Biomedical subjects

B Grassi

Publications and source records attributed to B Grassi.

At least 37 records · Page 2Linked to original sources

PubMed1998

Peripheral O2 diffusion does not affect V(O2)on-kinetics in isolated insitu canine muscle.

To test the hypothesis that muscle O2 uptake (V(O2)) on-kinetics is limited, at least in part, by peripheral O2 diffusion, we determined the V(O2) on-kinetics in 1) normoxia (Control); 2) hyperoxic gas breathing (Hyperoxia); and 3) hyperoxia and the administration of a drug (RSR-13, Allos Therapeutics), which right-shifts the Hb-O2 dissociation curve (Hyperoxia+RSR-13). The study was conducted in isolated canine gastrocnemius muscles (n = 5) during transitions from rest to 3 min of electrically stimulated isometric tetanic contractions (200-ms trains, 50 Hz; 1 contraction/2 s; 60-70% peak V(O2)). In all conditions, before and during contractions, muscle was pump perfused with constantly elevated blood flow (Q), at a level measured at steady state during contractions in preliminary trials with spontaneous Q x Adenosine was infused intra-arterially to prevent inordinate pressure increases with the elevated Q x Q was measured continuously, arterial and popliteal venous O2 concentrations were determined at rest and at 5- to 7-s intervals during contractions, and V(O2) was calculated as Q x arteriovenous O2 content difference. PO2 at 50% HbO2 saturation (P50) was calculated. Mean capillary PO2 (Pc(O2)) was estimated by numerical integration. P50 was higher in Hyperoxia+RSR-13 [40 +/- 1 (SE) Torr] than in Control and in Hyperoxia (31 +/- 1 Torr). After 15 s of contractions, Pc(O2) was higher in Hyperoxia (97 +/- 9 Torr) vs. Control (53 +/- 3 Torr) and in Hyperoxia+RSR-13 (197 +/- 39 Torr) vs. Hyperoxia. The time to reach 63% of the difference between baseline and steady-state V(O2) during contractions was 24.7 +/- 2.7 s in Control, 26.3 +/- 0.8 s in Hyperoxia, and 24.7 +/- 1.1 s in Hyperoxia+RSR-13 (not significant). Enhancement of peripheral O2 diffusion (obtained by increased PcO2 at constant O2 delivery) during the rest-to-contraction (60-70% of peak V(O2)) transition did not affect muscle V(O2) on- kinetics.

Animals↗

PubMed1997

Efficacy of paroxetine for the treatment of depression in the context of HIV infection.

Recent studies in the literature point out that HIV-infected subjects are affected by depression with a relatively high frequency. The aim of this study was to assess the efficacy and tolerability of paroxetine for the treatment of depression in the context of HIV infection. 15 HIV-infected subjects (10 patients with a major depressive episode and 5 patients with an adjustment disorder with depressed mood, according to the DSM IV diagnostic criteria) were administered paroxetine at a daily dosage of 20 mg. Depressive symptomatology was monitored by means of the Hamilton Rating Scale for Depression (HAM-D) at the time of enrollment and 2 weeks, 4 weeks, and 6 weeks later; at the same times adverse effects were recorded. 14 patients completed the study, and all of these recovered from depression; HAM-D mean scores significantly improved from baseline to final assessment, both when all subjects were considered (ANOVA for repeated measurements: p < or = 0.0001) and when only patients with a major depressive episode were included in the statistical analysis (ANOVA for repeated measurements: p < 0.0001). No significant adverse effects were recorded. Because of its efficacy and good tolerability paroxetine seems to be suitable for the treatment of depression in the context of HIV infection.

Adult↗

PubMed1997

Gas exchange and cardiovascular kinetics with different exercise protocols in heart transplant recipients.

