Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “cycle threshold value”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,027 records · Page 57Linked to original sources

[Gas exchange, blood acid-base balance and mechanical muscle efficiency during incremental levels of exertion in young healthy individuals].

UNLABELLED: In this study we have evaluated the changes in gas exchange variables, blood acid-base balance and the mechanical efficiency of muscle in healthy young men during an incremental exercise test. Twenty-six healthy men: age 22.1 +/- 1.4 (mean +/- SD) years, body mass 73.6 +/- 7.4 kg, height 179 +/- 8 cm, were subjects in this study. The subjects performed an incremental exercise test on a cycloergometer at a pedalling rate of 70 rev.min-1. The exercise test started at a power output of 30 W, followed by an increase of power output by 30 W every 3 minutes. Gas exchange variables were measured continuously (breath by breath). Antecubital blood samples for acid-base balance variables and plasma lactate concentration [La]pl were taken at the end of each 3-minute step. The lactate threshold (LT) in this study was defined as the highest power output above which [La]pl showed a sustained increase of > 0.5 mmol.l-1.step-1. The power output at LT amounted to 127 +/- 28 W. It corresponded to 45% of the maximal power output (MPO) reached at maximal oxygen uptake (VO2 max). The oxygen uptake at the LT amounted to 1734 +/- 282 ml.min-1 and corresponded to 48% of VO2 max (3726 +/- 363 ml.min-1). The minute ventilation at the LT amounted to 47.8 +/- 7.5 l, and its increase to the level of 125.7 +/- 19.7 l reached at the MPO was obtained mainly by intensification of breathing frequency from 23.8 +/- 3.31.min-1 to 43 +/- 5.91.min-1, for LT and MPO respectively. Analysis of the changes in PETCO2 during the incremental exercise test showed significant differences between subjects. One could recognise a group of subjects (n = 8) with high values of PETCO2 (above 45 mmHg) and a group of subjects (n = 8) with lower values of PETCO2 (below 43 mmHg). However, no significant differences in exercise tolerance, expressed by the level of MPO and maximal oxygen uptake, were found between those groups of subjects. The mechanical efficiency calculated on the basis of power output/net oxygen uptake ratio during cycling at a power output of 60 W amounted to 24.1 +/- 3.8 percent, at the LT 25.8 +/- 2.1%, whereas at the maximal power output a significant (p < 0.01) drop in muscle efficiency occurred, to the value of 23.1 +/- 1.6%. This drop in muscle efficiency occurring at the MPO may be an important factor limiting exercise tolerance when performing high power output exercise. IN CONCLUSION: The above presented data illustrate the physiological responses to incremental exercise and the level of exercise tolerance, which may serve as a reference point for the population of healthy, young physically active Polish students.

Acid-Base Equilibrium↗

Modeling soil organic matter dynamics as affected by soil water erosion.

Soil organic carbon (SOC) stock is an important component of the global carbon (C) cycle, which has the potential to influence global climate. In this paper we presented an overview of soil organic matter (SOM) models in the context of soil erosion and discussed basic processes driving erosion-induced SOC loss. Although the mechanism of this loss is poorly understood, erosion influences SOC in two ways: redistribution of C within the watershed or ecosystem, and loss of C to the atmosphere. Erosion disperses soil, altering its microbiological activity as well as water, air and nutrient regimes. This, along with sediment enrichment, has an impact on greenhouse gas emission from soil. For most of agricultural settings, field studies suggest that cultivation along with soil erosion are the primary reasons for SOC loss. Tracing the fate of eroded C is a challenging task. Modeling is the approach taken most often. In this paper we discuss approaches used in various SOC models to assess erosion-induced C loss from soil in agricultural ecosystems. An example with Century model applied to meadow and corn-soybean rotation under chisel-till demonstrated the model's ability to respond well to different erosion scenarios. It was estimated that at soil loss rate of 10 t ha(-1) year(-1) (value often considered a threshold for maintaining productivity) 19% of the total SOC loss would be attributed to erosion after 90 years of cultivation.

Agriculture↗

Oxygen uptake and muscle desaturation kinetics during intermittent cycling.

