In vitro effects of zinc gluconate and acetate on red cell aggregability.
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Biomedical subjects
Publications and source records attributed to C Préfaut.
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Previous studies have reported respiratory, cardiac and muscle changes at rest in triathletes 24 h after completion of the event. To examine the effects of these changes on metabolic and cardioventilatory variables during exercise, eight male triathletes of mean age 21.1 (SD 2.5) years (range 17-26 years) performed an incremental cycle exercise test (IET) before (pre) and the day after (post) an official classic triathlon (1.5-km swimming, 40-km cycling and 10-km running). The IET was performed using an electromagnetic cycle ergometer. Ventilatory data were collected every minute using a breath-by-breath automated system and included minute ventilation (V(E)), oxygen uptake (VO2), carbon dioxide production (VCO2), respiratory exchange ratio, ventilatory equivalent for oxygen (V(E)/VO2) and for carbon dioxide (V(E)/VCO2), breathing frequency and tidal volume. Heart rate (HR) was monitored using an electrocardiogram. The oxygen pulse was calculated as VO2/HR. Arterialized blood was collected every 2 min throughout IET and the recovery period, and lactate concentration was measured using an enzymatic method. Maximal oxygen uptake (VO2max) was determined using conventional criteria. Ventilatory threshold (VT) was determined using the V-slope method formulated earlier. Cardioventilatory variables were studied during the test, at the point when the subject felt exhausted and during recovery. Results indicated no significant differences (P > 0.05) in VO2max [62.6 (SD 5.9) vs 64.6 (SD 4.8) ml x kg(-1) x min(-1)], VT [2368 (SD 258) vs 2477 (SD 352) ml x min(-1)] and time courses of VO2 between the pre- versus post-triathlon sessions. In contrast, the time courses of HR and blood lactate concentration reached significantly higher values (P < 0.05) in the pre-triathlon session. We concluded that these triathletes when tested 24 h after a classic triathlon displayed their pre-event aerobic exercise capacity, bud did not recover pretriathlon time courses in HR or blood lactate concentration.
BACKGROUND: Single doses of zafirlukast attenuate exercise-induced bronchoconstriction (EIB), but previous studies have not measured zafirlukast's effects after regular dosing or its duration of effect beyond 4 hours. OBJECTIVE: The purpose of this study was to assess the effects of zafirlukast 20 mg and 80 mg twice daily compared with placebo on exercise challenges performed at 2 and 8 hours after the last dose of regular administration. METHODS: Twenty-four adult patients with stable asthma taking beta(2)-agonists, inhaled corticosteroids, or both received treatment with zafirlukast (20 mg and 80 mg) and placebo. The patients were treated twice daily for 14 days in a randomized, double-blind, 3-way cross-over fashion, with a 7-day washout period between each treatment. Exercise challenges were performed at 2 and 8 hours after the morning dose on day 14. FEV(1) was measured before exercise and at set intervals after exercise until it returned to within 7% of its baseline value. RESULTS: Both zafirlukast treatments significantly reduced EIB, as measured by the area under the FEV(1) time curve after the 2-hour (P <.001) and 8-hour (P <.001) exercise challenges and maximum fall in FEV(1) at the 2-hour challenge (P <.001). The comparison at 8 hours between treatments was affected by the unexpected finding that EIB was less in the placebo group after the 8-hour challenge than after the 2-hour challenge, as measured by the within-group change in the maximum fall in FEV(1) (P <.001) and the area under the FEV(1) time curve (P =.0023). CONCLUSION: Regular zafirlukast treatment protects against EIB for at least 8 hours after regular dosing. A refractory period, which may be caused by exercise-induced leukotriene release, may last for up to 6 hours after the initial response to exercise.
