Changes in Circulating Stem and Progenitor Cell Numbers Following Acute Exercise in Healthy Human Subjects: a Systematic Review and Meta-analysis.

Despite of the increasing number of investigations on the effects of acute exercise on circulating stem and progenitor cell (SC) numbers, and in particular on respective subgroups, i.e. endothelial (ESC), hematopoietic (HSC), and mesenchymal (MSC) stem and progenitor cells, a consensus regarding mechanisms and extent of these effects is still missing. The aim of this meta-analysis was to systematically evaluate the overall-effects of acute exercise on the different SC-subgroups and investigate possible subject- and intervention-dependent factors affecting the extent of SC-mobilization in healthy humans. Trials assessing SC numbers before and at least one timepoint after acute exercise, were identified in a systematic computerized search. Compared to baseline, numbers were significantly increased for early and non-specified SCs (enSCs) until up to 0.5 h after exercise (0-5 min: +0.64 [Standardized difference in means], p < 0.001; 6-20 min: +0.42, p < 0.001; 0.5 h: +0.29, p = 0.049), for ESCs until 12-48 h after exercise (0-5 min: +0.66, p < 0.001; 6-20 min: +0.43 p < 0.001; 0.5 h: +0.43, p = 0.002; 1 h: +0.58, p = 0.001; 2 h: +0.50, p = 0.002; 3-8 h: +0.70, p < 0.001; 12-48 h: +0.38, p = 0.003) and for HSCs at 0-5 min (+ 0.47, p < 0.001) and at 3 h after exercise (+ 0.68, p < 0.001). Sex, intensity and duration of the intervention had generally no influence. The extent and kinetics of the exercise-induced mobilization of SCs differ between SC-subpopulations. However, also definitions of SC-subpopulations are non-uniform. Therefore, finding a consensus with a clear definition of cell surface markers defining ESCs, HSCs and MSCs is a first prerequisite for understanding this important topic.

Acute Exercise-Induced Circulating Haematopoietic Stem and Progenitor Cells in Cardiac Patients - A Case Series.

BACKGROUND: Exercise-induced circulating haematopoietic stem and progenitor cell (HPC) number has been discussed in the context of regeneration in heart disease patients. OBJECTIVE: The aim of this pilot study was to compare the effect of different exercise protocols usually applied in cardiac rehabilitation on the number of acute, exercise-induced HPCs, related to potential mediators, e.g. biomarkers of sympathetic and oxidative stress, and inflammation. METHODS: This is a case series comprising seven patients suffering from coronary heart disease (CHD) undertaken at the Center for Ambulant Cardiac Rehabilitation. Patients (n=6) performed two exercise modes (constant-load, CLE; high-intensity interval, HIIE) in randomised order. Venous blood was drawn before and immediately after each test to assess CD34+/CD45+ HPC number by flow cytometry and biomarkers in blood plasma. The primary outcome was the change in HPC number, the secondary outcomes were changes in sympathetic/oxidative stress and markers of inflammation. RESULTS: Both exercise modes resulted in a non-significant increase in HPC number after exercise, even when the results of both tests were combined. Overall, free norepinephrine increased significantly and was positively related to exercise-induced HPC number (r=0.70, p<0.05). Markers of sympathetic activation (fNE), oxidative stress (myeloperoxidase) and inflammation (interleukin-6) significantly increased after CLE and HIIE with no difference between tests. CONCLUSIONS: Interestingly, acute CLE and HIIE did not stimulate significant HPC mobilisation in CHD, although both exercise modes elevated circulating concentrations of sympathetic activation. Haematopoietic stem and progenitor cell mobilisation could be blunted due to disease-related bone-marrow exhaustion.

Myocardial infarction does not affect circulating haematopoietic stem and progenitor cell self-renewal ability in a rat model.