PURPOSE: To investigate the kinetics of O2 uptake (VO2) and m. vastus lateralis [deoxyhemoglobin] ([Hb]) (near-infrared spectroscopy) for supramaximal intermittent cycling. METHODS: Six males performed a ramp test for determination of VO2peak and lactate threshold. On different days, they completed four intermittent "work:recovery" tests (10 s:20 s, 30 s:60 s, 60 s:120 s, 90 s:180 s) for 30 min or to the tolerable limit; "work" = 120% peak work rate (WRpeak) attained on the ramp, "recovery" = 20 W. RESULTS: Arterialized capillary [lactate] ([L]c) profiles were dependent on duty-cycle length and resembled those for constant-load exercise classically used to assign exercise intensity: 10 s:20 s-no increase (i.e., "moderate", with first-order VO2 kinetics); 30 s:60 s-increased but stable (i.e., "heavy," with first-order VO2 kinetics supplemented by a slow component (VO2 sc) that stabilizes); 60s:120s-progressive increase that was more marked for 90 s:180 s (i.e., "very heavy" or "severe," with first-order VO2 kinetics supplemented by a VO2 sc projecting to VO2peak). VO2 and Delta[Hb] oscillated with WR, the ensemble-averaged single-cycle oscillation amplitudes (peak-to-nadir) for each individual subject increasing with WR duty-cycle duration. In the 30-s:60-s test, with [L]c being elevated, there was also a tendency towards a modest VO2 sc, with an increase in individual VO2 peak values early in the test and VO2 not fully recovering back to baseline in recovery. This was more marked for the 60-s:120-s duty cycle: VO2 failed to recover completely back to baseline, and the peaks of the VO2 oscillations increased significantly with time (F = 30.7, P < 0.001); in some cases, VO2peak was attained and exhaustion rapidly ensued. CONCLUSION: VO2 kinetics in intermittent exercise over a range of duty-cycle durations tended to associate with blood [lactate] profiles, similarly to previous demonstrations for sustained constant-load exercise.

Adult↗

The effect of an aerobic interval training program on intermittent anaerobic performance.

The effects of a 9-week aerobic interval training program on anaerobic intermittent performance were investigated. Intermittent work consisted of four repeat 30-sec maximal efforts on a cycle ergometer (Wingate test) with 3-min recovery intervals. Thirteen men trained 3 days a week on the cycle ergometer, completing 3-min work-to-rest intervals and progressing from 5 to 10 reps. Relative and absolute values of aerobic power increased significantly for the training group (p < .05). No significant change was observed for the control group (n = 11). The training group demonstrated significant increases in the four anaerobic variables of short-term peak power (SPP), short-term anaerobic capacity (SAC), intermediate-term peak power (IPP), and total work (TW), and across the four 30-sec maximal repeats for anaerobic performance (T1-T4) (p < .05). Greater percentages of increase occurred for IPP and TW, especially during Repeats 3 and 4. The control group only demonstrated a significant increase in SPP for Repeat 3. These data suggest that the type of interval training program used in the study increased aerobic power and also enhanced performance in repeated high intensity, short duration work.

Adult↗

Gene expression changes in leukocytes during cardiopulmonary bypass are dependent on circuit coating.

BACKGROUND: Cardiopulmonary bypass (CPB) results in a systemic inflammatory response. Leukocytes play a crucial role in inflammatory reactions. Their gene expression profile in the context of CPB is unknown. METHODS AND RESULTS: In a prospective, randomized, and double-blind clinical trial, 12 male patients underwent elective coronary artery bypass grafting with either heparin-coated (group H) or protein-coated (group P) CPB circuits. Oligonucleotide microarray analyses of 22,283 genes were performed on circulating leukocytes, collected immediately before surgery and 6 hours after CPB. Microarray results were validated with real-time polymerase chain reaction. All patients had uneventful surgery, and no significant differences between groups were observed during the clinical course. Multiple statistical analyses with different methods were performed. Compared with preoperative expression at a threshold value of P<0.01, postoperative expression revealed 814 upregulated and 1187 downregulated genes in group H compared with 99 upregulated and 231 downregulated in group P (P<0.001). Fifty genes exhibited a >4-fold increase and 27 exhibited a >4-fold decrease in group H, whereas only 7 genes exhibited upregulation and 7 revealed downregulation in group P. Microarray-pathway-profile-finder analyses determined 1405 upregulated and 1454 downregulated pathways in group H compared with 552 upregulated and 818 downregulated pathways in group P (P<0.01). Pathways related to inflammatory response exhibited highest z scores in group H, reflecting cellular inflammatory activation. CONCLUSIONS: Heparin coating resulted in a more profound alteration in leukocyte gene expression when compared with protein coating. Microarray analyses present an innovative approach for the evaluation and understanding of inflammatory reactions associated with CPB.

