Cycling efficiency is not compromised for moderate exercise in moderately severe COPD

INTRODUCTION/PURPOSE: Hyperpnea and hyperinflation have been proposed as contributors to exaggerated energy demands in chronic obstructive pulmonary disease (COPD), yet there are incomplete data on exercise requirements. This study compared total-body energy demands of the internal (unloaded) and external work of cycling and delta mechanical efficiency in 40 patients (FEV1: 36+/-14% predicted) with COPD and 28 healthy age-matched controls while characterizing dynamic hyperinflation. METHODS: Steady-state V O2 was obtained at rest, during unloaded and 20-W cycling, and at 20, 50, and 65% peak cycling power. Delta mechanical efficiency was calculated between constant-load cycling at 65 and 20% peak power. Dynamic hyperinflation was assessed from inspiratory capacity maneuvers. RESULTS: Oxygen demands (L.min) at rest, for internal work (0.47+/-0.14 vs 0.45+/-0.11) or external work at 20 W (0.62+/-0.20 vs 0.57+/-0.13), were not different between patients and controls, although ventilation was elevated in COPD. Cycling at 65% of peak power induced dynamic hyperinflation in COPD, which indices were not related to cycling efficiency. Delta efficiency (%) was not different between patients (26.3+/-8.1) and controls (24.8+/-4.0). CONCLUSION: Findings suggest that bioenergetics of submaximal cycling is not compromised in moderately severe COPD despite tachypnea and dynamic hyperinflation.     

Reliability of submaximal exercise tests in patients with COPD. Chronic obstructive pulmonary disease.

Submaximal constant work rate exercise tests are often used to measure the efficacy of an exercise intervention, but the reliability of these tests in patients with chronic obstructive pulmonary disease (COPD) has not been established. PURPOSE: To examine the reproducibility of submaximal exercise responses of COPD patients compared with those of healthy elderly subjects. METHODS: Sixteen COPD patients and 15 healthy subjects performed four weekly submaximal exercise tests against two different constant work rates: 20 W and 50% of the peak work rate (PWR). Spirometry was performed before each exercise test. COPD patients and healthy subjects were: age 69 +/- 5 and 65 +/- 5 yr, body mass index 26.4 +/- 3.9 and 26.7 +/- 3.0 kg x m(-2), respectively. RESULTS: Both groups had no change in minute ventilation (V(E)), oxygen uptake (VO2), breathlessness (RPB), and leg fatigue (RPLF) for either work rate over repeated measures (P > 0.05). At 50% PWR test-retest reliability coefficients for V(E) and VO2 ranged from r = 0.88 to r = 0.96 for COPD patients and from r = 0.72 to r = 0.97 for healthy subjects; for RPB and RPLF test-retest reliability ranged from r = 0.76 to r = 0.89 for COPD patients and from r = 0.70 to r = 0.91 for healthy subjects. Intrasubject mean absolute differences for repeated measures of V(E), VO2, RPB, or RPLF were low and there were no group differences (P > 0.05). Percent error for V(E) and VO2 ranged from 6 +/- 3 to 9 +/- 7%, and for RPB and RPLF ranged from 19 +/- 18 to 68 +/- 65% for both groups at each work rate. CONCLUSIONS: Submaximal exercise responses were reliable over a 1-month period, and measures of the physiological and psychophysical responses of COPD patients were as reliable as those of healthy subjects.     

Performance and muscle oxygenation during isometric exercise and recovery in children with congenital heart diseases

