Biomedical subjects

S N Hussain

Publications and source records attributed to S N Hussain.

At least 19 recordsLinked to original sources

PubMed1992

Effects of diaphragmatic ischemia on the inspiratory motor drive.

To assess the effect of diaphragmatic ischemia on the inspiratory motor drive, we studied the in situ isolated and innervated left diaphragm in anesthetized, vagotomized, and mechanically ventilated dogs. The arterial and venous vessels of the left diaphragm were catheterized and isolated from the systemic circulation. Inspiratory muscle activation was assessed by recording the integrated electromyographic (EMG) activity of the left and right costal diaphragms and parasternal intercostal and alae nasi muscles. Tension generated by the left diaphragm during spontaneous breathing attempts was also measured. In eight animals, left diaphragmatic ischemia was induced by occluding the phrenic artery for 20 min, followed by 10 min of reperfusion. This elicited a progressive increase in EMG activity of the left and right diaphragms and parasternal and alae nasi muscles to 170, 157, 152, and 128% of baseline values, respectively, an increase in the frequency of breathing efforts, and no change in left diaphragmatic spontaneous tension. Thus the ratio of left diaphragmatic EMG to tension rose progressively during ischemia. During reperfusion, only the frequency of breathing efforts and alae nasi EMG recovered completely. In four additional animals, left diaphragmatic ischemia was induced after the left phrenic nerve was sectioned. Neither EMG activity of inspiratory muscles nor respiratory timing changed significantly during ischemia. In conclusion, diaphragmatic ischemia increases inspiratory motor drive through activation of phrenic afferents. The changes in alae nasi activity and respiratory timing indicate that this influence is achieved through supraspinal pathways.

Afferent Pathways↗

PubMed1992

Role of endothelium-derived relaxing factor in active hyperemia of the canine diaphragm.

To assess the effect of endothelium-derived relaxing factor (EDRF) on diaphragmatic vascular resistance at rest and during contractions, we studied an in situ isolated diaphragm preparation in anesthetized and mechanically ventilated dogs. The arterial supply of the left diaphragm (phrenic artery) was catheterized and perfused with arterial blood at a fixed flow rate. Drugs were infused through a side port of the arterial catheter at 1/100th of the phrenic arterial flow. The inferior phrenic vein was catheterized to complete the isolation from the systemic circulation. Three sets of experiments were performed. In set 1 (n = 3), we infused endothelium-dependent (acetylcholine, ACh) and endothelium-independent (sodium nitroprusside, SNP) dilators at increasing concentrations. ACh and SNP infusion elicited a dose-dependent decline in phrenic vascular resistance (Rphr) at concentrations greater than 10(-8) M and 0.50 micrograms/ml, respectively. In set 2 (n = 15), we infused an inhibitor of EDRF synthesis and release, L-argininosuccinic acid (ArgSA), at increasing concentrations (10(-4), 3 x 10(-4), and 6 x 10(-4) M). ArgSA produced a dose-dependent increase in Rphr. Infusion of another EDRF inhibitor (NG-nitro-L-arginine, LNA, 6 x 10(-4) M) elicited increase in Rphr similar to that induced by ArgSA. In set 3 (n = 25), we infused ArgSA or LNA (6 x 10(-4) M) simultaneously with ACh and SNP and during sustained (2-Hz) contractions of the diaphragm. Both ArgSA and LNA completely reversed ACh vasodilation, whereas SNP vasodilation was reversed by 26 and 11%, respectively. ArgSA or LNA infusion during contractions reversed vasodilation by 48 and 52%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1992

Effect of phrenic afferent stimulation on pattern of respiratory muscle activation.