NEW FINDINGS: What is the central question of this study? Although peripheral blood haematopoietic stem and progenitor cells are potentially important in regeneration after acute myocardial infarction, their self-renewal ability in the post-acute phase has not yet been addressed. What is the main finding and its importance? In rat peripheral blood, we show that myocardial infarction does not negatively affect circulating haematopoietic stem and progenitor cell self-renewal ability 2 weeks after acute infarction, which suggests a constant regenerative potential in the myocardial infarction post-acute phase. Given the importance of peripheral blood haematopoietic stem and progenitor cells (HPCs) in post-acute regeneration after acute myocardial infarction (MI), the aim of the present study was to investigate the number and secondary replating capacity/self-renewal ability of HPCs in peripheral blood before and 2 weeks after MI. In female Lewis inbred rats (n = 9), MI was induced by ligation of the left coronary artery, and another nine underwent sham surgery, without ligation, for control purposes. Myocardial infarction was confirmed by troponin I concentrations 24 h after surgery. Peripheral blood was withdrawn and fractional shortening and ejection fraction of the left ventricle were assessed before (day 0) and 14 days after MI or sham surgery (day 14). After mononuclear cell isolation, primary and secondary functional colony-forming unit granulocyte-macrophage (CFU-GM) assays were performed in order to detect the kinetics of functional HPC colony counts and cell self-renewal ability in vitro. The CFU-GM counts and cell self-renewal ability remained unchanged (P > 0.05) in both groups at day 14, without interaction between groups. In the intervention group, higher day 0 CFU-GM counts showed a relationship to lower fractional shortening on day 14 (ρ = -0.82; P < 0.01). Myocardial infarction did not negatively affect circulating HPC self-renewal ability, which suggests a constant regenerative potential in the post-acute phase. A relationship of cardiac contractile function 14 days after MI with circulating CFU-GM counts on day 0 might imply functional colony count as a predictive factor for outcome after infarction.

[Respiratory Muscle Training: State of the Art]. / Atemmuskeltraining: State-of-the-Art.

Specific respiratory muscle training (IMT) improves the function of the inspiratory muscles. According to literature and clinical experience, there are 3 established methods: 1.) resistive load 2.) threshold load and 3.) normocapnic hyperpnea. Each training method and the associated devices have specific characteristics. Setting up an IMT should start with specific diagnostics of respiratory muscle function and be followed by detailed individual introduction to training. The aim of this review is to take a closer look at the different training methods for the most relevant indications and to discuss these results in the context of current literature. The group of neuromuscular diseases includes muscular dystrophy, spinal muscular atrophy, amyotrophic lateral sclerosis, paralysis of the phrenic nerve, and injuries to the spinal cord. Furthermore, interstitial lung diseases, sarcoidosis, left ventricular heart failure, pulmonary arterial hypertension (PAH), kyphoscoliosis and obesity are also discussed in this context. COPD, asthma, cystic fibrosis (CF) and non-CF-bronchiectasis are among the group of obstructive lung diseases. Last but not least, we summarize current knowledge on weaning from respirator in the context of physical activity.

[Influence of bodily constitution and physical activity on postural stability]. / Einfluss von Konstitution und Belastung auf die posturale Stabilität.

CONTEXT AND OBJECTIVE: In order for balance to be maintained, the postural control system must process above all visual, vestibular and proprioceptive information and translate this input into appropriate motor responses. The influence of bodily constitution and physical activity on motor responses and thus on postural stability is still unclear. To use computerized dynamic posturography (CDP) to investigate the influence of body height, body mass index (BMI), regular sporting activity and acute maximal exercise on balance. SUBJECTS AND METHODS: Eighty-four subjects completed a standardized questionnaire on their height, BMI and sporting activity. We then assessed the postural stability of the subjects. Seventeen further subjects performed a maximal exercise test on a bicycle ergometer. We used CDP and a predefined protocol to assess balance at rest, at maximal exercise and then at 5-minute intervals until recovery. RESULTS: Body height and regular physical activity did not influence balance ability. By contrast, BMI and acute physical exercise had a strong effect. Immediately after maximal exercise, postural stability deteriorated by 44 % compared to the baseline level (p < 0.017). Complete recovery occurred within only 15 minutes. CONCLUSIONS: Whereas body height and regular physical activity do not influence balance performance, a high BMI value and acute maximal exercise lead to a considerable decrease in postural stability. Our results can thus explain the increasing risk of injury after strenuous physical activity, especially in association with sports that require excellent balance.

