[Preliminary reports of noninvasive accurate method to measure pulmonary vascular capacity in normal volunteers].

OBJECTIVE: Because the traditional loop of breathing control and regulation effect on blood circulation, there was rare study of pulmonary vein capacity. We need a noninvasive and accurate pulmonary vascular capacity measurement and analysis method. METHODS: Twelve normal volunteers were performed a total lung CT scan, image data analysis processing by computer software, the whole lungs from the apex to the base of lung with 40-50 layers by hand-cut, the connection between adjacent layers automatically by a computer simulation, the full pulmonary vascular (≥ 0.6 mm) were treated by high-accuracy three-dimensional imaging technology after removing the interference, and then calculate the whole lung and pulmonary vascular. RESULTS: The whole lung of the 12 normal volunteers from the apex to the base of lung CT scan image layers was 530 ± 98 (range, 431-841). The total capacity of lung and pulmonary vascular blood was 3705 ± 857 (range, 2398-5383) ml, and the total volume of the pulmonary vascular blood was 125 ± 32 (range, 94-201) ml. The pulmonary vein vascular blood volume was 63 ± 16 (range, 47-100) ml. CONCLUSION: The method of measuring the three-dimensional imaging of pulmonary vascular capacity by analyzing lung CT scan data is available and accurate.

[Normal reference values and predict equations of heart function].

OBJECTIVE: For heart functional parameters, we commonly used normal range. The reference values and predict formulas of heart functional parameters and their relationships with individual characteristics are still lack. METHODS: Left ventricular (LV) volumes (end-diastolic volume and end-systolic volume), stroke volume (SV), ejection fraction (EF) and cardiac output (CO) were measured by cardiac CT angiography (CAT) in 1 200 healthy Caucasian volunteers, men 807 and women 393, and age 20-90yr. The results are analyzed by high-accuracy three-dimensional imaging technology, and then measured the dynamic changes of the volumes of each atriam and ventricule during their contractions and relaxations. The gender, age, height and weight were analyzed by multiple linear regression to predict LV functional parameters. RESULTS: Except the LVEF was lower in man than in women (P < 0.001), all other LV functional parameters of EDV, ESV, SV, FE and CO were higher in man (P < 0.001). Multiple linear regression indicated that age, gender, height and weight are all independent factors of EDV, ESV and SV (P < 0.001). CO could be significantly predicted by age, gender and weight (P < 0.001), but not height (P > 0.05). The predict equation for CO (L x min(-1)) = 6.963+0.446 (Male) -0.037 x age (yr) +0.013 x weight (kg). CONCLUSION: Age, gender, height and weight are predictors of heart functions. The reference values and predict equations are important for noninvasive and accurate evaluation of cardiovascular disease and individualized treatment.

[The correlation of the stroke volume with pulmonary venous volume and left atrial volume].

OBJECTIVE: The same person's pulmonary venous blood volume, left atrial volume and stroke volume were measured by lung CT scans and cardiac CT angiography (CTA). Then their relationships were analyzed in order to investigate the mechanism of breathing control. METHODS: As we described before, full pulmonary vascular (-0.6mm) volume was accurately calculated by three-dimensional imaging technology from lung CT scan; left atrial volume and stroke volume of left ventricle were calculated from the CTA data. Then the relationships among them were analyzed for estimation of the lung-artery time. RESULTS: The total volume of lung and pulmonary vascular blood was 3486 ± 783 (2156-4418) ml, and the pulmonary vascular blood volume was 141 ± 20 (105-163) ml. The estimated pulmonary venous volume was 71 ± 10 (52-81) ml. Left atrial volume at the end diastolic was 97 ± 39 (53-165) ml, Stroke volume of left ventricle was 86 ± 16 (60-106) ml. Pulmonary venous volume and the left atrial volume were double of stroke volume(1.7-2.4). CONCLUSION: The estimated lung-artery time was three heart beat.

[Human experiments of metabolism, blood alkalization and oxygen effect on control and regulation of breathing. I: room air exercise test].