Ventilation and electromyogram (EMG) activities of the right hemidiaphragm, parasternal intercostal, triangularis sterni, transversus abdominis, genioglossus, and alae nasi muscles were measured before and during central stimulation of the left thoracic phrenic nerve in 10 alpha-chloralose anesthetized vagotomized dogs. Pressure in the carotid sinuses was fixed to maintain baroreflex activity constant. The nerve was stimulated for 1 min with a frequency of 40 Hz and stimulus duration of 1 ms at voltages of 5, 10, 20, and 30 times twitch threshold (TT). At five times TT, no change in ventilation or EMG activity occurred. At 10 times TT, neither tidal volume nor breathing frequency increased sufficiently to reach statistical significance, although the change in their product (minute ventilation) was significant (P less than 0.05). At 20 and 30 times TT, increases in both breathing frequency and tidal volume were significant. At these stimulus intensities, the increases in ventilation were accompanied by approximately equal increases in the activity of the diaphragm, parasternal, and alae nasi muscles. The increase in genioglossus activity was much greater than that of the other inspiratory muscles. Phrenic nerve stimulation also elicited inhomogeneous activation of the expiratory muscles. The transversus abdominis activity increased significantly at intensities from 10 to 30 times TT, whereas the activity of the triangularis sterni remained unchanged. The high stimulation intensities required suggest that the activation of afferent fiber groups III and IV is involved in the response. We conclude that thin-fiber phrenic afferent activation exerts a nonuniform effect on the upper airway, rib cage, and abdominal muscles and may play a role in the control of respiratory muscle recruitment.

Animals↗

PubMed1992

Oxygen delivery-independent effect of blood flow on diaphragm fatigue.

To determine the effect of blood flow on diaphragm fatigue independent of oxygen delivery, the left hemidiaphragm was vascularly isolated in 14 pentobarbital-anesthetized, mechanically ventilated dogs. Fatigue (decline in tension generation) of the left diaphragm was induced by phrenic nerve stimulation at 10 Hz, 12/min, duty cycle of 0.5 for 8 min. Two stimulation periods separated by 30 min of rest were performed in each animal. Diaphragmatic O2 delivery during the two periods was the same. In Group 1 (n = 8), the diaphragm was autoperfused from the femoral artery (high O2-low flow) during the first stimulation period. The tension generated by the diaphragm during this period declined progressively to 47.7% of initial values. In the second period in this group, the diaphragm was pump perfused with arterial blood, diluted with an equal volume of 6% dextran at a flow rate twice that of the first period (low O2-high flow). Tension in this period declined to 76% of initial tension (p less than 0.05 compared with high O2-low flow). In Group 2 (n = 6), stimulation performed while perfusing the diaphragm in the first period with diluted arterial blood at a flow rate twice that recorded during autoperfusion (low O2-high flow) produced a decline in tension to 70% of the initial values. In the second period, the diaphragm was perfused with undiluted arterial blood at a flow rate equal to 50% of that of the first period (high O2-low flow). Tension during this period declined to 56% of initial values (p less than 0.05 compared with low O2-high flow).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Respiratory muscle activation by limb muscle afferent stimulation in anesthetized dogs.

In 10 chloralose anaesthetized and spontaneously breathing dogs, we assessed the effect of limb muscle afferents on the peak integrated EMG activities of the genioglossus, alae nasi, costal diaphragm, parasternal intercostal, triangularis sterni, and transverse abdominis muscles. The influence of vagal and baroreceptor afferents were eliminated by vagotomy and perfusion of carotid sinuses at a constant pressure. Muscle afferents were activated by stimulating the central end of the gastrocnemius nerve for 1 min at 40 Hz and at different voltages. Stimulation at voltages equal to 5, 10 and 20 times twitch-threshold increased minute ventilation to 165, 216 and 250% of pre-stimulation values, respectively, which was achieved by increasing breathing frequency (shortening of the inspiratory and expiratory times) and tidal volume. The activity of the parasternal intercostal and alae nasi muscles increased by a similar degree to that of the diaphragm while the activities of the genioglossus and transverse abdominis were augmented to a greater degree than that of the diaphragm. On the other hand, the motor drive to triangularis sterni increased significantly only at 20 times twitch-threshold and to a lesser degree than that to the diaphragm. These results suggest that upper airway, inspiratory and expiratory rib cage and abdominal muscles may be independently regulated. Differences in the sensitivity of these muscles to the activation of limb muscle afferents can be explained by a complex pattern of central projections of these afferents on the central respiratory controllers or by intrinsic properties of the motor output of these controllers.

