Effect of chest wall vibration on breathlessness in normal subjects

This study evaluated the effect of chest wall vibration (115 Hz) on breathlessness. Breathlessness was induced in normal subjects by a combination of hypercapnia and an inspiratory resistive load; both minute ventilation and end-tidal CO2 were kept constant. Cross-modality matching was used to rate breathlessness. Ratings during intercostal vibration were expressed as a percentage of ratings during the control condition (either deltoid vibration or no vibration). To evaluate their potential contribution to any changes in breathlessness, we assessed several aspects of ventilation, including chest wall configuration, functional residual capacity (FRC), and the ventilatory response to steady-state hypercapnia. Intercostal vibration reduced breathlessness ratings by 6.5 +/- 5.7% compared with deltoid vibration (P less than 0.05) and by 7.0 +/- 8.3% compared with no vibration (P less than 0.05). The reduction in breathlessness was accompanied by either no change or negligible change in minute ventilation, tidal volume, frequency, duty cycle, compartmental ventilation, FRC, and the steady-state hypercapnic response. We conclude that chest wall vibration reduces breathlessness and speculate that it may do so through stimulation of receptors in the chest wall.     

Influence of vestibular activation on respiration in humans

The purpose of this study was to determine the effects of the semicircular canals and otolith organs on respiration in humans. On the basis of animal studies, we hypothesized that vestibular activation would elicit a vestibulorespiratory reflex. To test this hypothesis, respiratory measures, arterial blood pressure, and heart rate were measured during engagement of semicircular canals and/or otolith organs. Dynamic upright pitch and roll (15 cycles/min), which activate the otolith organs and semicircular canals, increased respiratory rate (Delta2 +/- 1 and Delta3 +/- 1 breaths/min, respectively; P < 0.05). Dynamic yaw and lateral pitch (15 cycles/min), which activate the semicircular canals, increased respiration similarly (Delta3 +/- 1 and Delta2 +/- 1, respectively; P < 0.05). Dynamic chair rotation (15 cycles/min), which mimics dynamic yaw but eliminates neck muscle afferent, increased respiration (Delta3 +/- 1; P < 0.05) comparable to dynamic yaw (15 cycles/min). Increases in respiratory rate were graded as greater responses occurred during upright (Delta5 +/- 2 breaths/min) and lateral pitch (Delta4 +/- 1) and roll (Delta5 +/- 1) performed at 30 cycles/min. Increases in breathing frequency resulted in increases in minute ventilation during most interventions. Static head-down rotation, which activates otolith organs, did not alter respiratory rate (Delta1 +/- 1 breaths/min). Collectively, these data indicate that semicircular canals, but not otolith organs or neck muscle afferents, mediate increased ventilation in humans and support the concept that vestibular activation alters respiration in humans.     

Effects of acute exposure to high altitude on ventilatory drive and respiratory pattern

To assess changes in ventilatory regulation in terms of central drive and timing, on exposure to high altitude, and the effects of induced hyperoxia at high altitude, six healthy normal lowland subjects (mean age 19.5 +/- 1.64 yr) were studied at low altitude (518 m) and on the first 4 days at high altitude (3,940 m). The progressive increase in resting expired minute ventilation (VE; control mean 9.94 +/- 1.78 to 14.25 +/- 2.67 l/min on day 3, P less than 0.005) on exposure to high altitude was primarily due to a significant increase in respiratory frequency (f; control mean 15.6 +/- 3.5 breaths/min to 23.8 +/- 6.2 breaths/min on day 3, P less than 0.01) with no significant change in tidal volume (VT). The increase in f was due to significant decreases in both inspiratory (TI) and expiratory (TE) time per breath; the ratio of TI to TE increased significantly (control mean 0.40 +/- 0.08 to 0.57 +/- 0.14, P less than 0.025). Mouth occlusion pressure did not change significantly, nor did the ratio of VE to mouth occlusion pressure. The acute induction of hyperoxia for 10 min at high altitude did not significantly alter VE or the ventilatory pattern. These results indicate that acute exposure to high altitude in normal lowlanders causes an increase in VE primarily by an alteration in central breath timing, with no change in respiratory drive. The acute relief of high altitude hypoxia for 10 min has no effect on the increased VE or ventilatory pattern.     