Reliability of non-invasive cardiac output measurement in individuals with tetraplegia.

STUDY DESIGN: The study is conducted on the basis of comparative-repeated measures. OBJECTIVES: The objective of this study is to assess the reliability of non-invasive cardiac output (CO) measurements in individuals with tetraplegia (TP) at rest and during exercise using Innocor, and to test the hypothesis that CO measurements are less reliable in TP than in able-bodied (AB) individuals. SETTING: Ambulatory volunteers, Switzerland. METHODS: Nine male motor-complete TP (C5-C7) and nine pair-matched AB performed repeated CO measurements at rest and during submaximal arm-crank and wheelchair exercises in four different test sessions. Within- and between-day reliabilities were compared between TP and AB. RESULTS: Mean differences between measurements at rest (TP vs AB, within-day: 0.1±0.5 vs 0.2±0.6 l min(-1), between-day: -0.7±0.6 vs -0.1±0.8 l min(-1)), during arm-crank (TP vs AB, within-day: 0.1±0.9 vs 0.5±0.7 l min(-1), between-day: -0.3±1.1 vs 0.0±1.1 l min(-1)) and wheelchair exercises (TP vs AB, within-day: 0.3±1.2 vs -0.1±0.8 l min(-1), between-day: 0.1±1.1 vs 0.5±0.9 l min(-1)) were not significantly different between TP and AB (all P>0.05). Coefficients of variation in TP (within-day, rest: 6.8%, arm-crank: 9.6% and wheelchair: 10.8%; between-day, rest: 11.9%, arm-crank: 11.2% and wheelchair: 10.3%) and in AB (within-day, rest: 7.7%, arm crank: 6.8% and wheelchair: 6.0%; between-day, rest: 9.2%, arm crank: 8.5% and wheelchair: 8.0%) indicated acceptable reliability. CONCLUSION: In contrast to our hypothesis, we found non-invasive CO measurements using Innocor to be as reliable in TP as they are in AB. Consequently, Innocor can be recommended for repeated assessments of CO in TP within routine diagnostics or for evaluation of training progress.

Expiratory muscle fatigue impairs exercise performance.

High-intensity, exhaustive exercise may lead to inspiratory as well as expiratory muscle fatigue (EMF). Induction of inspiratory muscle fatigue (IMF) before exercise has been shown to impair subsequent exercise performance. The purpose of the present study was to determine whether induction of EMF also affects subsequent exercise performance. Twelve healthy young men performed five 12-min running tests on a 400-m track on separate days: a preliminary trial, two trials after induction of EMF, and two trials without prior muscle fatigue. Tests with and without prior EMF were performed in an alternate order, randomly starting with either type. EMF was defined as a >or=20% drop in maximal expiratory mouth pressure achieved during expiratory resistive breathing against 50% maximal expiratory mouth pressure. The average distance covered in 12 min was significantly smaller during exercise with prior EMF compared to control exercise (2872+/-256 vs. 2957+/-325 m; P=0.002). Running speed was consistently lower (0.13 m s(-1)) throughout the entire 12 min of exercise with prior EMF. A significant correlation was observed between the level of EMF (decrement in maximal expiratory mouth pressure after resistive breathing) and the reduction in running distance (r2=0.528, P=0.007). Perceived respiratory exertion was higher during the first 800 m and heart rate was lower throughout the entire test of running with prior EMF compared to control exercise (5.3+/-1.6 vs. 4.5+/-1.7 points, P=0.002; 173+/-10 vs. 178+/-7 beats min(-1), P=0.005). We conclude that EMF impairs exercise performance as previously reported for IMF.

Intraoperative direct mechanical stimulation of the anterior cruciate ligament elicits short- and medium-latency hamstring reflexes.