Animals↗

PubMed1991

The effect of level of contraction on the electromyographic power spectrum of the diaphragm in pigs.

We investigated the relationship between the frequency components of myoelectric power spectra of the diaphragm and the level of diaphragmatic contraction in seven anaesthetized spontaneously breathing pigs. Electromyographic activity of the costal and crural portions of the diaphragm were recorded with fish-hook electrodes and the frequency-power spectra during inspiration were computed and expressed in terms of centroid frequency (fc). Diaphragmatic force was indirectly assessed as transdiaphragmatic pressure (Pdi) which was measured with balloon-catheter systems placed in the abdomen and oesophagus. The relationships between Pdi and costal and crural fc were assessed during brief (2 min) and incremental increases in diaphragmatic contraction, achieved by gradual occlusion of the inspiratory line of the breathing circuit. When Pdi was increased to 128, 191, 287 and 421% of the value measured during unobstructed breathing, costal and crural fc rose significantly in all animals because of an increase in the power of high-frequency components and a decline in the power of low-frequency components. Both costal and crural fc returned to control values within 5 min of the release of inspiratory occlusion. Our results indicate that the level of contraction is an important determinant of the diaphragmatic myoelectric power spectrum and should be taken into consideration when using power spectral analysis to diagnose diaphragmatic mechanical failure.

Animals↗

PubMed1991

Chemical activation of thin-fiber phrenic afferents. 2. Cardiovascular responses.

To assess the effects of groups III and IV (thin-fiber) phrenic afferents on arterial pressure, heart rate, and distribution of cardiac output, we injected capsaicin into phrenic arteries of in situ isolated and innervated left diaphragms of dogs anesthetized with chloralose, vagotomized, and mechanically ventilated. Blood flow in the ascending aorta, common carotid, renal, superior mesenteric, and femoral arteries was measured by electromagnetic and Doppler flow probes. Injection of 1 mg capsaicin into the left phrenic artery produced congruent to 15% increase in mean arterial pressure and congruent to 7% increase in heart rate with no change in aortic flow. Phrenic arterial flow decreased by 64%, renal arterial flow by 16%, and superior mesenteric arterial flow by 10%, whereas carotid flow increased by 13% and flow to the right gastrocnemius muscle did not change. Mean arterial pressure, heart rate, and blood flow distribution (with the exception of the decline in phrenic blood flow) returned to baseline within 60 s of the injection. Injection of 1.5 mg capsaicin into the right isolated and innervated gastrocnemius produced congruent to 35% increase in mean arterial pressure, 17% rise in heart rate, and no change in aortic blood flow. Phrenic and carotid arterial flow rose by 240 and 41%, respectively, whereas renal and superior mesenteric flow declined by 50 and 20%, respectively. In conclusion, thin-fiber phrenic afferents have an excitatory effect on arterial pressure and heart rate. They redistribute blood flow away from the renal and intestinal vascular beds and toward the carotid vascular bed. On the other hand, the cardiovascular reflex from thin-fiber phrenic afferents seems less potent than that from limb muscle afferents.

Afferent Pathways↗

PubMed1991

Diaphragmatic intramuscular pressure in relation to tension, shortening, and blood flow.