OBJECTIVE: Under the guidance of the holistic integrative physiology medicine, we reanalyzed the data during symptom-limited maximum cardiopulmonary exercise testing (CPET) in order to investigate control and regulatory mechanism of breathing. METHODS: This study investigated 5 normal volunteers who accepted artery catheter, performed CPET room air. Continuous measured pulmonary ventilation parameters and per minute arterial blood gas (ABG) analysis sample parameters during exercise. All CPET and ABG data changes were standard analyzed and calculated. RESULTS: With gradually increasing power, minute oxygen uptake(every breath oxygen uptake x respiratory rate = O2 paulse x heart rate) and minute ventilation (tidal volume x respiratory rate) showed nearly linear progressive increase during the CPET(compared with the rest stage, P < 0.05 - 0.001); Minute ventilation increased even more significant after the anaerobic threshold (AT) and respiratory compensation point. PaO2 was increased at recovery 2 minutes (P < 0.05); PaCO2 was decreased after anaerobic threshold 2 minutes (P < 0.05); [H+]a was increased from AT (P < 0.05), and rapidly raised at last 2 minutes, remained high at recovery. Lactate was increased rapidly from AT (compared with resting, P < 0.05); bicarbonate decreased rapidly from AT (compared with resting, P < 0.05) and it's changed direction was contrary to lactic acid. CONCLUSION: In order to overcome the resistance of the power during exercise, metabolic rate othe body increased, respiratory change depend upon the change metabolism, and the accumulation of acidic products exacerbated respiratory reactions at high intensity exercise.

[Human experiments of metabolism, blood alkalization and oxygen effect on control and regulation of breathing. II: room air exercise test after blood alkalization].

OBJECTIVE: Basis on the dynamic changes of the ventilation and arterial blood gas parameters to symptom-limited maximum cardiopulmonary exercise testing (CPET), we further investigate the effect of alkalized blood by drinking 5% NaHCO3 on ventilation during exercise. METHODS: After drinking 5% NaHCO3 75 ml (3.75 g) every 5 min, total dosage of 0.3 g/Kg, 5 volunteers repeated CPET. All CPET and ABG data changes were analyzed and calculated. At the same time, CPET and ABG parameters after alkalized blood were compared with those before alkalized blood (control) used paired t test. RESULTS: After alkalized blood, CPET response patterns of parameters of ventilation, gas exchange and arterial blood gas were very similar (P > 0.05). All minute ventilation, tidal volume, respiratory rate, oxygen uptake and carbon dioxide elimination were gradually increased from resting stage (P < 0.05-0.001), according to the increase of power loading. During CPET after alkalized blood, ABG parameters were compared with those of control: hemoglobin concentrations were lower, CaCO2 and pHa were increased at all stages (P < 0.05). The PaCO2 increased trend was clear, however only significantly at warm-up from 42 to 45 mmHg (P < 0.05). Compared with those of control, only the minute ventilation was decreased from 13 to 11 L/min at resting (P < 0.05). CONCLUSION: Even with higher mean CaCO2, PaCO2 and pHa, lower Hba and [H+]a, the CPET response patterns of ventilatory parameters after alkalized blood were similar.

[Human experiments of metabolism, blood alkalization and oxygen effect on control and regulation of breathing. III: pure oxygen exercise test after blood alkalization].

OBJECTIVE: After performed symptom-limited maximum cardiopulmonary exercise testing (CPET) before and after acute alkalized blood, we repeated CPET with pure oxygen. METHODS: Five volunteers, 3hr after alkalizing blood room air CPET, re-performed CPET inhaling from Douglas bag connected with pure oxygen tank. We compared with those of room air CPETs before and after alkalized blood. RESULTS: After alkalized blood oxygen CPET had a similar response pattern as those of CPETs before and after blood alkalization. During the CPET, all breath frequency, minute ventilation and tidal volume at each stage were similar to those of CPETs before and after alkalized blood (P > 0.05),except there was a lower peak tidal volume than those of both CPETs and a slightly higher resting minute ventilation only than CPET after alkalized blood (P > 0.05). After alkalized blood, oxygen CPET, all PaO2 and SaO2 and most Hb were lower than those of both CPETs (P < 0.05). The pHa and [HCO3-]a were higher than those of CPET before alkalized blood (P < 0.05); but were not CPET after alkalized blood (P > 0.05). PaCO2 was similar to that of CPET before alkalized blood (P > 0.05), but was lower than that of CPET after alkalized blood at resting and warm-up (P < 0.05); then was similar to both CPETs at anaerobic threshold (P > 0.05); but was higher at peak exercise higher than those of both CPETs (P < 0.01). Oxygen increased 2,3 volunteers' workload and time at AT and peak exercises. CONCLUSION: Respiratory response pattern to oxygen CPET after alkalized blood is similar to those of both CPETs before and after alkalized blood. The CPET response is dominantly depended upon metabolic rate, but not levels of pHa, PaCO2 and PaO2.