Influence of lung volume on oxygen cost of resistive breathing

We examined the relationship between the O2 cost of breathing (VO2 resp) and lung volume at constant load, ventilation, work rate, and pressure-time product in five trained normal subjects breathing through an inspiratory resistance at functional residual capacity (FRC) and when lung volume (VL) was increased to 37 +/- 2% (mean +/- SE) of inspiratory capacity (high VL). High VL was maintained using continuous positive airway pressure of 9 +/- 2 cmH2O and with the subjects coached to relax during expiration to minimize respiratory muscle activity. Six paired runs were performed in each subject at constant tidal volume (0.62 +/- 0.2 liters), frequency (23 +/- 1 breaths/min), inspiratory flow rate (0.45 +/- 0.1 l/s), and inspiratory muscle pressure (45 +/- 2% of maximum static pressure at FRC). VO2 resp increased from 109 +/- 15 ml/min at FRC by 41 +/- 11% at high VL (P less than 0.05). Thus the efficiency of breathing at high VL (3.9 +/- 0.2%) was less than that at FRC (5.2 +/- 0.3%, P less than 0.01). The decrease in inspiratory muscle efficiency at high VL may be due to changes in mechanical coupling, in the pattern of recruitment of the respiratory muscles, or in the intrinsic properties of the inspiratory muscles at shorter length. When the work of breathing at high VL was normalized for the decrease in maximum inspiratory muscle pressure with VL, efficiency at high VL (5.2 +/- 0.3%) did not differ from that at FRC (P less than 0.7), suggesting that the fall in efficiency may have been related to the fall in inspiratory muscle strength. During acute hyperinflation the decreased efficiency contributes to the increased O2 cost of breathing and may contribute to the diminished inspiratory muscle endurance.     

Increased vasoconstriction predisposes to hyperpnea and postural faint

Our prior studies indicated that postural fainting relates to splanchnic hypervolemia and thoracic hypovolemia during orthostasis. We hypothesized that thoracic hypovolemia causes excessive sympathetic activation, increased respiratory tidal volume, and fainting involving the pulmonary stretch reflex. We studied 18 patients 13-21 yr old, 11 who fainted within 10 min of upright tilt (fainters) and 7 healthy control subjects. We measured continuous blood pressure and heart rate, respiration by inductance plethysmography, end-tidal carbon dioxide (ET(CO(2))) by capnography, and regional blood flows and blood volumes using impedance plethysmography, and we calculated arterial resistance with patients supine and during 70 degrees upright tilt. Splanchnic resistance decreased until faint in fainters (44 +/- 8 to 21 +/- 2 mmHg.l(-1).min(-1)) but increased in control subjects (47 +/- 5 to 53 +/- 4 mmHg.l(-1).min(-1)). Percent change in splanchnic blood volume increased (7.5 +/- 1.0 vs. 3.0 +/- 11.5%, P < 0.05) after the onset of tilt. Upright tilt initially significantly increased thoracic, pelvic, and leg resistance in fainters, which subsequently decreased until faint. In fainters but not control subjects, normalized tidal volume (1 +/- 0.1 to 2.6 +/- 0.2, P < 0.05) and normalized minute ventilation increased throughout tilt (1 +/- 0.2 to 2.1 +/- 0.5, P < 0.05), whereas respiratory rate decreased (19 +/- 1 to 15 +/- 1 breaths/min, P < 0.05). Maximum tidal volume occurred just before fainting. The increase in minute ventilation was inversely proportionate to the decrease in ET(CO(2)). Our data suggest that excessive splanchnic pooling and thoracic hypovolemia result in increased peripheral resistance and hyperpnea in simple postural faint. Hyperpnea and pulmonary stretch may contribute to the sympathoinhibition that occurs at the time of faint.     