This study investigated performance, muscle oxygen saturation (StO2), and blood volume (BV) in patients with congenital heart diseases (CHD) and healthy children during and following sustained exercise. Maximal volunteered contraction (MVC) and endurance at 50 % of MVC (time to exhaustion, Tlim) of the knee extensor were measured in nine patients with CHD and 14 healthy control children. Near infrared spectroscopy was used to evaluated StO2 and BV in vastus lateralis. The drop in muscle oxygen saturation (D(mO2)), half time of recovery (T(SR)), and recovery speed to maximal oxygen saturation (Rs) were analyzed. Patients with CHD showed lower MVC (101.0 +/- 6.2 vs. 125.5 +/- 7.4 N x m, p < 0.01) and Tlim (67.0 +/- 7.5 vs. 127.5 +/- 11.1 s, p < 0.001) than control children. StO2 and BV values in both groups were similar at rest and decreased at the onset of contraction. D(mO2) was larger in patients, which reflected pronounced deoxygenation. During recovery, the patients exhibited a longer TSR (25.2 +/- 2.1 vs. 18.4 +/- 2.0 s, p < 0.05) and R(S) (64.6 +/- 5.5 vs. 42.7 +/- 4.6 s, p < 0.01) than control children. We concluded that reduced strength and endurance in patients with CHD were associated with an impairment of StO2 and BV, and a slower reoxygenation during recovery.     

Effects of oxygen on lower limb blood flow and O2 uptake during exercise in COPD

PURPOSE: To quantify the effects of acute oxygen supplementation on lower limb blood flow (QLEG), O2 delivery (QO2LEG), and O2 uptake (VO2LEG) during exercise and to determine whether the metabolic capacity of the lower limb is exhausted at peak exercise during room air breathing in patients with COPD. METHODS: Oxygen (FIO2 = 0.75) and air were randomly administered to 14 patients with COPD (FEV1: 35 +/- 2% pred, mean +/- SEM) during two symptom-limited incremental cycle exercise tests. Before exercise, a cannula was installed in a radial artery and a thermodilution catheter inserted in the right femoral vein. At each exercise step, five-breath averages of respiratory rate, tidal volume, and ventilation (VE), dyspnea and leg fatigue scores, arterial and venous blood gases, and QLEG were obtained. From these measurements, VO2LEG was calculated. RESULTS: Peak exercise capacity increased from 46 +/- 3 W in room air to 59 +/- 5 W when supplemental oxygen was used (P < 0.001). QLEG, QO2LEG, and VO2LEG were greater at peak exercise with O2 than with air (P < 0.05). During submaximal exercise, dyspnea score and VE were significantly reduced with O2 (P < 0.05), whereas QLEG, VO2LEG, and leg fatigue were similar under both experimental conditions. The improvement in peak exercise work rate correlated with the increase in peak QO2LEG (r = 0.66, P < 0.01), peak VO2LEG (r = 0.53, P < 0.05), and reduction in dyspnea at iso-exercise intensity (r = 0.56, P < 0.05). CONCLUSION: The improvement in peak exercise capacity with oxygen supplementation could be explained by the reduction in dyspnea at submaximal exercise and the increases in QO2LEG and VO2LEG, which enabled the exercising muscles to perform more external work. These data indicate that the metabolic capacity of the lower limb muscles was not exhausted at peak exercise during room air breathing in these patients with COPD.     

Cerebral cortex activity during supramaximal exhaustive exercise

AIM: The purpose of this study was to examine the effect of fatigue resulting from supramaximal dynamic exercise on cerebral cortex activity. METHODS: Five healthy male subjects (age 24.6+/-0.4 years, body weight 62.9+/-1.1 kg, height 175.3+/-1.2 cm, and maximal O2 uptake per body mass 48.4+/-1.3 ml/kg/min) participated in this study. All subjects performed at 120% of maximal oxygen uptake (VO2peak) on a cycle ergometer until reaching a state of volitional fatigue. Cerebral oxygenation was measured by near-infrared spectroscopy (NIRS) throughout the supramaximal constant exhaustive exercise. RESULTS: The mean exercise duration of the subjects was 147.2+/-3.4 s. The peak value of blood lactate concentration within 3-10 min after the exercise test was 14.4+/-0.1 mmol/l. Cerebral oxygenation (8.8+/-1.8 micromol/l) was increased significantly during the first minutes of exercise compared with the pre-exercise value (p<0.05) and cerebral oxygenation decreased with the passage of time during exercise. Cerebral oxygenation at the end of exercise decreased significantly compared with the resting value (-29.9+/-3.4 micromol/l, p<0.05). CONCLUSION: These findings suggest that the exhaustive exercise induces the decrease of cerebral function and that the fatigue resulting from dynamic exercise decreases the cerebral cortex activity.     

