Effect of hypercapnia and hypoxia on respiratory muscle activation in humans

Takasaki, Yoshito; Orr, David W.; Popkin, J.; Xie, Ailiang; Bradley, T. Douglas

doi:10.1152/jappl.1989.67.5.1776

Cited by 33 publications

(14 citation statements)

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“…However, the effects of body position on the ventilatory response to hypoxia have not been well characterized. In preliminary studies for previous investigations from our laboratory (Takasaki, Orr, Popkin, Xie & Bradley, 1989;Xie et al 1991) it was observed that the slope of the ventilatory response to hypoxia was lower in supine than upright human subjects. It therefore seemed possible that under hypoxic conditions, other respiratory output variables, such as respiratory force generation, might bear a more consistent relationship to oxyhaemoglobin saturation (Sa,2).…”

Section: Introductionmentioning

confidence: 84%

Influence of body position on pressure and airflow generation during hypoxia and hypercapnia in man.

Xie¹,

Takasaki²,

Popkin³

et al. 1993

The Journal of Physiology

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SUMMARY1. Inspiratory oesophageal pressure and ventilatory responses to hyperoxic, progressive hypercapnic rebreathing (HCVR) and isocapnic, progressive hypoxic rebreathing (HVR) were studied in five normal males in both supine and upright seated positions.2. No significant differences were found in the ventilatory response to hypercapnia between the supine and upright position. The slopes of the relationship between minute ventilation (VI) and the increase of end tidal Pco2 (APET, C02) were 3-27+0-23 and 2-76 + 024 1 min-mmHg-' supine and upright, respectively. However, the change in oesophageal pressure from the end expiratory level observed during quiet breathing to that at peak inspiration (AP.,es I) in relationship to APETCO2 was greater supine than upright (1-23+0 07 versus 0 79+0411 cmH20 mmHg-', P < 0-01).3. In contrast, during hypoxia-stimulated breathing the slope of the minute ventilation versus oxyhaemoglobin saturation curve (VI-Sa, 2) was flatter supine than upright (1P00+0-03 versus 175+0-05 1 min-(percentage fall in Sa, o2)1 P < 0-0001), but ApoI I in relation to Sa°2 during hypoxic rebreathing was similar supine and upright (0-38 + 0-03 versus 0 40 + 0-04 cmH2O (percentage fall in Sa' 02)' respectively).

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Section: Introductionmentioning

confidence: 84%

Influence of body position on pressure and airflow generation during hypoxia and hypercapnia in man.

Xie¹,

Takasaki²,

Popkin³

et al. 1993

The Journal of Physiology

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“…A number of papers have been devoted to investigating the effects of hypercapnia on both inspiratory and expiratory muscles in healthy humans (Grimby et al 1976;Grassino et al 1981;Lopata et al 1983;Henke et al 1988;Takasaki et al 1989;De Troyer et al 1990;Yan et al 1993;Tadashi et al 1996;Yan et al 1996) but no studies have described expiratory rib cage muscle recruitment. Grimby et al (1976) demonstrate that a _ V E of 40 l/min is reached with hypercapnic hyperpnoea before expiratory muscles are recruited phasically.…”

Section: Respiratory Muscle Recruitmentmentioning

confidence: 99%

“…This is not an unexpected finding owing to the effect of the hypercapnic stimulus on abdominal muscle recruitment. Studies of animals (Fregosi et al 1987;Easton et al 1995) and humans (Grimby et al 1976;Takasaki et al 1989;Yan et al 1996;Filippelli et al 2003) have shown that hypercapnia enhances abdominal expiratory activity. 4.…”

Section: Muscle Powermentioning

confidence: 99%

“…Studies on thoraco-abdominal motion in response to CO 2 have shown that, by decreasing end-expiratory abdominal volume (Vab,e), the expiratory muscles contribute to tidal volume (Takasaki et al 1989;Yan et al 1993;Gorini et al 2000). In contrast, it has been suggested by Henke et al (1988), using helium dilution, that end-expiratory lung volume (EELV) does not change significantly during CO 2 rebreathing.…”

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confidence: 99%

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Chest wall kinematics and respiratory muscle coordinated action during hypercapnia in healthy males

