Configuration of the chest wall and occlusion pressures in awake humans

Grassino, A.; Jp, Derenne; Almirall, Jaume; Milic–Emili, J.; Whitelaw, William A.

doi:10.1152/jappl.1981.50.1.134

Cited by 58 publications

(30 citation statements)

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“…The present finding of a gradual decrease in VAbd,EE are in line with results obtained by magnetometry or respiratory inductance plethysmography in healthy subjects [10,19,[25][26][27][28] and patients with ankylosing spondylitis [4]. The novel finding of the present study, in which a method that neither requires calibration nor depends on the degree of freedom was used [16], was the direct assessment of volume changes in the three chest wall compartments.…”

Section: Discussion Of the Resultssupporting

confidence: 91%

“…Respiratory muscle recruitment during hypercapnic stimulation has long been assessed in healthy humans [18, 26-28, 30, 31]. Some of these studies have shown that a decrease in the VAbd,EE optimises diaphragm configuration so that it can generate more pressure [26][27][28]. A novel finding of the present study is the direct assessment of PM,rc,I and PM,rc,E, PM,Abd and pressure production by the diaphragm in patients with ankylosing spondylitis.…”

Section: Discussion Of the Resultsmentioning

confidence: 99%

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Chest wall kinematics and respiratory muscle action in ankylosing spondylitis patients

et al. 2004

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No direct measurements of the pressures produced by the ribcage muscles, the diaphragm and the abdominal muscles during hyperventilation have been reported in patients with ankylosing spondylitis. Based on recent evidence indicating that abdominal muscles are important contributors to stimulation of ventilation, it was hypothesised that, in ankylosing spondylitis patients with limited ribcage expansion, a respiratory centre strategy to help the diaphragm function may involve coordinated action of this muscle with abdominal muscles.In order to validate this hypothesis, the chest wall response to a hypercapnic/hyperoxic rebreathing test was assessed in six ankylosing spondylitis patients and seven controls by combined analysis of: 1) chest wall kinematics, using optoelectronic plethysmography, this system is accurate in partitioning chest wall expansion into the contributions of the ribcage and the abdomen; and 2) respiratory muscle pressures, oesophageal, gastric and transdiaphragmatic (Pdi); the pressure/volume relaxation characteristics of both the ribcage and the abdomen allowed assessment of the peak pressure of both inspiratory and expiratory ribcage muscles, and of the abdominal muscles.During rebreathing, chest wall expansion increased to a similar extent in patients to that in controls; however, the abdominal component increased more and the ribcage component less in patients. Peak inspiratory ribcage, but not abdominal, muscle pressure was significantly lower in patients than in controls. End-inspiratory Pdi increased similarly in both groups, whereas inspiratory swings in Pdi increased significantly only in patients. No pressure or volume signals correlated with disease severity.The diaphragm and abdominal muscles help to expand the chest wall in ankylosing spondylitis patients, regardless of the severity of their disease. This finding supports the starting hypothesis that a coordinated response of respiratory muscle activity optimises the efficiency of the thoracoabdominal compartment in conditions of limited ribcage expansion.

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Section: Discussion Of the Resultssupporting

confidence: 91%

Section: Discussion Of the Resultsmentioning

confidence: 99%

Chest wall kinematics and respiratory muscle action in ankylosing spondylitis patients

et al. 2004

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“…Since the rate of CO2 elimination is directly proportional to 14, it seems appropriate that 1I would be maintained in the face of rising P., co regardless of body position. Our data and that from other investigators (Rigg et al 1974;Grassino, Derenne, Almirall, Milic-Emili & Whitelaw, 1981;Chapman & Rebuck, 1984a;Xie et al 1991) are consistent in this regard. In the present study, however, it was demonstrated that higher peak APOeS I was developed in order to maintain the same VT and P4 in the supine as in the upright position.…”

Section: Subjectssupporting

confidence: 92%

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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“…Second, the reduced EELV means that the diaphragm is lengthened, enabling this muscle to operate near its optimal length for force generation (101,114). Third, the reduced EELV allows for storage of elastic energy in the chest and abdominal walls during expiration that can be used to produce a portion of the work required during the ensuing inspiration (5, 35), although it is also possible that inspiration is aided in this situation by passive descent of the diaphragm (35). Importantly, accessory respiratory muscles are progressively recruited with increasing ventilatory demand during exercise, thereby sharing the load needed to support the exercise hyperpnea (6).…”

Section: Exercise Demands On the Respiratory Musclesmentioning

confidence: 99%

Exercise-induced respiratory muscle fatigue: implications for performance

Romer

Polkey²

2008

Journal of Applied Physiology

260

212

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Romer LM, Polkey MI. Exercise-induced respiratory muscle fatigue: implications for performance. J Appl Physiol 104: 879 -888, 2008. First published December 20, 2007 doi:10.1152/japplphysiol.01157.2007.-It is commonly held that the respiratory system has ample capacity relative to the demand for maximal O 2 and CO2 transport in healthy humans exercising near sea level. However, this situation may not apply during heavy-intensity, sustained exercise where exercise may encroach on the capacity of the respiratory system. Nerve stimulation techniques have provided objective evidence that the diaphragm and abdominal muscles are susceptible to fatigue with heavy, sustained exercise. The fatigue appears to be due to elevated levels of respiratory muscle work combined with an increased competition for blood flow with limb locomotor muscles. When respiratory muscles are prefatigued using voluntary respiratory maneuvers, time to exhaustion during subsequent exercise is decreased. Partially unloading the respiratory muscles during heavy exercise using low-density gas mixtures or mechanical ventilation can prevent exercise-induced diaphragm fatigue and increase exercise time to exhaustion. Collectively, these findings suggest that respiratory muscle fatigue may be involved in limiting exercise tolerance or that other factors, including alterations in the sensation of dyspnea or mechanical load, may be important. The major consequence of respiratory muscle fatigue is an increased sympathetic vasoconstrictor outflow to working skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb blood flow and increasing the severity of exerciseinduced locomotor muscle fatigue. An increase in limb locomotor muscle fatigue may play a pivotal role in determining exercise tolerance through a direct effect on muscle force output and a feedback effect on effort perception, causing reduced motor output to the working limb muscles. respiratory muscles; exercise; diaphragm; abdominals; magnetic stimulation; metaboreflex THE PURPOSE OF THIS MINIREVIEW is to address the question of whether the respiratory demands of exercise contribute significantly toward exercise limitation, either directly through limitations of the respiratory muscle pump or indirectly through effects on limb blood flow and locomotor muscle fatigue. We describe the mechanical and metabolic costs of meeting the ventilatory requirements of exercise. We then ask whether the respiratory muscles fatigue with exercise, what factors contribute to any such fatigue, and what the implications of these factors are for exercise tolerance. Finally, we deal with the potential mechanisms by which respiratory muscle fatigue could compromise exercise tolerance and whether it is possible to overcome this potential respiratory limitation. Our review focuses on the healthy young adult exercising near sea level. However, we also consider special circumstances that determine the balance between metabolic demand and respiratory system capacity in the highly trained endurance ...

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Configuration of the chest wall and occlusion pressures in awake humans

Cited by 58 publications

References 0 publications

Chest wall kinematics and respiratory muscle action in ankylosing spondylitis patients

Chest wall kinematics and respiratory muscle action in ankylosing spondylitis patients

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

Exercise-induced respiratory muscle fatigue: implications for performance

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