Effects of gravity and blood volume shifts on cardiogenic oscillations in respired gas.

During the cardiac cycle, cardiogenic oscillations of expired gas (x) concentrations (COS([x])) are generated. At the same time, there are heart-synchronous cardiogenic oscillations of airway flow (COS(flow)), where inflow occurs during systole. We hypothesized that both phenomena, although primarily generated by the heartbeat, would react differently to the cephalad blood shift caused by inflation of an anti-gravity (anti-G) suit and to changes in gravity. Twelve seated subjects performed a rebreathing-breath-holding-expiration maneuver with a gas mixture containing O2 and He at normal (1 G) and moderately increased gravity (2 G); an anti-G suit was inflated to 85 mmHg in each condition. When the anti-G suit was inflated, COS(flow) amplitude increased (P = 0.0028) at 1 G to 186% of the control value without inflation (1-G control) and at 2 G to 203% of the control value without inflation (2-G control). In contrast, the amplitude of COS of the concentration of the blood-soluble gas O2 (COS([O2/He])), an index of the differences in pulmonary perfusion between lung units, declined to 75% of the 1-G control value and to 74% of the 2-G control value (P = 0.0030). There were no significant changes in COS(flow) or COS([O2/He]) amplitudes with gravity. We conclude that the heart-synchronous mechanical agitation of the lungs, as expressed by COS(flow), is highly dependent on peripheral-to-central blood shifts. In contrast, COS([blood-soluble gas]) appears relatively independent of this mechanical agitation and seems to be determined mainly by differences in intrapulmonary perfusion.     

Effects of physical exercise and anti-G suit inflation on atrial natriuretic factor plasma level

The purpose of this study was to measure the effect of enhanced venous return on atrial natriuretic factor (ANF) secretion during exercise and upright posture and the consequences on renin angiotensin aldosterone system (RAAS) activity. Six healthy male subjects were submitted to four different procedures. All procedures were performed in the same position, i.e. riding on a support with legs hanging. Two procedures were performed at rest: the subjects were studied after a 25-min rest in this position, with and without the lower limb fitted with an anti-G suit inflated to 60 mmHg. Two procedures were carried out with physical exercise; arm-cranking was performed in the same position with and without the anti-G suit inflated to 60 mmHg. Venous blood was collected before and after each procedure in order to measure plasma ANF, plasma aldosterone concentration (PAC), plasma renin activity (PRA), corticotrophin (ACTH) and catecholamine level. The data mean +/- SEM showed that the ANF plasma level decreased significantly (p less than 0.05) from 32.5 +/- 4 to 28 +/- 6 pg.ml-1 after a 20-min rest in the upright posture, whereas this effect was absolished with anti-G suit inflation. Physical exercise with and without the anti-G suit increased the ANF level above control values (60 +/- 13.6 pg.ml-1 and 53 +/- 13 pg.ml-1): anti-G suit inflation had no significant effect. PRA increased after rest in an upright posture and during physical exercise; anti-G suit inflation abolished this increase in both conditions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Maximal oxygen uptake is not limited by a central nervous system governor.

We tested the hypothesis that the work of the heart was not a limiting factor in the attainment of maximal oxygen uptake (VO2 max). We measured cardiac output (Q) and blood pressures (BP) during exercise at two different rates of maximal work to estimate the work of the heart through calculation of the rate-pressure product, as a part of the ongoing discussion regarding factors limiting VO2 max. Eight well-trained men (age 24.4 +/- 2.8 yr, weight 81.3 +/- 7.8 kg, and VO2 max 59.1 +/- 2.0 ml x min(-1) x kg(-1)) performed two maximal combined arm and leg exercises, differing 10% in watts, with average duration of time to exhaustion of 4 min 50 s and 3 min 40 s, respectively. There were no differences between work rates in measured VO2 max, maximal Q, and peak heart rate between work rates (0.02 l/min, 0.3 l/min, and 0.8 beats/min, respectively), but the systolic, diastolic, and calculated mean BP were significantly higher (19, 5, and 10 mmHg, respectively) in the higher than in the lower maximal work rate. The products of heart rate times systolic or mean BP and Q times systolic or mean BP were significantly higher (3,715, 1,780, 569, and 1,780, respectively) during the higher than the lower work rate. Differences in these four products indicate a higher mechanical work of the heart on higher than lower maximal work rate. Therefore, this study does not support the theory, which states that the work of the heart, and consequently VO2 max, during maximal exercise is hindered by a command from the central nervous system aiming at protecting the heart from being ischemic.     