PURPOSE: Exercise-induced hypoxemia in highly trained athletes is associated with an increase in histamine release during exercise. The cells most implicated in blood histamine release are basophils. The aim of this study was to determine whether high-level endurance training induces modifications in histamine releasability from human basophils. METHODS: Seven young highly trained athletes (YA) [aged 26.1+/-1.3 yr (mean +/- SEM)] and seven master athletes (MA) (64.4+/-4.1 yr), all known to develop exercise-induced hypoxemia, were respectively compared with seven young untrained men (YC) (23.0+/-1.5 yr) and seven older untrained men (OC) (61.6+/-1.3 yr). During an incremental exhaustive exercise, blood samples for measurement of anti-IgE-induced histamine release from leukocytes were drawn at rest, VO2max, and recovery. RESULTS: Basophils from "leukocyte-rich" supernatant in YA and MA showed significantly higher histamine release induced by anti-IgE (1 microg x mL(-1) than, respectively, YC (P<0.01) and OC (P<0.05) at rest, VO2ax (P<0.01), and recovery (P<0.01). Basophils in YA and MA also showed a histamine release induced by anti-IgE that was higher at VO2max than at rest (respectively. P<0.01 and P<0.05), but this change was not found in the control groups. CONCLUSION: In conclusion, the basophils in highly trained endurance athletes, both young and older, showed higher anti-IgE-induced histamine release than those of untrained men. This effect of high-level training seemed to be potentiated by exercise.
PURPOSE: This study tests the reliability of a new device for assessing the oxygen consumption of the respiratory muscles (VO2 resp.). METHODS: Fourteen healthy male volunteers participated in the study. The device consists of an expandable external ventilatory dead space created with pieces of plastic tubing and a spirometer filled with 100% oxygen. It also incorporates a carbon dioxide absorber. Total VO2 (VO2 tot.) was recorded from the spirometric closed circuit and ventilation (V(E)), from the spirometer tracing. For each subject the test procedure was carried out in duplicate (T1 and T2) after an overnight fast. The dead space was increased at a constant rate of 260 mL every 90 s, and VO2 tot. and V(E) increased progressively. Because log VO2 tot. was linearly related to V(E), we calculated the slope value (log VO2-V(E)) and the Y-intercept (VE = 0) of the semilog regression representing, respectively, VO2 resp. and metabolic VO2 (VO2 met.). RESULTS: When compared with values in the literature, these values did not differ from those recorded in subjects of a similar age group. The VO2 resp. and VO2 met. calculated in T1 and T2 were not different (VO2 resp. = 0.0066 +/- 0.0005 for T1 vs 0.0067 +/- 0.0005 log mL x min(-1)/L x min(-1) for T2 and VO2 met. = 269.3 +/- 28.6 for T1 vs 281.9 +/- 24.1 mL x min(-1) for T2). The coefficients of variation were: 25% at T1 and 23% at T2 for VO2 resp. and 34% at T1 and 29% at T2 for VO2 met. Moreover, significant correlations (r = 0.96, P < 0.001 for VO2 resp., r = 0.95, P < 0.001 for VO2 met.), high coefficients of determination (r2 = 0.92 for VO2 resp., r2 = 0.90 for VO2 met.) and negligible SEE (0.0005 for VO2 resp., 0.2 mL x min(-1) for VO2 met.) were found between the two tests. When we plotted the mean values of VO2 resp. and VO2 met. measured at T1 and T2 against their respective differences, more than 95% of the slight differences ranged between the limits defined by mean value +/- 2 SD, reflecting the small discrepancy between duplicate measurements. CONCLUSION: The results confirm that the test performed with this device is useful and reliable for assessing the VO2 resp. in healthy subjects.
The effect of a single bout of exhaustive exercise on muscle lactate transport capacity was studied in rat skeletal muscle sarcolemmal (SL) vesicles. Rats were assigned to a control (C) group (n = 14) or an acutely exercised (E) group (n = 20). Exercise consisted of treadmill running (25 m/min, 10% grade) to exhaustion. SL vesicles purified from C and E rats were sealed because of sensitivity to osmotic forces. The time course of 1 mM lactate uptake in zero-trans conditions showed that the equilibrium level in the E group was significantly lower than in the C group (P < 0.05). The initial rate of 1 mM lactate uptake decreased significantly from 2.44 +/- 0.22 to 1.03 +/- 0.08 nmol. min(-1). mg protein(-1) (P < 0.05) after exercise, whereas that of 50 mM lactate uptake did not differ significantly between the two groups. For 100 mM external lactate concentration ([lactate]), exhaustive exercise increased initial rates of lactate uptake (219.6 +/- 36.3 to 465.4 +/- 80.2 nmol. min(-1). mg protein(-1), P < 0.05). Although saturation kinetics were observed in the C group with a maximal transport velocity of 233 nmol. min(-1). mg protein(-1) and a Michealis-Menten constant of 24.5 mM, saturation properties were not seen after exhaustive exercise in the E group, because initial rates of lactate uptake increased linearly with external [lactate]. We conclude that a single bout of exhaustive exercise significantly modified SL lactate transport activity, resulting in a decrease in 1 mM lactate uptake and was associated with alterations in the saturable properties at [lactate] above 50 mM. These results suggest that changes in sarcolemmal lactate transport activity may alter lactate and proton exchanges after exhaustive exercise.