Metabolic and cardiovascular adjustments to various submaximal exercises were evaluated in 82 heart transplant recipients (HTR) and in 35 control subjects (C). HTR were tested 21.5 +/- 25.3 (SD) mo (range 1.0-137.1 mo) posttransplantation. Three protocols were used: protocol A consisted of 5 min of rectangular 50-W load repeated twice, 5 min apart [5 min rest, 5 min 50 W (Ex 1), 5 min recovery, 5 min 50 W (Ex 2)]; protocol B consisted of 5 min of rectangular load at 25, 50, or 75 W; protocol C consisted of 15 min of rectangular load at 25 W. Breath-by-breath pulmonary ventilation (VE), O2 uptake (VO2), and CO2 output (VCO2) were determined. During protocol A, beat-by-beat cardiac output (Q) was estimated by impedance cardiography. The half times (t1/2) of the on- and off-kinetics of the variables were calculated. In all protocols, t1/2 values for VO2 on-, VE on-, and VCO2 on-kinetics were higher (i.e., the kinetics were slower) in HTR than in C, independently of workload and of the time post-transplantation. Also, t1/2 Q on- was higher in HTR than in C. In protocol A, no significant difference of t1/2 VO2 on- was observed in HTR between Ex 1 (48 +/- 9 s) and Ex 2 (46 +/- 8 s), whereas t1/2 Q on- was higher during Ex 1 (55 +/- 24 s) than during Ex 2 (47 +/- 15 s). In all protocols and for all variables, the t1/2 off-values were higher in HTR than in C, In protocol C, no differences of steady-state VE, VO2, and VCO2 were observed in both groups between 5, 10, and 15 min of exercise. We conclude that 1) in HTR, a "priming" exercise, while effective in speeding up the adjustment of convective O2 flow to muscle fibers during a second on-transition, did not affect the VO2 on-kinetics, suggesting that the slower VO2 on- in HTR was attributable to peripheral (muscular) factors; 2) the dissociation between Q on- and VO2 on-kinetics in HTR indicates that an inertia of muscle metabolic machinery is the main factor dictating the VO2 on-kinetics; and 3) the VO2 off-kinetics was slower in HTR than in C, indicating a greater alactic O2 deficit in HTR and, therefore, a sluggish muscle VO2 adjustment.

Adolescent↗

PubMed1996

Temporal lobe electroencephalogram power modifications during olfactory stimulation in HIV-infected patients.

Evidence derived from studies concerning brain metabolism and brain electrical activity suggests that temporal lobe functioning is impaired in the course of HIV infection. To test the hypothesis of temporal lobe dysfunction in HIV infection, we utilized computerized electroencephalogram (EEG) analysis to evaluate temporal lobe EEG power modifications induced by olfactory stimulation in 10 HIV-infected patients as compared with 10 seronegative control subjects. Our findings show that HIV-infected patients respond to olfactory stimulation with an increase in temporal lobe slow electrical activity (theta EEG power), whereas control subjects show a decrease in the same activity. The theta EEG power increase during olfactory stimulation in HIV-infected patients can be interpreted as a paradoxical response of the deep temporal regions to specific procedures, supporting the hypothesis of temporal lobe dysfunction in HIV infection.

Adult↗

PubMed1996

EEG power modifications in obsessive-compulsive disorder during olfactory stimulation.

Temporal lobe electroencephalogram (EEG) activity was quantitatively analyzed in obsessive-compulsive disorder (OCD) when subjects are at rest and during a temporal lobe activating procedure, i.e., olfactory stimulation. At rest with eyes closed, delta-1 and alpha-2 power differences were evident in OCD patients as compared with normal controls. During olfactory stimulation, differences between patients and normal groups were detectable in the slower beta frequencies: Normal subjects showed a power increase, whereas OCD patients showed no modification or slight decrease. Our results support previous findings of temporal lobe EEG abnormalities in OCD patients with an abnormal pattern of response to a temporal lobe activating procedure.

Adult↗

PubMed1996

Peak blood lactate and blood lactate vs. workload during acclimatization to 5,050 m and in deacclimatization.