We used an in situ isolated diaphragmatic preparation in anesthetized dogs to relate intramuscular pressure (IMP) to the blood flow, tension, and shortening of the diaphragm. In this preparation, the diaphragm shortens in a fashion similar to the intact diaphragm. Tension was measured by transducers attached to the left costal margin, which was detached from the rib cage and abdomen; IMP was measured by a miniature transducer placed between muscle fibers; length was measured by sonomicrometry; and diaphragmatic blood flow was monitored by measuring left phrenic arterial flow. In protocol 1, the relationships between tension, shortening, and IMP were assessed by stimulating the diaphragm for 2 s at various frequencies. Tension and shortening increased with increasing stimulation frequency up to 50 Hz with no change thereafter. Tension was linearly related to IMP. Similarly, there was a linear relationship between the degree of shortening and IMP; however, the slopes varied considerably between dogs. In protocol 2, the diaphragm was paced intermittently (12 trains/min, duty cycle of 0.5) with a gradual increase in stimulation frequency. Blood flow during contraction phase rose slightly at low tension and then declined significantly when tension exceeded 30% of maximum, whereas relaxation-phase flow increased with the increase in tension. IMP rose linearly with the increase in tension, and the IMP, at the point where contraction-phase flow became severely limited, was 50 +/- 14 mmHg (mean +/- SE). We conclude the following. 1) IMP is linearly related to tension and shortening; however, because tension and shortening changed simultaneously during contractions, the independent relationship of either tension or shortening and IMP remained untested.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Chemical activation of thin-fiber phrenic afferents: respiratory responses.

In supine chloralose-anesthetized and mechanically ventilated dogs, we assessed the effects of group III and IV thin-fiber phrenic afferents on cardiorespiratory control by injecting capsaicin into the phrenic artery of an in situ isolated and innervated left diaphragm. Inspiratory motor drive was assessed by measuring the electromyogram of left and right diaphragm, left parasternal, and mylohyoid muscles in five protocols. 1) Three boluses (2 ml) of capsaicin (1, 10, and 50 micrograms/ml) were injected 30 min apart. Only the 50-micrograms/ml injection elicited a significant increase in arterial pressure, heart rate, and inspiratory motor drive. 2) Repeated doses of capsaicin were tested. The pressor and hyperpneic responses were weakened. 3) High doses of capsaicin (100 and 500 micrograms/ml) were given. Hyperpneic and pressor responses were similar to those elicited by the 50-micrograms/ml dose. 4) When the left phrenic nerve was sectioned, the pressor and hyperpneic responses to the 50-micrograms/ml injection were abolished. 5) Capsaicin (50 micrograms/ml) was infused into the arterial supply of the in situ vascularly isolated and innervated gastrocnemius. Arterial pressure, breathing frequency, and inspiratory motor drive to all inspiratory muscles increased significantly and to a greater degree than in the diaphragm. In conclusion, diaphragmatic thin-fiber afferents have an excitatory effect on the inspiratory motor drive and arterial pressure that is similar to that seen in limb muscles.

Animals↗

PubMed1989

Effects of tension, duty cycle, and arterial pressure on diaphragmatic blood flow in dogs.

We investigated the selective effects of changes in transdiaphragmatic pressure (Pdi) and duty cycle on diaphragmatic blood flow in supine dogs at normal arterial pressure (N), moderate hypotension (MH), and severe hypotension (SH) [mean arterial pressure (Part) of 116, 75, and 50 mmHg, respectively]. The diaphragm was paced at a rate of 12/min by bilateral phrenic nerve stimulation. Left phrenic (Qphr-T) and left internal mammary (Qim-T) arterial flows were measured by electromagnetic flow probes. Changes in Pdi and duty cycle were achieved by changing the stimulation frequencies and the duration of contraction, whereas Part changes were produced by bleeding. With N and at a duty cycle of 0.5, incremental increases in Pdi produced peaks in Qphr-T and Qim-T at 30% maximum diaphragmatic pressure (Pdimax) with a gradual decline at higher Pdi. With MH and SH, blood flow peaked at 10% Pdimax. At any given Pdi, blood flow was lower with MH and SH in comparison to N. The effect of duty cycle was tested at two levels of Pdi. With N and at low Pdi (25% Pdimax), blood flow rose progressively with increases in duty cycle, whereas at moderate Pdi level (50% Pdimax) blood flow peaked at a duty cycle of 0.3, with no increase thereafter. With MH, blood flow at low Pdi rose linearly with increasing duty cycle but to a lesser extent than with N, and at a moderate Pdi flow peaked at a duty cycle of 0.3. With SH, blood flow at low and moderate Pdi was limited at duty cycles greater than 0.3 and 0.1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

In situ isolated perfused and innervated left hemidiaphragm preparation.

