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Jason H Mateika

Publications and source records attributed to Jason H Mateika.

13 recordsLinked to original sources

Long-term facilitation of ventilation and genioglossus muscle activity is evident in the presence of elevated levels of carbon dioxide in awake humans.

We hypothesized that long-term facilitation (LTF) of minute ventilation and peak genioglossus muscle activity manifests itself in awake healthy humans when carbon dioxide is sustained at elevated levels. Eleven subjects completed two trials. During trial 1, baseline carbon dioxide levels were maintained during and after exposure to eight 4-min episodes of hypoxia. During trial 2, carbon dioxide was sustained 5 mmHg above baseline levels during exposure to episodic hypoxia. Seven subjects were exposed to sustained elevated levels of carbon dioxide in the absence of episodic hypoxia, which served as a control experiment. Minute ventilation was measured during trial 1, trial 2, and the control experiment. Peak genioglossus muscle activity was measured during trial 2. Minute ventilation during the recovery period of trial 1 was similar to baseline (9.3 +/- 0.5 vs. 9.2 +/- 0.7 l/min). Likewise, minute ventilation remained unchanged during the control experiment (beginning vs. end of control experiment, 14.4 +/- 1.7 vs. 14.7 +/- 1.4 l/min). In contrast, minute ventilation and peak genioglossus muscle activity during the recovery period of trial 2 was greater than baseline (minute ventilation: 28.4 +/- 1.7 vs. 19.6 +/- 1.0 l/min, P < 0.001; peak genioglossus activity: 1.6 +/- 0.3 vs. 1.0 fraction of baseline, P < 0.001). We conclude that exposure to episodic hypoxia is necessary to induce LTF of minute ventilation and peak genioglossus muscle activity and that LTF is only evident in awake humans in the presence of sustained elevated levels of carbon dioxide.

Adult↗

Visual properties of objects affect manipulative forces and respiration differently.

Previously, we demonstrated that the respiratory and motor systems responded differently following consecutive lifts of an object whose weight could be altered (lighter or heavier) without changing the object's visual properties. When the weight of the object was altered in a manner unpredictable to the subject, the motor system response reflected the previous weight of the object (light or heavy) while the respiratory system reflected responses seen when lifting the heavier object regardless of whether a lighter or heavier object was lifted previously. It is possible that the default pattern of the respiratory system was due to a lack of visual size cues, which are known to have robust affects on grasp control. To test this hypothesis, 14 seated subjects performed self-initiated alternating lifts with objects whose size and weight covaried such that the weight of the upcoming lift was known despite the weight of the object previously lifted. Following both consecutive and alternating trials, the load force was scaled to the weight of the object (e.g., the heavier the object the larger the force) while the volume was scaled only following the consecutive trials. This suggests that the load forces were developed entirely based on visual information while lung volume was not. In addition, we suggest that following the consecutive trials, the volume increased as the object's weight increased in an effort to assist with trunk stabilization by indirectly increasing intra-abdominal pressure.

Adult↗

Heart rate variability in non-apneic snorers and controls before and after continuous positive airway pressure.

BACKGROUND: We hypothesized that sympathetic nervous system activity (SNSA) is increased and parasympathetic nervous system activity (PNSA) is decreased during non-rapid eye movement (NREM) sleep in non-apneic, otherwise healthy, snoring individuals compared to control. Moreover, we hypothesized that these alterations in snoring individuals would be more evident during non-snoring than snoring when compared to control. METHODS: To test these hypotheses, heart rate variability was used to measure PNSA and SNSA in 11 normotensive non-apneic snorers and 12 control subjects before and 7-days after adapting to nasal continuous positive airway pressure (nCPAP). RESULTS: Our results showed that SNSA was increased and PNSA was decreased in non-apneic snorers during NREM compared to control. However, these changes were only evident during the study in which snoring was eliminated with nCPAP. Conversely, during periods of snoring SNSA and PNSA were similar to measures obtained from the control group. Additionally, within the control group, SNSA and PNSA did not vary before and after nCPAP application. CONCLUSION: Our findings suggest that long-lasting alterations in autonomic function may exist in snoring subjects that are otherwise healthy. Moreover, we speculate that because of competing inputs (i.e. inhibitory versus excitatory inputs) to the autonomic nervous system during snoring, the full impact of snoring on autonomic function is most evident during non-snoring periods.

Adult↗

The ventilatory response to carbon dioxide and sustained hypoxia is enhanced after episodic hypoxia in OSA patients.

