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Biomedical subjects

G Ferretti

Publications and source records attributed to G Ferretti.

At least 199 records · Page 11Linked to original sources

Energy cost and efficiency of riding aerodynamic bicycles.

Traction resistance (Rt) was determined by towing two cyclists in fully dropped posture on bicycles with an aerodynamic frame with lenticular wheels (AL), an aerodynamic frame with traditional wheels (AT), or a traditional frame with lenticular wheels (TL) in calm air on a flat wooden track at constant speed (8.6-14.6 m.s-1). Under all experimental conditions, Rt increased linearly with the square of air velocity (v2a); r2 equal to greater than 0.89. The constant k = delta Rt/delta v2a was about 15% lower for AL and AT (0.157 and 0.155 N.s2 x m-2) than for TL bicycles (0.184 N.s2 x m-2). These data show firstly, that in terms of mechanical energy savings, the role of lenticular wheels is negligible and, secondly, that for TL bicycles, the value of k was essentially equal to that found by others for bicycles with a traditional frame and traditional wheels (TT). The energy cost of cycling per unit distance (Cc, J.m-1) was also measured for AT and TT bicycles from the ratio of the O2 consumption above resting to speed, in the speed range from 4.7 to 11.1 m.s-1. The Cc also increased linearly with v2a, as described by: Cc = 30.8 + 0.558 v2a and Cc = 29.6 + 0.606 v2a for AT and TT bicycles. Thus from our study it would seem that AT bicycles are only about 5% more economical than TT at 12.5 m.s-1 the economy tending to increase slightly with the speed.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerobiosis↗

Ventilatory response to exercise after heart and lung denervation in humans.

This study, aimed at investigating some aspects of breathing control at work, was conducted on 8 heart and lung transplant recipients (HLTR) (age 33 +/- 13 years, mean +/- SD; 10 +/- 6 months post-transplantation) and on two control groups, i.e. 11 heart transplant recipients (HTR) and 11 healthy untrained subjects (C). The patients performed a series of 2 to 6 1-min exercise bouts (at 25 or 50 W, corresponding to about 50% of their VO2max) on a bicycle ergometer, followed by a 5 min 25 or 50 W constant load. C exercised both at 50 W (C1) and at 50% of their VO2max (C2). Inspiratory (VI) and expiratory (VE) ventilation, tidal volume (VT), respiratory frequency (fR), end-tidal O2 and CO2 partial pressures (PETO2 and PETCO2 and gas exchange (VO2 and VCO) were measured breath-by-breath. "Phase I" ventilatory response (ph I) was determined as the mean changes of VI, VE, VT, fR, PETO2 and PETCO2, compared to rest, during the first two respiratory cycles following exercise onset. In HLTR ph I did not significantly differ from that of C1 and C2, whereas the response was lower in HTR. VE, VO2 and VCO2 responses during "phase II" (t 1/2 on-) and "phase III" (steady state exercise) were similar in HLTR and in HTR. t 1/2 on- were longer in HLTR and in HTR compared to C1. In 3 HLTR the ventilatory pattern during the 5 min constant loads was similar to that of HTR and C, whereas 4 HLTR presented higher VT and lower fR values. It is concluded that: 1) The ventilatory response to exercise, in all its phases, is substantially preserved despite lung denervation. When slight alterations are found (i.e. the slower phase II), they are presumably of peripheral origin. 2) The normal ph I in HLTR indicates that cardiac and/or pulmonary inputs to the respiratory centers are not involved in its regulation, or that their role can be subserved by other ventilatory control mechanisms.

Adolescent↗

Limitations to VO2max in humans after blood retransfusion.

Seven young, healthy male subjects performed maximal exercise on a cycloergometer with central venous and arterial catheters, before and after autologous retransfusion of red blood cells. Maximal oxygen consumption (VO2max), blood gas composition and haemodynamic variables were measured, in order to test the hypothesis of monofactorial vs. polyfactorial VO2max limitation. Autologous blood retransfusion led to significant increases in haemoglobin concentration and consequently arterial oxygen concentration during maximal exercise, while maximal cardiac output, heart rate and stroke volume were not significantly changed. The relationship between maximal oxygen delivery (cardiac output.arterial oxygen concentration; (Q.CaO2)max and maximal oxygen consumption in this study was VO2max (L.min-1) = 0.02 + 0.64.(Q.CaO2)max (L.min-1), the slope being significantly less than unity. These results suggest that (Q.CaO2)max plays but a fractional role in limiting VO2max, in agreement with recent models concerning the resistance to oxygen flow in the respiratory system (di Prampero and Ferretti, Respir. Physiol. 80: 113-128, 1990). The relative increase in VO2max after blood retransfusion matched the relative increase in 'aerobic performance', measured as the maximal power output that could be maintained aerobically for 30 min. Furthermore, the increase in maximal power output (15 +/- 3 watts) could account for almost all of the extra oxygen consumption. This match suggests that there is an inability to fully utilize muscle oxidative capacity in the normocythaemic state.

