Ex vivo biomechanical behavior of abdominal aortic aneurysm: Assessment using a new mathematical model

Knowledge of the biomechanical behavior of abdominal aortic aneurysm (AAA) as compared to nonaneurysmal aorta may provide information on the natural history of this disease. We have performed uniaxial tensile testing of excised human aneurysmal and nonaneurysmal abdominal aortic specimens. A new mathematical model that conforms to the fibrous structure of the vascular tissue was used to quantify the measured elastic response. We determined for each specimen the yield σ_y and ultimate σ_u strengths, the separate contribution to total tissue stiffness by elastin (E _E) and collagen (E _C) fibers, and a collagen recruitment parameter (A), which is a measure of the tortuosity of the collagen fibers. There was no significant difference in any of these mechanical properties between longitudinal and circumferential AAA specimens, nor inE _E andE _C between longitudinally oriented aneurysmal and normal specimens.A, σ_y, and σ_u were all significantly higher for the normal than for the aneurysmal group:A=0.223±0.046versus A=0.091±0.009 (mean ± SEM;p<0.0005), σ_y versus σ_y (p<0.05), and σ_u versus σ_u (p<0.0005), respectively. Our findings suggest that the AAA tissue is isotropic with respect to these mechanical properties. The observed difference inA between aneurysmal and normal aorta may be due to the complete recruitment and loading of collagen fibers at lower extensions in the former. Our data indicate that AAA rupture may be related to a reduction in tensile strength and that the biomechanical properties of AAA should be considered in assessing the severity of an individual aneurysm.     

Effect of repetitive stimulation on cell volume and its relationship to membrane potential in amphibian skeletal muscle

The effect of electrical stimulation on cell volume, V _c, and its relationship to membrane potential, E _m, was investigated in Rana temporaria striated muscle. Confocal microscope xz-plane scanning and histology of plastic sections independently demonstrated significant and reversible increases in V _c of 19.8±0.62% (n=3) and 27.1±8.62% (n=3), respectively, after a standard stimulation protocol. Microelectrode measurements demonstrated an accompanying membrane potential change, ΔE _m, of +23.6±0.98 mV (n=3). The extent to which this ΔE _m might contribute to the observed changes in V _c was explored in quiescent muscle exposed to variations in extracellular potassium concentration, [K⁺]_e. E _m and V _c varied linearly with log [K⁺]_e and [K⁺]_e, respectively, in the range 2.5–15 mM (R ²=0.99 and 0.96), and these results were used to reconstruct an approximately linear relationship between V _c and E _m (ΔV _c=0.85E _m+68.53; R ²=0.99) and hence derive the ΔV _c expected from the ΔE _m during stimulation. This demonstrated that both the time course and magnitude of the increase and recovery of V _c observed in active muscles could be reproduced by the corresponding [K⁺]_e-induced depolarisation in quiescent muscles, suggesting that the depolarisation associated with membrane activity makes a substantial contribution to the cell swelling during exercise. Furthermore, conditions of Cl⁻ deprivation abolished the relationship between E _m and V _c, supporting a mechanism in which the depolarisation of E _m drives a passive redistribution of Cl⁻ and hence cellular entry of Cl⁻ and K⁺ and an accompanying, osmotically driven, increase in V _c.     