Cardiovascular responses to lower body negative pressure in trained and untrained older men.

To determine whether aerobic conditioning alters the orthostatic responses of older subjects, cardiovascular performance was monitored during graded lower body negative pressure in nine highly trained male senior athletes (A) aged 59-73 yr [maximum O2 uptake (VO2 max) = 52.4 +/- 1.7 ml.kg-1 x min-1] and nine age-matched control subjects (C) (VO2 max = 31.0 +/- 2.9 ml.kg-1 x min-1). Cardiac volumes were determined from gated blood pool scintigrams by use of 99mTc-labeled erythrocytes. During lower body negative pressure (0 to -50 mmHg), left ventricular end-diastolic and end-systolic volume indexes and stroke volume index decreased in both groups while heart rate increased. The decreases in cardiac volumes and mean arterial pressure and the increase in heart rate between 0 and -50 mmHg were significantly less in A than in C. For example, end-diastolic volume index decreased by 32 +/- 4 ml in C vs. 14 +/- 2 ml in A (P < 0.01), mean arterial pressure declined 7 +/- 5 mmHg in C and increased by 5 +/- 3 mmHg in A (P < 0.05), and heart rate increased 13 +/- 3 beats/min in C and 7 +/- 1 beats/min in A (P < 0.05). These data suggest that increased VO2 max among older men is associated with improved orthostatic responses.     

Exercise VE and physical performance at altitude are not affected by menstrual cycle phase.

We hypothesized that progesterone-mediated ventilatory stimulation during the midluteal phase of the menstrual cycle would increase exercise minute ventilation (VE; l/min) at sea level (SL) and with acute altitude (AA) exposure but would only increase arterial O2 saturation (SaO2, %) with AA exposure. We further hypothesized that an increased exercise SaO2 with AA exposure would enhance O2 transport and improve both peak O2 uptake (VO2 peak; ml x kg-1 x min-1) and submaximal exercise time to exhaustion (Exh; min) in the midluteal phase. Eight female lowlanders [33 +/- 3 (mean +/- SD) yr, 58 +/- 6 kg] completed a VO2 peak and Exh test at 70% of their altitude-specific VO2 peak at SL and with AA exposure to 4,300 m in a hypobaric chamber (446 mmHg) in their early follicular and midluteal phases. Progesterone levels increased (P < 0.05) approximately 20-fold from the early follicular to midluteal phase at SL and AA. Peak VE (101 +/- 17) and submaximal VE (55 +/- 9) were not affected by cycle phase or altitude. Submaximal SaO2 did not differ between cycle phases at SL, but it was 3% higher during the midluteal phase with AA exposure. Neither VO2 peak nor Exh time was affected by cycle phase at SL or AA. We conclude that, despite significantly increased progesterone levels in the midluteal phase, exercise VE is not increased at SL or AA. Moreover, neither maximal nor submaximal exercise performance is affected by menstrual cycle phase at SL or AA.     

Cardiovascular responses of heart transplant recipients to graded exercise testing.

A group of orthotopic heart transplant (OHT, n = 28) and heart surgery (n = 19) patients, with similar ejection fractions and left ventricular end-diastolic pressures, were exercised to symptom-limited maximum to describe differences in cardiovascular and gas exchange responses. Testing was performed at a mean of 3 and 6 mo after surgery, respectively (P less than 0.05). OHT patients have a greater resting systolic and diastolic blood pressure (P less than 0.01) and a significantly greater (P less than 0.01) heart rate (HR) at rest in the supine and standing positions and during minutes 2 through 7 of supine recovery. Peak treadmill time was significantly less (P less than 0.01) in OHT patients. No significant differences were found for systolic blood pressure (SBP) during recovery, peak HR, ventilation, relative O2 uptake (VO2), body weight, ventilatory equivalents for O2 and CO2, O2 pulse, and HR-SBP product (peak HR x peak SBP). Peak pulse pressure, heart rate reserve, total VO2, and absolute VO2 at ventilatory threshold were significantly lower (P less than 0.01) in the OHT patients. We concluded that 1) complete cardiac decentralization is evident, 2) the significantly reduced VO2 at ventilatory threshold should be considered when activities of daily living are prescribed, and 3) SBP response is more appropriate than HR for assessing recovery of the decentralized heart after maximal exercise.     

