Differential costal and crural diaphragm compensation for posture changes

1985 ◽  
Vol 58 (6) ◽  
pp. 1895-1900 ◽  
Author(s):  
E. van Lunteren ◽  
M. A. Haxhiu ◽  
N. S. Cherniack ◽  
M. D. Goldman

The electromyographic (EMG) activities of the costal and crural diaphragm were recorded from bipolar fine-wire electrodes placed in the costal fibers adjacent to the central tendon and in the anterior portions of the crural fibers in 12 anesthetized cats. The EMG activities of costal and crural recordings were compared during posture changes from supine to head up and during progressive hyperoxic hypercapnia in both positions. The activity of both portions of the diaphragm was greater in the head up compared with supine posture at all levels of CO2; and increases in crural activity were greater than those in costal activity both as a result of changes in posture and with increasing CO2 stimuli. These results are consistent with the concept that diaphragm activation is modulated in response to changes in resting muscle length, and further, that neural control mechanisms allow separate regulation of costal and crural diaphragm activation.

2008 ◽  
Vol 104 (6) ◽  
pp. 1568-1573 ◽  
Author(s):  
Dimitri Leduc ◽  
André De Troyer

Although ascites causes abdominal expansion, its effects on abdominal muscle function are uncertain. In the present study, progressively increasing ascites was induced in supine anesthetized dogs, and the changes in abdominal (ΔPab) and airway opening (ΔPao) pressure obtained during stimulation of the internal oblique and transversus abdominis muscles were measured; the changes in internal oblique muscle length were also measured. As ascites increased from 0 to 100 ml/kg body wt, Pab and muscle length during relaxation increased. ΔPab also showed a threefold increase ( P < 0.001). However, ΔPao decreased ( P < 0.001). When ascites increased further to 200 ml/kg, resting muscle length continued to increase and muscle shortening during stimulation became very small so that active muscle length was 155% of the resting muscle length in the control condition. Concomitantly, ΔPab returned to the control value, and ΔPao continued to decrease. Similar results were obtained with the animals in the head-up posture, although the decrease in ΔPao appeared only when ascites was greater than 125 ml/kg. It is concluded that 1) ascites adversely affects the expiratory action of the abdominal muscles on the lung; 2) this effect results primarily from the increase in diaphragm elastance; and 3) when ascites is severe, the abdomen cross-sectional area is also increased and the abdominal muscles are excessively lengthened so that their active pressure-generating ability itself is reduced.


2019 ◽  
Vol 29 (5) ◽  
pp. 620-639 ◽  
Author(s):  
William Bechtel

Cognitive science has traditionally focused on mechanisms involved in high-level reasoning and problem-solving processes. Such mechanisms are often treated as autonomous from but controlling underlying physiological processes. I offer a different perspective on cognition which starts with the basic production mechanisms through which organisms construct and repair themselves and navigate their environments and then I develop a framework for conceptualizing how cognitive control mechanisms form a heterarchical network that regulates production mechanisms. Many of these control mechanisms perform cognitive tasks such as evaluating circumstances and making decisions. Cognitive control mechanisms are present in individual cells, but in metazoans, intracellular control is supplemented by a nervous system in which a multitude of neural control mechanisms are organized heterarchically. On this perspective, high-level cognitive mechanisms are not autonomous, but are elements in larger heterarchical networks. This has implications for future directions in cognitive science research.