The aim of the present study was to determine the effects of 40 km of cycling on the biomechanical and cardiorespiratory responses measured during the running segment of a classic triathlon, with particular emphasis on the time course of these responses. Seven male triathletes underwent four successive laboratory trials: (1) 40 km of cycling followed by a 10-km triathlon run (TR), (2) a 10-km control run (CR) at the same speed as TR, (3) an incremental treadmill test, and (4) an incremental cycle test. The following ventilatory data were collected every minute using an automated breath-by-breath system: pulmonary ventilation VE, l x min[-1]), oxygen uptake (VO2, ml x min(-1) x kg[-1]), carbon dioxide output (ml x min[-1]), respiratory equivalents for oxygen (VE/VO2) and carbon dioxide (VE/VCO2), respiratory exchange ratio (R) respiratory frequency (f, breaths x min[-1]), and tidal volume (ml). Heart rate (HR, beats x min[-1]) was monitored using a telemetric system. Biomechanical variables included stride length (SL) and stride frequency (SF) recorded on a video tape. The results showed that the following variables were significantly higher (analysis of variance, P < 0.05) for TR than for CR: VO2 [51.7 (3.4) vs 48.3 (3.9) ml x kg(-1) x min(-1), respectively], VE [100.4 (1.4) l x min(-1) vs 84.4 (7.0) l x min(-1)], VE/VO2 [24.2 (2.6) vs 21.5 (2.7)] VE/VCO2 [25.2 (2.6) vs 22.4 (2.6)], f[55.8 (11.6) vs 49.0 (12.4) breaths x min(-1)] and HR [175 (7) vs 168 (9) beats x min(-1)]. Moreover, the time needed to reach steady-state was shorter for HR and VO2 (1 min and 2 min, respectively) and longer for VE (7 min). In contrast, the biomechanical parameters, i.e. SL and SF, remained unchanged throughout TR versus CR. We conclude that the first minutes of the run segment after cycling in an experimental triathlon were specific in terms of VO2 and cardiorespiratory variables, and nonspecific in terms of biomechanical variables.
Exercise-induced hypoxaemia (EIH) in master athletes may be related to a diminished exercise hyperpnoea. The aim of this study was to determine whether EIH is associated with a change in the sensitivity of the ventilation response to activation of the central chemoreceptors. The ventilation response to CO2 was measured in nine elderly untrained men (UT) [mean age 66.3 (SEM 3.1) years] and nine master athletes (MA) [mean age 62.7 (SEM 0.8) years] at rest, during moderate exercise (40% maximal oxygen uptake, VO2max), and during strenuous exercise (70% VO2max) using the rebreathing method. Our results showed that the ventilation response to CO2 did not differ with endurance training and/or exercise, that the threshold of the CO2 response (Th) increased with exercise (P < 0.001), that the increase in Th in MA was higher than in UT between rest and moderate exercise [deltaTh(0-40): 8.55 (SEM 1.8) vs 3.06 (SEM 1.72) mmHg, P < 0.05], and that deltaTh(0-40) and Th during moderate exercise were negatively correlated with arterial O2 saturation during maximal exercise (r=0.50, P<O0.05). We concluded therefore that exercise-induced hypoxaemia in master athletes may not be due to a lower ventilation response to CO2, but may be partly related to a greater increase in Th during moderate exercise.