Aged↗

[A chapter in systematic schizophrenia research--the search for causal explanations for sex differences in age of onset].

With the aim of detecting causal processes contributing to the onset of schizophrenic symptoms a systematic search strategy was worked out. One of the few epidemiological findings on schizophrenia consistently diverging from expected values, the sex difference in age at first admission, was taken as a basis and replicated on data from the Danish and the Mannheim case registers by controlling for selection and diagnostic artefacts. Danish psychiatrists turned out to have underdiagnosed schizophrenia to a considerable extent at least in 1976, the year from which the analysed case-register data dated. After the exclusion of alternative explanations, the time when symptoms appeared for the first time and the first acute episode occurred was determined for a representative sample of 267 first-admitted cases with a diagnosis of non-affective functional disorder by using the IRAOS interview designed for this purpose. At any of the definitions of first onset applied the mean age of females was significantly higher than that of males, the difference ranging from 3.2 to 4.1 years. The distribution of onsets across the female life cycle showed a clearly delayed increase at young age and a second, lower peak of onsets at the age of 45-54, whereas the cumulative incidence up to the age of 60 years was equal for males and females. On assessing the plausibility of psychosocial versus biological explanations it was hypothesized that due to the effect of estrogens the vulnerability threshold for schizophrenia is raised in females until the menopause. Animal experiments and postmortem analysis showed that chronic estrogen applications significantly shortened dopamine-induced behaviour and reduced D2 receptor sensitivity in the brain. The applicability of this pathophysiological mechanism on human schizophrenia was tested on acutely schizophrenic females with normal menstrual cycles. A significant negative correlation was found between measures of symptomatology and plasma estrogen levels. Apparently, the manifestation of schizophrenic symptoms is influenced by a sufficiently sensitive D2 receptor system in the brain, blocked by neuroleptics and modulated by estrogens.

Adolescent↗

Aerobic and anaerobic correlates of multiple sprint cycling performance.

The aims of this study were to examine (a) the relationship between maximal oxygen uptake (VO(2)max) and several performance indices of multiple sprint cycling; (b) the relationship between maximal accumulated oxygen deficit (MAOD) and those same performance indices; and (c) the influence of recovery duration on the magnitude of those relationships. Twenty-five physically active men completed a VO(2)max test, a MAOD test, and 2 maximal intermittent (20 x 5 seconds) sprint cycling tests with contrasting recovery periods (10 seconds or 30 seconds). Mean +/- SD for age, height, and body mass were 20.6 +/- 1.5 years, 177.2 +/- 5.4 cm, and 78.2 +/- 8.2 kg, respectively. All tests were conducted on a friction-braked cycle ergometer with subsequent data normalized for body mass. Moderate (0.3 < or = r < 0.5) positive correlations were observed between power output data and MAOD (range, 0.31-0.46; 95% confidence limits, -0.10 to 0.72). Moderate to large positive correlations also were observed between power output data and VO(2)max, the magnitude of which increased as values were averaged across all sprints (range, 0.45-0.67; 95% confidence limits 0.07-0.84). Correlations between fatigue and VO(2)max were greater in the intermittent protocol with 30-second recovery periods (r = -0.34; 95% confidence limits, 0.06 to -0.65). The results of this study reflect the complex energetics associated with multiple sprint work. Though the findings add support to the idea that multiple sprint sports demand a combination of speed and endurance, further longitudinal research is required to confirm the relative importance of these parameters.

Adult↗

Spontaneous otoacoustic emissions in an active feed-forward model of the cochlea.