A vagally mediated response to metabolic acidosis in anesthetized rabbits

Pentobarbital sodium-anesthetized rabbits received 10-min infusions of acetic, lactic, or propionic acid delivered via a catheter to the right atrium at a rate of 1 mmol/min (n = 14). Arterial [H+] increased by 35.8 +/- 7.6 (SD) nmol/l, a decrease in pH of 0.27 +/- 0.04. By the end of the infusion period respiratory frequency (f), tidal volume (VT), and minute ventilation (V) had increased by 15.5 +/- 6.2 breaths/min, 7.3 +/- 2.7 ml, and 0.86 +/- 0.34 l/min, respectively. Arterial PCO2 (PaCO2) increased initially, but isocapnia was established during the latter half of the infusion (delta PaCO2 = 0.4 +/- 2.0 Torr). Bilateral cervical vagotomy eliminated the f response to acid infusions (n = 9, delta f = 0.6 +/- 2.4 breaths/min). The increase in VT (12.6 +/- 3.1 ml) was greater, but that in V (0.39 +/- 0.11 l/min) was less than in intact animals (P less than 0.05). PaCO2 remained elevated throughout the infusion (delta PaCO2 = 5.5 +/- 2.6 Torr), resulting in a greater rise in arterial [H+] (delta[H+]a = 53.6 +/- 6.6 nmol/l, delta pHa = -0.37 +/- 0.04). It is concluded that vagal afferents play a role in the f response to acute metabolic acidosis in rabbits.     

Respiratory pattern changes produced by intercostal muscle/rib vibration

Large-amplitude vibration of the intercostal muscles/ribs has an inhibitory effect on inspiratory motor output. This effect has been attributed, in part, to the stimulation of intercostal muscle tendon organs. Intercostal muscle/rib vibration can also produce a decrease or increase in respiratory frequency. Studies were conducted 1) to determine whether, in addition to intercostal tendon organs, costovertebral joint mechanoreceptors (CVJR's) contribute to the inspiratory inhibitory effect of intercostal muscle/rib vibration (IMV) and 2) to explain the different respiratory frequency responses to IMV previously reported. Phrenic (C5) activity was monitored in paralyzed thoracotomized, artificially ventilated cats. Vibration (125 Hz) at amplitudes greater than 1,200 micron of one T6 intercostal space in decerebrated vagotomized rats reduced phrenic activity. This response was still present but weaker in some animals after denervation of the T6 intercostal muscles. Subsequent denervation of the T6 CVJR's by dorsal root sections eliminated this effect. Respiratory frequency decreased during simultaneous vibration (greater than 1,200 micron) of the T5 and T7 intercostal spaces in vagotomized cats. Respiratory frequency increased during IMV of two intercostal spaces (greater than 1,300 micron) in vagal intact cats. The use of different anesthetics (pentobarbital, allobarbital) did not alter these results. We conclude that CVJR's may contribute to the inhibitory effect of IMV on medullary inspiratory activity. The presence or absence of pulmonary vagal afferents can account for the different respiratory frequency responses to IMV, and different anesthetics did not influence these results.     

Ventilatory response to hypoxia in unanesthetized newborn kittens

We studied the ventilatory response to hypoxia in 11 unanesthetized newborn kittens (n = 54) between 2 and 36 days of age by use of a flow-through system. During quiet sleep, with a decrease in inspired O2 fraction from 21 to 10%, minute ventilation increased from 0.828 +/- 0.029 to 1.166 +/- 0.047 l.min-1.kg-1 (P less than 0.001) and then decreased to 0.929 +/- 0.043 by 10 min of hypoxia. The late decrease in ventilation during hypoxia was related to a decrease in tidal volume (P less than 0.001). Respiratory frequency increased from 47 +/- 1 to 56 +/- 2 breaths/min, and integrated diaphragmatic activity increased from 14.9 +/- 0.9 to 20.2 +/- 1.4 arbitrary units; both remained elevated during hypoxia (P less than 0.001). Younger kittens (less than 10 days) had a greater decrease in ventilation than older kittens. These results suggest that the late decrease in ventilation during hypoxia in the newborn kitten is not central but is due to a peripheral mechanism located in the lungs or respiratory pump and affecting tidal volume primarily. We speculate that either pulmonary bronchoconstriction or mechanical uncoupling of diaphragm and chest wall may be involved.     