Aerobic exercise training as a potential source of natural antibodies protective against human immunodeficiency virus-1.

Despite the effectiveness of HAART in controlling HIV-1 replication, the emergence of drug-resistant viruses in infected patients and the severe side effects caused by the currently used drug regimens and the lack of an effective vaccine necessitate the continued search for new therapeutic strategies for prevention and therapy of HIV disease. Previously we reported that natural autoantibodies, recognizing peptide FTDNAKTI (peptide NTM1) derived from the C2 domain of HIV-1 gp120, contribute to the control of HIV disease. Here we demonstrated that sera from well-trained athletic (HIV-negative) subjects showed high reactivity with peptide NTM1. This result confirms that aerobic exercise training stimulates production of natural autoantibodies, which recognize peptide NTM1. Bioinformatics analysis indicates that these natural autoantibodies could slow down disease progression by blocking the superantigenic site on HIV-1 gp120. The results suggest that aerobic exercise training may be a promising non-toxic and inexpensive adjunctive anti-HIV therapy.

Clinical relevance of constant power exercise duration changes in COPD.

The endurance time during constant high work-rate exercise (t(LIM)) is used to assess exercise capacity in patients with chronic obstructive pulmonary disease and as an outcome measure for pulmonary rehabilitation. Our study was designed to establish the minimum clinically important difference for the t(LIM). t(LIM) was measured in 105 patients (86 males) before and after an 8-week outpatient pulmonary rehabilitation programme. Subjects were asked to identify, from a five-point Likert scale, the perceived change in their exercise performance immediately upon completion of the exercise tests. The scale ranged from "better" to "worse". The mean+/-sd age was 64+/-5 yrs, forced expiratory volume in 1 s (FEV(1)) 47+/-10% and FEV(1)/forced vital capacity 54.7+/-16.3%. Baseline t(LIM) at 75% of the peak work rate was 397+/-184 s, which increased by 62+/-63% after rehabilitation. In subjects who felt their exercise tolerance was "slightly better", the mean improvement was 34% in the relative improvement over the baseline value (95% CI 29-39)% or 101 (86-116) s compared with 121 (109-134)% in those who reported that their exercise tolerance was "better" and 8 (2-14)% in those who felt their exercise tolerance was "about the same". Minimum clinically important improvement for t(LIM) averaged approximately 33% of baseline. Patients were able to distinguish at least one further additional level of benefit at 120% of baseline.

The role of passive immunization in hiv-positive patients : a case report.

An HIV-positive patient presented with pulmonary tuberculosis as her AIDS-defining diagnosis in 1993 and was effectively treated with 12 months of standard antituberculosis medications (isoniazide, rifampin, and pyrazinamide for 2 months). She received zidovudine for 6 weeks at the time of her diagnosis; however, because of patient preference, she has not received subsequent standard HIV medications (7 years). Her CD4 count at the time of diagnosis (1993) was 297/microL. Monthly passive immunotherapy was administered (fresh frozen plasma from HIV-negative blood donors with a significant titer for the anti-vasoactive intestinal peptide [VIP]/NTM antibody) from December 1993 to June 1994. Her CD4 count increased to > 400/microL during the passive immunotherapy and has remained stable for the past 6 years. The rational for the use of anti-VIP/NTM antibodies preparations in HIV, the possible mode of action of anti-VIP/NTM antibodies, the use of Ig preparations, and the role of exercise as a natural source of anti-VIP/NTM antibodies are discussed. This case report supports the potential therapeutic use of anti-VIP antibodies for treatment of HIV disease.

Carbon dioxide pressure-concentration relationship in arterial and mixed venous blood during exercise.