Numerical simulation of spontaneous otoacoustic emissions (SOAE) was done using a 1-dimensional macromechanical cochlear model with an active 'feed-forward' force in every section of the basilar membrane (BM). When the activity of the force was increased the model showed more stability than a 'feed-back' model and could have excitation curves with larger tips without divergence of the solution. The stability broke up when either (1) the damping of the BM was made slightly irregular throughout the BM or (2) the feed-forward force was switched off at a certain part of the BM, and limit cycle oscillations (LCO) emerged within the cochlea. Critical feed-forward value for the emergence of LCO in the first setting of BM (1), which was intended to simulate physiological variations in the distribution of outer hair cells, was searched utilizing the 'ringing' of delayed evoked otoacoustic emissions (DEOAE). In the course of the search, smooth transition from a DEOAE to a set of SOAEs was found to occur keeping the same spectral fine structure of the emissions when the feed-forward force surpassed a certain value. It was, as a result suggested that the two kinds of emissions may have the same origin. In the second setting of BM (2), which was intended to simulate pathological cases. LCOs tended to be stronger than in the first one and they had similarity not only to real SOAEs but also to tinnitus in the way they showed up very close to or at the "edge' of the switched-off part of the BM.

Auditory Threshold↗

Cumulative glycemic exposure and microvascular complications in insulin-dependent diabetes mellitus. The glycemic threshold revisited.

BACKGROUND: The development of microvascular insulin-dependent diabetes mellitus (IDDM) complications has been shown to be related to both duration of diabetes and the degree of glycemic exposure. However, controversy exists as to whether there is a threshold of glycemic exposure, below which there is minimal risk. Furthermore, there are few data describing the relationship of total glycemic exposure (duration x degree) to complications rates-a potentially useful research and clinical tool. OBJECTIVES: To determine a cumulative glycemic exposure variable that combines the effect of both degree and duration of hyperglycemia and to evaluate this variable in terms of its relation to microvascular complications. The association between cumulative glycemic exposure and complication risk was also examined to evaluate whether there was a threshold effect. METHODS: A total of 353 patients with IDDM who had completed the first 6 years of follow-up in the Pittsburgh Epidemiology of Diabetes Complications Study were included in this analysis. These subjects had a mean age of 27.9 years, and the mean duration of the disease was 19.4 years. Subjects were examined at baseline (cycle 1) and then biennially (cycle 2, cycle 3, and cycle 4) for diabetes complications. Total glycosylated hemoglobin (HbA1) was measured at each cycle. A cumulative glycemic exposure variable, named A1months, was calculated by multiplying the number of HbA1 units above normal at each cycle by the number of months between the midpoints of the preceding and succeeding cycle intervals. RESULTS: The mean number of A1months experienced at the time of diagnosis of proliferative retinopathy (914), microalbuminuria (952), overt nephropathy (1043), and distal symmetrical polyneuropathy (1043) did not vary by duration of diabetes. Thus, approximately 1000 A1months were needed (on average) for the advanced complications to develop. Although the risk for developing proliferative retinopathy rose gradually as A1months increased, a more abrupt increase in the risk was seen (again at approximately 1000 A1months) for microalbuminuria (odds ratio, 6.9; 95% confidence interval, 2.5-19.1), overt nephropathy (odds ratio, 6.5; 95% confidence interval, 2.0-21.7), and distal symmetrical polyneuropathy (odds ratio, 6.5; 95% confidence interval, 2.4-17.8). Nonetheless, complications developed in the majority of cases at glycemic exposures below 1000 A1months. The cumulative glycemic exposure variable A1months does not predict complications any better than its component variables (duration and HbA1). Furthermore, formal statistical testing failed to show a definitive threshold for any complication. CONCLUSIONS: Although A1months does not enhance prediction of complications, it may be a useful summary measure of glycemic exposure for both patients and physicians. However, although subjects with 1000 A1months or more appear to be at increased risk of developing most microvascular complications, because the majority of complications arise in subjects with less than this exposure, this threshold value should only be considered a minimal goal. For example, our data suggest that for most microvascular complications to develop, it would take, on average, 83 years with an HbA1 unit at 1% above normal, 42 years at 2% above normal, 28 years at 3% above normal. 21 years at 4% above normal, and 18 years at 5% above normal.