Adrenergic regulation of HSL serine phosphorylation and activity in human skeletal muscle during the onset of exercise

Skeletal muscle hormone-sensitive lipase (HSL) activity is increased by contractions and increases in blood epinephrine (EPI) concentrations and cyclic AMP activation of the adrenergic pathway during prolonged exercise. To determine the importance of hormonal stimulation of HSL activity during the onset of moderate- and high-intensity exercise, nine men [age 24.3 +/- 1.2 yr, 80.8 +/- 5.0 kg, peak oxygen consumption (VO2 peak) 43.9 +/- 3.6 ml x kg(-1) x min(-1)] cycled for 1 min at approximately 65% VO2 peak, rested for 60 min, and cycled at approximately 90% VO2 peak for 1 min. Skeletal muscle biopsies were taken pre- and postexercise, and arterial blood was sampled throughout exercise. Arterial EPI increased (P < 0.05) postexercise at 65% (0.45 +/- 0.10 to 0.78 +/- 0.27 nM) and 90% VO2 peak (0.57 +/- 0.34 to 1.09 +/- 0.50 nM). HSL activity increased (P < 0.05) following 1 min of exercise at 65% VO2 peak [1.05 +/- 0.39 to 1.78 +/- 0.54 mmol x min(-1) x kg dry muscle (dm)(-1)] and 90% VO2 peak (1.07 +/- 0.24 to 1.91 +/- 0.62 mmol x min(-1) x kg dm(-1)). Cyclic AMP content also increased (P < 0.05) at both exercise intensities (65%: 1.52 +/- 0.67 to 2.75 +/- 1.12, 90%: 1.85 +/- 0.65 to 2.64 +/- 0.93 micromol/kg dm). HSL Ser660 phosphorylation (approximately 55% increase) and ERK1/2 phosphorylation ( approximately 33% increase) were augmented following exercise at both intensities, whereas HSL Ser563 and Ser565 phosphorylation were not different from rest. The results indicate that increases in arterial EPI concentration during the onset of moderate- and high-intensity exercise increase cyclic AMP content, which results in the phosphorylation of HSL Ser660. This adrenergic stimulation contributes to the increase in HSL activity that occurs in human skeletal muscle in the first minute of exercise at 65% and 90% VO2 peak.     

Gender differences in the endocrine and metabolic responses to hypoxic exercise.

This study tested the hypothesis that women would have blunted physiological responses to acute hypoxic exercise compared with men. Fourteen women taking oral contraceptives (28 +/- 0.9 yr of age) and 15 men (30 +/- 1.0 yr of age) with similar peak O(2) consumption (VO(2 peak)) values (56 +/- 1.1 vs. 57 +/- 0.8 ml x kg fat-free mass(-1) x min(-1)) were studied under hypoxic (H; fraction of inspired oxygen = 13%) vs. normoxic (fraction of inspired oxygen = 20.93%) conditions. Cardiopulmonary, metabolic, and neuroendocrine measures were taken before, during, and 30 min after three 5-min consecutive workloads at 30, 45, and 60% VO(2 peak). In women compared with men, glucose levels were greater during recovery from H (P < 0.05) and lactate levels were lower at 45% VO(2 peak), 60% VO(2 peak), and up to 20 min of recovery (P < 0.05), regardless of trial (P < 0.0001). Although the women had greater baseline levels of cortisol and growth hormone (P < 0.0001), gender did not affect these hormones during H or exercise. Catecholamine responses to H were also similar between genders. Thus the endocrine response to hypoxia per se was not blunted in women as we had hypothesized. Other mechanisms must be at play to cause the gender differences in metabolic substrates in response to hypoxia.     

Mechanistic basis for the gas exchange threshold in Thoroughbred horses.