Peak blood lactate ([Labl]peak) and blood lactate concentration ([Labl]) vs. workload (W) relationships during acclimatization to altitude and in the deacclimatization were evaluated in 10 Caucasian lowlanders at sea level (SL0); after approximately 1 wk (Alt1wk), 3 wk (Alt3wk), and 5 wk (Alt5wk) at 5,050 m; and weekly during the first 5 wk after return to sea level (SL1wk-SL5wk). Incremental bicycle ergometer exercises (30 W added every 4 min up to exhaustion) were performed. At Alt1wk and at Alt5wk, the experiments were repeated in hypobaric normoxia (Alt1wk-O2 and Alt5wk-O2). [Labl] was determined at rest and during the last approximately 30 s of each W. [Labl]peak was taken as the highest [Labl] during recovery. Acid-base status (pH and concentration of HCO-3 in arterialized capillary blood) was determined at rest. Mean [Labl]peak values were 11.5 (SL0), 8.0 (Alt1wk), 6.4 (Alt3wk), 6.3 (Alt5wk), 8.0 (SL1wk), 9.4 (SL2wk), 10.8 (SL3wk), 11.3 (SL4wk), and 11.6 (SL5wk) mM. At Alt1wk-O2 and Alt5wk-O2, peak W increased, compared with Alt1wk and Alt5wk, whereas no changes were observed for [Labl]peak. [Labl] vs. W was shifted to the left (i.e., higher [Labl] values were found for the same W) at Alt1wk compared with SL0 and partially shifted back to the right (i.e., lower [Labl] values were found for the same W) at Alt3wk and Alt5wk. At Alt1wk-O2 and Alt5wk-O2, [Labl] vs. W values were superimposed on that at SL0. At SL1wk-SL5wk, [Labl] vs. W values were shifted to the right compared with that at SL0. At Alt1wk, a condition of respiratory alkalosis was found, which was only partially compensated for during acclimatization. At SL1wk, the acid-base status was back to normal. We conclude that 1) the reduced [Labl]peak at altitude is still present for 2-3 wk after return from altitude; is not attributable to reduced peak W nor to hypoxia per se, nor to a reduced buffer capacity; alternatively, it could be related to some central determinants of fatigue. 2) The [Labl] vs. W leftward shift at altitude was due to hypoxia per se. 3) The factor(s) responsible for the [Labl] vs. W partial rightward shift during acclimatization could still be effective during the first weeks after return to sea level.

Acclimatization↗

PubMed1996

Muscle O2 uptake kinetics in humans: implications for metabolic control.

Muscle O2 uptake (VO2) kinetics in response to an augmented energetic requirement (on-transition) has never been directly determined in humans. We have developed a constant-infusion thermodilution technique that allowed rapid measurements of leg blood flow (Qleg) and, in conjunction with frequent serial measurement of arteriovenous O2 content difference across the leg [(Ca - Cv)O2leg], permitted the determination of the VO2 of the leg (VO2leg) at 3- to 4-s time intervals. VO2leg kinetics during the on-transition was taken as a close approximation of muscle VO2 (VO2mus) kinetics. Alveolar VO2 (VO2A), Qleg, leg O2 delivery [(Q.CaO2leg)], (Ca - Cv)O2leg, and VO2leg kinetics were determined in six trained subjects [age 22.8 +/- 4.4 (SD) yr; maximal O2 uptake 59.1 +/- 5.3 ml.kg-1.min-1] during the transition from unloaded pedaling to a workload (loaded pedaling; LP) (183 +/- 20 W) well below the previously determined ventilatory threshold. For all variables, two distinct phases were recognized. During the first 10-15 s of loaded pedaling (phase I), VO2A, Qleg, and (Q.CaO2)leg increased rapidly, whereas VO2leg increased only slightly and (Ca - Cv)O2leg actually decreased. After phase I, all variables showed a monoexponential increase (phase II), with similar time courses [slightly faster for (Ca - CV)O2leg]. In a consideration of both phases, the half times of the responses among variables were not significantly different: 25.5 +/- 2.6 s for VO2A, 26.6 +/- 7.6 s for Qleg, 26.9 +/- 8.3 s for (Q.CaO2leg, 23.5 +/- 1.3 s for (Ca - Cv)O2leg, and 27.9 +/- 5.7 s for VO2leg. We conclude that during the on-transition the kinetics of VO2A and VO2leg, as measured by these methods, are similar. The analysis of the early phase (first 10-15 s) of the on-transition indicates that bulk delivery of O2 to the working muscles is not limiting VO2leg kinetics. However, the present results cannot discriminate between maldistribution of blood flow/VO2 vs. inertia the intracellular oxidative machinery as the limiting factor.

Adult↗

PubMed1996

Blood flow distribution in working in situ canine muscle during blood flow reduction.