The anterior cruciate ligament (ACL) has not only a mechanical but also a sensorimotor function. Patients with injuries of the ACL frequently complain of knee instability despite good mechanical stabilization after surgical reconstruction. Compared with healthy subjects, their latencies of hamstring reflexes after anterior tibia translation are considerably increased. There is evidence for the existence of a reflex arc between the ACL and the hamstrings. The aim of this study was to determine if there is a direct reflex response after an isolated mechanical stimulation of the ACL in humans. In 10 patients who underwent arthroscopy, hamstring electromyographic (EMG) responses were assessed intraoperatively after applying an isolated load on the ACL. Latencies, amplitudes, and integrals of the EMG responses were analyzed. In four patients, the measurements were repeated after injection of local anesthetics into the ACL. In all subjects, responses with mean latencies of 42 +/- 4.4 (SD) ms corresponding to a medium latency response (MLR) were found. In seven subjects, they were preceded by responses with a short-latency (SLR) of 24 +/- 2.7 ms. The maximum amplitude was 8.6 +/- 7 mV, the integral 0.064 +/- 0.05 mV*s. The injection of local anesthetics reduced the amplitude by 34 +/- 12% and the integral by 50 +/- 20%. Direct mechanical stimulation of the ACL evokes considerably smaller SLRs and MLRs than anterior tibia translation during standing. It is argued that latency changes observed in patients with ACL ruptures may be rather due to changes in the sensorimotor integration of the afferent input from the knee joint than to the absence of the direct ACL reflex.

Chemoreceptive mechanisms elucidated by studies of congenital central hypoventilation syndrome.

Humans born with the condition of central hypoventilation during non-rapid eye movement sleep, termed congenital central hypoventilation syndrome (CCHS), invariably have absent or greatly diminished central hypercapnic ventilatory chemosensitivity. Genetic and pathological studies of CCHS may enable identification of the genes or areas of the central nervous system involved in the syndrome and thus implicated in central hypercapnic ventilatory chemosensitivity. Functional studies of CCHS permit a more quantitative assessment of the importance of ventilatory chemosensitivity in the regulation of breathing during wakefulness and sleep. The experimental evidence suggests that central hypercapnic ventilatory chemosensitivity is crucial in regulating alveolar ventilation during non-rapid eye movement sleep but not during rapid eye movement sleep or during many of the behaviors occurring during wakefulness. Presumably, other neural drives to breathe supervene to enable adequate ventilation. However, although physiological studies in CCHS subjects have been greatly instructive, their accurate interpretation will have to await future determination of the potential genetic and/or neuroanatomic basis of the syndrome.

Respiratory muscle training increases cycling endurance without affecting cardiovascular responses to exercise.

We tested whether the increased cycling endurance observed after respiratory muscle training (RMT) in healthy sedentary humans was associated with a training-induced increase in cardiac stroke volume (SV) during exercise, similar to the known effect of endurance training. Thirteen subjects underwent RMT by normocapnic hyperpnea, nine underwent aerobic endurance training (cycling and/or running) and fifteen served as non-training controls. Training comprised 40 sessions performed within 15 weeks, where each session lasted 30 min. RMT increased cycling endurance at 70% maximal aerobic power (Wmax) by 24% [mean (SD) 35.6 (11.9) min vs 44.2 (17.6) min, P < 0.05], but SV at 60% Wmax was unchanged [94 (21) ml vs 93 (20) ml]. Aerobic endurance training increased both SV [89 (24) ml vs 104 (32) ml, P < 0.01] and cycling endurance [37.4 (12.8) min vs 52.6 (16.9) min, P < 0.01]. In the control group, no changes were observed in any of these variables. It is concluded that the increased cycling endurance that is observed after RMT is not due to cardiovascular adaptations, and that the results provide evidence for the role of the respiratory system as an exercise-limiting factor.

Respiratory muscle endurance training in humans increases cycling endurance without affecting blood gas concentrations.