Adult↗

Maximal lactic capacity at altitude: effect of bicarbonate loading.

The aim of the present study was to test the hypothesis that the net maximal blood lactate accumulation ([La]max) during heavy exercise in lowlanders acclimatized to chronic hypoxia may be limited by the reduced bicarbonate stores. Six men [age 32 +/- 4 (SD) yr] performed supramaximal exercise until voluntary exhaustion at sea level (204 +/- 54 W) and after sojourning for 1 mo at 5,050 m (175 +/- 23 W), without (C) and with (B) oral sodium-bicarbonate loading (0.3 g/kg body wt). Exhaustion time, arterial blood lactate concentration, arterial pH (pHa), arterial PCO2, and intramuscular pH were measured at rest and after exercise. At sea level, exhaustion time increased from 6.5 +/- 2.8 min in C to 7.5 +/- 2.7 min in B (P < 0.05). At altitude, exhaustion times were similar to the sea level C values and the same in C and B. At sea level, resting pHa increased from 7.41 +/- 0.02 in C to 7.46 +/- 0.03 in B (P < 0.001); the corresponding values at altitude were 7.46 +/- 0.04 and 7.55 +/- 0.03 (P < 0.001). Postexercise pHa at sea level was 7.22 +/- 0.02 in C and 7.25 +/- 0.08 in B (NS). After exercise at altitude, pHa was 7.32 +/- 0.04 and 7.44 +/- 0.03 in C and B, respectively (P < 0.001). [La]max increased from 12.86 +/- 1.45 mM in C to 16.63 +/- 1.76 mM in B (P < 0.01) at sea level and from 6.85 +/- 1.40 mM in C to 7.95 +/- 1.74 mM in B (NS) at altitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

Changes of plasma lipids and erythrocyte membrane fluidity in psoriatic children.

Psoriasis has been associated with an abnormal plasma lipid metabolism, and changes of erythrocyte membrane lipid composition and fluidity have been shown in adult patients. To investigate whether the alterations of plasma lipids appear also in pediatric patients, we have studied plasma lipids and lipoproteins in 15 prepubertal children affected by mild-to-moderate psoriasis with respect to healthy controls. The patients showed higher levels of plasma total cholesterol (4.44 +/- 0.78 versus 4.03 +/- 0.58 mmol/L), a significant increase of cholesterol associated with HDL (1.39 +/- 0.26 versus 1.13 +/- 0.28 mmol/L, p = 0.02), and a significant decrease of the ratio LDL cholesterol to HDL cholesterol (1.73 +/- 0.6 versus 2.46 +/- 0.8, p = 0.02). By using fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene, we have shown a significant increase in fluidity in erythrocyte membrane of psoriatic children that was associated with a slight, but not significant, decrease in the cholesterol to protein ratio (422 +/- 127 versus 503 +/- 117 nmol/mg). No significant changes of phospholipid fatty acid composition have been shown, in disagreement with previous studies in adult patients. Our results support the relation between childhood psoriasis and plasma lipid changes, which are likely related to the slight compositional changes in erythrocytes. However, the observed abnormalities are expressed differently in children than in adults.

Apolipoproteins↗

[Intrathoracic hydatid cyst. Contribution of tomodensitometry. Apropos of 25 cases].

Twenty-five cases of thoracic hydatic disease, studied by CT since 1982, are reviewed. Fifteen patients were Maghrebin, 10 were native. The lungs were interested 22 times, the mediastinum 3 times and the heart only once. Complications of hydatic disease were present 8 times. We compare contribution of CT to the other diagnosis criterious. Our results show the accuracy of CT for the diagnosis of non complicated cyst and the lack of specificity for complicated cysts.

Echinococcosis↗

Physico-chemical properties of copper-oxidized high density lipoprotein: a fluorescence study.