The exercising Thoroughbred horse (TB) is capable of exceptional cardiopulmonary performance. However, because the ventilatory equivalent for O2 (VE/VO2) does not increase above the gas exchange threshold (Tge), hypercapnia and hypoxemia accompany intense exercise in the TB compared with humans, in whom VE/VO2 increases during supra-Tge work, which both removes the CO2 produced by the HCO buffering of lactic acid and prevents arterial partial pressure of CO2 (PaCO2) from rising. We used breath-by-breath techniques to analyze the relationship between CO2 output (VCO2) and VO2 [V-slope lactate threshold (LT) estimation] during an incremental test to fatigue (7 to approximately 15 m/s; 1 m x s(-1) x min(-1)) in six TB. Peak blood lactate increased to 29.2 +/- 1.9 mM/l. However, as neither VE/VO2 nor VE/VCO2 increased, PaCO2 increased to 56.6 +/- 2.3 Torr at peak VO2 (VO2 max). Despite the presence of a relative hypoventilation (i.e., no increase in VE/VO2 or VE/VCO2), a distinct Tge was evidenced at 62.6 +/- 2.7% VO2 max. Tge occurred at a significantly higher (P < 0.05) percentage of VO2 max than the lactate (45.1 +/- 5.0%) or pH (47.4 +/- 6.6%) but not the bicarbonate (65.3 +/- 6.6%) threshold. In addition, PaCO2 was elevated significantly only at a workload > Tge. Thus, in marked contrast to healthy humans, pronounced V-slope (increase VCO2/VO2) behavior occurs in TB concomitant with elevated PaCO2 and without evidence of a ventilatory threshold.     

Human ventilatory responsiveness to hypoxia is unrelated to maximal aerobic capacity.

Ventilatory responsiveness to hypoxia (HVR) has been reported to be different between highly trained endurance athletes and healthy sedentary controls. However, a linkage between aerobic capacity and HVR has not been a universal finding. The purpose of this study was to examine the relationship between HVR and maximal oxygen consumption (VO2 max) in healthy men with a wide range of aerobic capacities. Subjects performed a HVR test followed by an incremental cycle test to exhaustion. Participants were classified according to their maximal aerobic capacity. Those with a VO2 max of >or=60 ml x kg(-1) x min(-1) were considered highly trained (n = 13); those with a VO2 max of 50-60 ml x kg(-1) x min(-1) were considered moderately-trained (n = 18); and those with a VO2 max of <50 ml x kg(-1) x min(-1) were considered untrained (n = 24). No statistical differences were detected between the three groups for HVR (P > 0.05), and the HVR values were variable within each group (range: untrained = 0.28-1.61, moderately trained = 0.23-2.39, and highly trained = 0.08-1.73 l x min.%arterial O2 saturation(-1)). The relationship between HVR and VO2 max was not statistically significant (r = -0.1723; P > 0.05). HVR was also unrelated to maximal minute ventilation and ventilatory equivalents for O2 and CO2. We found that a spectrum of hypoxic ventilatory control is present in well-trained endurance athletes and moderately and untrained men. We interpret these observations to mean that other factors are more important in determining hypoxic ventilatory control than physical conditioning per se.     

Time course for recovery of peak aerobic power after blood donation

Peak aerobic power (VO2peak) is decreased after blood donation, but the time course for full recovery is unknown. We measured VO2peak and exercise time to fatigue before and weekly for 4 weeks after 450-ml blood donation at a blood donor clinic, to determine the time course of recovery. Twelve moderately active individuals (2 women, 10 men; 24.3 ± 5.2 years) of average aerobic fitness (based on their VO2peak relative to normative values) completed VO2peak exercise tests before donation, the day after donation, and at weekly intervals for 4 weeks after donation. VO2peak was determined by an incremental exercise test on a cycle ergometer. At baseline, mean absolute and relative VO2peak values were 4.06 ± 0.92 L·min(-1) and 46.6 ± 7.0 ml·kg(-1)·min(-1), respectively. VO2peak was significantly decreased on day 1 (3.85 ± 0.89 L·min(-1); 44.0 ± 6.5 ml·kg(-1)·min(-1)) and during week 2 (3.91 ± 0.97 L·min(-1); 44.5 ± 7.2 ml·kg(-1)·min(-1)) after blood donation (p < 0.05), and recovered at week 3 after donation. Time to fatigue and peak heart rate were not significantly affected by blood donation. We conclude that blood donation causes a significant decrease in VO2peak for between 2 and 3 weeks. The practical application of this study is that aerobic power in people of average fitness will be decreased, up to 3 weeks after donating blood. Despite this, there is no effect of blood donation on performance as measured by time to fatigue during an incremental test on a cycle ergometer.     