Amplitude of human head movements associated with horizontal saccades

 Human saccades may or may not be associated with head movements. To date, little attention has been devoted to the mechanisms determining head movement recruitment and scaling. Normal human subjects made horizontal, centrifugal saccades along an encircling array of light-emitting diodes. Measurements of gaze, head, and eye-in-head angle were made at the conclusion of the head movement (or at the end of the eye movement in eye-only saccades). We found that head movement amplitude (ΔH) related in a simple fashion to the eye eccentricity that would have resulted if the gaze shift had been performed without a head movement. Plots of ΔH vs this predicted eye eccentricity (E _PRED) had a central flat region in which gaze shifts were unaccompanied by head movements (the eye-only range) and two flanking lobes in which ΔH was a linear function of E _PRED (the eye-head ranges). ΔH correlated with E _PRED better than with gaze shift amplitude, as would be expected if head movements were controlled so as to keep eye eccentricity within a particular range. Head movement tendencies were quantified by the width of the eye-only range, the slope of the eye-head range, and the width of the region within which the eye was likely to be found at the conclusion of the completed gaze-shifting behavior (the customary ocular motor range). The measures ranged widely in these normal subjects: 35.8±31.9° for the eye-only range (mean±SD), 0.77±0.16 for the slope of the eye-head range, and 44.0±23.8° for the customary ocular motor range. Yet for a given subject, the measurements were reproducible across experimental sessions, with the customary ocular motor range being the most consistent measure of the three. The form of the ΔH vs E _PRED plots suggests that the neural circuitry underlying eye-head coordination carries out two distinct functions – gating the head movement and scaling the head movement. The reason for the large intersubject variability of head movement tendencies is unknown. It does not parallel intersubject differences in full-scale eye (in orbit) range or full-scale neck range. Received: 25 June 1998 / Accepted: 23 November 1998     

V˙E and V˙CO2 remain tightly coupled during incremental cycling performed after a bout of high-intensity exercise

The purpose of the present study was to determine whether the linear relationship between CO₂ output (V˙CO₂) and pulmonary ventilation (V˙ _E) is altered during incremental cycling performed after exercise-induced metabolic acidosis. Ten untrained, female subjects performed two incremental cycling tests (15 W · min⁻¹ up to 165 W) on separate days. One incremental exercise test was conducted without prior exercise, whereas the other test was preceded by a 1-min bout of maximal cycling. The ventilatory equivalent for O₂ (V˙ _E/V˙O₂) was only elevated above control values at 15–60 W during incremental cycling performed after high-intensity exercise. In contrast, the ventilatory equivalent for CO₂ (V˙ _E/V˙CO₂) was significantly increased above control levels at nearly every work stage of incremental work (all except 165 W). Hyperventilation relative to V˙CO₂ was confirmed by the significantly lower end-tidal CO₂ tension (P _ETCO₂) obtained throughout the incremental cycling that was performed after high-intensity exercise (except at 165 W). V˙ _E and V˙CO₂ were significantly correlated under both treatment conditions (r > 0.99; P < 0.001). Moreover, both the slope and y-intercept of the linear regression were found to be significantly elevated during the incremental cycling performed after high-intensity cycling compared to control conditions (P < 0.01). The increase in the slope of the V˙ _E-V˙CO₂ relationship during incremental exercise performed under these conditions does not represent an uncoupling of V˙ _E from V˙CO₂, but could be accounted for by the significantly lower P _ETCO₂ observed during exercise. Accepted: 20 June 1997     

Streaming potentials during the confined compression creep test of normal and proteoglycan-depleted cartilage

The streaming potential response of cartilage in the confined compression creep configuration was assessed theoretically and measured experimentally in normal and proteoglycan-depleted tissue. The analytical solution, using the linear biphasic continuum model including electrokinetics and assuming homogeneous material properties, predicted that: (i) the peak streaming potentials is ΔV=k_e·Δσ, where k_e is the electrokinetic coefficient and Δσ is the change in compressive stress; (ii) the potential is maintained at 95 to 100% of the peak value of 0<t<0.10τ, where τ is the gel diffusion time constant; and (iii) during short times, 0<t<0.01 τ, 90% of the peak streaming potential occurs over a region extending 23% into the tissue sample. Experimentally, adult bovine cartilage disks, 0.5 mm thick, were subjected to step changes of compressive stress. The measured changes in potential indicated a linear response for changes in stress up to 0.10 MPa. The k_e of normal cartilage, estimated from the short time (0<t<2 sec) change in potential, was −1.65±1.25 mV/MPa. Digestion of cartilage by chondroitinase ABC resulted in an increased (less negative) k_e of −0.75±0.70 mV/MPa and a 33±29% depletion of anionic glycosaminoglycan, whereas digestion with trypsin resulted in a further increase in k_e to +1.64±0.95 mV/MPa and a 98±1% depletion of glycosaminoglycan. The streaming potential measurement may be a useful addition to the widely used confined compression creep test to assess cartilage material properties.     