Our primary hypothesis was that the acute ventilatory response to carbon dioxide in the presence of sustained hypoxia {VRCO2 (hypoxia)} or hyperoxia {VRCO2 (hyperoxia)} would increase in subjects with obstructive sleep apnea (OSA) after exposure to episodic hypoxia. Secondarily, we hypothesized that chronic (i.e. years) exposure to episodic hypoxia, a hallmark of OSA, would facilitate persistent augmentation of respiratory activity (i.e. long-term facilitation) after acute (i.e. minutes) exposure to episodic hypoxia. Nine healthy males with OSA that were healthy otherwise completed a series of rebreathing trials before and after exposure to eight 4 min episodes of hypoxia. On a separate occasion, the rebreathing trials were repeated before and after exposure to atmospheric air for a duration equivalent to the episodic hypoxia protocol (i.e. sham episodic hypoxia). During the rebreathing trials, subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (P(ET)CO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr) or high oxygen gas mixture (140 Torr). During the trials, P(ET)CO2 increased while the selected level of oxygen was maintained. The point at which ventilation began to rise in a linear fashion as P(ET)CO2 increased was the ventilatory threshold. The ventilatory response below and above the threshold was determined. The results showed that the VRCO2 (hypoxia) and the VRCO2 (hyperoxia) was increased after exposure to episodic hypoxia {VRCO2 (hypoxia): 7.9 +/- 1.3 versus 10.5 +/- 1.3, VRCO2 (hyperoxia): 5.9 +/- 1.1 versus 6.7 +/- 1.1 L/min/Torr}. However, only the increase in the VRCO2 (hypoxia) after episodic hypoxia was greater than the increase measured after exposure to sham episodic hypoxia. Long-term facilitation of ventilation, tidal volume and breathing frequency was not evident after episodic hypoxia. We conclude that the VRCO2 (hypoxia) is enhanced after exposure to acute episodic hypoxia and that enhancement of the VRCO2 (hypoxia) occurs even though long-term facilitation is not evident.

Adult↗

Treatment with leuprolide acetate decreases the threshold of the ventilatory response to carbon dioxide in healthy males.

This investigation was designed to determine if suppression of testosterone alters the ventilatory response to carbon dioxide in the presence of high and low levels of oxygen. Eleven healthy male subjects completed a series of rebreathing trials during wakefulness, before and after treatment with a long-acting gonadotropin-releasing hormone agonist. Five subjects also completed studies during non-rapid eye movement (NREM) sleep. During wakefulness, subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (P(ET,CO2)) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr) or high oxygen (140 Torr) gas mixture. During each trial P(ET,CO2) increased while oxygen was maintained at a constant level. The threshold of the ventilatory response to carbon dioxide was considered to be the point at which minute ventilation began to rise in a linear fashion as P(ET,CO2) increased. The slope of the ventilatory response above the threshold was used as a measure of sensitivity to carbon dioxide. During NREM sleep, hypocapnia was induced via nasal mechanical ventilation. Several trials were completed until the cessation of mechanical ventilation resulted in a central apnoea which demarcated the threshold of the ventilatory response to carbon dioxide. In response to treatment with leuprolide acetate, the threshold measured in wakefulness decreased during carbon dioxide rebreathing in the presence of low (41.05 +/- 0.77 versus 39.40 +/- 0.83 Torr; P = 0.01) and high (46.32 +/- 0.56 versus 44.78 +/- 0.83 Torr; P = 0.01) oxygen levels. An increase in sensitivity (4.82 +/- 0.61 versus 7.17 +/- 1.20 l min(-1) Torr(-1); P = 0.02) was also observed during rebreathing in the presence of high but not low oxygen levels. The increase in sensitivity was accompanied by an increase in carbon dioxide production. The findings observed during NREM sleep were similar to those observed during wakefulness, since the P(ET,CO2) that demarcated the threshold was decreased after leuprolide treatment (42.1 +/- 0.6 versus 39.6 +/- 0.6 Torr; P = 0.002). Additionally, the decrease in P(ET,CO2) required to induce an apnoea was greater after treatment with leuprolide (2.56 +/- 0.25 versus 4.06 +/- 0.29 Torr; P = 0.004). We conclude that suppression of testosterone decreases the threshold of the ventilatory response to carbon dioxide during both wakefulness and sleep.

Adult↗

Ventilatory responses to carbon dioxide at low and high levels of oxygen are elevated after episodic hypoxia in men compared with women.