We developed a vascularly isolated in situ preparation of the left hemidiaphragm in which arterial blood was only provided through the left phrenic artery and the venous blood only drained through the phrenic vein. The costal margins were secured and connected to three force transducers. Muscle shortening was measured by sonomicrometry. The presence of arterial collaterals between the left hemidiaphragm and the systemic circulation was excluded by the systemic injection of a vital dye (Lissamine Green), a neuromuscular blocking agent (succinylcholine), and by the injection of epinephrine. Left phrenic nerve stimulation produced homogeneous shortening and tension. The degree of shortening in the isolated and intact left diaphragm at the same resting length was similar. The preparation was stable for 2 h with less than 10% decline in maximum tension. Two advantages of this preparation are particularly important. 1) Diaphragmatic energetics can be studied independently of systemic factors, and 2) the role of phrenic nerve afferents in the control of breathing and systemic circulation can easily be assessed without activating nonphrenic nerve afferents.

Animals↗

PubMed1988

Autoregulation of diaphragmatic blood flow in dogs.

In eight anesthetized spontaneously breathing dogs, we determined whether diaphragmatic blood flow is dependent on arterial blood pressure (Pa) or whether it is autoregulated. We also determined whether diaphragmatic muscular activity affects the degree of autoregulation. We measured blood flow through the left phrenic artery (Qphr) with an electromagnetic flow probe and decreased Pa in steps by controlled hemorrhage. Phrenic venous blood was sampled to allow the calculation of diaphragmatic O2 consumption (VO2phr). Diaphragmatic energy demands were varied by using three inspiratory resistances (R1, R2, and R3), which increased peak transdiaphragmatic pressure two-, three-, and fourfold, respectively. During quiet breathing, Qphr was independent of Pa between Pa of 90 and 120 mmHg (i.e., plateau of pressure-flow relation), but at lower Pa, Qphr was directly related to Pa. During inspiratory loading, the Qphr plateau ended at a higher Pa than with quiet breathing, but within the normal ranges of Pa there still was a plateau. VO2phr at a given work load was constant between Pa of 70 and 120 mmHg, but at Pa of 50-55 mmHg, VO2phr declined with all work loads. We conclude that in spontaneously breathing dogs 1) Qphr is autoregulated over the normal range of blood pressures and 2) VO2phr is maintained over wider ranges of Pa than Qphr.

Animals↗

PubMed1988

Diaphragmatic energetics and blood flow during pulmonary edema and hypotension.

We studied the role of O2 supply and demand factors for producing diaphragmatic failure in a canine model of cardiogenic shock with pulmonary edema. We produced pulmonary edema with oleic acid and then hypotension with cardiac tamponade and followed the animals until respiratory failure began, which was defined by a 50% fall in frequency of breathing and diaphragmatic pressure-time index (PTI; cmH2O.s-1.min-1) with no decrease in the diaphragmatic electromyogram. Regional blood flows were measured with radiolabeled microspheres. Diaphragmatic O2 consumption (VO2 di) (ml.min-1.100 g-1) was determined from the diaphragmatic blood flow (Qdi) and the arterial and phrenic venous O2 contents. With oleic acid-induced pulmonary edema, PTI Qdi, and VO2 di increased from control of 101.7 +/- 31.7, 17 +/- 1.8, and 0.81 +/- 0.11, respectively, to 187.2 +/- 27.6, 42.2 +/- 7.2, and 3.32 +/- 0.35 (P less than 0.05). With tamponade, PTI did not change (186.7 +/- 60.0), whereas VO2 di increased further to 3.98 +/- 0.98 (P less than 0.05) due to increased O2 extraction and no significant change in Qdi (32.8 +/- 4.0). As fatigue developed, VO2 di decreased to 2.30 +/- 0.23 due to the combined effects of small declines in Qdi and the arterial O2 content but remained higher than control even though the energy demands returned to control values. In conclusion, when cardiogenic shock is added to pulmonary edema VO2 di and energy output do not increase further and eventually fall.