Adolescent↗

An alternative method to determine maximal accumulated O2 deficit in runners.

An accepted measure of anaerobic capacity is the maximal O2 deficit. But it is not feasible to use O2 deficit if > or =10 submaximal runs are needed to extrapolate the O2 demand of high velocity running (Medbø et al. 1988). Recently, an alternative method to determine O2 deficit was proposed (Hill 1996) using only results of supramaximal cycle ergometer tests. The purpose of this study was to evaluate this alternative method with data from treadmill tests. Twenty-six runners ran at 95%, 100%, 105%, and 110% of their velocity at VO2max. Times to exhaustion, velocity, and accumulated oxygen uptake (VO2) from each individual's four tests were fit to the following equation using iterative nonlinear regression: accumulated VO2 = (O2 demand x velocity x time)-O2 deficit. The mean value s derived for O2 demand and O2 deficit were 0.198+/-0.031 ml x kg(-1) x m(-1) and 42+/-22 ml x kg(-1). SEE for the parameters were 0.007+/-0.007 ml x kg(-1) x m(-1) and 8+/-10 ml x kg(-1), respectively. Mean R2 was 0.998+/-0.003. It was concluded that O2 deficit can be determined from all-out treadmill tests without the need to perform submaximal tests.

Adult↗

Kinetics of VO(2) in professional cyclists.

PURPOSE: To analyze the kinetics of oxygen uptake (VO(2)) in professional road cyclists during a ramp cycle ergometer test and to compare the results with those derived from well-trained amateur cyclists. METHODS: Twelve professional cyclists (P group; 25 +/- 1 yr; maximal power output (W(max)), 508.3 +/- 9.3 watts) and 10 amateur cyclists (A group; 22 +/- 1 y; W(max), 429.9 +/- 8.6 watts) performed a ramp test until exhaustion (power output increases of 25 watts x min(-1)). The regression lines of the VO(2):power output (W) relationship were calculated for the following three phases: phase I (below the lactate threshold (LT)), phase II (between LT and the respiratory compensation point (RCP)), and phase III (above RCP). RESULTS: In group P, the mean slope (Delta VO(2):Delta W) of the VO(2):W relationship decreased significantly (P < 0.01) across the three phases (9.9 +/- 0.1, 8.9 +/- 0.2, and 3.8 +/- 0.6 mL O(2) x watts(-1) x min(-1) for phases I, II, and III, respectively). No significant differences (P > 0.05) were found between phases I and II (P > 0.05) in group A, whereas Delta VO(2):Delta W significantly increased in phase III (P < 0.01), compared with phase II (10.2 +/- 0.3, 9.2 +/- 0.4, and 10.1 +/- 1.1 mL O(2) x watts(-1) x min(-1) in phases I, II, and III, respectively). The mean value of Delta VO(2):Delta W for phase III was significantly lower in group P than in group A (P < 0.01). CONCLUSION: Contrary to the case in amateur riders, the rise in VO(2) in professional cyclists is attenuated at moderate to high workloads. This is possibly an adaptation to the higher demands of their training/competition schedule.

Adult↗

Apoptosis regulating genes, bcl-2 and bax, and human telomerase reverse transcriptase messenger RNA expression in adrenal tumors: possible diagnostic and prognostic importance.

BACKGROUND: Apoptosis-suppressing gene, bcl-2, and apoptosis-inducing gene, bax, are expressed in various tumors. Human telomerase reverse transcriptase (hTERT) expression is increased in many cancers. The purpose of this investigation was to determine whether bcl-2 or bax gene expression differs between benign and malignant adrenal tumors, and whether hTERT gene expression correlates with the prognosis of patients with adrenal cancer. METHODS: Expression of bcl-2 and bax from 52 adrenal surgical specimens was analyzed by reverse transcription-polymerase chain reaction. Expression of hTERT was analyzed by real-time quantitative reverse transcription-polymerase chain reaction, and expressed using the delta-delta threshold cycle method. RESULTS: All normal adrenal tissues (n = 7) and benign adrenal tumors (n = 41) expressed bcl-2 and bax, whereas all adrenocortical cancers (n = 4) expressed bcl-2 but not bax. Expression of hTERT was increased in adrenocortical cancers compared with that in normal tissues (P <.05), cortical adenomas (n = 17) (P <.05), cortical hyperplasias (n = 4) (P <.05), and pheochromocytomas (n = 20) (P <.05). The one patient with an adrenocortical cancer without increased hTERT expression is alive with distant metastasis 5 years after adrenalectomy. The other 3 patients with adrenocortical cancer died 5 to 24 months after adrenalectomy. CONCLUSIONS: Expression of bax gene appears to distinguish adrenal cancer from benign adrenal tumors. Gene expression of hTERT should be investigated as a prognostic marker in adrenal cortical cancers.