We hypothesized that the acute ventilatory response to carbon dioxide in the presence of low and high levels of oxygen would increase to a greater extent in men compared with women after exposure to episodic hypoxia. Eleven healthy men and women of similar race, age, and body mass index completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the end-tidal partial pressure of carbon dioxide (PetCO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr), or high oxygen gas mixture (150 Torr). During the trials, PetCO2 increased while the selected level of oxygen was maintained. The point at which minute ventilation began to rise in a linear fashion as PetCO2 increased was considered to be the carbon dioxide set point. The ventilatory response below and above this point was determined. The results showed that the ventilatory response to carbon dioxide above the set point was increased in men compared with women before exposure to episodic hypoxia, independent of the oxygen level that was maintained during the rebreathing trials (50 Torr: men, 5.19 +/- 0.82 vs. women, 4.70 +/- 0.77 l x min(-1) x Torr(-1); 150 Torr: men, 4.33 +/- 1.15 vs. women, 3.21 +/- 0.58 l x min(-1) x Torr(-1)). Moreover, relative to baseline measures, the ventilatory response to carbon dioxide in the presence of low and high oxygen levels increased to a greater extent in men compared with women after exposure to episodic hypoxia (50 Torr: men, 9.52 +/- 1.40 vs. women, 5.97 +/- 0.71 l x min(-1) x Torr(-1); 150 Torr: men, 5.73 +/- 0.81 vs. women, 3.83 +/- 0.56 l x min(-1) x Torr(-1)). Thus we conclude that enhancement of the acute ventilatory response to carbon dioxide after episodic hypoxia is sex dependent.

Adult↗

Baroreflex sensitivity in nonapneic snorers and control subjects before and after nasal continuous positive airway pressure.

HYPOTHESIS: We hypothesized that baroreflex sensitivity is decreased during wakefulness and non-rapid eye movement sleep in normotensive, nonapneic snorers who are otherwise healthy. Moreover, we hypothesized that nocturnal alterations in baroreflex sensitivity are abolished during the application of nasal continuous positive airway pressure (nCPAP). DESIGN: The sequencing technique was used to measure baroreflex sensitivity in 16 normotensive nonapneic snorers and 16 control subjects matched for age, height, weight, gender, and race. Subsequently, baroreflex sensitivity was measured in 12 of 16 snorers and 14 of 16 control subjects during the application of nCPAP. RESULTS: Mean (+/- SE) baroreflex sensitivity was reduced during sleep in the nonapneic snoring group (wakefulness, 20.99 +/- 1.46 ms/mm Hg; sleep, 15.85 +/- 1.49 ms/mm Hg), but not in the control group (wakefulness, 21.82 +/- 2.48 ms/mm Hg; sleep, 23.54 +/- 2.18 ms/mm Hg). This reduction was abolished by the application of nCPAP in the snoring group (before nCPAP therapy, 16.30 +/- 2.17 ms/mm Hg; during nCPAP therapy, 20.63 +/- 2.40 ms/mm Hg). The application of nCPAP did not alter baroreflex sensitivity in the control group (before nCPAP therapy, 23.54 +/- 2.18 ms/mm Hg; during nCPAP therapy, 22.56 +/- 1.73 ms/mm Hg). BP was not significantly different between the snoring and control groups either before or during nCPAP application. CONCLUSIONS: Our findings suggest that nocturnal alterations in baroreflex sensitivity may exist in nonapneic snoring subjects prior to alterations in other cardiovascular variables.

Adult↗

Peripheral chemoreflex responsiveness is increased at elevated levels of carbon dioxide after episodic hypoxia in awake humans.

We hypothesized that the acute ventilatory response to hypoxia is enhanced after exposure to episodic hypoxia in awake humans. Eleven subjects completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (Pet(CO(2))) below 25 Torr. Subjects then breathed from a bag containing normocapnic (42 Torr), low (50 Torr), or high oxygen (140 Torr) gas mixtures. During the trials, Pet(CO(2)) increased while a constant oxygen level was maintained. The point at which ventilation began to rise in a linear fashion as Pet(CO(2)) increased was considered to be the ventilatory recruitment threshold. The ventilatory response below and above the recruitment threshold was determined. Ventilation did not persist above baseline values immediately after exposure to episodic hypoxia; however, Pet(CO(2)) levels were reduced compared with baseline. In contrast, compared with baseline, the ventilatory response to progressive increases in carbon dioxide during rebreathing trials in the presence of low but not high oxygen levels was increased after exposure to episodic hypoxia. This increase occurred when carbon dioxide levels were above but not below the ventilatory recruitment threshold. We conclude that long-term facilitation of ventilation (i.e., increases in ventilation that persist when normoxia is restored after episodic hypoxia) is not expressed in awake humans in the presence of hypocapnia. Nevertheless, despite this lack of expression, the acute ventilatory response to hypoxia in the presence of hypercapnia is increased after exposure to episodic hypoxia.