Electromyographic activity and rate of muscle fatigue of the quadriceps femoris during cycling exercise in the severe domain

This study compared the activation pattern and the fatigue rate among the superficial muscles of the quadriceps femoris (QF) during severe cycling exercise. Peak oxygen consumption (VO(2)peak) and maximal accumulated oxygen Deficit (MAOD) were established by 10 well-trained male cyclists (27.5 ± 4.1 years, 71.0 ± 10.3 kg, 173.4 ± 6.6 cm, mean VO(2)peak 56.7 ± 4.4 ml·kg·min(-1), mean MAOD 5.7 ± 1.1 L). Muscle activity (electromyographic [EMG] signals) was obtained during the supramaximal constant workload test (MAOD) and expressed by root mean square (RMS) and median frequency (MF slope). The RMS of the QF, vastus lateralis (VL) and vastus medialis (VM) muscles were significantly higher than at the beginning after 75% of exercise duration, whereas for the rectus femoris (RF), this was observed after 50% of exercise duration (p ≤ 0.05). The slope of the MF was significantly higher in the RF, followed by the VL and VM (-3.13 ± 0.52 vs. -2.61 ± 0.62 vs. -1.81 ±0.56, respectively; p < 0.05). We conclude that RF may play an important role in limiting performance during severe cycling exercise.     

Peak oxygen uptake during arm cranking for men and women

To determine upper body peak O2 uptake (VO2) in a group of young females and to obtain information on possible sex differences, 40 subjects, 20 females and 20 males, mean age 26 +/- 4 (SD) and 31 +/- 6 yr, respectively, were studied during maximal arm-cranking exercise. Peak values for power output, VO2, minute ventilation (VE), and heart rate (HR) were determined for each subject. In addition, arm-shoulder volume (A-SV) was measured before exercise. Significant differences between males and females (P less than 0.05) were found for peak power output (134 +/- 18 vs. 86 +/- 13 W), peak VO2 expressed in liters per minute (2.55 +/- 0.45 vs. 1.81 +/- 0.36) and milliliters per kilogram per minute (34.2 +/- 5.3 vs. 29.2 +/- 4.9), peak VE (95.4 +/- 14.5 vs. 70.1 +/- 19.2 1 X min-1), and A-SV (3,126 +/- 550 vs. 2,234 +/- 349 ml), whereas peak HR was not significantly different between the two groups (174 +/- 14 vs. 174 +/- 36 beats X min-1). However, when peak VO2 was corrected for arm and shoulder size there was no significant difference between the groups (0.82 +/- 0.13 vs. 0.78 +/- 0.13 ml X ml A-SV-1 X min-1). These results suggest that the observed differences between men and women for peak VO2 elicited during arm cranking when expressed in traditional terms (1 X min-1 and ml X kg-1 X min-1) are a function of the size of the contracting muscle mass and are not due to sex-related differences in either O2 delivery or the O2 utilization capacity of the muscle itself.     

Hemodynamic effects of anti-G suit inflation in a 1-G environment

This study evaluated effects of various anti-G inflation pressures on cardiac volumes and the relationship of these volume changes to mean arterial pressure changes. Ventricular volumes were calculated using two-dimensional echocardiography. An anti-G suit was inflated to 2, 4, and 6 psi in the standing and supine positions for 10 male subjects. In the supine position, mean arterial pressure increased from base line for all three inflation pressures (P = 0.05). The end-diastolic volume increased after 2-psi inflation (P = 0.03). Cardiac output or stroke volume did not change. After standing, mean arterial pressure (P = 0.002), end-diastolic volume (P = 0.002), and stroke volume (P = 0.05) fell after suit deflation. Peripheral vascular resistance fell in the 2- and 4-psi inflation profiles. In the standing protocol, mean arterial pressure, end-diastolic volume, stroke volume, and cardiac output rose with all three inflation pressures (P less than 0.05). After reclining, heart rate increased (P = 0.02) and mean arterial pressure fell (P less than 0.05) in the 4- and 6-psi inflation profiles after suit deflation. Increases in mean arterial pressure are caused by increases in cardiac preload and cardiac output after inflation of the anti-G suit while subjects were standing. Increased cardiac preload was not consistently seen after inflation while subjects were supine. Changes in end-diastolic volume and mean arterial pressure were dependent on the pressure used to inflate the anti-G suit.     