2008 ◽  
Vol 16 (S 1) ◽  
pp. 138-141 ◽  
Author(s):  
B. Frier ◽  
E. A. S. Al-Dujaili ◽  
R. J. M. Corrall ◽  
J. Pritchard ◽  
C. R. W. Edwards

1987 ◽  
Vol 63 (4) ◽  
pp. 1622-1628 ◽  
Author(s):  
P. A. Easton ◽  
J. W. Fitting ◽  
A. E. Grassino

Changes in length of costal and crural segments of the canine diaphragm were measured by sonomicrometry within the first 100–300 ms of inspiration during CO2 rebreathing in anesthetized animals. Both segments showed small but significant decreases in end-expiratory length during progressive hypercapnia. Although both costal and crural segments showed electromyographic activity within the first 100 ms of inspiration, in early inspiration crural shortening predominated with minimal costal shortening. Neither segment contracted isometrically early in inspiration in the presence of airway occlusion. The amount of crural shortening during airway occlusion exceeded costal shortening; both segments showed increased shortening with prolonged occlusion and increasing CO2. Costal and crural shortening at 100 ms was not different for unoccluded and occluded states. These observations suggest that neural control patterns evoke discrete and unequal contributions from the diaphragmatic segments at the beginning of an inspiration; the crural segment may be predominately recruited in early inspiration. Despite traditional assumptions about occlusion pressure measurement (P0.1), diaphragm segments do not contract isometrically during early inspiratory effort against an occluded airway.


2019 ◽  
Vol 126 (4) ◽  
pp. 1117-1128 ◽  
Author(s):  
Tetsunori Ikegami ◽  
Michael Ji ◽  
Naoyuki Fujimura ◽  
Jenny V. Suneby Jagers ◽  
Teresa M. Kieser ◽  
...  

In humans and other mammals, isocapnic hypoxia sustained for 20–60 min exhibits a biphasic ventilation pattern: initial increase followed by a significant ventilatory decline (“roll-off”) to a lesser intermediate plateau. During sustained hypoxia, the mechanical action and activity of the diaphragm have not been studied; thus we assessed diaphragm function in response to hypoxic breathing. Thirteen spontaneously breathing awake canines were exposed to moderate levels of sustained isocapnic hypoxia lasting 20–25 min (80 ± 2% pulse oximeter oxygen saturation). Breathing pattern and changes in muscle length and electromyogram (EMG) activity of the costal and crural diaphragm were continuously recorded. Mean tidal shortening and EMG activity of the costal and crural diaphragm exhibited an overall biphasic pattern, with initial brisk increase followed by a significant decline ( P < 0.01). Although costal and crural shortening did not differ significantly with sustained hypoxia, this equivalence in segmental shortening occurred despite distinct and differing EMG activities of the costal and crural segments. Specifically, initial hypoxia elicited a greater costal EMG activity compared with crural ( P < 0.05), whereas sustained hypoxia resulted in a lesser crural EMG decline/attenuation than costal ( P < 0.05). We conclude that sustained isocapnic hypoxia elicits a biphasic response in both ventilation and diaphragmatic function and there is clear differential activation and contribution of the two diaphragmatic segments. This different diaphragm segmental action is consistent with greater neural activation of costal diaphragm during initial hypoxia, then preferential sparing of crural activation as hypoxia is sustained. NEW & NOTEWORTHY In humans and other mammals, during isocapnic hypoxia sustained for 20–60 min ventilation exhibits a biphasic pattern: initial increase followed by significant ventilatory decline (“roll-off”). During sustained hypoxia, the function of the diaphragm is unknown. This study demonstrates that the diaphragm reveals a biphasic action during the time-dependent hypoxic “roll-off” in ventilation. These results also highlight that the two diaphragm segments, costal and crural, show differing, distinctive contributions to diaphragm function during sustained hypoxia.