Reproducibility of muscle oxygen saturation

The present study evaluated the reproducibility of tissue oxygenation in relation to oxygen consumption (VO2) across cycle exercise intensities in a test-retest design. 12 subjects (25.7±2.1 years; 24.7±1.9 kg · m(-2)) twice performed an incremental bicycle exercise protocol, while tissue oxygen saturation (StO2) in the vastus lateralis muscle was monitored by a commercially available NIRS unit and VO2 determined by an open-circuit indirect calorimetric system. Coefficients of variation across rest, workloads corresponding to 25, 50 and 75% of individual maximum capacity, and maximum load were 5.8, 4.6, 6.1, 8.0, 11.0% (StO2) and 7.6, 6.0, 3.7, 3.4, 3.1% (VO2), respectively. 95 % CI of relative test-retest differences ranged from -5.6 to +5.4% at 25% load to -17.2 to +7.5% at maximum load for StO2 and from -7.3 to +7.7% at rest to -3.3 to +3.2% at maximum load for VO2. With advancing exercise intensity, within-subject variability of StO2 was augmented, whereas VO2 variability slightly attenuated. NIRS measurements at higher workloads need to be interpreted with caution.     

Influence of endurance exercise on respiratory muscle performance

PURPOSE: During high-intensity, exhaustive, constant-load exercise above 85% of maximal oxygen consumption, the diaphragm of healthy subjects can fatigue. Although a decrease in trans-diaphragmatic pressure is the most objective measure of diaphragmatic fatigue, possible extra-diaphragmatic muscle fatigue would not be detected by this method. The aim of the present study was to investigate the impact of exhaustive, constant-load cycling exercise at different intensities on global respiratory performance determined by the time to exhaustion while breathing against a constant resistance. METHODS: Ten healthy, male subjects performed an exhaustive cycling endurance test at 65, 75, 85, and 95% of peak oxygen consumption (VO2peak). Before cycling (to) as well as at 10 min (t10) and 45 min (t45) after cycling, respiratory performance was determined. RESULTS: Breathing endurance was equivalently reduced after exhaustive cycling at either 65% (8.4 +/- 4.1 min [t0] vs 3.9 +/- 2.8 min [t10]), 75% (9.9 +/- 6.1 vs 4.4 +/- 2.8 min), 85% (9.3 +/- 6.0 vs 3.8 +/- 2.9 min), or 95% VO2peak (8.5 +/- 5.1 vs 4.0 +/- 2.5 min) and, therefore, was independent of exercise intensity. CONCLUSION: This result contradicts previous findings, possibly due to the fact that extra-diaphragmatic muscles are tested in addition to the diaphragm during resistive breathing.     

Noninvasive evaluation of skeletal muscle oxidative metabolism after heart transplant

PURPOSE: The main aim of the present study was to investigate skeletal muscle oxidative metabolism in heart transplant recipients (HTR) by noninvasive tools. METHODS: Twenty male HTR (age 50.4 +/- 2.6 yr; mean +/- SE) and 17 healthy untrained age-matched controls (CTRL) performed an incremental exercise (IE) and a series of constant-load (CLE) moderate-intensity exercise tests on a cycloergometer. The following variables were determined: heart rate (HR); breath-by-breath pulmonary O2 uptake (VO2); and skeletal muscle (vastus lateralis) oxygenation indices by continuous-wave near-infrared spectroscopy. Changes in concentration of deoxygenated hemoglobin (Hb) and myoglobin (Mb) (Delta[deoxy(Hb + Mb)]), expressed as a fraction of values obtained during a transient limb ischemia, were taken as an index of skeletal muscle O2 extraction. "Peak" values were determined at exhaustion during IE. Kinetics of adjustment of variables were determined during CLE. RESULTS: VO2peak, HRpeak, and Delta[deoxy(Hb + Mb)] peak were significantly lower in HTR than in CTRL (17.1 +/- 0.7 vs 34.0 +/- 1.9 mL.kg(-1).min(-1), 133.8 +/- 3.8 vs 173.0 +/- 4.8 bpm, and 0.42 +/- 0.03 vs 0.58 +/- 0.04, respectively). In HTR, Delta[deoxy(Hb + Mb)] increase at submaximal workloads was steeper than in CTRL, suggesting an impaired O2 delivery to skeletal muscles, whereas the lower Delta[deoxy(Hb + Mb)] peak values suggest an impaired capacity of O2 extraction at peak exercise. VO2 and HR kinetics during CLE were significantly slower in HTR than in CTRL, whereas, unexpectedly, no significant differences were found for Delta[deoxy(Hb+Mb)] kinetics (mean response time: 21.3 +/- 1.1 vs 20.2 +/- 1.2 s). CONCLUSION: The findings confirm the presence of both "central" (cardiovascular) and "peripheral" (at the skeletal muscle level) impairments to oxidative metabolism in HTR. The noninvasiveness of the measurements will allow for serial evaluation of the patients, in the presence and/or absence of rehabilitation programs.     