In order to assess the performance of subjects with sickle cell trait (SCT) during brief and explosive exercise involving mainly alactic anaerobic metabolism, the percentage of athletes with SCT was determined in Ivory Coast track and field throw and jump champions, both men and women, for the period 1956-1995. Thirty-four (27.8%) sickle cell trait carriers (SCTC) were identified among the 122 national champions that we were able to contact. These 34 SCTC had won 78 national titles (24.5%) and established 37 national records (43.5%), distributed among the throw and jump events. These percentages were significantly higher than the prevalence of SCT in the general Ivory Coast population (12.0%). The women's high jump and men's shot put events had the highest percentages of SCTC record holders (90.9% and 87.5%, respectively). Moreover, the two top national record holders and title winners, one man and one woman, were SCTC athletes, and their hemoglobin S percentage (HbS: 39.1% and 39.4%, respectively) and mean corpuscular volume (MCV) excluded an associated alpha-thalassemia. We conclude that the significantly higher percentage of SCTCs among Ivory Coast track and field champions, as compared to the percentage in the general population suggests that SCT may be a determinant factor for success in brief and explosive track and field events involving mainly alactic anaerobic metabolism.
To test whether orthotopic heart transplant (OHT) patients with low pulmonary diffusion capacity have a greater limitation to exercise than OHT patients with normal pulmonary diffusion capacity, we investigated cardiorespiratory responses and blood gases in two groups of OHT patients, one with low (LdG) and the other with normal pulmonary diffusion capacity (NdG), during a graded exercise test. The results showed 1) significantly reduced peak power (P < 0.05), peak oxygen uptake (VO2, P < 0.001), peak oxygen pulse (VO2/heart rate, P < 0.01), peak minute ventilation (VE, P < 0.05), and delta PaO2 (peak PaO2 - rest PaO2, P < 0.05) in LdG versus NdG; 2) a nonsignificant decrease in peak heart rate in LdG (P < 0.13, P = 24%); and 3) significant increases in peak respiratory equivalent for oxygen (VE/VO2, P < 0.05) and delta P(A-a)O2 (peak P(A-a)O2 - resting P(A-a)O2, P < 0.05) in LdG versus NdG. No significant difference was found for PaO2 and PaCO2 at rest or at peak exercise between the groups. A strong correlation was found between pulmonary diffusion capacity (TLCO/VA) and peak VO2 (r = 0.81, P < 0.01); that is, TLCO/VA explains 66% of the variance in peak VO2. We conclude that OHT patients with decreased pulmonary diffusion capacity have a lower exercise tolerance than patients with normal pulmonary diffusion capacity. However, because of the lack of exercise-induced hypoxemia, diffusion abnormalities are not the main limiting factor for exercise tolerance in the low diffusion group.
Exercise intolerance in COPD patients appears to be in part because of skeletal muscle dysfunction. Studies using biopsy techniques and magnetic resonance spectroscopy have demonstrated changes in enzyme activities and metabolism that indicate reduced oxidative capacity in the peripheral muscles of these patients. Regarding the respiratory muscles, the biochemical characteristics have been studied in only a few works and the results seem to depend on the specific muscle group studied. Several factors, such as hypoxemia, nutritional status, pharmacological treatment, and deconditioning, may be responsible for these skeletal muscle abnormalities. This brief review describes the changes in peripheral and respiratory muscles in COPD patients based on data from the literature. The causes of these muscle abnormalities, their contribution to exercise intolerance, and the effects of training are then discussed. We conclude with suggested directions for future investigation using contemporary noninvasive technologies.