To calculate cardiac output by the indirect Fick principle, CO(2) concentrations (CCO(2)) of mixed venous (Cv(CO(2))) and arterial blood are commonly estimated from PCO(2), based on the assumption that the CO(2) pressure-concentration relationship (PCO(2)-CCO(2)) is influenced more by changes in Hb concentration and blood oxyhemoglobin saturation than by changes in pH. The purpose of the study was to measure and assess the relative importance of these variables, both in arterial and mixed venous blood, during rest and increasing levels of exercise to maximum (Max) in five healthy men. Although the mean mixed venous PCO(2) rose from 47 Torr at rest to 59 Torr at the lactic acidosis threshold (LAT) and further to 78 Torr at Max, the Cv(CO(2)) rose from 22.8 mM at rest to 25.5 mM at LAT but then fell to 23.9 mM at Max. Meanwhile, the mixed venous pH fell from 7.36 at rest to 7.30 at LAT and to 7.13 at Max. Thus, as work rate increases above the LAT, changes in pH, reflecting changes in buffer base, account for the major changes in the PCO(2)-CCO(2) relationship, causing Cv(CO(2)) to decrease, despite increasing mixed venous PCO(2). Furthermore, whereas the increase in the arteriovenous CCO(2) difference of 2.2 mM below LAT is mainly due to the increase in Cv(CO(2)), the further increase in the arteriovenous CCO(2) difference of 4.6 mM above LAT is due to a striking fall in arterial CCO(2) from 21.4 to 15.2 mM. We conclude that changes in buffer base and pH dominate the PCO(2)-CCO(2) relationship during exercise, with changes in Hb and blood oxyhemoglobin saturation exerting much less influence.

Metabolic Syndromes Associated With HIV: Mitigating the Side Effects of Drug Therapy.

HIV infection and highly active antiretroviral therapy (HAART) are associated with a variety of metabolic disorders such as AIDS wasting syndrome, cachexia, sarcopenia, metabolic dysregulation, lipodystrophy, abnormalities of serum lipids, and lactic acidosis. Adjunctive therapies (eg, diet, antilipid therapy), risk-factor modification (eg, smoking cessation, blood pressure control), aerobic exercise, and anabolic treatments can be used to mitigate the effects of HIV infection and the adverse effects of HAART, thereby improving long-term health in individuals infected with HIV.

Comparison of exercise cardiac output by the Fick principle using oxygen and carbon dioxide.

BACKGROUND AND STUDY OBJECTIVE: Theoretically, cardiac output (CO) calculated by the Fick principle should be the same using O(2) (CO[O2]) or CO2 (CO[CO2]) as the test gas. However, agreement depends on the accuracy of gas exchange and blood gas measurements and the validity of the equations to convert measured variables into blood gas contents. Considering the widespread use of indirect estimates of pulmonary artery blood PCO2 and CO2 content to measure Fick principle CO during exercise, we wished to determine whether CO[O2] and CO[CO2] were equal during exercise and whether CO[CO2] could be accurately and precisely determined using direct measures of pulmonary artery blood. PREPARATION AND METHODS: Five healthy young nonsmoking volunteer men performed incremental exercise from rest to peak exercise on two separate occasions with intervening rest. Catheters were placed in brachial and pulmonary arteries to allow repeated blood sampling every minute during concurrent breath-by-breath gas exchange measurements from rest to peak exercise. CO[O2] was compared with CO[CO2] at multiple levels of exercise. Using standard equations, arterial and mixed venous O2 contents were calculated from hemoglobin concentration (Hb), oxyhemoglobin saturation (SO2), and PO2, whereas CO2 contents were calculated from PCO2, pH, Hb, and SO2. Blood gas analyzers were used for measurement of pH, PCO2, and PO2, and a co-oximeter was used for measurement of Hb and SO2. Initial calculations suggested that exercise CO[CO2] was 14% higher than CO[O2] and helped disclose small systematic measurement errors in PCO(2) for values > 45 mm Hg detected by proficiency testing surveys and documented with blood tonometry in the blood gas analyzer. RESULTS: After correcting PCO2 for the small systematic measurement error found, the measures and equations used to calculate arterial and mixed venous O2 and CO2 contents were adequate to provide mean CO values that are reasonably similar. However CO[CO2] values were more than twice as variable as CO[O2]. CONCLUSIONS: The increased variability of Fick principle CO[CO2] compared with CO[O2] is attributable to the much lower extraction ratio for CO2 and the greater complexity in calculation of blood CO2 than O2 contents. These results raise concerns about the accuracy and precision of estimating CO and stroke volume using CO2 as a test gas, even with direct measurement of blood CO2 contents in normal subjects.