Causes of differences in exercise-induced changes of base excess and blood lactate

It has been concluded from comparisons of base excess (BE) and lactic acid (La) concentration changes in blood during exercise-induced acidosis that more H⁺ than La⁻ leave the muscle and enter interstitial fluid and blood. To examine this, we performed incremental cycle tests in 13 untrained males and measured acid–base status and [La] in arterialized blood, plasma, and red cells until 21 min after exhaustion. The decrease of actual BE (−ΔABE) was 2.2 ± 0.5 (SEM) mmol l⁻¹ larger than the increase of [La]_blood at exhaustion, and the difference rose to 4.8 ± 0.5 mmol l⁻¹ during the first minutes of recovery. The decrease of standard BE (SBE), a measure of mean BE of interstitial fluid (if) and blood, however, was smaller than the increase of [La] in the corresponding volume (Δ[La]_if+blood) during exercise and only slightly larger during recovery. The discrepancy between −ΔABE and Δ[La]_blood mainly results from the Donnan effect hindering the rise of [La]_erythrocyte to equal values like [La]_plasma. The changing Donnan effect during acidosis causes that Cl⁻ from the interstitial fluid enter plasma and erythrocytes in exchange for HCO₃⁻. A corresponding amount of La⁻ remains outside the blood. SBE is not influenced by ion shifts among these compartments and therefore is a rather exact measure of acid movements across tissue cell membranes, but changes have been compared previously to Δ[La]_blood instead to Δ[La]_if+blood. When performing correct comparisons and considering Cl⁻/HCO₃⁻ exchange between erythrocytes and extracellular fluid, neither the use of ΔABE nor of ΔSBE provides evidence for differences in H⁺ and La⁻ transport across the tissue cell membranes.     

Extracellular bicarbonate and non-bicarbonate buffering against lactic acid during and after exercise

Defense of extracellular pH constancy against lactic acidosis can be estimated from changes (Δ) in lactic acid ([La]), [HCO₃⁻], pH and PCO₂ in blood plasma because it is equilibrated with the interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 13 untrained (UT) and 21 endurance-trained (TR) males to find out if acute and chronic exercise influence the defense. During exercise the capacity of non-bicarbonate buffers (β_nbi = −Δ[La] · ΔpH⁻¹ − Δ[HCO₃⁻] · ΔpH⁻¹) available for the extracellular fluid (mainly hemoglobin, dissolved proteins and phosphates) amounted to 32 ± 2(SEM) and 20 ± 2 mmol l⁻¹ in UT and TR, respectively (P < 0.02). During recovery β_nbi decreased to 14 (UT) and 12 (TR) mmol l⁻¹ (both P < 0.001) corresponding to values previously found at rest by in vivo CO₂ titration. Bicarbonate buffering (β_bi) amounted to 44–48 mmol l⁻¹ during and after exercise. The large exercise β_nbi seems to be mainly caused by an increasing concentration of all buffers due to shrinking of the extracellular volume, exchange of small amounts of HCO₃⁻ or H⁺ with cells and delayed HCO₃⁻ equilibration between plasma and interstitial fluid. Increase of [HCO₃⁻] during titration by these mechanisms augments total β and thus the calculated β_nbi more than β_bi because it reduces ΔpH and Δ[HCO₃⁻] at constant Δ[La]. The smaller rise in exercise β_nbi in TR than UT may be caused by an increased extracellular volume and an improved exchange of La⁻, HCO₃⁻ and H⁺ between trained muscles and blood.     