Adenoma↗

Energetics of best performances in track cycling.

VO2max and best performance times (BPTs) obtained during maximal voluntary trials over 1, 2, 5, and 10 km from a stationary start were assessed in 10 elite cyclists. Steady-state VO2 and peak blood lactate concentration ([La]b) were also determined in the same subjects pedaling on a track at constant submaximal speeds. The energy cost of cycling (Cc, J.m-1) was calculated as the ratio of VO2, corrected for glycolytic energy production and expressed in W, to v (m.s-1). Individual relationships between Cc and v were described by: Cc = Ccrr + k1 v2 where Ccrr is the energy spent against friction and k1 v2 is that spent against drag. Overall energy cost of cycling (Cctot) was obtained, adding to Cc the energy spent to accelerate the total moving mass from a stationary start. Individual theoretical BPTs were then calculated and compared with the actual ones as follows. The maximal metabolic power sustained at a constant level by a given subject (Emax, W) is a known function of the exhaustion time (te). It depends on his VO2max and maximal anaerobic capacity; it was obtained from individual VO2max and [La]b values. The metabolic power (Ec, W) necessary to cover any given distance (d) is a known function of the performance time over d (td); it is given by Ec = Cctot v = Cctot d td. For all subjects and distances, the t values solving the equalities Emax F(te) = Ec F(td) were calculated and assumed to yield theoretical BPTs. Calculations showed a fairly good agreement between actual and calculated BPTs with an average ratio of 1.035 +/- 0.058.

Adolescent↗

Airborne concentrations of benzene due to diesel locomotive exhaust in a roundhouse.

Concentrations of airborne benzene due to diesel exhaust from a locomotive were measured during a worst-case exposure scenario in a roundhouse. To understand the upper bound human health risk due to benzene, an electromotive diesel and a General Electric four-cycle turbo locomotive were allowed to run for four 30-min intervals during an 8-h workshift in a roundhouse. Full-shift and 1-h airborne concentrations of benzene were measured in the breathing zone of surrogate locomotive repairmen over the 8-h workshift on 2 consecutive days. In addition, carbon monoxide was measured continuously; elemental carbon (surrogate for diesel exhaust) was sampled with full-shift area samples; and nitrogen dioxide/nitric oxide was sampled using full-shift and 15-min (nitrogen dioxide only) area samples. Peak concentrations of carbon monoxide ranged from 22.5 to 93 ppm. The average concentration of elemental carbon for each day of the roundhouse study was 0.0543 and 0.0552 microg/m(3 )for an 8-h workshift. These were considered "worst-case" conditions since the work environment was intolerably irritating to the eyes, nose, and throat. Short-term nitrogen dioxide concentrations ranged from 0.81 to 2.63 ppm during the diesel emission events with the doors closed. One-hour airborne benzene concentrations ranged from 0.001 to 0.015 ppm with 45% of the measurements below the detection limit of 0.002-0.004 ppm. Results indicated that the 8-h time-weighted average for benzene in the roundhouse was approximately 100-fold less than the current threshold limit value (TLV) of 0.5 ppm. These data are consistent with other studies, which have indicated that benzene concentrations due to diesel emissions, even in a confined environment, are quite low.

Air Pollution, Indoor↗

Significant effects of mild endogenous hormonal changes in humans: considerations for low-dose testing.