Mechanisms of exercise limitation in HIV+ individuals.

Cardiopulmonary exercise testing (CPX) is an important diagnostic tool for both clinical and research purposes in HIV positive (HIV+) individuals. Important information can be obtained from the gas exchange responses that can elucidate heart, lung, peripheral vascular, pulmonary vascular, and muscle abnormalities in this population. A large percentage of these patients are deconditioned, respond well to exercise training, and have no intrinsic limitation to exercise. Results of a progressively increasing CPX can be used to: 1) design an exercise prescription for aerobic training in HIV+ individuals; 2) identify and refer patients with subtle abnormalities of gas exchange for further diagnostic studies to exclude early infectious complications: and 3) evaluate the improvements in maximal oxygen uptake, lactic acidosis threshold, and gas exchange kinetics as result from an aerobic exercise training program. Gas exchange kinetic analysis of constant work rate tests can provide similar information in a nonmaximal, reproducible, readily obtainable format. Both progressively increasing and constant work rate CPX tests provide important information on the changes in oxygen flow from the environment to the exercising muscle that occur with aerobic exercise training. Finally, a case study involving the exercise prescription for HIV+ individuals is reviewed as well as the risk of transmission of HIV during competitive sports competition events.

HIV and aerobic exercise. Current recommendations.

Aerobic exercise training is an important therapy to offer individuals who are HIV positive (HIV+). Six to 12 weeks of moderate exercise sessions (3 times per week for 1 hour) significantly improves aerobic capacity (VO2max and lactic acidosis threshold), apparently without detrimental effects on the immune system. In addition, small but significant beneficial effects on the immune system (skin test reactivity) and quality of life are obtained. The effects on lean body mass with aerobic exercise training have been less marked, but are clearly less costly than androgenic hormone administration in this population. Aerobic exercise training can be recommended with confidence in HIV+ patients.

The effect of exercise training on aerobic fitness, immune indices, and quality of life in HIV+ patients.

PURPOSE: Thirty four HIV+ patients participated in a 6-wk aerobic exercise training program to determine whether exercise improved aerobic fitness, immune indices, and quality of life. METHODS: Subjects were assigned to three groups: control (no regular aerobic exercise), moderate exercise, and heavy exercise training. At study entry and exit (in each subject) we evaluated aerobic function with a symptom limited cardiopulmonary exercise test, immune indices with CD4 counts and Candida skin tests, viral replication with plasma HIV RNA measurements, and quality of life with a HIV+ population validated questionnaire. RESULTS: Aerobic fitness increased significantly in both exercise groups relative to the control group; immune indices changed very little among all three groups; however, the Candida skin tests (mm2) increased significantly in the moderate group; viral replication was essentially unchanged in all three groups; quality of life (QOL) markers improved in both exercising groups but not the control group. There were no opportunistic infections during the study. CONCLUSIONS: Exercise training resulted in a substantial improvement in aerobic function while immune indices were essentially unchanged. Quality of life markers improved significantly with exercise. Exercise training is safe and effective in this patient group and should be promoted for HIV+ patients.

Mechanism of the exercise hyperkalemia: an alternate hypothesis.