Near infrared spectroscopy in the diagnosis of chronic exertional compartment syndrome

BACKGROUND: Patients with chronic exertional compartment syndrome (CECS) experience pain during exercise. An abnormal increase in intracompartmental pressure (ICP) leads to impaired local tissue perfusion resulting in ischemia and pain. At cessation of exercise, pain subsides. Diagnosis is confirmed through postexercise ICP. Near infrared spectroscopy (NIRS) can measure tissue oxygen saturation (StO(2)) noninvasively. HYPOTHESIS: NIRS can diagnose CECS by showing tissue deoxygenation. STUDY DESIGN: Prospective, nonrandomized clinical trial. METHOD: Volunteers completed a standardized exercise protocol. Those suspected of CECS did so preoperatively and postoperatively. StO(2) and ICP were monitored. Data were compared between volunteers and patients and prefasciotomy and postfasciotomy. RESULTS: Significant differences between the StO(2) values of volunteers and patients with CECS were found. Average peak exercise StO(2) value for those with CECS was lower than for the healthy (27 versus 56, P <.05). Patients showed more absolute and percentage change between baseline and peak exercise StO(2) (absolute: 60 versus 35, P <.05; percentage: 67 versus 38, P <.05). StO(2) values in legs with confirmed CECS returned to normal range postfasciotomy. All changes differed significantly with preoperative values. CONCLUSION: StO(2) can distinguish healthy from diseased legs. This study provides evidence supporting NIRS as a noninvasive, painless alternative to ICP in the diagnosis of CECS.     

Effects of sildenafil on exercise capacity in hypoxic normal subjects

The phosphodiesterase-5 inhibitor sildenafil has been reported to improve hypoxic exercise capacity, but the mechanisms accounting for this observation remain incompletely understood. Sixteen healthy subjects were included in a randomized, double-blind, placebo-controlled, cross-over study on the effects of 50-mg sildenafil on echocardiographic indexes of the pulmonary circulation and on cardiopulmonary cycle exercise in normoxia, in acute normobaric hypoxia (fraction of inspired O2, 0.1), and then again after 2 weeks of acclimatization at 5000 m on Mount Chimborazo (Ecuador). In normoxia, sildenafil had no effect on maximum VO2 or O2 saturation. In acute hypoxia, sildenafil increased maximum VO2 from 27 +/- 5 to 32 +/- 6 mL/min/kg and O2 saturation from 62% +/- 6% to 68% +/- 9%. In chronic hypoxia, sildenafil did not affect maximum VO2 or O2 saturation. Resting mean pulmonary artery pressure increased from 16 +/- 3 mmHg in normoxia to 28 +/- 5 mmHg in normobaric hypoxia and 32 +/- 6 mmHg in hypobaric hypoxia. Sildenafil decreased pulmonary vascular resistance by 30% to 50% in these different conditions. We conclude that sildenafil increases exercise capacity in acute normobaric hypoxia and that this is explained by improved arterial oxygenation, rather than by a decrease in right ventricular afterload.     