Extracellular pH defense against lactic acid in untrained and trained altitude residents

The assumption that buffering at altitude is deteriorated by bicarbonate (bi) reduction was investigated. Extracellular pH defense against lactic acidosis was estimated from changes (Δ) in lactic acid ([La]), [HCO₃ ⁻], pH and PCO₂ in plasma, which equilibrates with interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 10 untrained (UT) and 11 endurance-trained (TR) highlanders (2,600 m). During exercise the capacity of non-bicarbonate buffers (β _nbi = −Δ[La] · ΔpH⁻¹ − Δ[HCO₃ ⁻] · ΔpH⁻¹) amounted to 40 ± 2 (SEM) and 28 ± 2 mmol l⁻¹ in UT and TR, respectively (P < 0.01). During recovery β _nbi decreased to 20 (UT) and 16 (TR) mmol l⁻¹ (P < 0.001) corresponding to values expected from hemoglobin, dissolved protein and phosphate concentrations related to extracellular fluid (ecf). This was accompanied by a larger decrease of base excess after than during exercise for a given Δ[La]. β _bi amounted to 37–41 mmol l⁻¹ being lower than at sea level. The large exercise β _nbi was mainly caused by increasing concentrations of buffers due to temporary shrinking of ecf. Tr has lower β _nbi in spite of an increased Hb mass mainly because of an expanded ecf compared to UT. In highlanders β _nbi is higher than in lowlanders because of larger Hb mass and reduced ecf and counteracts the decrease in [HCO₃ ⁻]. The amount of bicarbonate is probably reduced by reduction of the ecf at altitude but this is compensated by lower maximal [La] and more effective hyperventilation resulting in attenuated exercise acidosis at exhaustion.     

Thermoregulatory responses of circum-pubertal children

Passive temperature lability of nine circumpubertal children [11.4 (1.2) years] was compared to that of nine young adult males [26.6 (5.2) years]. Each subject completed a 20-min period of exercise, followed immediately by post-exercise immersion in water at 28°C. The aim of the exercise protocol was to induce a steady rate of sweating (E _SW) while the postexercise immersion period induced cooling of the core region (tympanic temperature:T _ty). TheT _ty values (relative to rest, ΔT _ty) at which sweating abated and at which shivering commenced were defined as the thresholds for the cessation of sweating and onset of shivering, respectively. While there was no significant difference between the ΔT _ty sweating thresholds, the onset of shivering, as reflected in the oxygen uptake response, occurred at significantly higher (P < 0.05) ΔT _ty values in the children [mean (SD): −0.07 (0.07)°C] than in the adults [−0.22 (0.10)°C]. The slope of theE _SW/ΔT _ty relationship was found to be significantly lower in the children (z = −5.64;P < 0.05), while the slopes of the /ΔT _ty relationship were not significantly different (z = −0.84;P > 0.05). Skin blood perfusion was measured at the forehead (SkBP), and the slope of the SkBP/ΔT _ty relationship across the nullzone was significantly less in the children than in the adults (z = −2.13;P < 0.05) with the greatest reduction in perfusion occurring prior to the offset of sweating in the children. The subjective ratings of thermal comfort indicated that the children were more sensitive to changes in core temperature than the adults. It is concluded that maturation plays an important role in modifying thermoregulatory responses to deviations in core temperature. These results suggest that there may be differences in thermoregulatory “strategies” which are maturationally related.     

Attenuated β-adrenoceptor-mediated cardiac contractile responses following androgenic steroid administration to sedentary rats