Isolated respiratory muscle endurance training (RMT) can prolong constant-intensity cycling performance. We tested whether RMT affects O2 supply during exercise, i.e. whether the partial pressure of oxygen in arterial blood (Pa,O2) and/or its oxygen saturation (SaO2) are higher during exercise after RMT than before. A group of 28 sedentary subjects were randomly assigned to either an RMT (n = 13) or a control group (n = 15). The RMT consisted of 40x30 min sessions of normocapnic hyperpnoea. The control group did not perform any training. Breathing and cycling endurance time as well as PaO2 and SaO2 during cycling at a constant intensity of 70% maximum power output were measured before and after the RMT or the control period. Mean breathing endurance increased significantly after RMT compared to control [RMT 5.2 (SD 2.9) vs 38.1 (SD 6.8) min, control 6.5 (SD 5.7) vs 6.4 (SD 7.6) min; P < 0.01], as did mean cycling endurance [RMT 35.6 (SD 11.9) vs 44.0 (SD 17.2) min, control 32.8 (SD 11.6) vs 31.4 (SD 14.4) min; P<0.05]. The RMT did not affect PaO2 which ranged from 11.6 to 12.3 kPa (87-92 mmHg), and SaO2 which ranged from 96% to 98% throughout all tests. In conclusion, RMT substantially increased breathing and cycling endurance in sedentary subjects. These changes, however, cannot be attributed to increased O2 supply, as neither PaO2 nor SaO2 were increased during exercise after RMT.

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.

Respiratory muscle endurance training in chronic obstructive pulmonary disease: impact on exercise capacity, dyspnea, and quality of life.

Inspiratory muscle training may have beneficial effects in certain patients with chronic obstructive pulmonary disease (COPD). Because of the lack of a home training device, normocapnic hyperpnea has rarely been used as a training mode for patients with COPD, and is generally considered unsuitable to large-scale application. To study the effects of hyperpnea training, we randomized 30 patients with COPD and ventilatory limitation to respiratory muscle training (RMT; n = 15) with a new portable device or to breathing exercises with an incentive spirometer (controls; n = 15). Both groups trained twice daily for 15 min for 5 d per week for 8 wk. Training-induced changes were significantly greater in the RMT than in the control group for the following variables: respiratory muscle endurance measured through sustained ventilation (+825 +/- 170 s [mean +/- SEM] versus -27 +/- 61 s, p < 0.001), inspiratory muscle endurance measured through incremental inspiratory threshold loading (+58 +/- 10 g versus +21.7 +/- 9.5 g, p = 0.016), maximal expiratory pressure (+20 +/- 7 cm H(2)O versus -6 +/- 6 cm H(2)O, p = 0.009), 6-min walking distance (+58 +/- 11 m versus +11 +/- 11 m, p = 0.002), V O(2peak) (+2.5 +/- 0.6 ml/kg/min versus -0.3 +/- 0.9 ml/kg/min, p = 0.015), and the SF-12 physical component score (+9.9 +/- 2.7 versus +1.8 +/- 2.4, p = 0.03). Changes in dyspnea, maximal inspiratory pressure, treadmill endurance, and the SF-12 mental component score did not differ significantly between the RMT and control groups. In conclusion, home-based respiratory muscle endurance training with the new device used in this study is feasible and has beneficial effects in subjects with COPD and ventilatory limitation.

Endogenous circadian rhythm of pulmonary function in healthy humans.