Animals↗

PubMed1988

Relationship among EMG and contractile responses of the diaphragm elicited by hypotension.

In a canine model, we investigated the effects of severe hypotension on the indexes of diaphragmatic failure. We measured 1) the transdiaphragmatic pressure obtained in response to 20- and 100-Hz stimulation of phrenic nerves (Pdi20 and Pdi100), 2) the power spectrum of diaphragmatic electromyogram (EMG), 3) the ratio of integrated diaphragmatic EMG to Pdi (Edi/Pdi), and 4) the rate of relaxation of Pdi100 and Pdi20. Arterial blood pressure (Pa) was reduced to 40-50 mmHg by a balloon inflated in the inferior vena cava and was maintained at this level until Pdi100 declined to 75% of the control value (100% shock time, ST). A recovery period of 60 min at normal Pa was allowed. During hypotension, Pdi100 and Pdi20 declined only at 100% ST [95.0 +/- 13.0 (SE) min]; however, only Pdi100 recovered within 15 min. The power spectrum shifted to low frequencies early and progressively during shock period. Edi/Pdi rose significantly at 80 and 100% ST and recovered within 15 min. The relaxation rate of Pdi20 and Pdi100 increased significantly at 100% ST only. We conclude that 1) diaphragmatic contractility is depressed during severe hypotension, 2) changes in the power spectrum occurred first in the shock state, followed by alterations in Edi/Pdi, and subsequently both changes in the frequency-pressure curve and relaxation rate occurred last.

Animals↗

PubMed1987

Effects of norepinephrine and fluid administration on diaphragmatic O2 consumption in septic shock.

The effects of norepinephrine infusion and fluid administration on diaphragmatic O2 consumption during endotoxic shock were assessed in spontaneously breathing anesthetized dogs. Blood flow was measured with the microsphere technique, and diaphragmatic venous blood was obtained via a catheter inserted into the left inferior phrenic vein. One group of dogs (n = 6) received 10 mg/kg Escherichia coli endotoxin intravenously (E group). In the second and third groups, blood pressure after endotoxin injection was restored by continuous infusion of norepinephrine tartrate (N group) or by infusion of normal saline and dextran infusion (F group). The animals were observed for 2 h after endotoxin injection. Cardiac output fell significantly in the E and N group, whereas it was restored in the F group. Minute ventilation and diaphragmatic pressure-time index rose twofold in the three groups of dogs. Diaphragmatic O2 consumption (VO2 di) increased substantially in the E group to a mean value of 3.46 ml X 100 g-1 X min-1, which was achieved by higher blood flow and by an increase in O2 extraction. In the N group, VO2 di was higher than control but was lower than that of the E group (mean value of 1.43 ml X 100 g-1 X min-1), which was achieved solely by increasing O2 extraction. In the F group, VO2 di was also lower than that of the E group (mean value of 1.51 ml X 100 g-1 X min-1), which was achieved by high diaphragmatic blood flow. Thus, at any given diaphragmatic task, the diaphragm consumed less O2 in the N and F group than in the E group.

Animals↗

PubMed1986

Respiratory muscle energetics during endotoxic shock in dogs.

Respiratory muscle O2 consumption, lactate production, and endogenous substrate utilization during endotoxic shock were assessed in two groups of anesthetized spontaneously breathing dogs. In the endotoxin group (Escherichia coli endotoxin 10 mg/kg iv) and the sham group (saline iv), we sampled diaphragm, external intercostal, and gastrocnemius muscle tissue for glycogen and lactate concentrations before and after 3 h of the experimental period. Only in the endotoxin group did blood pressure and cardiac output decline significantly. Arterial O2 content did not change significantly during shock, whereas mixed venous, phrenic venous, and femoral venous O2 contents dropped to 8.0 +/- 1.1, 5.8 +/- 0.8, and 3.6 +/- 0.6 ml/dl at 60 min of shock, respectively, with little change thereafter. At 30 min of shock, femoral venous lactate rose higher than arterial values, whereas at 90 min of shock, onward, phrenic venous lactate was significantly higher than arterial concentrations. All muscle tissues showed significant lactate production and glycogen depletion after shock. In a second set of experiments we measured respiratory muscle blood flow during shock with radioactive microspheres. At 60 min of shock, diaphragmatic and intercostal blood flow rose by six- and twofold, respectively, whereas gastrocnemius blood flow declined significantly. We conclude that during endotoxin shock 1) the increased demands of the respiratory muscles are met by increasing blood flow and O2 extraction; 2) anaerobic metabolism and respiratory muscle substrate depletion, or both, may contribute to the observed fatigue.