The purpose of this study was to determine whether reduction in apparent muscle O2 diffusing capacity (Dmo2) calculated during reduced blood flow conditions in maximally working muscle is a reflection of alterations in blood flow distribution. Isolated dog gastrocnemius muscle (n = 6) was stimulated for 3 min to achieve peak O2 uptake (VO2) at two levels of blood flow (controlled by pump perfusion): control (C) conditions at normal perfusion pressure (blood flow = 111 +/- 10 ml.100 g-1.min-1) and reduced blood flow treatment [ischemia (I); 52 +/- 6 ml.100 g-1.min-1]. In addition, maximal vasodilation was achieved by adenosine (A) infusion (10(-2)M) at both levels of blood flow, so that each muscle was subjected randomly to a total of four conditions (C, CA, I, and IA; each separated by 45 min of rest). Muscle blood flow distribution was measured with 15-microns-diameter colored microspheres. A numerical integration technique was used to calculate Dmo2 for each treatment with use of a model that calculates O2 loss along a capillary on the basis of Fick's law of diffusion. Peak VO2 was reduced significantly (P < 0.01) with ischemia and was unchanged by adenosine infusion at either flow rate (10.6 +/- 0.9, 9.7 +/- 1.0, 6.7 +/- 0.2, and 5.9 +/- 0.8 ml.100 g-1.min-1 for C, CA, I, and IA, respectively). Dmo2 was significantly lower by 30-35% (P < 0.01) when flow was reduced (except for CA vs. I; 0.23 +/- 0.03, 0.20 +/- 0.02, 0.16 +/- 0.01, and 0.13 +/- 0.01 ml.100 g-1.min-1.Torr-1 for C, CA, I, and IA, respectively). As expressed by the coefficient of variation (0.45 +/- 0.04, 0.47 +/- 0.04, 0.55 +/- 0.03, and 0.53 +/- 0.04 for C, CA, I, and IA, respectively), blood flow heterogeneity per se was not significantly different among the four conditions when examined by analysis of variance. However, there was a strong negative correlation (r = 0.89, P < 0.05) between Dmo2 and blood flow heterogeneity among the four conditions, suggesting that blood flow redistribution (likely a result of a decrease in the number of perfused capillaries) becomes an increasingly important factor in the determination of Dmo2 as blood flow is diminished.

Animals↗

PubMed1996

Pulmonary hemodynamic response to exercise in subjects with prior high-altitude pulmonary edema.

Individuals with a prior history of (susceptible to high altitude pulmonary edema (HAPE-S) have high resting pulmonary arterial pressures, but little data are available on their vascular response to exercise. We studied the pulmonary vascular response to exercise in seven HAPE-S and nine control subjects at sea level and at 3,810 m altitude. At each location, both normoxic (inspired PO2 = 148 Torr) and hypoxic (inspired PO2 = 91 Torr) studies were conducted. Pulmonary hemodynamic measurements included pulmonary arterial and pulmonary arterial occlusion pressures. A multiple regression analysis demonstrated that the pulmonary arterial pressure reactivity to exercise was significantly greater in the HAPE-S group. This reactivity was not influenced by altitude or oxygenation, implying that the response was intrinsic to the pulmonary circulation. Pulmonary arterial occlusion pressure reactivity to exercise was also greater in the HAPE-S group, increasing with altitude but independent of oxygenation. These findings suggest an augmented flow-dependent pulmonary vasoconstriction and/or a reduced vascular cross-sectional area in HAPE-S subjects.

Adult↗

PubMed1996

Exercise-induced VA/Q inequality in subjects with prior high-altitude pulmonary edema.

Ventilation-perfusion (VA/Q) mismatch has been shown to increase during exercise, especially in hypoxia. A possible explanation is subclinical interstitial edema due to high pulmonary capillary pressures. We hypothesized that this may be pathogenetically similar to high-altitude pulmonary edema (HAPE) so that HAPE-susceptible people with higher vascular pressures would develop more exercise-induced VA/Q mismatch. To examine this, seven healthy people with a history of HAPE and nine with similar altitude exposure but no HAPE history (control) were studied at rest and during exercise at 35, 65, and 85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m) breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) gas at both locations. We measured cardiac output and respiratory and inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard deviation of the perfusion distribution) increased with exercise. At sea level, log standard deviation of the perfusion distribution was slightly higher in the HAPE-susceptible group than in the control group during heavy exercise. At altitude, these differences disappeared. Because a history of HAPE was associated with greater exercise-induced VA/Q mismatch and higher pulmonary capillary pressures, our findings are consistent with the hypothesis that exercise-induced mismatch is due to a temporary extravascular fluid accumulation.