Use of facemask and mouthpiece to assess constant-workrate exercise capacity in COPD

PURPOSE: To compare the response to constant-workrate cycling exercise between the mouthpiece and the facemask in patients with chronic obstructive pulmonary disease (COPD). METHODS: Ten patients with COPD (FEV1: 48 +/- 14% pred, mean +/- SD) performed two symptom-limited constant-workrate cycling exercise tests at 80% of their predetermined peak exercise capacity. One test was performed using a mouthpiece and the other with a facemask, in a random order. The endurance time to constant-workrate exercise was compared between the two interfaces. VO2, VCO2, ventilation (VE), inspiratory capacity, dyspnea Borg score, and heart rate responses during exercise were also compared. RESULTS: Endurance time was similar between the two interfaces (mean difference +/- SD, 30 +/- 74 s, P = 0.23). Except for the end-exercise values, which were lower with the facemask, the VO2, VCO2, and VE responses to submaximal exercise were similar between the two interfaces. Perception of dyspnea, inspiratory capacity, and heart rate kinetics were similar during the two exercise tests. No clear preference about either interface was expressed by the patients. CONCLUSION: The mouthpiece and the facemask can be used with comparable results to determine the endurance time to constant-workrate cycling exercise in patients with COPD. Compared with the mouthpiece, the end-exercise values for VO2, VCO2, and VE were underestimated when a facemask was used. The similar responses in heart rate and symptom perception suggest that this could be due to an air leak at end-exercise with the facemask.     

Comparison of fingertip to arterial blood samples at rest and during exercise.

OBJECTIVE: The purpose was to determine whether arterialized fingertip blood-gas samples are comparable to arterial samples at rest and at exercise. DESIGN: Repeated measures, with subjects serving as their own controls. SETTING: Department of Anesthesia, Montreal General Hospital, Montreal, Quebec, Canada, (January to April 2004). PARTICIPANTS: Fifteen healthy men (age = 25 +/- 4 y; weight = 76.4 +/- 11.4 kg; height = 180.7 +/- 8.0 cm; peak oxygen uptake or VO2peak = 46.0 +/- 9.0 mL . kg . min). MAIN OUTCOME MEASURES: Arterial blood gases, metabolites, electrolytes. RESULTS: Blood sampled simultaneously from the radial artery and warmed fingertip at rest and during 2 levels of exercise (vigorous 181 W or 70% VO2peak; maximal 261 W or 100% VO2peak) on a electronically braked ergometer. Arterial partial pressure of oxygen in blood combining rest and the 2 exercise levels was on average 13.6 +/- 9.0 mm Hg higher than arterialized fingertip samples, with the largest difference occurring at rest (18.8 +/- 6.5 mm Hg; 95% CI = 15.5, 22.1) and the smallest difference occurring at the highest level of exercise (8.3 +/- 9.2 mm Hg; 95% CI = 3.6, 13.0; P < 0.05). The pattern for oxyhemoglobin saturation was the same, showing statistical differences between the sampling sites with the differences reduced at the highest exercise intensity. In contrast, there was no difference in arterial and arterialized partial pressure of carbon dioxide in blood (-1.0 +/- 1.5 mm Hg; 95% CI = -1.4, -0.6), or plasma lactate, glucose, pH, hemoglobin, and electrolytes between both sampling sites at rest or at the 2 exercise levels. CONCLUSION: Arterialized fingertip blood samples at rest and during exercise can predict arterial carbon dioxide pressure, and can predict arterial plasma lactate, glucose, pH, hemoglobin, and electrolytes; but not arterial oxyhemoglobin saturation or arterial oxygen pressure.     

