UT < or = 50 ml x kg(-1) x min(-1)). Resting (BASE) DLCO, DM and VC were obtained, then subjects cycled to fatigue at the highest workrate attained during the preliminary tests. Diffusion measurements were then made at 1, 2, 4, 6 and 24 h. DLCO was depressed at 1 h, lowest at 6 h and approached BASE values at 24 h in all groups. The DLCO change was paralleled by a change in VC. Alterations to VC were similar between groups except at 24 h where MT and HT subjects had returned to BASE while UT did not. DM was significantly lower than BASE at 1, 2, 4, and 6 h, and was similar between groups. The changes in DLCO post-exercise appear to be primarily due to a decrease in VC. Comparable diffusion decrements were observed in all subjects. The results of this study suggest that post-exercise alterations in DLCO, DM and VC are not related to aerobic capacity.

The purpose of this investigation was to quantify the difference in energy expenditure between traditional cycling handlebars and aero-bars during outdoor submaximal cycling. Eleven trained cyclists (age = 29.3 ± 1.9 years, weight = 69.4 ± 3.8 kg, VO2max = 58.1 ± 2.0 ml∙kg−1∙min−1) were randomly assigned a sequence of three hand positions: brake hoods (BH), drop-bars (DB), and aero-bars (AB). Subjects cycled at 30 km∙h−1 in one position for 5 minutes, then recovered until HR fell below 120 bpm. This was then repeated for the other hand positions. All cycling was completed on a standard racing bike fitted with aero-bars. Tire pressure was held constant for all trials. A portable telemetric system (Cosmed K-2) was used to measure VO2, VE and heart rate (HR) during the trials. No statistical differences were observed between AB and DB. Significant differences (p E = 66.1 ± 2.7 L∙min−1; HR = 152 ± 4 bpm; VO2 = 1.56 ±.15 L∙min−1) and AB (VE = 61.3 ± 2.8 L∙min−1; HR = 146 ± 4 bpm; VO2 = 1.31 ±.10 L∙min−1). AB provides an energy savings over the traditional BH cycling posture. Key words: aerodynamic handlebars, oxygen consumption, field testing, portable telemetric system

to the editor: We appreciate the interest and input of the accompanying commentaries (see Ref. [7][1]). However, we wish to restate that this Point:Counterpoint is related to human athletes performing sea-level exercise. Reports of edema with exercise at altitude or breath-hold diving, while

There is increasing interest in head-up-displays (HUDs) for automotive use. A number of technologies could be employed for the combiner function including plain glass reflection, dielectric enhancement, and holography. This paper will consider the potential role for conformal holography as the combiner element by initially reviewing the system requirements from an optical design view, how these differ significantly from an avionic HUD, and how they relate to material characteristics and process features. This will involve a consideration in some detail of the effects of specified hologram properties and lamination features on the optical performance and image characteristic of a car HUD. In particular, we shall examine such features as hologram efficiency, bandwidth, tuning position, environmental stability, tolerances, and film lamination effects and how these may influence the key optical characteristics of the image, i.e., distortions, blur, brightness, double imaging (separation and contrast) outside world view, etc.. A theoretical model based on Kogelnik coupled wave theory will be used to illustrate the various tradeoffs between hologram properties and process, image features, and display characteristics (bandwidth, polarization, etc.). This analysis will be related to properties of currently available holographic materials with reference to recent experimental work.