We investigated in rats the effect of 4 wk of hypodynamia on the respiration of mitochondria isolated from four distinct muscles [soleus, extensor digitorum longus, tibial anterior, and gastrocnemius (Gas)] and from subsarcolemmal (SS) and intermyofibrillar (IMF) regions of mixed hindlimb muscles that mainly contained the four cited muscles. With pyruvate plus malate as respiratory substrate, 4 wk of hindlimb suspension produced an 18% decrease in state 3 respiration for IMF mitochondria compared with those in the control group (P < 0.05). The SS mitochondria state 3 were not significantly changed. Concerning the four single muscles, the mitochondrial respiration was significantly decreased in the Gas muscle, which showed a 59% decrease in state 3 with pyruvate + malate (P < 0.05). The other muscles presented no significant decrease in respiratory rate in comparison with the control group. With succinate + rotenone, there was no significant difference in the respiratory rate compared with the respective control group, whatever the mitochondrial origin (SS, or IMF, or from single muscle). We conclude that 4 wk of hindlimb suspension alters the respiration of IMF mitochondria in hindlimb skeletal muscles and seems to act negatively on complex I of the electron-transport chain or prior sites. The muscle mitochondria most affected are those isolated from the Gas muscle.
STUDY OBJECTIVE: The aims of this work were to determine (1) whether patients with COPD have impaired skeletal muscle performance (ie, maximal strength and endurance) compared with healthy subjects, and (2) whether the level of physical activity, body composition, and lung function are related to skeletal muscle performance in COPD patients. METHODS: Seventeen COPD patients and eight healthy age-matched control subjects performed maximum voluntary contraction (MVC) of the quadriceps and an endurance test consisting of dynamic contractions of the quadriceps against 20% of MVC at an imposed regular pace until exhaustion. The endurance test duration determined the muscle "limit time" (Tlim). A score of physical activity (PA score) was obtained using an adapted physical activity questionnaire for the elderly, and body composition was measured by the bioelectrical impedance method. Symptom-limited oxygen uptake (VO2 sl) was also assessed in COPD patients using a maximal incremental exercise test. RESULTS: The results showed that Tlim and PA score were significantly decreased in COPD patients (p<0.05). Significant positive correlations were found in the COPD group between Tlim and the PA score (r=0.60; p<0.05), FEV1 (r=0.52; p<0.05), and PaO2 (r=0.63; p<0.05). The same results were found between the PA score and VO2 sl (r=0.57; p<0.05) and FEV1 (r=0.63; p<0.05). CONCLUSION: These findings indicate impaired skeletal muscle endurance in COPD patients related to altered lung function and associated physical inactivity.
Since iron deficiency is associated with abnormal erythrocyte rheology, we investigated relationships between plasma ferritin and blood rheology in 36 male elite sportsmen (age: 22.38+/-0.9 years). On the whole, ferritin was negatively correlated with blood viscosity (r = -0.36, p < 0.05). When 23 subjects with low ferritin levels suggesting mild iron deficiency were compared with 13 matched sportsmen with normal ferritin levels, iron-deficient sportsmen were shown to have a higher blood viscosity at 1000 s(-l) (3.17+/-0.09 vs. 2.85+/-0.06 mPas, p < 0.05), explained by a higher plasma viscosity (1.38+/-0.02 vs. 1.31+/-0.02 mPa s, p < 0.05), while hematocrit and RBC rigidity index Tk were similar in the two groups. RBC aggregability index M (4.59+/-0.58 vs. 2.95+/-0.43 mPas, p < 0.05) and M1 (8.46+/-0.58 vs. 6.07+/-0.55, p < 0.01) were higher in iron-deficient subjects. Serum zinc was lower in iron-deficient sportsmen (0.73+/-0.02 vs. 0.83+/-0.02 mg/l, p < 0.01), but the score of early signs of overtraining was higher in this group (10.84+/-1.61 vs. 4.08+/-1.11, p < 0.01). These data suggest that mild iron deficiency as commonly seen in athletes, before anemia occurs, is associated with an increase in plasma viscosity and RBC aggregation, together with an increased subjective feeling of exercise overload.
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While it is well established that blood viscosity is decreased in sportsmen and related to fitness, the involvement of fibrinogen in this relationship is less well defined. Relationships among fitness, rheology and fibrinogen were investigated in 32 football players (age 17-33 years: 19 professionals and 13 leisure players). A submaximal 25 min exercise-test was performed and allowed the calculation of aerobic working capacity. Aerobic working capacity (W170 and VO2 max) was negatively correlated to fibrinogen (r = -0.531, p < 0.01 and r = -0.623, p < 0.01), while on the whole sample the correlation to viscosity and erythrocyte aggregation was not significant. When subjects were divided into two subgroups according to their plasma fibrinogen concentration, the aerobic working capacity (either expressed as W170 or VO2 max) is higher when plasma fibrinogen level is lower than 2.7 g/l. Thus, there is a highly significant negative correlation between fibrinogen and fitness in these sportsmen, independent of blood rheology. These data suggest that rheology and fibrinogen are to some extent separate determinants of an individual's fitness.