The validity of physiological variables to assess training intensity in kayak athletes

It appears that training benefits are compromised if excessive training is performed at intensities that are either too low or too high. This suggests a need for accurate methods to monitor training intensity. It has been suggested that heart rate (HR) or lactate concentration ([La -]) can be used to accurately monitor training intensity. The purpose of the present study therefore, was to examine whether the relationship between HR, [La -] and intensity determined during a kayak graded exercise test (GXT) remained stable during constant-intensity kayak exercise. Sixteen trained kayak paddlers, (22 +/- 4 y, peak V.O (2) = 3.7 +/- 0.9 l x min (-1)) performed a GXT on a wind-braked kayak ergometer. They then performed a 20-min constant-load test on the kayak ergometer at a power output corresponding to their lactate inflection (LI) intensity. Eight subjects also performed a 20-min constant-load test at a power output corresponding to their lactate threshold (LT) intensity. Differences between constant-load and GXT values were determined using one-way ANOVA (p < 0.05). There were no significant differences between values for HR and V.O (2) derived from the GXT and those measured during both constant-load tests. However, while [La -] also provided a valid marker of the LI training intensity (1.8 +/- 0.3 v 2.1 +/- 0.8 mmol x l (-1)), [La -] did not provide a valid marker of the LT training intensity (3.8 +/- 0.7 v 5.1 +/- 1.4 mmol x l (-1)). These results suggest that HR, but not [La -1], is similar during both a GXT and constant-load exercise at the LT intensity.     

Is hemoglobin desaturation related to blood viscosity in athletes during exercise?

Several studies have suggested that athletes with low hemoglobin saturation during exercise may experience impaired pulmonary blood gas exchange during maximal exercise. Blood viscosity may be implicated in exercise-induced pulmonary hemorrhage in race horses. We hypothesized that blood rheology may contribute to impaired gas exchange and reduced hemoglobin saturation during exercise in humans. A group of 20 highly trained endurance athletes participated in this study, 9 with low hemoglobin saturation during exercise (Low-SpO (2) group) and 11 with normal hemoglobin saturation (High-SpO (2) group). All subjects performed a progressive exercise test conducted to V.O (2max). Venous blood was sampled at rest, 50 % V.O (2max) and maximal exercise. Blood viscosity (etab) was measured at very high shear rate (1000 s (-1)) and 37 degrees C with a falling ball viscometer. The erythrocyte rigidity coefficient, "Tk", was calculated using the Dintenfass equation. At rest, no significant difference in etab was observed between the two groups (3.00 +/- 0.08 mPa . s vs. 3.01 +/- 0.04 mPa . s for the Low-SpO (2) and High-SpO (2) group, respectively). At 50 % V.O (2max) and maximal exercise, etab was higher in Low-SpO (2) (p < 0.01). Tk decreased in High-SpO (2) (p < 0.01) but remained unchanged in the other group during testing. The greater increase in etab in the Low-SpO (2) group during exercise may therefore have been due to the lack of reduction in Tk. As suggested by previous studies, the greater increase in blood viscosity in athletes with low hemoglobin saturation may lead to vascular shear stress. Whether this could impair the blood gas barrier and result in exercise-induced hypoxemia requires further study.     

Influence of peak VO2 and muscle fiber type on the efficiency of moderate exercise

PURPOSE: The purpose of this study was to determine if %Type I fibers and/or aerobic fitness (as peak .VO(2)) would predict Delta efficiency (DeltaEff) and Delta.VO(2)/Deltawork rate (WR) for moderate (below lactate threshold 0.05). CONCLUSION: These results suggest that aerobic fitness affects the energetic response to changes in power output during moderate exercise, such that the more aerobically fit a subject, the greater the increase in oxygen cost (.VO(2)) (reduced efficiency) as work rate increases. Further, Delta.VO(2)/DeltaWR reflects the inverse of DeltaEff for moderate-intensity exercise in healthy fed subjects.     

Influence of work rate incremental rate on the exercise responses in patients with COPD

