Noninvasive profiling of exercise-induced hypoxemia in competitive cyclists

The purpose of this case study was to profile maximal exercise and the incidence of exercise-induced arterial hypoxemia (EIAH) at three different altitudes within a group of competitive cyclists residing and training at 1,500 m. Ten male cyclists (category I or II professional road cyclists: ages, 27.7 +/- 6.1; weight, 69.9 +/- 6.9 kg) participated in three randomly assigned VO2max tests at sea level (SL), 1,500 m and 3000 m. Arterial saturation (pulse oximetry), ventilation, and power output (PO) were recorded continuously throughout the test. The SaO2 percentages at VO2max were significantly higher at SL when compared with 1500 m (p < 0.001); however, no difference was observed between VO2max values at either altitude (SL: 72.3 +/- 2.5 mL.kg-1.min-1, 1,500 m: 70.6 +/- 2.3 mL.kg-1.min-1), only when compared with 3,000 m: 63.9 +/- 2.1 mL.kg-1.min-1, p < 0.021. Percent SaO2 did correspond with maximal PO, and there was an overall main effect observed between POs as they continually declined from SL to 3,000 m (SL: 403.3 +/- 10.6 W; 1,500 m: 376.1 +/- 9.8 W; 3,000 m: 353.9 +/- 7.8 W; p < 0.0001). The results of this case study revealed that training and residing at 1,500 m did not reduce the incidence of EIAH during maximal exercise at 1,500 m for this selected group of cyclists.     

Prevalence of exercise-induced arterial hypoxemia in healthy women

PURPOSE: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.     

Caffeine stimulates ventilation in athletes with exercise-induced hypoxemia

INTRODUCTION/PURPOSE: Many athletes with exercise-induced hypoxemia (EIH) show an insufficient ventilatory response to exercise and low resting ventilatory responsiveness. The purpose of this project was to determine whether a moderate dosage of caffeine, a common ventilatory stimulant, could augment resting ventilatory responsiveness, exercise ventilation (V E), end-tidal O2 partial pressure (PetO2), and arterial oxyhemoglobin saturation (HbSaO2) in athletes with EIH. METHODS: Eight highly trained males ([formula: see text], 69.2 +/- 4.0 mL.[kg.min]) who demonstrated EIH at [formula: see text] (HbSaO2, 88.0 +/- 1.7%), ingested in a randomized design a placebo or caffeine (CAF, 8 mg.kg body wt) 1 h before testing. Ventilatory responsiveness at rest was assessed via the isocapnic hypoxic and hyperoxic hypercapnic ventilatory responses (HVR and HCVR, respectively). Dependent measures of metabolic variables, ventilation, and saturation were determined during progressive treadmill exercise to exhaustion. RESULTS: V E was higher at 75%, 80%, and 100% of [formula: see text] with CAF (P < 0.05). V E/V O2, PetO2, and HbSaO2 were increased at 75%, 80%, and 90% of [formula: see text] with CAF but were not different at [formula: see text] despite an increase in V e. No change in [formula: see text] was observed between treatments. HVR and HCVR were not different between the two conditions, indicating that the increased V E likely came from central stimulation or secondary effects of CAF. CONCLUSION: The failure of HbSaO2 to increase at [formula: see text] despite an increase in V E suggests that mechanisms influencing HbSaO2 other than an inadequate hyperventilatory response may operate to different degrees across individuals as [formula: see text] is approached.     

Attenuated ANF response to exercise in athletes with exercise-induced hypoxemia

Some highly trained endurance athletes develop an exercise-induced hypoxemia (EIH) at least partially due to a hemodynamic factor with a potential stress failure on pulmonary capillaries. Atrial natriuretic factor (ANF) is a pulmonary vasodilatator and its release during exercise could be reduced with endurance training. We hypothesized that athletes exhibiting EIH, who have a greater training volume than non-EIH athletes, have a reduced ANF release during exercise explaining the pathophysiology of EIH. Ten highly trained EIH-athletes (HT-EIH), ten without EIH (HT-nEIH), and nine untrained (UT) males performed incremental exercise to exhaustion. No between group differences occurred in resting ANF plasma levels. In contrast to HT-nEIH and UT (p < 0.05), HT-EIH showed a smaller increase in ANF concentration between rest and maximal exercise (HT-EIH: 8.12 +/- 0.69 vs. 14.1 +/- 1.86 pmol x l (-1); HT-nEIH: 10.46 +/- 1 vs. 18.7 +/- 1.8 pmol x l (-1); UT: 6.23 +/- 0.95 vs. 20.38 +/- 2.79 pmol x l (-1)). During the recovery, ANF levels decreased significantly in HT-nEIH and UT groups (p < 0.05). Electrolyte values increased in all groups during exercise but were higher in both trained groups. In conclusion, this study suggested that ANF response to exercise may be important for exercise-induced hypoxemia.     