Adult↗

PubMed1995

The role of pulmonary CO2 flow in the control of the phase I ventilatory response to exercise in humans.

To gain an insight into the origin of the phase I ventilatory response to exercise (ph I) in humans, pulmonary ventilation (VE) and end-tidal partial pressures of oxygen and carbon dioxide (PETO2 and PETCO2, respectively) were measured breath-by-breath in six male subjects during constant-intensity exercise on the cycle ergometer at 50, 100 and 150 W, with eupnoeic normocapnia (N) or hyperpnoeic hypocapnia (H) established prior to the exercise test. Cardiac output (Qc) was also determined beat-by-beat by impedance cardiography on eight subjects during moderate exercise (50 W), and the CO2 flow to the lungs (Qc.Cv-CO2 where Cv-CO2 is concentration of CO2 in mixed veneous blood) was estimated with a time resolution of one breathing cycle. In N, the initial abrupt increase of VE during ph I (delta VE approximately 18 1.min-1 above rest) was followed by a transient fall. When PETCO2 started to increase (and PETO2 decreased) VE increased again (phase II ventilatory response, ph II). In H, during ph I delta VE was similar to that of N. By contrast, during ph II delta VE kept gradually decreasing and started to increase only when PETCO2 had returned to approximately 40 mmHg (5.3 kPa). Thus, as a result of the prevailing initial conditions (N or H) a temporal shift of the time-course of VE during ph II became apparent. No correlation was found between CO2 flow to the lungs and VE during ph I. These results are interpreted as suggesting that an increased CO2 flow to the lungs does not constitute an important factor for the initial hyperventilatory response to exercise. They are rather compatible with a neural origin of ph I, and would support the "neurohumoral" theory of ventilatory control during exercise.

Adult↗

PubMed1995

Evaluation of resistance index of several anticancer agents on parental and resistant P-388 cell lines.

Multidrug resistance is frequently detected in haematological malignancies and in acute leukaemias with a poor prognosis. In the last few years, several reports seem to suggest that the new anthracycline derivative idarubicin and the anthraquinone mitoxantrone have some advantages in the management of untreated or relapsed acute leukaemias compared with older anthracyclines. This could be due to a different interaction of these drugs with multidrug resistance. To evaluate this possibility, we compared the activity of doxorubicin (DOXO), epirubicin (EPI), idarubicin (IDA) and mitoxantrone (MITO) on a murine, multidrug resistant, leukaemic cell line (P-388/Dx) cultured in vitro. ID50 of IDA and MITO was in the ng range whereas that of DOXO and EPI was in the microgram(s) range. Moreover, IDA has a resistance index of 50 whereas DOXO has one of 250. Verapamil is able to almost completely abolish the resistance to IDA. Efflux experiments confirm that verapamil increases IDA intracellular concentration. IDA and MITO appear to be less involved in multidrug resistance than older anthracyclines.

Animals↗

PubMed1995

Notes on the use of fluvoxamine as treatment of depression in HIV-1-infected subjects.

Fluvoxamine belongs to the class of selective serotonin reuptake inhibitors (SSRIs) which have recently gained large popularity as antidepressant agents essentially because they lack the most troublesome adverse effects of older antidepressants (i.e. tricyclic antidepressants) such as anticholinergic effects and cardiotoxicity. Recent studies in the literature suggest that HIV-1 infected subjects are affected by depressive episodes with a relatively high frequency, often requiring an antidepressant treatment. Due to its favorable adverse effects profile, we used fluvoxamine as first line treatment for sixteen depressed HIV-1 infected subjects. They were administered the drug at a daily dosage of 100 mg in the evening. Fluvoxamine provided a good clinical efficacy for six of these patients, whereas the other ten had to discontinue the drug because of the presence of severe adverse effects such as acute total insomnia, gastro-intestinal disturbances together with anorexia, aggressive and impulsive behavior and excessive sedation. The observed fluvoxamine side-effects are not typical or specific for this particular patient group since they are also described in seronegative subjects taking fluvoxamine; however, our findings seem to indicate that they become more frequent and more severe when the drug is administered to HIV-1 infected patients.