A progressive hyperkalemia is observed as exercise intensity increases. The current most popular hypothesis for the hyperkalemia is that the Na+-K+ pump cannot keep pace with the K+ efflux from muscle during the depolarization-repolarization process of the sarcolemmal membrane during muscle contraction. In this report, we present data that suggest an alternate hypothesis to those previously described. Because phosphocreatine (PCr) is a highly dissociated acid and creatine is neutral at cell pH, the concentration of nondiffusible anions decreases, and an alkaline reaction takes place when PCr hydrolyzes. This creates a state of cation (K+) excess and H+ depletion in the cell. To examine the balance of K+ and H+ for exercising muscle during the early period of exercise when PCr changes most rapidly, catheters were inserted into the brachial artery and femoral vein (FV) in five healthy subjects who performed two 6-min cycle ergometer exercise tests at 40 and 85% of peak oxygen uptake. FV blood was sampled every 5 s during the first 2 min, then every 30 s for the remaining 4 min of exercise and the first 3 min of recovery, and then less frequently for the next 12 min. Arterial sampling was every 30 s during exercise and simultaneous with FV sampling during recovery. Arterial K+ concentration ([K+]) increase lagged FV [K+] increase. The hyperkalemia observed during early exercise results from K+ release from skeletal muscle. FV [K+] increased by 5 s of the start of exercise and followed the rate of H+ loss from the FV blood for the first 30 s of exercise. FV lactate and Na+ kinetics differed from K+ kinetics during exercise and recovery. As predicted from the PCr hydrolysis reaction, the exercising limb took up H+ and released K+ at the start of exercise (first 30 s) at both exercise intensities, resulting in a FV metabolic alkalosis. K+ release was essentially complete by 3 min, the time at which oxygen uptake (and, presumably, PCr) reached its asymptote. These findings lead us to hypothesize that the early K+ release by the cell takes place with H+ exchange and that the major mechanism for the exercise hyperkalemia is the reduction in nondiffusible intracellular anions in the myocyte as PCr hydrolyzes.

Effect of acute bicarbonate administration on exercise responses of COPD patients.

Patients with severe chronic obstructive pulmonary disease (COPD) are limited in their exercise tolerance by the level of ventilation (VE) they can sustain. We determined whether acutely increasing blood bicarbonate levels decreased acid stimulation to the respiratory chemoreceptors during exercise, thereby improving exercise tolerance. Responses were compared with those obtained during 100% O2 breathing (known to reduce VE in these patients) and to the responses of healthy young subjects. Participants were six patients with severe COPD (forced expired volume in 1 s = 31 +/- 11% predicted) but without chronic CO2 retention and 5 healthy young subjects. Each subject performed three incremental cycle ergometer exercise tests: 1) control, 2) after ingestion of 0.3 g.kg-1 of sodium bicarbonate and 3) while breathing 100% O2. During these tests VE was measured continuously and arterialized venous blood (patients) or arterial blood (healthy subjects) was sampled serially to assess acid base variables. Bicarbonate loading increased standard bicarbonate by 4-6 mmol.L-1 and this elevation persisted during exercise. In both groups, bicarbonate loading resulted in a substantially higher arterial pH; arterial PCO2 was either unchanged (healthy subjects) or mildly (averaging 5 torr) higher (COPD patients). However, in neither group did bicarbonate loading result in an altered VE response to exercise or an increase in exercise tolerance. In contrast, superimposing hyperoxia on bicarbonate ingestion yielded, on average, 24% reduction in VE and 50% increase in peak work rate in the patients (but not in the healthy young subjects). We conclude that acute bicarbonate loading is not an ergogenic aid in patients with severe COPD.

Cardiac output estimated noninvasively from oxygen uptake during exercise.

Because gas-exchange measurements during cardiopulmonary exercise testing allow noninvasive measurement of oxygen uptake (Vo2), which is equal to cardiac output (CO) x arteriovenous oxygen content difference [C(a-vDo2),] CO and stroke volume could theoretically be estimated if the C(a-vDo2) increased in a predictable fashion as a function of % maximum Vo2 (Vo2max) during exercise. To investigate the behavior of C(a-vDo2) during progressively increasing ramp pattern cycle ergometry exercise, 5 healthy subjects performed 10 studies to exhaustion while arterial and mixed venous blood were sampled. Samples were analyzed for blood gases (pH, Pco2, Po2) and oxyhemoglobin and hemoglobin concentration with a CO-oximeter. The C(a-vDo2) (ml/100 ml) could be estimated with a linear regression [C(a-vDo2) = 5.72 + 0.105 x % Vo2max; r = 0.94]. The CO estimated from the C(a-vDo2) by using the above linear regression was well correlated with the CO determined by the direct Fick method (r = 0.96). The coefficient of variation of the estimated CO was small (7-9%) between the lactic acidosis threshold and peak Vo2. The behavior of C(a-vDo2), as related to peak Vo2, was similar regardless of cardiac function compared with similar measurements from studies in the literature performed in normal and congestive heart failure patients. In summary, CO and stroke volume can be estimated during progressive work rate exercise testing from measured Vo2 (in normal subjects and patients with congestive heart failure), and the resultant linear regression equation provides a good estimate of C(a-vDo2).