The modifications of the physico-chemical properties of the high density lipoprotein (HDL) before and after in vitro induced oxidation by copper ions have been studied using the fluorescence polarization (Pf) of the phosphatidylcholine derivative of 1,6-diphenyl-1,3,5-hexatriene (DPH-PC) and of the cationic derivative (TMA-DPH). We have observed that HDL oxidation is associated with a decrease of the molecular order at the lipoprotein surface as demonstrated by the increase in Pf with respect to untreated HDL. Moreover in oxidized HDL the polarity-sensitive probe laurdan has shown a decrease of the polarity in its microenvironment. It has been suggested that a decrease in HDL fluidity would inhibit cholesterol reverse transport from peripheral tissues in form of HDL core cholesteryl esters. Peroxidation of HDL, if occurring in vivo, could contribute to the progress of atherogenesis by decreasing cholesterol efflux from peripheral tissues.

Copper↗

Central sleep apnoea syndrome with upper airway collapse.

We report on an 83 yr old man with hypersomnia and central sleep apnoea (CSA). He had several possible causes for CSA, including a central nervous system lesion, hypocapnia and anatomical narrowing of the airway at the hypopharyngeal level. We postulate that reduced central respiratory drive occurring in conjunction with upper airway narrowing may have led to central apnoeas. These in turn could have facilitated a complete passive hypopharyngeal collapse at the end of each apnoea, as visualized by somnofluoroscopy. The CSA could also have been favoured by respiratory instability due to chronic hypocapnia.

Aged↗

The energy cost of walking or running on sand.

Oxygen uptake (VO2) at steady state, heart rate and perceived exertion were determined on nine subjects (six men and three women) while walking (3-7 km.h-1) or running (7-14 km.h-1) on sand or on a firm surface. The women performed the walking tests only. The energy cost of locomotion per unit of distance (C) was then calculated from the ratio of VO2 to speed and expressed in J.kg-1.m-1 assuming an energy equivalent of 20.9 J.ml O2-1. At the highest speeds C was adjusted for the measured lactate contribution (which ranged from approximately 2% to approximately 11% of the total). It was found that, when walking on sand, C increased linearly with speed from 3.1 J.kg-1.m-1 at 3 km.h-1 to 5.5 J.kg-1.m-1 at 7 km.h-1, whereas on a firm surface C attained a minimum of 2.3 J.kg-1.m-1 at 4.5 km.h-1 being greater at lower or higher speeds. On average, when walking at speeds greater than 3 km.h-1, C was about 1.8 times greater on sand than on compact terrain. When running on sand C was approximately independent of the speed, amounting to 5.3 J.kg-1.m-1, i.e. about 1.2 times greater than on compact terrain. These findings could be attributed to a reduced recovery of potential and kinetic energy at each stride when walking on sand (approximately 45% to be compared to approximately 65% on a firm surface) and to a reduced recovery of elastic energy when running on sand.

Adult↗

Effects of temperature on the maximal instantaneous muscle power of humans.

The maximal instantaneous muscle power (wi,max) probably reflects the maximal rate of adenosine 5'-triphosphate (ATP) hydrolysis (ATPmax), a temperature-dependent variable, which gives rise to the hypothesis that temperature, by affecting ATPmax, may also influence wi,max. This hypothesis was tested on six subjects, whose vastus lateralis muscle temperature (Tmuscle) was monitored by a thermocouple inserted approximately 3 cm below the skin surface. The Wi,max was determined during a series of high jumps off both feet on a force platform before and after immersion up to the abdomen for 90 min in a temperature controlled (T = 20 +/- 0.1 degrees C) water bath. Control Tmuscle was 35.8 +/- 0.7 degrees C, with control Wi,max being 51.6 (SD 8.7) W.kg-1. After cold exposure, Tmuscle decreased by about 8 degrees C, whereas wi,max 27% lower. The temperature dependence of Wi,max was found to be less (Q10 less than 1.5, where Q10 is the temperature coefficient as calculated in other studies) than reported in the literature for ATPmax. Such a low Q10 may reflect an increase in the mechanical equivalent of ATP splitting, as a consequence of the reduced velocity of muscle contraction occurring at low Tmuscle.

Adenosine Triphosphate↗

Heart rate overshoot at the beginning of muscle exercise.

A characteristic notch in the heart rate (fc) on-response at the beginning of square-wave exercise is described in 7 very fit marathon runners and 12 sedentary young men, during cycle tests at 30% and 60% of maximal oxygen consumption (VO2max). The fc notch revealed a fc overshoot with respect to the fc values predicted from exponential beat-by-beat fitted models. While at 30% of VO2max all subjects showed a fc overshoot, at 60% of VO2max it occurred in the marathon runners but not in the sedentary subjects. The mean time of occurrence of the fc overshoot from the onset of the exercise was 16.7 (SD 4.7) s and 12.2 (SD 3.2) s at 30% of VO2max in the runners and the sedentary subjects respectively, and 23.8 (SD 8.8) s at 60% of VO2max in the runners. The amplitude of the overshoot, with respect to rest, was 41 (SD 12) beats.min-1 and 31 (SD 4) beats.min-1 at 30% of VO2max in the runners and the sedentary subjects respectively, and 46 (SD 19) beats.min-1 at 60% of VO2max in the runners. The existence and the amplitude of the fc overshoot may have been related to central command and muscle heart reflex mechanisms and thus may have been indicators of changes in the balance between sympathetic and parasympathetic activity occurring in fit and unfit subjects.