We review the significant and adverse health effects that can occur with relatively small endogenous hormonal changes in pubertal and adult humans. We discuss the effects of hormonal changes that occur within normal physiologic ranges--such as the rising levels of estrogen in peripuberty, which cause growth spurts at low levels and then the fusion of epiphyses at higher levels--and the hormonal variations during the menstrual cycle and their relation to genital phenotypic changes and intercurrent disease evolution. We turn next to adaptive changes in gonadal and other functions during aging, exercise, stress, starvation, and chronic diseases, which can serve as models for the effects of exogenous, hormonally active compounds. Then we review the states of borderline hormonal imbalances such as subclinical (having few or very mild symptoms, if any) hypothyroidism or hyperthyroidism, glucose intolerance, and other endocrine conditions. Finally, we review the deleterious systemic effects of gonadal imbalance. Information stemming from clinical observations leads to the concept of "no threshold" within the endocrine system and thus illustrates the importance of considering low-dose testing for chemicals that interfere with hormonal activity. We also urge attention to more sensitive, less visible end points such as osteoporosis, increased risk for cardiovascular disease, or cognitive changes.

Adolescent↗

Recombinant follicle-stimulating hormone (FSH; Puregon) is more efficient than urinary FSH (Metrodin) in women with clomiphene citrate-resistant, normogonadotropic, chronic anovulation: a prospective, multicenter, assessor-blind, randomized, clinical trial. European Puregon Collaborative Anovulation Study Group.

OBJECTIVE: To compare the safety and efficacy of recombinant FSH (follitropin beta, Puregon; NV Organon, Oss, the Netherlands) and urinary FSH (urofollitropin, Metrodin; Ares-Serono, Geneva, Switzerland). DESIGN: A prospective, multicenter, assessor-blind, randomized, clinical trial. SETTING: Twelve European infertility clinics. PATIENT(S): One hundred seventy-two women (recombinant FSH: n = 105; urinary FSH: n = 67) with clomiphene citrate-resistant normogonadotropic chronic anovulation (World Health Organization group II). INTERVENTION(S): Eligible subjects were randomized (ratio of recombinant to urinary FSH, 3:2) and treated for a maximum of three cycles. A low-dose step-up regimen was used, with 75 IU of FSH given IM daily for a maximum of 14 days and, if needed, weekly increments of half an ampule given thereafter until the threshold dose for follicular development was achieved. MAIN OUTCOME MEASURE(S): Cumulative ovulation rate after three cycles, total FSH dose, and treatment period needed to achieve ovulation. RESULT(S): The cumulative ovulation rates after three treatment cycles were 95% and 96% for the recombinant and urinary FSH groups, respectively. Overall, ovulation was seen in 155 of 223 treatment cycles (69.5%) in the recombinant FSH group, compared with 92 of 138 treatment cycles (66.7%) in the urinary FSH group. In the first cycle, a statistically significantly lower total dose (750 versus 1,035 IU) and a shorter treatment period (10 versus 13 days) were needed in the recombinant FSH group to reach ovulation. Only one case of ovarian hyperstimulation syndrome led to hospitalization. Two sets of twins (one in each treatment group) and one set of triplets (in the recombinant FSH group) were born. CONCLUSION(S): Recombinant FSH (Puregon) is more efficient than urinary FSH (Metrodin) in inducing follicular development.

Adult↗

Trained versus untrained men: different immediate post-exercise responses of pituitary adrenal axis. A preliminary study.