Numerous studies have demonstrated a diurnal rhythm in indices of pulmonary function in both healthy subjects and subjects with asthma, with minima occurring during the night. To determine whether such diurnal changes are caused by an endogenous circadian rhythm or by diurnal alterations in behavior or the environment, we measured indices of pulmonary function throughout a "constant routine" protocol designed to unmask underlying circadian rhythms. After two acclimation days in the laboratory, 10 healthy adults maintained relaxed wakefulness in a semirecumbent posture in a constant environment with low light (10 lux) for 41 h. Measurements of FEV(1), FEVC, PEF, blood cortisol, and core body temperature (CBT) were performed every 2 h. Results of cosinor analysis of group data aligned to CBT circadian minimum revealed significant circadian variations in FEV(1) and FEV(1)/FEVC, cortisol, and CBT, and lack of significant circadian variations in FEVC and PEF. The ranges (peak to trough) of mean circadian changes in spirometric variables were 2. 0-3.2% of the mesor. The circadian minima of all variables occurred within the usual sleep period (although subjects remained awake). Because of differences in phase relationships between CBT and pulmonary function among subjects, the circadian rhythms within subjects were generally larger than the group average circadian changes, being significant for FEV(1)/FEVC in 5 of 10 subjects and for PEF in 6 of 10 subjects. Sleep deprivation (24 h) failed to cause a significant change in any pulmonary function variable (when controlled for circadian phase). Thus, endogenous circadian rhythms contribute to diurnal changes in pulmonary function in healthy subjects.

An endogenous circadian rhythm of respiratory control in humans.

Many physiological and behavioural functions have circadian rhythms - endogenous oscillations with a period of approximately 24 h that can occur even in the absence of sleep. We determined whether there is an endogenous circadian rhythm in breathing, metabolism and ventilatory chemosensitivity in humans. Ten healthy, adult males were studied throughout 4 days in a stable laboratory environment. After two initial baseline days (16 h wakefulness plus 8 h sleep) that served to achieve a steady state, subjects were studied under constant behavioural and environmental conditions throughout 41 h of wakefulness. Ventilation, metabolism and the magnitude of the hypercapnic ventilatory response (HCVR) were measured every 2 h. Individuals' data were aligned according to circadian phase (core body temperature minimum; CBTmin) and averaged. In the group average data, there was a significant and large amplitude circadian variation in HCVR slope (average of +/-0.4 l min-1 mmHg-1; corresponding to +/-12.1 % of 24 h mean), and a smaller amplitude rhythm in the HCVR x-axis intercept (average of +/-1.1 mmHg; +/-2.1 % of 24 h mean). Despite a significant circadian variation in metabolism (+/-3.2 % of 24 h mean), there were no detectable rhythms in tidal volume, respiratory frequency or ventilation. This small discrepancy between metabolism and ventilation led to a small but significant circadian variation in end-tidal PCO2 (PET,CO2; +/-0.6 mmHg; +/-1.5 % of 24 h mean). The circadian minima of the group-averaged respiratory variables occurred 6-8 h earlier than CBTmin, suggesting that endogenous changes in CBT across the circadian cycle have less of an effect on respiration than equivalent experimentally induced changes in CBT. Throughout these circadian changes, there were no correlations between HCVR parameters (slope or x-axis intercept) and either resting ventilation or resting PET,CO2. This suggests that ventilation and PET,CO2 are little influenced by central chemosensory respiratory control in awake humans even when at rest under constant environmental and behavioural conditions. The characteristic change in PET,CO2 during non-rapid eye movement sleep was shown to be independent of circadian variations in PET,CO2, and probably reflects a change from predominantly behavioural to predominantly chemosensory respiratory control. This study has documented the existence and magnitude of circadian variations in respiration and respiratory control in awake humans for the first time under constant behavioural and environmental conditions. These results provide unique insights into respiratory control in awake humans, and highlight the importance of considering the phase of the circadian cycle in studies of respiratory control.

Sleep deprivation per se does not decrease the hypercapnic ventilatory response in humans.