Androgenic steroids administered in doses at pharmacological levels to sedentary animals have been shown to result in a reduced β-adrenoceptor-mediated increase in systolic cardiac performance when assessed in vivo. Whether the attenuated adrenergic response occurs as a consequence of alterations in either cardiac loads, heart rate, modifications in left ventricular (LV) geometry, or a decrease in myocardial contractile performance has not been determined. In this study the effect of chronic administration (over 3 months) of an androgenic steroid (nandrolone decanoate, 5 mg · kg⁻¹ biweekly) on the response of load-insensitive indices of myocardial contractile function [the slope of the LV systolic stress-strain relationship (LV-Eⁿ _max, where Eⁿ _max is systolic myocardial elastance)] to an adrenergic-inotropic stimulus was examined ex vivo in paced rat hearts. Systolic cardiac performance was assessed at 300 beats · min⁻¹ in isolated constant flow perfused heart preparations both before and during 10^−8.5 mol · l⁻¹ isoproterenol (ISO) infusion (approximate concentration of ISO eliciting 50% maximal inotropic response to ISO). Steroid administration resulted in left-shifted LV systolic and diastolic pressure-volume (P-V ) relationships. The leftshifted P-V relationships were attributed, in part, to increased slopes of these relationships. However, the steroid-mediated increment in the slope of the systolic P-V relationship (systolic chamber elastance, E_max) was not associated with a similar change in LV Eⁿ _max [control 19.2 (SEM 2.1) g · cm⁻², steroid 18.3 (SEM 2.4) g . cm⁻²] as determined in the absence of ISO. Isoproterenol infusion resulted in an increase in both E_max and Eⁿ _max in the control rats, without altering systolic performance in the steroid treated rats. Consequently, in the presence of ISO, the steroid treated rats exhibited a similar E_max, but a reduction in Eⁿ _max compared to the control rats [control 25.6 (SEM 1.9) g · cm⁻², steroid 18.5 (SEM 1.5) g · cm⁻²; P < 0.05]. In conclusion, these results would suggest that chronic high dose androgenic steroid administration produces a decrease in myocardial contractile reserve to β-adrenoceptor stimulation. Accepted: 3 September 1999     

Extracellular pH defense against lactic acid in normoxia and hypoxia before and after a Himalayan expedition

The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios −Δ[La] · ΔpH⁻¹ (where Δ[La] is change in lactic acid concentration and ΔpH is change in pH) and Δ[HCO₃ ⁻] · ΔpH⁻¹ (where Δ[HCO₃ ⁻] is change in bicarbonate concentration) in blood plasma. The difference between −Δ[La] · ΔpH⁻¹ and Δ[HCO₃ ⁻] · ΔpH⁻¹ yields the capacity of available non-bicarbonate buffers (mainly hemoglobin). In turn, Δ[HCO₃ ⁻] · ΔpH⁻¹ can be separated into a pure bicarbonate buffering (as calculated at constant carbon dioxide tension) and a hyperventilation effect. These quantities were measured in 12 mountaineers during incremental exercise tests before, and 7–8 days (group 1) or 11–12 days (group 2) after their return from a Himalayan expedition (2800–7600 m altitude) under conditions of normoxia and acute hypoxia. In normoxia −Δ[La] · ΔpH⁻¹ amounted to [mean (SEM)] 92 (6) mmol · l⁻¹ before altitude, of which 19 (4), 48 (1) and 25 (3) mmol · l⁻¹ were due to hyperventilation, bicarbonate and non-bicarbonate buffering, respectively. After altitude −Δ[La] · ΔpH⁻¹ was increased to 128 (12) mmol · l⁻¹ (P < 0.01) in group 1 and decreased to 72 (5) mmol · l⁻¹ in group 2 (P < 0.05), resulting mainly from apparent large changes of non-bicarbonate buffer capacity, which amounted to 49 (14) mmol · l⁻¹ in group 1 and to 10 (2) mmol · l⁻¹ in group 2. In acute hypoxia the apparent increase in non-bicarbonate buffers of group 1 was even larger [140 (18) mmol · l⁻¹]. Since the hemoglobin mass was only modestly elevated after descent, other factors must play a role. It is proposed here that the transport of La⁻ and H⁺ across cell membranes is differently influenced by high-altitude acclimatization. Accepted: 14 September 2000     

Estimation of transmembrane potential of thymic lymphocytes during dexamethasone-induced apoptosis