PURPOSE: The peak work rate (Wpeak) measured during a progressive stepwise exercise test is commonly used to select the target training intensity for an exercise training program. In healthy subjects, a greater Wpeak is achieved when a faster rate of increase in work rate is used, whereas VO2 peak is independent of the rate of increase in work rate. This effect might be even more pronounced in chronic obstructive pulmonary disease (COPD) patients, in whom the VO2 kinetics during exercise are slower compared with healthy subjects. METHODS: To investigate this, we studied 10 COPD patients (9 M/1 F, age: 65+/-5 yr [mean +/- SD], FEV1: 33+/-8%). They underwent, on separate days, three stepwise exercise tests on an ergocycle. For each test, increments of 5, 10, or 20 W x min(-1) were used in random order; the investigator was blinded as to which increment was used. VO2, VCO2, heart rate (HR), minute ventilation (VE), breathlessness and leg fatigue at rest, at each work rate, and at maximal capacity were obtained. RESULTS: Wpeak averaged 40+/-13, 53+/-14, and 66+/-19 W for the 5-, 10-, and 20-W protocol, respectively (P < 0.001), whereas VO2 peak was comparable at 0.96+/-0.16, 1.02+/-0.18, and 1.03+/-0.20 L x min(-1). As the rate of increase in work rate became faster, the VO2/work rate relationship shifted to the right. This is exemplified by the VO2 at 40 W, which averaged 0.98+/-0.06, 0.90+/-0.09, and 0.83+/-0.10 L x min(-1) for the 5-, 10-, and 20-W protocol, respectively (P < 0.05). Similar observations were made for the relationship between HR, VE, and symptom scores, and work rate. There was no significant differences in peak values for HR and VE, and symptoms scores. CONCLUSIONS: We conclude that the work rate incremental rate influences the Wpeak achieved, whereas the peak values for VO2, HR, VE, and symptom scores remain comparable. These findings have practical implications for the exercise evaluation of patients with COPD.     

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.     

Respiratory muscle deoxygenation and ventilatory threshold assessments using near infrared spectroscopy in children

The aim of this study was to assess respiratory muscles deoxygenation and to determine ventilatory threshold using near infrared spectroscopy (NIRS) in children during incremental cardiopulmonary exercise. Fourteen healthy children with a mean +/- SD age of 12.8 +/- 1.4 yrs performed an incremental exercise test on a cycle ergometer. NIRS was used to assess deoxygenation of the respiratory muscles. Ventilatory parameters (oxygen uptake, carbon dioxide production, and ventilation minute), power output, and tissue saturation (StO2) were measured. Ventilatory threshold was determined by the two following methods: the V-slope method which corresponds to the breakpoint in VCO2 as a function VO2 relationship (VT(V-slope)) and the NIRS method which corresponds to the point of rapid fall in StO2 (VT(nirs)). During exercise, the respiratory muscles deoxygenated as the exercise intensity increased. StO2 decrease progressively until an abrupt decrease was observed. No significant differences were observed between cardiorespiratory variables corresponding either to VT(V-slope) or to VT(nirs). The two methods showed a good agreement (data were inside the 95 % confidence interval). Likewise, a significant relationship was found between VT(V-slope) and VT(nirs) for each parameter measured (r = 0.87 to 0.94, p < 0.001). We concluded that respiratory muscles deoxygenate during incremental exercise in children and that ventilatory threshold could be determined by NIRS.     

Exercise induced arterial hypoxemia in swimmers

AIM: Exercise induced arterial hypoxemia (EIAH) is a reduction in arterial oxygenation, which may result from a drop in arterial oxygen pressure and therefore in oxygen saturation. We examined EIAH in swimmers, while till now it was known to occur in cyclists and runners. METHODS: We studied 8 male highly trained swimmers (age: 23+/-1.7; (.-)VO(2peak), 5.3+/-0.1 l/min and 8 male ex-swimmers (age: 21.5+/-0.6; (.-)VO(2peak), 3.4+/-0.3 l/min). All subjects performed 200-meter freestyle at maximum effort. Hemoglobin saturation (SaO(2)%) was measured using a finger pulse oximeter before exercise in the water in an upright position and immediately after exercise, within 5 seconds. RESULTS: Highly trained swimmers developed a statistically significant decrease in SaO(2)% (from 98.3+/-0.3 to 94+/-0.9, p= or <0.01) after exercise, while ex-swimmers did not (from 98.4+/-0.3 to 96.8+/-0.3 ns). The 4% decrease in SaO(2)% observed in highly trained swimmers can be characterized as mild EIAH. CONCLUSIONS: Our study suggests that highly trained swimmers but not ex-swimmers may develop mild EIAH after 200 meters freestyle swimming at maximum effort.