Romagnoli

Gigliotti

Lanini

et al. 2004

European Journal of Applied Physiology

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The present study was designed to verify whether during hypercapnic stimulation, as we had previously found during exercise or walking, the partitioning of the respiratory motor output is equally distributed to the muscles of chest wall compartments to assist diaphragm function. We studied chest wall kinematics and respiratory muscle recruitment in seven healthy men during rebreathing of a hypercapnic-hyperoxic gas mixture (CO(2) RT). Data were compared with those previously obtained during either cycling exercise or walking. The chest wall volume ( Vcw), assessed by optoelectronic plethysmography (OEP), was modeled as the sum of the volumes of the lung-apposed rib cage ( Vrc,p), diaphragm-apposed rib cage ( Vrc,a) and abdomen ( Vab). Esophageal ( Pes), gastric ( Pga) and transdiaphragmatic ( Pdi= Pga- Pes) pressures were simultaneously recorded. Velocity of shortening ( V') and power ( W'= Px V') of the diaphragm ( W'di), rib cage muscles ( W'rcm) and abdominal muscles ( W'abm) were also calculated. During CO(2) RT the progressive increase in end-inspiratory Vcw resulted from an increase in both end-inspiratory Vrc,p and Vrc,a, while the progressive decrease in end-expiratory Vcw was entirely due to the decrease in end-expiratory Vab. The increase in Vrc,p was proportionally slightly greater than that in Vrc,a. The end-inspiratory increase and end-expiratory decrease in Vcw were accounted for by inspiratory rib cage (RCM,i) and abdominal (ABM) muscle recruitment, respectively. W'di, W'rcm and W'abm progressively increased. However, while most of W'di was expressed in terms of velocity of shortening, most of W'rcm and W'abm was expressed as force or pressure. A comparison of CO(2) results with data obtained during exercise revealed: (1). a gradual vs. an immediate response, (2). a similar decrease in Vab,e and Pabm, (3). an apparent lack of any difference in ABM recruitment, (4). less gradual ABM relaxation, (5). no drop in Pdi but a similar Wdi change and decrease in pressure-to-velocity ratio of the diaphragm. We have found that in healthy humans: (1). the increased motor output with hypercapnia is equally distributed between RCM and ABM to minimize transdiaphragmatic pressure and (2). data on chest wall kinematics and respiratory muscle recruitment are only partly in line with those obtained during walking or cycling exercise.

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“…However, considering that ours was a model of hyperpnea generated primarily by a chemical stimulus, it is important to recognize that CO 2-stimulated hyperpnea recruits expiratory muscles at a lower minute ventilation than hypoxic hyperpnea (24). For this reason, pleural pressure drive changes in flow.…”

Section: Discussionmentioning

confidence: 99%

Hyperpnea limits the volume recruited by positive end-expiratory pressure.

Chandra¹,

Coggeshall²,

Ravenscraft³

et al. 1994

Am J Respir Crit Care Med

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The effectiveness of positive end-expiratory pressure (PEEP) relates directly to alveolar recruitment. We tested the hypothesis that active use of expiratory muscles during labored breathing impairs the ability of PEEP to increase end-expiratory lung volume. Eight healthy volunteers naive to the purposes of our study were exposed to targeted end-expiratory pressures of 0, 5, and 10 cm H2O during mechanical ventilation applied by mouthpiece and noseclips at three levels of ventilation: resting and two levels (moderate and high) of CO2 stimulation (10.9 +/- 0.4, 19.9 +/- 0.5 and 27.5 +/- 0.5 L/min, respectively). Inductive plethysmography demonstrated that end-expiratory lung volume rose by an average of 98 +/- 5 ml/cm H2O PEEP during quiet breathing but by much less during the two levels (moderate and high) of CO2 stimulation: 78 +/- 6 ml/cm H2O and 47 +/- 5 ml/cm H2O (p < 0.05). Hyperpnea also shifted the distribution of the recruited volume toward regions sampled by the rib cage band of the plethysmograph. Whatever advantage expiratory muscle activity may have for minimizing the workload of the inspiratory muscles, the cost may be reduced effectiveness of PEEP in increasing lung volume and improving oxygen exchange.

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Effect of hypercapnia and hypoxia on respiratory muscle activation in humans

Cited by 33 publications

References 0 publications

Influence of body position on pressure and airflow generation during hypoxia and hypercapnia in man.

Influence of body position on pressure and airflow generation during hypoxia and hypercapnia in man.

Chest wall kinematics and respiratory muscle coordinated action during hypercapnia in healthy males

Hyperpnea limits the volume recruited by positive end-expiratory pressure.

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