The use of potential-sensitive fluorescent probes allowed us to estimate transmembrane potentials of the plasma (Δφ_p) and mitochondrial (Δφ_m) membranes of rat thymocytes, which were −58±3 mV and −169±7 mV, respectively. Dexamethasone-induced apoptosis led to a significant decrease in Δφ_p (by 55%) and Δφ_m (by 17%). This effects of dexamethasone was dose- and time-dependent. Changes in Δφ_m were greater and preceded those in Δφ_p. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 127, No. 1, pp. 117–120, January, 1999     

Elastic modulus of prepared canine jejunum,a new vascular graft material

The submucosal connective tissue of the jejunum has been shown to be suitable for use as a vascular graft in preliminary dog studies. To partially characterize the mechanical properties of this new graft material, longitudinal stress (σ)-strain (ε)-data were obtained on 13 specimens of canine jejunum, stripped of its mucosal and external smooth-muscle layers. The ratio of stress to strain is the modulus of elasticity (E). It was found that the stress σ-strain ε-data fitted the expressionγ=K∈ ^α very well. For a typical specimenγ=2.69×10⁶∈^2.33. The modulus of elasticity (E=γ ^1-1/α K ^1/α) was found to increase with increasing stress, ranging from about 2,000 to 9,000 mmHg. For the average specimenE=573γ ^0.57, where σ is in mmHg, (1 mmHg=133.3 Pascals).     

Noninvasive measurement of arterial elasticity in various human limbs

Arterial elasticity expressed by such indices as volume elastic modulus E_v and compliance C_a were noninvasively measured in various human limb segments; the upper arms, forearms, fingers, thighs, calves and toes. These indices are defined, respectively, as and C_a=ΔV/ΔP, where ΔP is pulse pressure, mean arterial volume and ΔV its pulsatile variation. ΔP was calculated from systolic P_as and mean P_am arterial pressures determined by volume oscillometric sphygmomanometry using the following equation: and the ΔV were detected by electrical admittance plethysmography at various transmural pressure P_t levels controlled by a compression cuff. The values obtained in these limb segments were compared with each other at P_t levels 0,30 and 60 mm Hg and the differences between them were discussed.     

Estimation of cardiomyocyte transmembrane potential with potential-sensitive fluorescent probes

Transmembrane potentials on the plasma (Δφ₄) and mitochondrial (Δφ_m) membrane of isolated rat cardiomyocytes were estimated using the potential-sensitive fluorescent probe DSM. The values were −93±4 and −196±11 mV, respectively. Sufan significantly decreased the reduction of Δφ_m induced by chemical hypoxia. The effects of antiarrhythmic drugs on changes in Δφ_p were studied using the fluorescent probe dis-C₃-(5). Lidocaine, novocainamide, richlocaine, and leocaine blocked depolarization of the myocyte plasma membrane induced by electrical stimulation and did not affect the Δφ_m. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 126, No. 11, pp. 594–597, November, 1998     

A Numerical Model of the Respiratory Modulation of Pulmonary Shunt and PaO<Subscript>2</Subscript> Oscillations for Acute Lung Injury

It is an accepted hypothesis that the amplitude of the respiratory-related oscillations of arterial partial pressure of oxygen (ΔPaO₂) is primarily modulated by fluctuations of pulmonary shunt (Δs), the latter generated mainly by cyclic alveolar collapse/reopening, when present. A better understanding of the relationship between ΔPaO₂, Δs, and cyclic alveolar collapse/reopening can have clinical relevance for minimizing the severe lung damage that the latter can cause, for example during mechanical ventilation (MV) of patients with acute lung injury (ALI). To this aim, we numerically simulated the effect of such a relationship on an animal model of ALI under MV, using a combination of a model of lung gas exchange during tidal ventilation with a model of time dependence of shunt on alveolar collapse/opening. The results showed that: (a) the model could adequately replicate published experimental results regarding the complex dependence of ΔPaO₂ on respiratory frequency, driving pressure (ΔP), and positive end-expiratory pressure (PEEP), while simpler models could not; (b) such a replication strongly depends on the value of the model parameters, especially of the speed of alveolar collapse/reopening; (c) the relationship between ΔPaO₂ and Δs was overall markedly nonlinear, but approximately linear for PEEP ≥ 6 cmH₂O, with very large ΔPaO₂ associated with relatively small Δs.     