Adult↗

PubMed1995

GST-pi and P-170 co-expression in multiple myeloma.

Bone marrow samples from 40 patients affected by multiple myeloma either treated or untreated were examined for expression of glutathione-S-transferase pi (GST-pi), P-glycoprotein and the protein product of ras oncogenes family, p-21, on plasma cells, by immunocytochemical detection. 72% of evaluated samples were positive for P-170 and 82% for GST-pi without any correlation with clinical or prognostic parameters. A significant relationship between GST-pi expression and P-170 positivity was found and co-expression was observed in 91% of evaluated samples. Expression of P-170 and GST-pi was found both in treated and untreated patients. However, patients evaluated before and after therapy showed an increase in the percentage of plasma cells positive for GST-pi or P-170 or both. Expression of p-21 was not associated with these mechanisms of drug resistance. These data suggest that different resistance mechanisms are present in multiple myeloma.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1995

Determinants of maximal exercise VO2 during single leg knee-extensor exercise in humans.

Previously, a reduction in fractional inspired O2 (FIO2) during dynamic exercise of the human quadriceps muscles of one leg resulted in increased muscle blood flow (Q) and a fall in femoral venous O2 tension (PO2) but no change in peak O2 uptake (VO2). These data can be interpreted as reflecting an increase in muscle O2 diffusive capacity (DO2) in hypoxia or, alternatively, that maximum O2 uptake (VO2max) was not reached for these muscles when air was breathed, in which case the theory of diffusion limitation to VO2max is not applicable to these data. Therefore, the primary goal of this study was to test the hypothesis that VO2max would be reduced in hypoxia as a result of the decreased O2 supply and a constant diffusional conductance from blood to exercising muscle. To resolve this, five trained men were studied performing single leg incremental knee-extensor exercise to VO2max while breathing air (N) and again while breathing 12% O2 (H). The maximum work rate (WRmax) was 30-50 W greater and produced even greater associated maximum leg Q (N = 9.1 +/- 0.61 and H = 8.2 +/- 0.65 l/min, P < 0.05) and leg O2 than in previous studies. Hypoxia reduced quadriceps muscle VO2max (N = 1.4 +/- 0.1 and H = 1.1 +/- 0.1 l/min, P < 0.05). In the two conditions the relationships between 1) measured femoral venous PO2 (N = 18 +/- 0.5 and H = 13 +/- 0.5 Torr) and VO2max and 2) calculated mean capillary PO2 (N = 37 +/- 0.4 and H = 28 +/- 0.8 Torr) and VO2max were each one of proportionality.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Maximal rate of blood lactate accumulation during exercise at altitude in humans.

The lower peak lactate accumulation in blood ([La(b)]p) at altitude may be associated with a reduced maximal glycolytic flux. Based on certain assumptions, the latter can be indirectly evaluated in vivo, during short supramaximal exercises, by measuring the maximal rate of lactate accumulation in blood (delta [La(b)]max). delta [La(b)]max was determined on six white subjects at sea level (SL1), after approximately 1 wk (Alt1) and 4 wk (Alt2) of a 35-day sojourn at 5,050 m, and 1 wk after return to sea level (SL2). The subjects performed exercises of increasing duration (5, 15, 25, 35, 45 s or until exhaustion) on a bicycle ergometer at loads = 200% of the individual Wmax. The latter was previously determined in each condition as the greatest work rate that could be sustained for 2-4 min during an incremental exercise. Net [La(b)] accumulation (delta [La(b)]) was measured after each exercise bout. delta [La(b)] resulted to be linearly related to exercise duration. The slopes of the individual delta [La(b)] vs. exercise duration lines were taken as delta [La(b)]max. Exhaustion times were approximately 30-45 s in all conditions. [La(b)]p (in mM) during recovery after the exhaustive load was higher at SL1 (10.22 +/- 1.09; means +/- SD) than at Alt1 (5.08 +/- 0.82), Alt2 (8.13 +/- 2.67), and SL2 (8.18 +/- 1.43). delta [La(b)]max was lower at Alt1 (0.09 +/- 0.02) and at Alt2 (0.17 +/- 0.05) than at SL1 (0.25 +/- 0.05) and SL2 (0.23 +/- 0.06). Both [La(b)]p and delta [La(b)]max increased during acclimatization.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1995

Effect of [Hb] on blood flow distribution and O2 transport in maximally working skeletal muscle.