The hypothalamo-pituitary-adrenal axis is involved throughout the exercise-recovery cycle. Nevertheless, differences in hormone responses during early recovery between sedentary and endurance trained subjects are not well known. The aim of this preliminary study was to monitor plasma cortisol and adrenocorticotropic hormone (ACTH) concentrations both during and after the end of running exercise performed by four endurance trained adults (marathon men) compared to four sedentary subjects. Two parameters, i.e. intensity and duration, were changed on 4 consecutive days. The 1st day (D0) was spent in the laboratory: all blood samples were obtained at rest to determine diurnal variations of each hormone. On the following days (D1-D4) the subjects exercised: D1 and D2 brief (20 min), light (50% maximal heart rate HRmax, D1) or strenuous (80% HRmax, D2), D3 and D4 prolonged (120 min), light (D3) or strenuous (D4). In both groups, neither brief (D1, D2) nor prolonged light exercise (D3) induced any significant variation in plasma ACTH or cortisol concentrations. Plasma ACTH and cortisol concentrations increased only if the exercise was intense and prolonged (D4). The training factor did not modify the intensity or duration thresholds for the activation of the pituitary-adrenocortical response to exercise in the conditions of our experiment. However, during immediate recovery from the four exercise regimens, the plasma ACTH concentrations of the marathon men were constantly above the values of the sedentary subjects, although plasma cortisol concentration remained similar in both groups. As an indirect means of evaluating the relationships between ACTH and cortisol we compared the areas under the cortisol and ACTH curves (AUC) from 0.5 to 3.5 h during recovery from D1 to D4 compared to D0 at the same time. Cortisol AUC were similar in the sedentary subjects and marathon men although the ACTH AUC were different in the sedentary subjects and marathon men, suggesting a change in the pituitary-adrenal relationship at some yet indeterminate level. During the immediate recovery from exercise whatever its intensity, the magnitude of the ACTH response was increased in the trained subjects but with a reduced effect upon its target, the adrenal glands. This phenomenon has not been described in the literature. Two non-exclusive phenomena may be involved, i.e. a decreased adrenal sensitivity to ACTH stimulation, and/or a decreased hypothalamo-pituitary axis sensitivity to cortisol negative feedback.

Adrenal Glands↗

Detection of the change point in oxygen uptake during an incremental exercise test using recursive residuals: relationship to the plasma lactate accumulation and blood acid base balance.

The purpose of this study was to develop a method to determine the power output at which oxygen uptake (VO2) during an incremental exercise test begins to rise non-linearly. A group of 26 healthy non-smoking men [mean age 22.1 (SD 1.4) years, body mass 73.6 (SD 7.4) kg, height 179.4 (SD 7.5) cm, maximal oxygen uptake (VO2max) 3.726 (SD 0.363) l x min(-1)], experienced in laboratory tests, were the subjects in this study. They performed an incremental exercise test on a cycle ergometer at a pedalling rate of 70 rev x min(-1). The test started at a power output of 30 W, followed by increases amounting to 30 W every 3 min. At 5 min prior to the first exercise intensity, at the end of each stage of exercise protocol, blood samples (1 ml each) were taken from an antecubital vein. The samples were analysed for plasma lactate concentration [La]pl, partial pressure of O2 and CO2 and hydrogen ion concentration [H+]b. The lactate threshold (LT) in this study was defined as the highest power output above which [La-]pl showed a sustained increase of more than 0.5 mmol x l(-1) x step(-1). The VO2 was measured breath-by-breath. In the analysis of the change point (CP) of VO2 during the incremental exercise test, a two-phase model was assumed for the 3rd-min-data of each step of the test: Xi = at(i) + b + epsilon(i) for i = 1,2, ..., T, and E(Xi) > at(i) + b for i = T + 1, ..., n, where X1, ..., Xn are independent and epsilon(i) approximately N(0, sigma2). In the first phase, a linear relationship between VO2 and power output was assumed, whereas in the second phase an additional increase in VO2 above the values expected from the linear model was allowed. The power output at which the first phase ended was called the change point in oxygen uptake (CP-VO2). The identification of the model consisted of two steps: testing for the existence of CP and estimating its location. Both procedures were based on suitably normalised recursive residuals. We showed that in 25 out of 26 subjects it was possible to determine the CP-VO2 as described in our model. The power output at CP-VO2 amounted to 136.8 (SD 31.3) W. It was only 11 W -- non significantly -- higher than the power output corresponding to LT. The VO2 at CP-VO2 amounted to 1.828 (SD 0.356) l x min(-1) was [48.9 (SD 7.9)% VO2max]. The [La-]pl at CP-VO2, amounting to 2.57 (SD 0.69) mmol x l(-1) was significantly elevated (P < 0.01) above the resting level [1.85 (SD 0.46) mmol x l(-1)], however the [H+]b at CP-VO2 amounting to 45.1 (SD 3.0) nmol x l(-1), was not significantly different from the values at rest which amounted to 44.14 (SD 2.79) nmol x l(-1). An increase of power output of 30 W above CP-VO2 was accompanied by a significant increase in [H+]b above the resting level (P = 0.03).

Acid-Base Equilibrium↗