Exercise-induced changes in blood levels of alpha-tocopherol

Levels of α-tocopherol (αT) in plasma and red blood cells (RBC) are assumed to be modulated by exercise. The mechanisms involved remain to be established. We examined the influence of different running bouts on the content of αT in RBC (αT_RBC), the concentration in plasma (αT_plasma), and their relationship with lipolysis, as indicated by changes (Δ) in plasma glycerol concentration ([glycerol]). Eleven healthy runners [mean (SD) age 35 (9) years, height 177.3 (7.6) cm, body mass 69.6 (9.4) kg, and peak oxygen consumption, , 57.8 (4.8) ml^.kg^–1.min^–1] performed an incremental treadmill test [duration 17 (2) min, peak velocity, v _peak 4.8 (0.4) m^.s^–1], a training run [173 (12) min, 57 (4)% v _peak] and a marathon [197 (24) min, 75 (5)% v _peak]. Before (pre) and after (post) each run, haematological and lipid parameters, αT_RBC and αT_Plasma were determined. Haemoconcentration was observed after each run. Δ[glycerol] was +0.10 (0.10) mmol^.l^–1, +0.40 (0.14) mmol^.l^–1 and +0.51 (0.15) mmol^.l^–1 in the treadmill test, training run and marathon, respectively. When corrected for haemoconcentration, values of αT_plasma decreased [–5.4 (7.5)%, P<0.05] in the treadmill test, were unchanged [+0.7 (8.7)%] in the training run and increased [+7.8 (8.3)%, P<0.05] in the marathon. αT_RBC decreased [pre vs post: 22.7 (3.2) nmol^.g haemoglobin^–1 (nmol^.g Hb^–1) vs 18.9 (3.8) nmol^.g Hb^–1, P<0.05] in the treadmill test and was not significantly changed in either the training run [20.8 (1.9) nmol^.g Hb^–1 vs 19.1 (3.0) nmol^.g Hb^–1] or the marathon [21.6 (2.9) nmol^.g Hb^–1 vs 23.4 (2.7) nmol^.g Hb^–1]. ΔαT_RBC and ΔαT_plasma were positively related to Δ[glycerol]. The reduction in αT_RBC and αT_plasma after short-lasting heavy exercise indicates the consumption of αT, whereas the association between ΔαT and Δ[glycerol] suggests mobilisation of αT, especially in long-lasting exercises. However, although αT appears to be influenced by exercise, the results suggest a well-balanced regulation of αT during exercise resulting in small, and only in part, significant ΔαT in blood. Electronic Publication     

Estimation of the retainer height biomechanical contribution in posterior resin-bonded fixed partial dentures: a structural-thermal coupled finite element analysis

This study determines the RBFPD (resin-bonded fixed partial dentures) biomechanical aspects to retainer height using structural-thermal coupled finite element (FE) analysis under normal (37°C) and high (51°C) oral temperatures. Three RBFPD FE models with different retainer heights (100, 75, and 50% of the distance from 2 mm above the CE (cementum-enamel) junction to the occlusal surface) were created using image processing, contour stacking, and mapping mesh procedures. After FE model validation, the maximum first principal and von Mises stresses in the remaining tooth (σ_T) and prosthesis (σ_P), were recorded for all models under structural-thermal coupled analyses. The simulation results showed that the σ_T and σ_p values decreased with greater retainer height as a result of the increasing prosthesis stiffness and maximizing bonding area between the enamel and retainer at normal oral temperature (37°C). However, no significant stress differences were found according to the retainer height varying dimensions at high (51°C) temperatures. The RBFPD retainer height biomechanical response is dominated by the structural analysis result (at 37°C) and it is recommended that the prosthesis retainer have as great a height as possible to decrease the stress values.     