Effects of changes in inspiratory muscle strength on the sensation of respiratory force

The sensation of respiratory muscle force was compared in seven normal subjects before and after inspiratory muscle strength training. Subjects performed 20 sustained maximal inspiratory maneuvers daily for 6-18 wk. Maximal inspiratory pressures (MIP) increased from 124 +/- 10 to 187 +/- 9 (SE) cmH2O (P less than 0.005). Exponents of the power function relationships between mouth pressure (Pm) and the intensity of the sensation of force, corrected for inspiratory duration, during magnitude scaling of resistive and elastic ventilatory loads were the same before and after training (P greater than 0.05). However, absolute sensation intensity (S) during resistive and elastic loading was reduced significantly after strength training but returned toward baseline levels greater than or equal to 8 wk after the cessation of training when the MIP had fallen to 150 +/- 5 cmH2O. The absolute S at a given Pm during ventilatory loading changed inversely with changes in MIP (P less than 0.001). Furthermore the relationship between absolute S and Pm expressed as a proportion of the MIP (Pm/MIP) was constant over testing periods. These results suggest that the sensation of respiratory muscle force reflects the proportion of the maximum force utilized in breathing and may be based on the level of respiratory motor command signals.     

Sustained isocapnic hypoxia suppresses the perception of the magnitude of inspiratory resistive loads.

The sensation of increased respiratory resistance or effort is likely to be important for the initiation of alerting or arousal responses, particularly in sleep. Hypoxia, through its central nervous system-depressant effects, may decrease the perceived magnitude of respiratory loads. To examine this, we measured the effect of isocapnic hypoxia on the ability of 10 normal, awake males (mean age = 24.0 +/- 1.8 yr) to magnitude-scale five externally applied inspiratory resistive loads (mean values from 7.5 to 54.4 cmH(2)O. l(-1). s). Each subject scaled the loads during 37 min of isocapnic hypoxia (inspired O(2) fraction = 0.09, arterial O(2) saturation of approximately 80%) and during 37 min of normoxia, using the method of open magnitude numerical scaling. Results were normalized by modulus equalization to allow between-subject comparisons. With the use of peak inspiratory pressure (PIP) as the measure of load stimulus magnitude, the perception of load magnitude (Psi) increased linearly with load and, averaged for all loaded breaths, was significantly lower during hypoxia than during normoxia (20.1 +/- 0.9 and 23.9 +/- 1.3 arbitrary units, respectively; P = 0. 048). Psi declined with time during hypoxia (P = 0.007) but not during normoxia (P = 0.361). Our result is remarkable because PIP was higher at all times during hypoxia than during normoxia, and previous studies have shown that an elevation in PIP results in increased Psi. We conclude that sustained isocapnic hypoxia causes a progressive suppression of the perception of the magnitude of inspiratory resistive loads in normal subjects and could, therefore, impair alerting or arousal responses to respiratory loading.     

Reversal by tolazoline hydrochloride of xylazine hydrochloride-ketamine hydrochloride immobilizations in free-ranging desert mule deer

We captured 10 free-ranging desert mule deer (Odocoileus hemionus crooki) (five males and five females) by net-gun from a helicopter and immobilized them with xylazine hydrochloride (HCl) (100 mg) and ketamine HCl (300 to 400 mg) injected intramuscularly. Arousal and ambulation times were 13.9 +/- 4.2 and 14.3 +/- 4.2 min in eight deer injected intravenously with tolazoline HCl (3.0 mg/kg). We observed a curvilinear relationship (R = 0.50, P less than 0.01) between rectal temperature and time after induction of anesthesia. Mean peak temperature (41.4 C) occurred at 23.7 +/- 3.2 min postinduction and was greater (P less than 0.01) than the mean temperature measured initially (40.8 C). Heart and respiratory rates (108 beats/min and 75 breaths/min) were elevated prior to immobilization. Mean heart rate increased (P less than 0.05) from 90 +/- 9 beats/min in anesthetized deer to 120 +/- 13 beats/min after tolazoline HCl injection. A 20% capture-related mortality rate suggests this combination of physical and chemical capture has serious limitations. Captive deer permitted to recover from xylazine HCl-ketamine HCl immobilization without a reversal agent were able to walk in 290 +/- 79 min.     