1981 ◽  
Vol 241 (6) ◽  
pp. H789-H794
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw

The carotid sinus control of hindlimb hemodynamics was determined in halothane-anesthetized vagotomized dogs. The carotid sinuses were bilaterally isolated and perfused under controlled conditions. The hindlimb was perfused under conditions of 1) physiological inflow, 2) constant pressure, and 3) constant flow. The variation of hindlimb resistance with mean carotid sinus perfusion pressure was largest under conditions of constant-pressure perfusion and smallest with physiological inflow. Values for constant-flow perfusion were intermediate. The effects of different values of constant-flow perfusion on the carotid sinus control of hindlimb hemodynamics was also determined. Values of hindlimb resistance increased with decreasing flow rate as did the variation with carotid sinus perfusion pressure. No evidence of a contribution of local control mechanisms related to changes in perfusion pressure or bed inflow could be demonstrated. The differences in the variation of hindlimb resistance with carotid sinus pressure under the various perfusion conditions can be explained on the basis of the mechanics of vascular smooth muscle. The amount of lumen constriction associated with changes in degree of activation depends on the conditions under which shortening occurs as well as upon the initial muscle length. It appears that local factors do not contribute to the control of hindlimb hemodynamics under the conditions in which these studies were performed.


2011 ◽  
Vol 106 (2) ◽  
pp. 667-679 ◽  
Author(s):  
Yongqiang Feng ◽  
Vincent L. Gracco ◽  
Ludo Max

We investigated auditory and somatosensory feedback contributions to the neural control of speech. In task I, sensorimotor adaptation was studied by perturbing one of these sensory modalities or both modalities simultaneously. The first formant (F1) frequency in the auditory feedback was shifted up by a real-time processor and/or the extent of jaw opening was increased or decreased with a force field applied by a robotic device. All eight subjects lowered F1 to compensate for the up-shifted F1 in the feedback signal regardless of whether or not the jaw was perturbed. Adaptive changes in subjects' acoustic output resulted from adjustments in articulatory movements of the jaw or tongue. Adaptation in jaw opening extent in response to the mechanical perturbation occurred only when no auditory feedback perturbation was applied or when the direction of adaptation to the force was compatible with the direction of adaptation to a simultaneous acoustic perturbation. In tasks II and III, subjects' auditory and somatosensory precision and accuracy were estimated. Correlation analyses showed that the relationships 1) between F1 adaptation extent and auditory acuity for F1 and 2) between jaw position adaptation extent and somatosensory acuity for jaw position were weak and statistically not significant. Taken together, the combined findings from this work suggest that, in speech production, sensorimotor adaptation updates the underlying control mechanisms in such a way that the planning of vowel-related articulatory movements takes into account a complex integration of error signals from previous trials but likely with a dominant role for the auditory modality.


1964 ◽  
Vol 207 (3) ◽  
pp. 705-715 ◽  
Author(s):  
S. Evans Downing ◽  
Edmund H. Sonnenblick

Studies were designed to determine parameters of force and velocity derived from isolated cardiac muscle mechanics which would permit comparison with related performance characteristics in the intact ventricle. In the papillary muscle, for a wide range of resting muscle lengths, tension developed isometrically (Po) was found a linear function of initial muscle length and proportional to the extent of isotonic shortening (δL). Length-tension curves obtained isotonically were virtually identical to those obtained isometrically. In the intact heart stroke volume is a function of δL. Ventricular end-diastolic pressure is a function of resting muscle length. As increments of resting muscle length increased δL, increasing ventricular end-diastolic pressure augmented stroke volume. Increasing the load carried by the muscle (afterload) at a given resting muscle length increased work performed by the papillary muscle. Similarly, increasing aortic pressure increased stroke work for a given ventricular end-diastolic pressure in the intact heart. In the papillary muscle time to maximal δL was an inverse function of maximal velocity of shortening (Vmax), but independent of both Lr and afterload. The inverse relation of time to max δL and Vmax were shown for norepinephrine and frequency. In the intact heart time to peak ventricular pressure, was found to be largely independent of ventricular end-diastolic and aortic pressures and inversely related to the inotropic state of the myocardium. Contractility of the papillary muscle strictly defined by Vmax and Po, was thus characterized by time to maximal δL, as well as δL. Contractility of the ventricle at a given ventricular end-diastolic pressure could then be defined by stroke volume and peak pressure time, which are indices of force and velocity.


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