Nutritional status and chronic pulmonary hyperinflation can alter respiratory muscle function in cystic fibrosis (CF). This study investigated: 1) whether inspiratory muscle function is reduced in children with stable CF in comparison with healthy controls; and 2) the mechanisms leading to inspiratory muscle weakness, which probably predispose to respiratory muscle fatigue. We determined the tension-time index of the inspiratory muscles (TTMUS) noninvasively at rest in 16 children with mild to moderate CF (mean age, 11 +/- 2 years) and 10 healthy controls (mean age, 11 +/- 2 years). The TTMUS was determined as follows: TTMUS = TI/TTOT.PI/PIMAX, where PI is the mean inspiratory pressure estimated from the measure of mouth occlusion pressure (P0.1), PIMAX is the maximal inspiratory pressure, and TI/TOT is the duty cycle. The results showed similar nutritional status in both groups, as well as mild to moderate airway obstruction, hyperinflation, and trapped gas in the CF group. In this group only, a significant inverse relationship was found between TI/TOT and PI/PIMAX[TITTOT = 0.482 - (0.388PI/PIMAX), r = -0.53; p < 0.05]. These patients also had greater TTMUS (TTMUS = 0.087 +/- 0.030 in CF vs. 0.056 +/- 0.014 in controls, P < 0.01) that increased with decreasing lean body mass (r = -0.70, P < 0.005), with increasing percent predicted functional residual capacity (r = 0.70, P < 0.05), and increasing volumes of trapped gas (r = 0.77, P < 0.01). The multiple linear regression analysis for these factors was significant (R2 = 0.84, P < 0.01); however, the partial regression coefficient was significant only for lean body mass (r2 = 0.60, P < 0.05). Therefore, muscle mass appeared as the strongest determinant of TTMUS in CF. This study used a noninvasive method to assess the inspiratory muscle performance in children with CF. The results suggest impairment in inspiratory muscle function in these children despite good nutritional status and only mild to moderate alteration in pulmonary function tests. In addition, we were able to investigate some of the determinants of inspiratory muscle weakness, namely, muscle mass, hyperinflation, and trapped gas, and found that muscle mass played a predominant role.
We investigated metabolic and hormonal responses during repeated bouts of brief and intense exercise (a force-velocity test; Fv test) and examined the effect of glucose ingestion on these responses and on exercise performance. The test was performed twice by seven subjects [27 (2) years] according to a double-blind randomized crossover protocol. During the experimental trial (GLU), the subjects ingested 500 ml of glucose polymer solution containing 25 g glucose 15 min before starting the exercise. During the control trial (CON), the subjects received an equal volume of sweet placebo (aspartame). Exercise performance was assessed by calculating peak anaerobic power (W(an,peak)). Venous plasma lactate concentration increased significantly during the Fv test (P < 0.001), but no difference was found between CON and GLU. Blood glucose first decreased significantly from the beginning of exercise up to the 6-kg load (P < 0.001) and then increased significantly at W(an,peak) and for up to 10 min during the recovery period (P < 0.001) in both CON and GLU. Insulin concentrations decreased significantly in both groups, but were higher at W(an,peak) in GLU compared with CON (P < 0.05). Glucagon and epinephrine did not change significantly in either group, but epinephrine was significantly lower in GLU after glucose ingestion (P < 0.05) and at W(an,peak) (P < 0.05). W(an,peak) was not significantly different between CON and GLU. In conclusion, blood glucose and insulin concentrations decreased during repeated bouts of brief and intense exercise, while blood lactate concentration increased markedly without any significant change in glucagon and epinephrine concentrations. Glucose ingestion altered metabolic and hormonal responses during the Fv test, but the performance as measured by W(an,peak) was not changed.