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

A group of 15 competitive male cyclists [mean peak oxygen uptake, VO2peak 68.5 (SEM 1.5 ml x kg(-1) x min(-1))] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% VO2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (VO2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P(A)O2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P(A-a)O2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At VO2peak PaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P(A)O2 and P(A-a)O2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and VO2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and P(A)O2 with the first exercise intensity and at VO2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.     

Maximal aerobic power and leg muscle mass and strength related to age in non-athletic males and females

To investigate the relationships between the age-associated decline in peak oxygen uptake (peak VO2), leg muscle mass (LMM) and leg strength (LS) under the modulating effect of gender and level of physical activity (LPA, as assessed by questionnaire), we evaluated 71 sedentary subjects [males(M):females(F), 34:37], aged 20-80 years. Peak VO2 at maximum cycle ergometry was related to LMM (dual energy X-ray absorptiometry) and LS (isokinetic dynamometry) using both standard (y x x(-1)) and power function ratios (allometry). Absolute values of all variables were higher in males and declined with age (P < 0.01). Differences between the genders disappeared after peak VO2 x LS(-1.46(M)or -1.62(F)) adjustment but remained significant between peak VO2 LMM-(-0.51 (M)or -0.45(F)) and LS LMM- (-091(M) or -1.10(F)) corrected values. Allometric correction of peak VO2 and LS by LMM slowed their age-related declines; the flattening effect however, was more evident in the females. Interestingly, while no age-related decrement in peak VO2 LS(-1) was found, power function ratio values also declined with age, and at a slower rate in females. These findings are consistent with those obtained following a multiple regression analysis using LPA as an independent covariate (P < 0.01). We conclude that using adequate scaling methods and controlling by LPA: (1) no gender differences are observed in peak VO2 adjusted for LS, (2) loss of LS and LMM are important determinants of the age-associated reduction in physical fitness in both genders but (3) age per se has an LS- and LMM-independent influence on the functional decline, although this intrinsic effect of senescence is less pronounced in females.     

The major surface antigens of Entamoeba histolytica trophozoites are GPI-anchored proteophosphoglycans

Trophozoites of the parasitic protozoa, Entamoeba histolytica, synthesize a cell surface lipoglycoconjugate, termed lipophosphoglycan, which is thought to be an important virulence factor and potential vaccine candidate against invasive amebiasis. Here, we show that the E. histolytica lipophosphoglycans are in fact glycosylphosphatidylinositol (GPI)-anchored proteophosphoglycans (PPGs). These PPGs contain a highly acidic polypeptide component which is rich in Asp, Glu and phosphoserine residues. This polypeptide component is extensively modified with linear glycan chains having the general structure, [Glcalpha1-6](n)Glcbeta1-6Gal (where n=2-23). These glycan chains can be released after mild-acid hydrolysis with trifluoroacetic or hydrofluoric acid and are probably attached to phosphoserine residues in the polypeptide backbone. The PPGs are further modified with a GPI anchor which differs from all other eukaryotic GPI anchors so far characterized in containing a glycan core with the structure, Gal(1)Man(2)GlcN-myo-inositol, and in being heterogeneously modified with chains of alpha-galactose. Trophozoites of the pathogenic HM-1:IMSS strain synthesize two distinct classes of PPG which have polydisperse molecular masses of 50-180 kDa (PPG-1) and 35-60 kDa (PPG-2) and are modified with glucan side-chains of different average lengths. In contrast, the non-pathogenic Rahman strain synthesizes one class of PPG which is only elaborated with short disaccharide side-chains (i.e. Glcbeta1-6Gal). However, the PPGs are abundant in all strains (8x10(7) copies per cell) and are likely to form a protective surface coat.     

Left ventricular function during arm exercise: influence of leg cycling and lower body positive pressure.