Sound Waves Effectively Assist Tobramycin in Elimination of Pseudomonas aeruginosa Biofilms In vitro

Microbial biofilms are highly refractory to antimicrobials. The aim of this study was to investigate the use of low-frequency vibration therapy (20–20 kHz) on antibiotic-mediated Pseudomonas aeruginosa biofilm eradication. In screening studies, low-frequency vibrations were applied on model biofilm compositions to identify conditions in which surface standing waves were observed. Alginate surface tension and viscosity were also measured. The effect of vibration on P. aeruginosa biofilms was studied using a standard biofilm assay. Subminimal inhibitory concentrations (sub-MIC) of tobramycin (5 μg/ml) were added to biofilms 3 h prior, during, and immediately after vibration and quantitatively assessed by (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) reduction assay (XTT) and, qualitatively, by confocal laser scanning microscopy (CLSM). The standing waves occurred at frequencies <1,000 Hz. Biofilms vibrated without sub-MIC tobramycin showed a significantly reduced metabolism compared to untreated controls (p < 0.05). Biofilms treated with tobramycin and vibrated simultaneously (450, 530, 610, and 650 Hz), or vibrated (450 and 650 Hz) then treated with tobramycin subsequently, or vibrated (610Hz, 650Hz) after 3 h of tobramycin treatment showed significantly lower metabolism compared to P. aeruginosa biofilm treated with tobramycin alone (p < 0.05). CLSM imaging further confirmed these findings. Low frequency vibrations assisted tobramycin in killing P. aeruginosa biofilms at sub-MIC. Thus, sound waves together with antibiotics are a promising approach in eliminating pathogenic biofilms.KEY WORDS: alginate, biofilm, Pseudomonas, tobramycin, vibration     

Temporal association of nitric oxide levels and airflow in asthma after whole lung allergen challenge.

Exhaled nitric oxide (NO) levels are high in asthmatic subjects and increase with exacerbations. We hypothesized that higher levels of NO observed during asthma exacerbations are due to increased synthesis of NO. Exhaled NO and peak flows were measured in 11 asthmatic and 9 healthy control subjects before and after experimental asthmatic response induced by whole lung allergen challenge. Baseline peak flows of asthmatics were significantly lower than controls and decreased significantly immediately after challenge (P = 0.004). NO was measured by collecting exhaled breaths without breath hold (NO0) and after a 15-s breath hold (NO15). The rate of NO accumulation over time [parts/billion per second (ppb/s)] was calculated by DeltaNO/Deltat = (NO15 - NO0)/15, where Delta denotes a change and t is time. The NO accumulation rates in asthmatic and control subjects were similar at baseline; however, NO accumulation at 24 h increased threefold from baseline in asthmatic compared with control subjects (asthmatic subjects, 0.6 +/- 0.2 ppb/s; control subjects, 0.2 +/- 0.1 ppb/s; P = 0.01). Our study suggests that increased NO during an asthma exacerbation is due to increased synthesis, perhaps by increased expression of NO synthases.     

Control of breathing in the echidna (Tachyglossus aculeatus) during hibernation

Resting non-hibernating echidnas are characterised by low metabolic rates, but also have a very low respiratory frequency and a variable respiratory minute volume, often resulting in low levels of arterial O(2) and high CO(2). As the echidna lies at one physiological extreme among the hibernators, in terms of its large size and low metabolism and ventilatory requirement when not hibernating, a study of control of breathing during hibernation in echidnas should provide a useful test of the generality of various models. We used non-invasive techniques to study breathing patterns and the control of ventilation in 6 echidnas. Hibernating echidnas (T(b) range 7-10 degrees C) showed episodic breathing with bursts of breaths (average 36+/-16 breaths in 24+/-5 min) followed by a period of apnea (76+/-17 min) then a series (8+/-4) of slow breaths at 14+/-1 min intervals leading up to the next burst. Increasing CO(2) levels in the inspired air increased the number of breaths in a burst, eventually leading to continuous breathing. Inter burst breaths were controlled by O(2): hypoxia increased inter burst breaths, and decreased burst length, while hyperoxia abolished inter burst breaths and increased the apneic period. Overall, while CO(2) was a strong respiratory stimulus in hibernating echidnas, O(2) had little effect on total ventilation, but did have a strong effect on the breathing pattern.     