Adult↗

Effects of muscle temperature on the VO2 kinetics at the onset of exercise in man.

The kinetics (i.e. the rate of readjustment) of O2 uptake (VO2) at the mouth of muscle blood flow in the vastus lateralis muscle (Qm), and the net accumulation of lactate in the rest-to-exercise transient (early lactate) were assessed in 6 untrained men (age 31 +/- 8 (SD) yrs) during constant-load 5-min duration exercises on the cyclo ergometer of 75 and 125 W, performed at muscle temperatures (Tm) of 35.5 +/- 0.9 degrees C (N) and of 28.0 +/- 1.65 degrees C (C). VO2 was measured breath-by-breath; Qm was assessed from 133Xe clearance; early lactate was calculated as the difference between the venous lactate concentrations observed after and before exercise. At both work loads, steady-state VO2 was slightly higher in N than in C (P less than 0.05 at 75 W; NS at 125 W). The half-times of VO2 kinetics were: in N, 36.2 +/- 6.7 s at 75 W and 41.6 +/- 8.6 s at 125 W; in C, 41.4 +/- 10.0 at 75 W and 43.8 +/- 14.0 at 125 W (NS). Mean steady state Qm was 8.5 ml.min-1.100 g-1 in C, and 13.4 in N at 75 W (NS); at 125 W, Qm was 18.3 ml.min-1.100 g-1 in C vs. 25.0 in N (NS). The half-times of the Qm kinetics tended to be slower in C than in N (NS). At both work loads, early lactate was slightly greater in C than in N (NS). It is concluded that, at submaximal exercise, (a) steady state VO2 and the VO2 kinetics are not affected by Tm, and (b) at the onset of exercise Qm does not affect VO2 kinetics.

Adult↗

Metabolic transient studies by NMR.

The time course of phosphocreatine (PC) hydrolysis in humans was measured by 31P-NMR spectroscopy (31P-NMRS) with a time resolution of 10.8 s in the gastrocnemius muscle and a relationship between muscle O2 consumption (VO2) and [PC] was derived from a bioenergetic model. This allowed a direct estimate of the half-time of the intracellular VO2 kinetics (t1/2 VO2) of the contracting human gastrocnemius in aerobic conditions. t1/2 VO2 was found to be approximately 16 s and independent of the work load. This value corresponds to the shortest t1/2 VO2 determined at the mouth of the subject in the absence of lactate accumulation in the rest to work transient. t1/2 VO2 may now be assessed in man at low muscle temperatures. To this aim a procedure was developed allowing corrections of the 31P-NMR spectra based on the muscle temperature profiles obtained by a simultaneously acquired proton image.

Adenosine Triphosphate↗

Cold and muscle performance.

The effects of muscle temperature on the development of muscular power are discussed. Temperature influences power (both metabolic and mechanical) by means of its effects on the rate of ATP hydrolysis and/or resynthesis. One would therefore expect reduced power outputs at cold muscle temperatures in humans. However, this is not the case during submaximal aerobic exercise. In fact, no changes in metabolic power output at any given submaximal work load were found at cold muscle temperatures, despite the reduced rate of ATP resynthesis and/or splitting. To explain this, it has been postulated that the fraction of active muscle mass at any given time instant could increase in the cold, thus compensating for the reduced ATP splitting rate. This means that the aerobic ATP resynthesis in the cold may be carried out at a slower rate by a greater activated muscle mass. This compensation cannot be operational when maximal power is attained, for in this case the instantaneously activated muscle mass is constant and limited. In fact the maximal aerobic power and the maximal instantaneous anaerobic power decrease with decreasing muscle temperature, as indicated by an average Q10 of 1.4 in the physiological muscle temperature range. The reduction in maximal aerobic power in the cold may be the consequence particularly of a decrease in O2 supply associated with reduced maximal cardiac output and muscle blood flow. On the other hand, the Q10 of the maximal anaerobic power should strictly depend on the reduced rate of ATP hydrolysis. The Q10 of the latter, however, according to Arrhenius law, should be 2 to 3 instead of 1.4.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

Regulation of perfusive O2 transport during exercise in humans: effects of changes in haemoglobin concentration.