The purpose of this study was to characterize left ventricular (LV) diastolic filling and systolic performance during graded arm exercise and to examine the effects of lower body positive pressure (LBPP) or concomitant leg exercise as means to enhance LV preload in aerobically trained individuals. Subjects were eight men with a mean age (+/-SE) of 26.8 +/- 1.2 yr. Peak exercise testing was first performed for both legs [maximal oxygen uptake (Vo(2)) = 4.21 +/- 0.19 l/min] and arms (2.56 +/- 0.16 l/min). On a separate occasion, LV filling and ejection parameters were acquired using non-imaging scintography using in vivo red blood cell labeling with technetium 99(m) first during leg exercise performed in succession for 2 min at increasing grades to peak effort. Graded arm exercise (at 30, 60, 80, and 100% peak Vo(2)) was performed during three randomly assigned conditions: control (no intervention), with concurrent leg cycling (at a constant 15% leg maximal Vo(2)) or with 60 mmHg of LBPP using an Anti G suit. Peak leg exercise LV ejection fraction was higher than arm exercise (60.9 +/- 1.7% vs. 55.9 +/- 2.7%; P < 0.05) as was peak LV end-diastolic volume was reported as % of resting value (110.3 +/- 4.4% vs. 97 +/- 3.7%; P < 0.05) and peak filling rate (end-diastolic volume/s; 6.4 +/- 0.28% vs. 5.2 +/- 0.25%). Concomitant use of either low-intensity leg exercise or LBPP during arm exercise failed to significantly increase LV filling or ejection parameters. These observations suggest that perturbations in preload fail to overcome the inherent hemodynamic conditions present during arm exercise that attenuate LV performance.     

Comparison of heart rate deflection and ventilatory threshold during a field cross-country roller-skiing test

This study was to assess whether the point of deflection from linearity of heart rate (HRd) could be an accurate predictor of ventilatory threshold (VT2) during a specific cross-country roller-skiing (RS) test. Ten well-trained cross-country skiers performed a maximal and incremental RS test in the field and a standardized maximal and incremental treadmill running (TR) test in the laboratory. Values of oxygen uptake (VO2) and heart rate (HR) were continuously recorded during all exercises by a portable breath-by-breath gas exchange measurement system and a wireless Polar monitoring system, respectively. The VT2 and HRd points were individually determined by visual analysis during RS. Maximal VO2 (VO2 max) and HR were higher (p < 0.05) during TR (67.1 +/- 7.3 ml x min(-1) x kg(-1) and 196.0 +/- 14.1 bpm, respectively) compared with RS (64.2 +/- 7.3 ml x min(-1) x kg(-1) and 191.5 +/- 13.1 bpm, respectively). However, a high correlation (r = 0.94, p < 0.01) between TR and VO2 max was observed. Paired t-tests showed no significant differences in HR (183.6 +/- 15.1 vs. 185.2 +/- 13.9 bpm) and VO2 (55.5 +/- 7.1 vs. 55.8 +/- 6.1 ml x min(-1) x kg(-1)) at intensities corresponding to HRd and VT2 during the RS test, respectively; Pearson product-moment correlation coefficients demonstrated significant relationships for HR at the HRd and VT2 points (r = 0.99, p < 0.001) as well as for VO2 (r = 0.95, p < 0.001). Our results indicate that the specific incremental RS test is effective in eliciting HRd in the field for all skiers and is an accurate predictor of VT2. These findings give very interesting practical applications to cross-country coaches and skiers to evaluate and control specific aerobic training loads.     

Oxygen uptake during swimming in a hypobaric hypoxic environment

The purpose of this study was to determine oxygen uptake (VO2) at various water flow rates and maximal oxygen uptake (VO2max) during swimming in a hypobaric hypoxic environment. Seven trained swimmers swam in normal [N; 751 mmHg (100.1 kPa)] and hypobaric hypoxic [H; 601 mmHg (80.27 kPa)] environments in a chamber where atmospheric pressure could be regulated. Water flow rate started at 0.80 m.s-1 and was increased by 0.05 m.s-1 every 2 min up to 1.00 m.s-1 and then by 0.05 m.s-1 every minute until exhaustion. At submaximal water flow rates, carbon dioxide production (VCO2), pulmonary ventilation (VE) and tidal volume (VT) were significantly greater in H than in N. There were no significant differences in the response of submaximal VO2, heart rate (fc) or respiratory frequency (fR) between N and H. Maximal VE, fR, VT, fc, blood lactate concentration and water flow rate were not significantly different between N and H. However, VO2max under H [3.65 (SD 0.11) l.min-1] was significantly lower by 12.0% (SD 3.4)% than that in N [4.15 (SD 0.18) l.min-1]. This decrease agrees well with previous investigations that have studied centrally limited exercise, such as running and cycling, under similar levels of hypoxia.