Exercise with hypoventilation induces lower muscle oxygenation and higher blood lactate concentration: role of hypoxia and hypercapnia

Eight men performed three series of 5-min exercise on a cycle ergometer at 65% of normoxic maximal O₂ consumption in four conditions: (1) voluntary hypoventilation (VH) in normoxia (VH_0.21), (2) VH in hyperoxia (inducing hypercapnia) (inspired oxygen fraction [F_IO₂] = 0.29; VH_0.29), (3) normal breathing (NB) in hypoxia (F_IO₂ = 0.157; NB_0.157), (4) NB in normoxia (NB_0.21). Using near-infrared spectroscopy, changes in concentration of oxy-(Δ[O₂Hb]) and deoxyhemoglobin (Δ[HHb]) were measured in the vastus lateralis muscle. Δ[O₂Hb − HHb] and Δ[O₂Hb + HHb] were calculated and used as oxygenation index and change in regional blood volume, respectively. Earlobe blood samples were taken throughout the exercise. Both VH_0.21 and NB_0.157 induced a severe and similar hypoxemia (arterial oxygen saturation [SaO₂] < 88%) whereas SaO₂ remained above 94% and was not different between VH_0.29 and NB_0.21. Arterialized O₂ and CO₂ pressures as well as P50 were higher and pH lower in VH_0.21 than in NB_0.157, and in VH_0.29 than in NB_0.21. Δ[O₂Hb] and Δ[O₂Hb − HHb] were lower and Δ[HHb] higher at the end of each series in both VH_0.21 and NB_0.157 than in NB_0.21 and VH_0.29. There was no difference in Δ[O₂Hb + HHb] between testing conditions. [La] in VH_0.21 was greater than both in NB_0.21 and VH_0.29 but not different from NB_0.157. This study demonstrated that exercise with VH induced a lower tissue oxygenation and a higher [La] than exercise with NB. This was caused by a severe arterial O₂ desaturation induced by both hypoxic and hypercapnic effects.     

Mechanisms of reduced mitochondrial Ca2+ accumulation in failing hamster heart

Mitochondrial Ca²⁺ plays important roles in the regulation of energy metabolism and cellular Ca²⁺ homeostasis. In this study, we characterized mitochondrial Ca²⁺ accumulation in Syrian hamster hearts with hereditary cardiomyopathy (strain BIO 14.6). Exposure of isolated mitochondria from 70 nM to 30 μM Ca²⁺ ([Ca²⁺]_o) caused a concentration-dependent increase in intramitochondrial Ca²⁺ concentrations ([Ca²⁺]_m). The [Ca²⁺]_m was significantly lower in cardiomyopathic (CMP) hamsters than in healthy hamsters when [Ca²⁺]_o was higher than 1 μM and a decrease of about 52% was detected at [Ca²⁺]_o of 30 μM (916 ± 67 nM vs 1,932 ± 132 nM in control). A possible mechanism responsible for the decreased mitochondrial Ca²⁺ uptake in CMP hamsters is the depolarization of mitochondrial membrane potential (Δψ _m). Using a tetraphenylphosphonium (TPP⁺) electrode, the measured Δψ _m in failing heart mitochondria was −136 ± 1.5 mV compared with −159 ± 1.3 mV in controls. Analyses of mitochondrial respiratory chain demonstrated a significant impairment of complex I and complex IV activities in failing heart mitochondria. In summary, a less negative Δψ _m resulting from defects in the respiratory chain may lead to attenuated mitochondrial Ca²⁺ accumulation, which in turn may contribute to the depressed energy production and myocardial contractility in this model of heart failure. In addition to other known impairments of ion transport in sarcoplasmic reticulum and plasma membrane, results from this paper on mitochondrial dysfunctions expand our understanding of the molecular mechanisms leading to heart failure.