Adult↗

Chemoreflex control of ventilation is altered during wakefulness in humans with OSA.

We hypothesized that patients with obstructive sleep apnea (OSA) have a different awake ventilatory response to carbon dioxide above and below eupnea compared with normal. Eight male subjects with OSA and control subjects matched for gender, race, age, height and weight voluntarily hyperventilated during wakefulness to reduce the partial pressure of carbon dioxide (PET(CO2)) below 25 mmHg. Subjects were then switched into a rebreathing bag containing a normocapnic (42 mmHg) hypoxic [partial pressure of end tidal oxygen (PET(O2))=50 mmHg (H50)] or hyperoxic [PET(O2)=140 mmHg (H140)] gas mixture. During the trial PET(CO2) increased while PET(O2) was maintained at a constant level. The point at which ventilation and PET(CO2) increased linearly was considered to be the carbon dioxide ventilatory recruitment threshold (VRT(CO2)). Measurements of ventilation and its components (i.e. tidal volume and breathing frequency) were made below this threshold and the slope of the minute ventilation; tidal volume or breathing frequency response above the threshold was determined. Four trials for a given oxygen level were completed. The PET(CO2) that demarcated the VRT(CO2) was increased (H(50)=43.43+/-0.92 vs. 41.05+/-0.67; H(140)=47.65+/-0.80 vs. 45.28+/-0.75), as were measures of ventilation below the threshold (H(50)=18.50+/-2.11 vs. 13.44+/-1.43; H(140)=19.66+/-2.71 vs. 10.83+/-1.24) in the OSA subjects compared with control. In contrast the OSA and control subjects did not respond differently to changes in PET(CO2) above the threshold. We conclude that the PET(CO2) that delineates the VRT(CO2) and ventilation below this threshold is elevated in subjects with OSA.

Adult↗

Internal representations underlying respiration during object manipulation.

We examined the presence of anticipatory control and the resulting interactions of the respiratory and motor systems during discrete object manipulation. In response to an auditory signal, subjects reached forward, grasped, and lifted an instrumented object weighing 150 or 1000 g while the breathing pattern, fingertip forces, and movements were measured. Following every block of five lifts, the object was removed from sight and replaced with the same or an alternate mass. Thus, the object's weight was predictable during the last lift of each block and unpredictable during the first lift after the transition. When the object's weight was predictable, the force application was faster and inspiratory duration and the tidal volume were reduced for the breath associated with the lift for 1000-g compared to 150-g lifts. Following the transition, when the object's weight was unpredictable, the force application reflected the weight of the object during the previous lift while the respiratory output, regardless of the preceding weight, resembled that used for 1000-g lifts. Additionally, inspiratory duration was significantly correlated with the reach duration in three of the four unpredictable lifting conditions. We conclude that these system-specific anticipatory alterations may arise from a common internal representation that was formed through past manipulatory weight experience.

Adult↗

Respiratory-related activation of human abdominal muscles during exercise.

We tested the hypothesis that abdominal muscles are active during the expiratory phase of the respiratory cycle during exercise. Electromyographic (EMG) activities of external oblique and rectus abdominis muscles were recorded during incremental exercise to exhaustion and during 30 min of constant work rate exercise at an intensity of 85 % of the peak oxygen consumption rate (V(O(2))). High amplitude intramuscular EMG activities of both abdominal muscles could be evoked with postural manoeuvres in all subjects. During cycling, respiratory-related activity of the external obliques was evoked in four of seven subjects, whereas rectus abdominis activity was observed in six of the seven subjects. We measured only the activity that was confined exclusively to the expiratory phase of the respiratory cycle. Expiratory activity of both muscles increased with exercise intensity, although peak values averaged only 10-20 or 20-40 % of the peak activity (obtained during maximal, voluntary expiratory efforts) for the external oblique and rectus abdominis muscles, respectively. To estimate how much of the recorded abdominal muscle activity was supporting leg movements during exercise, we compared the activity at the very end of incremental exercise to that recorded during the first five respiratory cycles after the abrupt cessation of exercise, when ventilation was still very high. Although external oblique activity was reduced after exercise stopped, clear expiratory activity remained. Rectus abdominis activity remained high after exercise cessation, showing a gradual decline that approximated the decline in ventilation. During constant work rate exercise, EMG activities increased to 40-50 and 5-10 % of peak in rectus and external oblique muscles, respectively, and then plateaued for the remainder of the bout in spite of a continual upward drift in (V(O(2))) and pulmonary ventilation. Linear regression analysis showed that the rise in respiratory-related expiratory muscle activity during progressive intensity exercise was significantly correlated with ventilation, although weakly. In constant work rate exercise, expiratory EMG activities increased, but the changes were highly variable and did not change as a function of exercise time, even though ventilation drifted significantly with time. These experiments suggest that abdominal muscles play a role in regulating the ventilatory response to progressive intensity bicycle exercise, although some of the observed activity may support postural adjustments or limb movements. The contribution of abdominal muscles to ventilation during constant work rate exercise is variable, and expiratory activity does not 'drift' significantly with time.