1. Recently it was suggested that submaximal cardiac output (Q) could vary in response to changes in arterial O2 concentration (Ca,O2), so that arterial O2 delivery (Qa,O2 = Q x Ca,O2, in ml min-1) is kept constant. 2. This hypothesis was tested on eight healthy male subjects, at rest and during exercise (50, 100 and 150 W) in three conditions: normaemia (N), after 6 weeks of endurance training (T), and 2 days after subsequent autologous blood reinfusion (P). 3. Measured variables were oxygen consumption (VO2), by open circuit method, Q, by a CO2 rebreathing method, and haemoglobin concentration ([Hb]), by a photometric method. Ca,O2 was calculated as the product of [Hb], arterial O2 saturation (0.97), and the O2 binding coefficient. 4. [Hb] and thus Ca,O2 increased by 2.6% (T vs. N) and subsequently by further 5.8% (P vs. T). VO2 and Qa,O2 were linear functions of power (w), both relationships being unaffected by changes in Ca,O2. As a consequence, the linear Q vs. VO2 relationships were shifted downward as Ca,O2 increased. 5. The VO2 vs. w and the Qa,O2 vs. w relationships had the same slope. Therefore, the difference between Qa,O2 (w) and VO2 (w), equal to O2 flow in mixed venous blood (Qv,O2), was constant. 6. In conclusion, the tested hypothesis was supported by the present results. The observed constancy of Qv,O2 suggested that Qv,O2 may play a key role in regulating the cardiovascular response to exercise.

Adult↗

Somnofluoroscopy, computed tomography, and cephalometry in the assessment of the airway in obstructive sleep apnoea.

BACKGROUND: Assessments of the upper airways in patients with the obstructive sleep apnoea syndrome are usually carried out on awake patients who are upright. The dynamics of the airway in a patient who is asleep and lying down may be different. METHODS: Somnofluoroscopy, computed tomography of the upper airway, and cephalometry were carried out in 11 patients with the obstructive sleep apnoea syndrome (10 male; mean (SD) age 53 (10) years) to examine the airway while they were awake and asleep. RESULTS: At somnofluoroscopy 10 patients were in stage 2 sleep and only one in REM sleep. At least five obstructive events were visualised by lateral fluoroscopy in each patient. Imaging allowed observation of the dynamics of airway collapse, which began in the oropharynx in all cases, progressing to the hypopharynx in 10 cases and to the laryngopharynx in five. At fluoroscopy the soft palate was seen to hook up during airway occlusion in 10 patients, thereby increasing its cross sectional area. It was then sucked down into the hypopharynx. Somnofluoroscopic and cephalometric findings agreed, eight of the 10 patients with hypopharyngeal collapse shown by somnofluoroscopy having an inferiorly placed hyoid bone according to cephalometry (distance from the mandibular plane to the hyoid bone (MP-H distance) increased); the one patient with no hypopharyngeal collapse had a normal MP-H. By contrast, six of the 11 patients had a normal or supranormal hypopharyngeal cross sectional area of the airway on the computed tomogram. CONCLUSIONS: Somnofluoroscopy allows examination of the dynamics of airway closure in this disorder and shows the important role of the soft palate in acting as a plug in the oropharynx. Dynamic studies are required to determine the pattern of pharyngeal obstruction in obstructive sleep apnoea.

Adult↗

Phosphocreatine hydrolysis by 31P-NMR at the onset of constant-load exercise in humans.

The kinetics of phosphocreatine (PC) breakdown in human plantar flexors at the onset of constant-load aerobic exercise was determined by high-resolution 31P-nuclear magnetic resonance spectroscopy (NMRS). The half time of the process (t1/2PC) was obtained by fitting curves (n = 13) from five subjects at various aerobic work loads for which muscle pH was not different from that at rest. Steady-state PC concentration ([PC]) was not < 70% of the resting value and was linearly related to the work load (w) ([PC] = -3.01 +/- 0.08 w + 1 (r = 0.48, 2P < 0.1)). The average t1/2PC was 16.2 s and was independent of work load. Because the half time of the muscle PC kinetics reflects the half time of the O2 uptake (MO2) kinetics (t1/2MO2), the latter is equal to that found earlier in the isolated perfused dog gastrocnemius. Whereas in the dog the above t1/2MO2 compares well with the homologous half time of the O2 uptake at the alveolar level, in humans such equivalence is found only at extremely low work loads, when the transient contribution by anaerobic glycolysis is negligible.

Adult↗