We investigated whether the reduction in calculated muscle diffusion capacity for O2 (DmO2) previously shown to occur with lowered hemoglobin concentration ([Hb]) perfusion of maximally working muscle is related to changes in the blood flow distribution. If blood flow distribution is altered during low [Hb] conditions, the reduction in the calculated DmO2 may in fact be due to increasing heterogeneity and not to some other hemoglobin-related factor. Color-stained (15-microns-diam) microspheres were injected into the artery supplying maximally working isolated in situ dog gastrocnemius muscle (n = 6) while it was being perfused (flow controlled by pump perfusion) with whole blood at three different levels of [Hb] (14.1 +/- 0.5, 8.9 +/- 0.4, and 5.7 +/- 0.4 (SE) g/100 ml] in a blocked-order design. Muscle blood flow and arterial PO2 were not changed as [Hb] was altered. Maximal O2 uptake (11.8 +/- 1.3, 8.2 +/- 0.8, and 6.0 +/- 0.9 ml.100 g-1 min-1 for those [Hb] values, respectively) and the associated estimate of DmO2 (0.25 +/- 0.03, 0.18 +/- 0.03, and 0.15 +/- 0.03 ml.100 g-1.min-1.Torr-1) declined significantly (P < 0.05) with [Hb]. However, the dispersion of the blood flow distribution did not change significantly and, if anything, indicated less heterogeneity at lower [Hb] (coefficient of variation - 0.52 +/- 0.06, 0.46 +/- 0.05, and 0.43 +/- 0.03). These results suggest that in maximally working canine muscle in situ, when O2 delivery is reduced by lowering [Hb] (at constant blood flow), changes in blood flow distribution play no significant role in the reduction of maximal O2 uptake and calculated DmO2. The apparent increase in the resistance to O2 diffusion (i.e., reduction in the DmO2) during anemia may therefore be a result of increased red blood cell spacing in the capillary, slow chemical off-loading kinetics of O2 from Hb, or some other effect that remains to be determined.

Animals↗

PubMed1994

Ventilatory responses to hypercapnia and hypoxia in elite breath-hold divers.

It was recently hypothesized that elite breath-hold divers may display blunted ventilatory responses to hypoxia and/or hypercapnia (Ferretti et al., J. Appl. Physiol. 70: 794-802, 1991). To test this hypothesis, the following measurements were made on three elite breath-hold divers (members of the same family), and on 9 healthy untrained control subjects (C): (1) Steady-state pulmonary ventilation (VE) at rest in the supine posture while breathing room air or normoxic CO2-enriched mixtures. (2) Breath-by-breath VE changes (delta VE), with respect to baseline conditions, after 4 breaths of 100% O2, under the following conditions: normoxia (PIO2 = 146 Torr) at rest (NR); normoxic exercise (60 watt on a bicycle ergometer) (NE); hypoxia (PIO2 = 77 Torr) at rest (HR); hypoxic exercise (HE). The results were as follows: (1) In hypercapnic experiments VE (normalized per unit of body surface area) was significantly lower in the divers than in C (4.32 +/- 0.04 [mean +/- SD]L.min-1.m-2 vs. 5.31 +/- 0.62 at FICO2 = 1.5%; 5.21 +/- 0.17 vs. 7.72 +/- 1.39 at FICO2 = 3%; 8.86 +/- 0.76 vs. 13.14 +/- 2.27 at FICO2 = 5%), as well as than in subjects described by previous authors as being characterized by 'low CO2 sensitivity'. (2) The 100% O2-breathing maneuvers did not induce significant delta VE both in NR and in HR, whereas peak delta VE were -6.73 +/- 1.38 L.min-1 (divers) vs. -5.24 +/- 3.10 (C) in NE, and -17.39 +/- 4.92 (divers) vs. -17.52 +/- 6.32 (C) in HE (no significant differences). It is concluded that the divers, compared to C, had a blunted ventilatory response to hypercapnia, but not to hypoxia. The former may represent an adaptive or genetically inherited phenomenon.

Adaptation, Physiological↗