Effect of a long- and short-acting beta2-agonist on exercise-induced arterial hypoxemia

PURPOSE: determine the effect of formoterol and salbutamol on the arterial oxygen saturation (SaO(2)) of highly trained nonasthmatic athletes with exercise-induced arterial hypoxemia (EIAH). METHODS: Ten male athletes (age = 27.1 +/- 0.7, [OV0312]O(2max) = 65.2 +/- 2.5 mL.kg-1.min-1, SaO(2min) = 91.0 +/- 2.1%) with minimal bronchial reactivity to aerosols (i.e., negative methacholine challenge test) completed three identical exercise sessions differing only by the medication administered. Formoterol (F), a long-acting beta-2 agonist, was compared with salbutamol (S) and a placebo (P). F (12 microg), S (400 microg), or P was administered by a Turbuhaler, 10 min before exercise testing in a double-blind, randomized, three-way crossover design. Testing sessions included an incremental cycle ergometer test to exhaustion, while monitoring SaO(2) and ventilation, and a pre- and postexercise pulmonary function test. RESULTS: There were no significant differences between the groups in SaO(2) nadir with exercise (F = 92.0 +/- 1.0; S = 92.0 +/- 1.0; P = 91.0 +/- 0.7%). During the maximal incremental test, no differences were observed in SaO(2) or minute ventilation between the three experimental conditions. Pulmonary function tests revealed a significant increase in FEV(1) and FEV(1)/FVC after exercise in all conditions. Drug administration increased FEV(1)/FVC postexercise compared with placebo (F = 87.9 +/- 2.3, S = 87.6 +/- 1.7 > P = 85.6 +/- 2.1%; P < 0.05). CONCLUSION: An acute, inhaled, therapeutic dose of formoterol or salbutamol did not affect SaO(2) nadir or ventilation kinetics in a group of highly trained nonasthmatic athletes with EIAH.     

Effect of prolonged exercise on arterial oxygen saturation in athletes susceptible to exercise-induced hypoxemia

This study examined the effect of prolonged endurance exercise on the development of exercise-induced hypoxemia (EIH) in athletes who had previously displayed EIH during an incremental maximal exercise test. Five male and three female endurance-trained athletes participated. Susceptibility to EIH was confirmed through a maximal incremental exercise test and defined as a reduction in the saturation of arterial oxygen (SpO(2)) of >/=4% from rest. Sixty minutes of running was conducted, on a separate day, at an oxygen consumption corresponding to 95% of ventilatory threshold. Immediately following the 60 min exercise bout, athletes commenced a time trial to exhaustion at 95% maximal oxygen consumption (VO(2max)). The reduction in SpO(2) was significantly greater during the maximal incremental test, than during the 60 min, or time trial to exhaustion (-8.8+/-1.4%, -3.3+/-1.1%, and -4.1+/-2.3%, P<0.05, respectively). The degree of desaturation during the 60 min was significantly related to the relative intensity of exercise at 95% ventilatory threshold (adjusted r(2)=0.54, P=0.02). In conclusion, athletes who did not exercise at greater than 73% VO(2max) during 60 min of endurance exercise did not display EIH, despite being previously susceptible during an incremental maximal test.     

Rectal temperature after marathon running.

Rectal temperature was measured in 62 male runners who competed in the 1983 Dundee marathon race: all measurements were made immediately after the race. Competitors' times were noted at 5, 10, 15 and 20 miles (8.0, 16.1, 24.1, 32.2 km) and at the finish (26.2 miles, 42.2 km). Mean finishing time of the group was 3 hr 33 min +/- 48 min (mean +/- S.D.; range = 2 hr 17 min-5 hr 11 min). Mean running speed of the group decreased progressively as the distance covered increased. Mean post-race rectal temperature was 38.7 +/- 0.9 degrees C (range 35.6-40.3 degrees C). The post-race temperature was correlated (p less than 0.01) with the time taken to cover the last 6.2 miles (10 km) of the race, but not with the overall finishing time (p greater than 0.05). Only the fastest runners were able to maintain an approximately constant pace throughout the race, whereas the slower runners slowed down progressively. The runners with the highest post-race temperature, although not necessarily the fastest runners, also tended to maintain a steady pace throughout. The runners with the lowest post-race temperature slowed down markedly only over the last 6.2 mile section of the race. The results clearly indicate that runners forced by fatigue or injury to slow down in the latter stages of races held at low ambient temperatures may already be hypothermic or at serious risk of hypothermia.     