Breathlessness during exercise with and without resistive loading

The purpose of this study was to quantify the intensity of breathlessness associated with exercise and respiratory resistive loading, with the specific purpose of isolating the quantitative contributions of inspiratory pressure, length, velocity, and frequency of inspiratory muscle shortening and duty cycle to breathlessness. The intensity of inspiratory pressure was quantified by measurement of estimated esophageal pressure (Pes = pressure at the mouth plus lung pressure), the extent of shortening by tidal volume (VT), and the velocity of shortening by inspiratory flow rate (VI). Six normal subjects underwent five incremental (100 kpm X min-1 X min-1) exercise tests on a cycle ergometer to maximum capacity. The first and last test were unloaded and the intervening tests were performed with external added resistances of 33, 57, and 73 cm H2O X l-1 X s in random order. The resistances were selected to provide a range of pressures, tidal volumes, flow rates, and patterns of breathing. At rest and at the end of each minute during exercise the subjects estimated the intensity of breathlessness (psi) by selecting a number ranging from 0 to 10 (Borg rating scale, 0 indicating no appreciable breathlessness and 10 the maximum tolerable sensation). Breathlessness was significantly and independently related to Pes (P less than 0.0001), VI (P less than 0.0001), frequency of breathing (fb) (P less than 0.01), and duty cycle [ratio of inspiratory duration to total breath duration (TI/TT)] (P less than 0.01): psi = 0.11 Pes + 0.61 VI + 1.99 TI/TT + 0.04 fb - 2.60 (r = 0.83). The results suggest that peak pressure (tension), VI (velocity of inspiratory muscle shortening), TI/TT, and fb contribute independently and collectively to breathlessness. The perception of respiratory muscle effort is ideally suited to subserve this sensation. The neurophysiological mechanism purported is a conscious awareness of the intensity of the outgoing motor command by means of corollary discharge within the central nervous system.     

Airway blood flow response to eucapnic dry air hyperventilation in sheep

Eucapnic hyperventilation, breathing dry air, produces a two- to fivefold increase in airway blood flow in the dog. To determine whether airway blood flow responds similarly in the sheep we studied 16 anesthetized sheep. Seven sheep (1-7) were subjected to two 30-min periods of eucapnic hyperventilation breathing 1) warm humid air [100% relative humidity (rh)] followed by 2) warm dry air [0% rh] at 40 breaths/min. To determine whether there was a dose-response effect on blood flow of increasing levels of hyperventilation of dry air, another nine sheep (8-16) were subjected to four 30-min periods of eucapnic hyperventilation breathing warm humid O2 followed by warm dry O2 at 20 or 40 breaths/min in random sequence. Five minutes before the end of each period of hyperventilation, hemodynamics, blood gases, and tracheal mucosal temperature were measured, and tracheal and bronchial blood flows were determined by injection of 15- or 50-micron-diam radiolabeled microspheres. After the last measurements had been made, all sheep were killed, and the lungs and trachea were removed for determination of blood flow to trachea, bronchi, and parenchyma. In sheep 1-7, warm dry air hyperventilation at 40 breaths/min produced an increase in blood flow to trachea (7.6 +/- 3.5 to 17.0 +/- 6.2 ml/min, P less than 0.05) and bronchi (9.0 +/- 5.4 to 18.2 +/- 8.2 ml/min, P less than 0.05) but not to the parenchyma. When blood flow was compared with the two ventilatory rates (sheep 8-16), tracheal blood flow increased (9.1 +/- 3.3 to 18.2 +/- 6.1 ml/min, P less than 0.05) at a rate of 40 breaths/min but not at 20 breaths/min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Treadmill economy in girls and women matched for height and weight.

We investigated differences in walking (80 m/min) and running (147 m/min) economy [submaximal oxygen consumption (VO(2) (submax))] between adolescent girls (n = 13; age = 13.3 +/- 0.9 yr) and young women (n = 23; age = 21.0 +/- 1.5 yr). Subjects were matched for height (158.7 +/- 2.9 cm) and weight (52.1 +/- 3.0 kg). Anthropometric measures (height, weight, breadths, skinfolds) and preexercise oxygen consumption were obtained on all subjects before submaximal and maximal treadmill exercise. Anthropometric measures were similar between groups, as was maximal oxygen consumption (girls, 47.7 +/- 5.2; women, 47.5 +/- 5.7 ml. kg(-1). min(-1)). VO(2) (submax) was significantly greater (P < 0.0002) in girls compared with women during both walking (16.4 +/- 1.7 vs. 14.4 +/- 1. 1 ml. kg(-1). min(-1)) and running (38.1 +/- 3.7 vs. 33.9 +/- 2.4 ml. kg(-1). min(-1)). Preexercise oxygen consumption (4.4 vs. 3.9 ml. kg(-1). min(-1)) accounted for only a fraction of the differences found in exercise economy. Although heart rate and respiratory frequency were greater in the girls in both walking (118 +/- 11 vs. 104 +/- 12 beats/min and 31 +/- 3 vs. 25 +/- 4 breaths/min, respectively; P < 0.002) and running (180 +/- 15 vs. 163 +/- 17 beats/min and 47 +/- 11 vs. 38 +/- 8 breaths/min; P < 0.005), this did not likely account for a large part of the difference in VO(2) (submax) between groups.     