Animals↗

PubMed1985

Effects of separate rib cage and abdominal restriction on exercise performance in normal humans.

We assessed the effects of selective restriction of movements of the rib cage (Res,rc) and abdomen (Res,ab) on ventilatory pattern, transdiaphragmatic pressure (Pdi), and electrical activity of the diaphragm (Edi) in five normal subjects exercising at a constant work rate (80% of maximum power output) on a cycle ergometer till exhaustion. Restriction of movements was achieved by an inelastic corset applied tightly around the rib cage or abdomen. Edi was recorded by an esophageal electrode, rectified, and then integrated, and peak values during inspiration were measured. Each subject exercised at the same work rate on 3 days: with Res,rc, with Res,ab, and without restriction (control). Res,rc but not Res,ab reduced exercise time (tlim). Up to tlim, minute ventilation (VE) was similar in all three conditions. At any level of VE, however, Res,rc decreased tidal volume and inspiratory and expiratory time, whereas Res,ab had no effect on the pattern of breathing. Res,ab was associated with higher inspiratory Pdi swings at any level of VE, whereas peak Edi was similar to control. Inspiratory Pdi swings were the same with Res,rc as control, but the peak Edi for a given Pdi was greater with Res,rc (P less than 0.05). During Res,rc the abdominal pressure swings in expiration were greater than with Res,ab and control. We conclude that Res,rc altered the pattern of breathing in normal subjects in high-intensity exercise, decreased diaphragmatic contractility, increased abdominal muscle recruitment in expiration, and reduced tlim. On the other hand, Res,ab had no effect on breathing pattern or tlim but was associated with increased diaphragmatic contractility.

Abdomen↗

PubMed1985

Inspiratory muscle function with restrictive chest wall loading during exercise in normal humans.

The effects of selective restriction of rib cage (Res,rc) and abdominal wall (Res,ab) movements on endurance of short-term constant-load heavy exercise and on diaphragmatic function during such exercise were examined in five normal young men. An inelastic surgical corset was used to achieve Res,rc and Res,ab. Subjects exercised on a cycle ergometer at 80% of their maximum power output to exhaustion on three occasions: with Res,rc, with Res,ab, and without restriction of chest wall movements (control). Transdiaphragmatic (Pdi), esophageal, and gastric pressures were measured. Electromyogram of the diaphragm was recorded by an esophageal electrode, and the ratio of the power content of a high-frequency to low-frequency band (H/L ratio) was measured. In addition, maximum Pdi (Pdimax) pre- and immediately postexercise was recorded. Res,rc was associated with a shorter endurance time, a progressive decline of the H/L ratio, and a significant reduction of Pdimax postexercise, whereas no such changes were found with Res,ab. We conclude that diaphragmatic function was well defended with abdominal wall loading, whereas limitation of rib cage expansion reduced diaphragmatic endurance during exercise. The diaphragmatic tension-time index (TTdi) in exercise was always less than the critical value of 0.15 found by Bellemare and Grassino (J. Appl. Physiol. 53: 1190-1195, 1982) when subjects inspired against large resistive loads at normal minute ventilations. We suggest that the higher inspiratory flow rate (P less than 0.05) and breathing frequency (P less than 0.05) account for the occurrence of diaphragmatic fatigue in exercise with Res,rc when the TTdi was 0.06 +/- 0.02.

Abdominal Muscles↗