Several studies have found that sleep deprivation reduces the hypercapnic ventilatory response (HCVR). Such results may have been affected by uncontrolled activities or environmental influences during the sleep deprivation period. The current study determined the "pure" effect of sleep deprivation on respiratory control under strictly controlled behavioral and environmental conditions. After 2 d of acclimation in the laboratory, 10 subjects maintained wakefulness (confirmed by EEG), a constant semirecumbent posture, ate regular small meals, had constant interaction with experimenters, and stayed in an environment with constant low light (10 lux) and constant room temperature for 41 consecutive hours. Measurements of HCVR, resting ventilation, V O(2) and V CO(2) were performed every 2 h. Comparisons were made of six pairs of measurements, with each pair separated by 24 h of sleep deprivation. None of the respiratory variables changed significantly with 24 h of sleep deprivation. Mean HCVR increased by 17% with sleep deprivation (3.12 versus 3.54 L x min(-1) x mm Hg(-1); not significant). These results show that sleep deprivation per se does not reduce the sensitivity of central chemoreceptors nor change resting ventilation or metabolism. The reduced HCVR after sleep loss found in previous studies may have been affected by uncontrolled activities or environmental influences during sleep deprivation periods.

Breathing pattern and exercise endurance time after exhausting cycling or breathing.

The aim of the present study was to investigate whether the changes in breathing pattern that frequently occur towards the end of exhaustive exercise (i.e., increased breathing frequency, fb, with or without decreased tidal volume) may be caused by the respiratory work itself rather than by leg muscle work. Eight healthy, trained subjects performed the following three sessions in random order: (A) two sequential cycling endurance tests at 78% peak O2 consumption (VO2peak) to exhaustion (A1, A2); (B) isolated, isocapnic hyperpnea (B1) at a minute ventilation (VE) and an exercise duration similar to that attained during a preliminary cycling endurance test at 78% VO2peak, followed by a cycling endurance test at 78% VO2peak (B2); (C) isolated, isocapnic hyperpnea (C1) at a VE at least 20% higher than that of the preliminary cycling test and the same exercise duration as the preliminary cycling test, followed by a cycling endurance test at 78% VO2peak (C2). Neither of the two isocapnic hyperventilation tasks (B1 or C1) affected either the breathing pattern or the endurance times of the subsequent cycling tests. Only cycling test A2 was significantly shorter [mean (SD) 26.5 (8.3) min] than tests A1 [41.0(9.0) min], B2 [41.9 (6.0) min], and C2 [42.0 (7.5) min]. In addition, compared to test A1, only the breathing pattern of test A2 was significantly different [i.e., VE: + 10.5 (7.6) 1 min(-1), and fb: + 12.1 (8.5) breaths min(-1)], in contrast to the breathing patterns of cycling tests B2 [VE: -2.5 (6.2) 1 min(-1), f(b): +0.2 (3.6) breaths min(-1)] and C2 [VE: -3.0 (7.0) 1 min(-1), fb: +0.6 (6.1) breaths min(-1)]. In summary, these results suggest that the changes in breathing pattern that occur towards the end of an exhaustive exercise test are a result of changes in the leg muscles rather than in the respiratory muscles themselves.

Noninvasive measurement of respiratory muscle performance after exhaustive endurance exercise.

The use of noninvasive techniques to measure respiratory muscle performance after different types of endurance exercise has not been entirely successful, as the results have not consistently indicated diminished performance for similar types of exercise. The aim of the present study was 1) to compare different, noninvasive methods to assess respiratory muscle performance before and after an exhaustive cycling endurance test (which has previously been shown to induce diaphragmatic fatigue) and 2) to determine which of the tests best reflect published results of measurements of diaphragmatic fatigue. Twelve healthy subjects participated in the study and performed three different test series in a random order on three different days. These tests were performed before, and 5, 40 and 75 min after an exhausting task (a cycling endurance run at 85% of maximal oxygen uptake (V'O2,max)). The tests of the three test series were 1) breathing against a constant inspiratory resistance to task failure, 2) determination of 12-min sustained ventilatory capacity, and 3) spirometric and maximal inspiratory and expiratory mouth pressure measurements. The only measurement that was affected by exhaustive cycling was the time to task failure breathing against inspiratory resistance. It was significantly reduced from (mean+/-sD) 364+/-88 s before exercise to 219+/-122 s at 5 min after cessation of exercise. It is concluded that the constant-load resistive breathing test to task failure is the only noninvasive respiratory muscle performance test evaluated in this study which shows a decrease in respiratory muscle performance after exhaustive endurance exercise.