Effect of elastic loading on ventilatory pattern during progressive exercise

Ventilatory responses to progressive exercise, with and without an inspiratory elastic load (14.0 cmH2O/l), were measured in eight healthy subjects. Mean values for unloaded ventilatory responses were 24.41 +/- 1.35 (SE) l/l CO2 and 22.17 +/- 1.07 l/l O2 and for loaded responses were 24.15 +/- 1.93 l/l CO2 and 20.41 +/- 1.66 l/l O2 (P greater than 0.10, loaded vs. unloaded). At levels of exercise up to 80% of maximum O2 consumption (VO2max), minute ventilation (VE) during inspiratory elastic loading was associated with smaller tidal volume (mean change = 0.74 +/- 0.06 ml; P less than 0.05) and higher breathing frequency (mean increase = 10.2 +/- 0.98 breaths/min; P less than 0.05). At levels of exercise greater than 80% of VO2max and at exhaustion, VE was decreased significantly by the elastic load (P less than 0.05). Increases in respiratory rate at these levels of exercise were inadequate to maintain VE at control levels. The reduction in VE at exhaustion was accompanied by significant decreases in O2 consumption and CO2 production. The changes in ventilatory pattern during extrinsic elastic loading support the notion that, in patients with fibrotic lung disease, mechanical factors may play a role in determining ventilatory pattern.     

Fluctuations in plantar flexion force are reduced after prolonged tendon vibration.

The purpose of the study was to examine the effect of prolonged vibration on the force fluctuations during a force-matching task performed at low-force levels. Fourteen young healthy men performed a submaximal force-matching task of isometric plantar flexion before and after Achilles tendon vibration (n = 8, vibration subjects) or lying without vibration (n = 6, control subjects) for 30 min. The target forces were 2.5-10% of the previbration maximal voluntary contraction force. The standard deviation of force decreased by a mean of 29 +/- 20% across target forces after vibration, whereas it did not decrease significantly in control subjects (-5 +/- 12%). This change was significantly greater compared with control subjects (P < 0.01 for both). Power spectral density of the force was predominantly composed of signals of low-frequency bandwidth (相似文献   

Effect of intestinal afferent stimulation on pattern of respiratory muscle activation

The purpose of the present study was to examine the reflex effects of mechanical stimulation of intestinal visceral afferents on the pattern of respiratory muscle activation. In 14 dogs anesthetized with pentobarbital sodium, electromyographic activity of the costal and crural diaphragm, parasternal intercostal, and upper airway respiratory muscles was measured during distension of the small intestine. Rib cage and abdominal motion and tidal volume were also recorded. Distension produced an immediate apnea (11.16 +/- 0.80 s). During the first postapneic breath, costal (43 +/- 7% control) and crural (64 +/- 6% control) activity were reduced (P less than 0.001). In contrast, intercostal (137 +/- 11%) and upper airway muscle activity, including alae nasi (157 +/- 16%), genioglossus (170 +/- 15%), and posterior cricoarytenoid muscles (142 +/- 7%) all increased (P less than 0.005). There was greater outward rib cage motion although the abdomen moved paradoxically inward during inspiration, resulting in a reduction in tidal volume (82 +/- 6% control) (P less than 0.005). Postvagotomy distension produced a similar apnea and subsequent reduction in costal and crural activity. However, enhancement of intercostal and upper airway muscle activation was abolished and there was a greater fall in tidal volume (65 +/- 14%). In conclusion, mechanical stimulation of intestinal afferents affects the various inspiratory muscles differently; nonvagal afferents produce an initial apnea and subsequent depression of diaphragm activity whereas vagal pathways mediate selective enhancement of intercostal and upper airway muscle activation.