Evidence of decrease in peak heart rate in acute hypoxia: effect of exercise-induced arterial hypoxemia

This study focuses on the influence of the arterial oxygen saturation level at exhaustion on peak heart rate under acute moderate hypoxia, in endurance-trained subjects. Nineteen competing male cyclists performed exhaustive ramp exercise (cycle ergometer) under normoxia and normobaric hypoxia (15 % O (2)). After the normoxic trial, the subjects were divided into those demonstrating exercise-induced arterial hypoxemia during exercise (> 5 % decrease in SaO (2) between rest and the end of exercise, n = 10) and those who did not (n = 9). O (2) uptake, heart rate and arterial O (2) saturation (ear-oximeter) levels were measured. Under hypoxia, peak heart rate decreased for both groups (p < 0.001) and to a greater extent for hypoxemic subjects (p < 0.01). Arterial O (2) saturation under hypoxia was lower for the hypoxemic than for the non-hypoxemic subjects (p < 0.001) and it was correlated to the fall in peak heart rate between normoxia and hypoxia for all subjects (p < 0.01; r = 0.65). Hypoxemic subjects presented greater decrease in maximal O (2) uptake than non-hypoxemic ones (19.6 vs. 15.6 %; p < 0.05). The results confirm the greater decrement in arterial O (2) saturation under hypoxia in hypoxemic subjects and demonstrates a more pronounced reduction in peak heart rate in those subjects compared with non-hypoxemic ones. These data confirm the possible influence of arterial oxygenation on the decrease in peak heart rate in acute hypoxia.     

History of exercise-induced asthma

Strenuous exercise prolonged for several minutes can cause airway obstruction in asthmatic subjects. Initial obstruction becomes most extreme 5-10 min after the completion of exercise and usually remits within a few minutes but may recur 3-6 h later. The response to exercise depends upon the type of exercise. Swimming is less likely to cause exercise-induced asthma than running. Recent exercise or pretreatment with a bronchodilator or cromolyn can inhibit exercise-induced asthma. Nasal breathing or inhalation of warm, fully humidified air during exercise can minimize exercise-induced asthma. Local changes in osmolarity or cooling of mast cells probably causes release of mediators that cause airway obstruction.     

14 C-deoxyglucose imaging overestimates myocardial viability in subacute infarction of rats

Clinical studies using 18F-fluorodeoxyglucose suggest that this tracer may overestimate myocardial viability. This study aimed to elucidate whether 2-deoxyglucose accurately indicates myocardial viability at the early phase of myocardial infarction. Autoradiography with 14C-deoxyglucose was performed in fasting rats whose left coronary artery was occluded for 60 min and then reperfused. 14C-deoxyglucose was injected 30 min after the reperfusion (acute; n=10) or 1 week later (subacute; n=9). Infarction and risk areas were identified by triphenyl tetrazolium chloride or haematoxylin-eosin staining and methylene blue, respectively. Immuno-histochemical staining using anti-glucose transporter 1 and 4 antibodies was performed. At the acute stage, the uptake of deoxyglucose was consistent with the grade of anti-glucose transporter 4 expression. At the subacute stage, the uptake of deoxyglucose in poorly viable myocardium (543.4+/-343.7%: normalized with the uptake at the right ventricle) as well as in the viable one (335.2+/-149.8%) in the risk area was significantly greater than that in the remote area (116.4+/-94.9%, P<0.01). Anti-glucose transporter 1 was expressed in the poorly viable area where inflammatory cells infiltrated. It is concluded that deoxyglucose uptake by inflammatory cells which express anti-glucose transporter 1 causes overestimation of myocardial viability at subacute stage.     

Pathophysiology of exercise-induced asthma

The initiating stimulus for exercise-induced asthma in airway mucosal cooling or drying is caused by heat and water losses during exercise-related hyperventilation. It is not known how this stimulus is translated to bronchoconstriction, but the most convincing evidence is that mast cells are activated and release bronchospastic chemical mediators. The obstructive response appears to depend on the existence of abnormally reactive airways characteristically found in asthmatics. A number of modifying factors may be found during exercise, including plasma changes in catecholamines and metabolite and acid-base status.     

Detection and correction of frequency instabilities for volumetric 1H echo-planar spectroscopic imaging.

Spectral quality in 1H magnetic resonance spectroscopic imaging (MRSI) critically depends on the stability of the main magnetic field. For echo-planar MRSI implemented at 3 T, temperature variation in the passive steel shims of the magnet system can lead to a significant drift in the resonance frequency. A method is presented that incorporates interleaved measurement of the instantaneous resonance frequency of a reference water signal into a volumetric MRSI sequence and allows correction for the drift during postprocessing. Results from normal human brain at 3 T indicate that the correction largely removes lineshape distortions, recovers metabolite signal loss, and improves spectral quality by reducing the width of spectral lines; however, particularly in inferior regions, other sources of distortion may be present that cause broadening of spectral lines.     

Evidence-based management of exercise-induced asthma

Exercise-induced asthma (EIA) is a common, yet often unrecognized condition occurring in both known asthmatics and otherwise healthy individuals. Misdiagnosis, both over- and underdiagnosis, is not uncommon. In order to accurately diagnose EIA, a bronchoprovocation challenge test must be performed; the current recommended test is a eucapnic hyperventilation (EVH) challenge test. Although there are a number of treatment options available, both pharmacologic and nonpharmacologic, in most cases medications are required. A range of medications are currently available to either treat or prevent EIA. It is important that the medications used are individualized to the patients needs and monitored to ensure efficacy.