Abdominal Muscles↗

Effects of lung volume and chemoreceptor activity on blood pressure and R-R interval during the Valsalva maneuver.

STUDY OBJECTIVES: The purpose of the present investigation was to examine the effect of lung volume and inspiration of 100% oxygen on blood pressure and R-R interval responses during the Valsalva maneuver. DESIGN AND PARTICIPANTS: Fourteen healthy subjects completed eight Valsalva maneuvers. Four of the maneuvers were completed after inspiring to total lung capacity while the remaining maneuvers were completed at end-expiratory lung volume. Two maneuvers completed at a given lung volume were performed under hyperoxic conditions while the remaining maneuvers were completed under normoxic conditions. RESULTS: Overall, a significant increase in blood pressure and decrease in R-R interval occurred throughout phases I-IV of the Valsalva maneuvers that were initiated from end-expiratory lung volume as compared to total lung capacity. These changes were accompanied by a concomitant increase in baroreflex sensitivity during phase IV. Furthermore, independent of lung volume the baroreflex response was attenuated under hyperoxic conditions. CONCLUSIONS: We conclude that the lung volume that exists prior to the onset of the maneuver alters the blood pressure and R-R interval response during phases I-IV of the Valsalva maneuver. Furthermore, we suggest that these responses are mediated in part by changes in chemoreceptor activity since the baroreflex was reset and the sensitivity was reduced under hyperoxic conditions. Given these findings, we recommend that lung volume be controlled when patients are completing a Valsalva maneuver to obtain reliable and reproducible measures of blood pressure, R-R interval duration and baroreflex sensitivity.

Administration, Inhalation↗

Arterial stiffness increases during obstructive sleep apneas.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) appears to be an independent risk factor for diurnal systemic hypertension, but the specific biologic markers for this association have not been well established. Increased arterial stiffness is an important measure of increased left ventricular load and a predictor of cardiovascular morbidity and may precede the onset of systemic hypertension in humans. However, arterial stiffness has not been measured in association with obstructive apneas in patients with OSA, nor related to systemic blood pressure (BP) activity in this setting. Our objective was to test the hypothesis that arterial stiffness may be utilized as a sensitive measure of arterial vasomotor perturbation during obstructive events in patients with OSA, by demonstrating that (1) arterial stiffness increases acutely in association with obstructive apnea and hypopnea, and that (2) such increased stiffness may occur in the absence of acute BP increase. DESIGN: Prospective, cross-sectional. SETTING: A tertiary-care university-based sleep and ventilatory disorders center. PATIENTS: Forty-four normo- and hypertensive adult patients (11 women, 33 men) with polysomnographically diagnosed moderate to severe OSA. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Beat-to-beat BP was recorded from the radial artery by applanation tonometry during nocturnal polysomnography. Arterial augmentation index (AAI), a measure of arterial stiffness, was calculated as the ratio of augmented systolic BP (SBP) to pulse pressure and expressed as a percentage for the following conditions: awake, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events, and the first 15 cardiac cycles following apnea termination ("post apnea"). Mean AAI (+/-SD) for the group was significantly increased during NREM sleep from early apnea to late apnea (12.02 +/- 2.70% vs 13.35 +/- 3.54%, p<0.05, ANOVA). During REM (analyzed in 20 patients), MI again significantly increased from early apnea to late apnea (11.75 +/- 2.81% vs 13.43 +/- 4.97%). Conversely, neither mean SBP nor mean arterial BP was significantly changed from early apnea to late apnea in NREM (SBP 130 +/- 14 mmHg vs 129 +/- 14 mmHg) or REM (SBP 128 +/- 22 mmHg vs 127 +/- 21 mmHg). CONCLUSIONS: Arterial stiffness increases acutely during obstructive apneas in both NREM and REM sleep, in the absence of measurable BP change. These data suggest that arterial stiffness may be a sensitive measure of acute arterial vasomotor perturbation in this setting and may have implications concerning cardiovascular sequelae in patients with OSA.

Adult↗