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Biomedical subjects

T Mohr

Publications and source records attributed to T Mohr.

At least 37 records · Page 2Linked to original sources

Caffeine ingestion and metabolic responses of tetraplegic humans during electrical cycling.

Normally, caffeine ingestion results in a wide spectrum of neural and hormonal responses, making it difficult to evaluate which are critical regulatory factors. We examined the responses to caffeine (6 mg/kg) ingestion in a group of spinal cord-injured subjects [7 tetraplegic (C5-7) and 2 paraplegic (T4) subjects] at rest and during functional electrical stimulation of their paralyzed limbs to the point of fatigue. Plasma insulin did not change, caffeine had no effect on plasma epinephrine, and there was a slight increase (P < 0. 05) in norepinephrine after 15 min of exercise. Nevertheless, serum free fatty acids were increased (P < 0.05) after caffeine ingestion after 60 min of rest and throughout the first 15 min of exercise, but the respiratory exchange ratio was not affected. The exercise time was increased (P < 0.05) by 6% or 1.26 +/- 0.57 min. These data suggest that caffeine had direct effects on both the adipose tissue and the active muscle. It is proposed that the ergogenic action of caffeine is occurring, at least in part, by a direct action of the drug on muscle.

Adult↗

Increased bone mineral density after prolonged electrically induced cycle training of paralyzed limbs in spinal cord injured man.

Spinal cord injured (SCI) individuals have a substantial loss of bone mass in the lower limbs, equaling approximately 50% of normal values in the proximal tibia, and this has been associated with a high incidence of low impact fractures. To evaluate if this inactivity-associated condition in the SCI population can be reversed with prolonged physical training, ten SCI individuals [ages 35.3 +/- 2.3 years (mean +/- standard error [SE]); post injury time: 12.5 +/- 2.7 years, range 2-24 years; level of lesion: C6-Th4; weight: 78 +/- 3.8 kg] performed 12 months of Functional Electrical Stimulated (FES) upright cycling for 30 min per day, 3 days per week, followed by six months with only one weekly training session. Bone mineral density (BMD) was determined before training and 12 and 18 months later. BMD was measured in the lumbar spine, the femoral neck, and the proximal tibia by dual energy absorptiometry (DEXA, Nordland XR 26 MK1). Before training, BMD was in the proximal tibia (52%), as well as in the femoral neck, lower in SCI subjects than in controls of same age (P < 0.05). BMD of the lumbar spine did not differ between groups (P > 0.05). After 12 months of training, the BMD of the proximal tibia had increased 10%, from 0.49 +/- 0.04 to 0. 54 +/- 0.04 g/cm2 (P < 0.05). After a further 6 months with reduced training, the BMD in the proximal tibia no longer differed from the BMD before training (P > 0.05). No changes were observed in the lumbar spine or in the femoral neck in response to FES cycle training. It is concluded that in SCI, the loss of bone mass in the proximal tibia can be partially reversed by regular long-term FES cycle exercise. However, one exercise session per week is insufficient to maintain this increase.

Absorptiometry, Photon↗

Long-term adaptation to electrically induced cycle training in severe spinal cord injured individuals.

Spinal cord injured (SCI) individuals most often contract their injury at a young age and are deemed to a life of more or less physical inactivity. In addition to the primary implications of the SCI, severe SCI individuals are stigmatized by conditions related to their physically inactive lifestyle. It is unknown if these inactivity related conditions are potentially reversible and the aim of the present study was, therefore, to examine the effect of exercise on SCI individuals. Ten such individuals (six with tetraplegia and four with paraplegia; age 27-45 years; time since injury 3-23 years) were exercise trained for 1 year using an electrically induced computerized feedback controlled cycle ergometer. They trained for up to three times a week (mean 2.3 times), 30 min on each occasion. The gluteal, hamstring and quadriceps muscles were stimulated via electrodes placed on the skin over their motor points. During the first training bouts, a substantial variation in performance was seen between the subjects. A majority of them were capable of performing 30 min of exercise in the first bout; however, two individuals were only able to perform a few minutes of exercise. After training for 1 year all of the subjects were able to perform 30 min of continuous training and the work output had increased from 4 +/- 1 (mean +/- SE) to 17 +/- 2 Kilo Joules per training bout (P < 0.05). The maximal oxygen uptake during electrically induced exercise increased from 1.20 +/- 0.08 litres per minute measured after a few weeks habituation to the exercise to 1.43 +/- 0.09 litres per minute after training for 1 year (P < 0.05). Magnetic resonance cross sectional images of the thigh were performed to estimate muscle mass and an increase of 12% (mean, P < 0.05) was seen in response to 1 year of training. In biopsies taken before exercise various degrees of atrophy were observed in the individual muscle fibres, a phenomenon that was partially normalized in all subjects after training. The fibre type distribution in skeletal muscles is known to shift towards type IIB fibres (fast twitch, fast fatiguable, glycolytic fibres) within the first 2 years after the spinal cord injury. The muscle in the present investigation contained of 63% myosin heavy chain (MHC) isoform IIB, 33% MHC isoform IIA (fast twitch, fatigue resistant) and less than 5% MHC isoform I (slow twitch) before training. A shift towards more fatigue resistant contractile proteins was found after 1 year of training. The percentage of MHC isoform IIA increased to 61% of all contractile protein and a corresponding decrease to 32% was seen in the fast fatiguable MHC isoform IIB, whereas MHC isoform I only comprised 7% of the total amount of MHC. This shift was accompanied by a doubling of the enzymatic activity of citrate synthase, as an indicator of mitochondrial oxidative capacity. It is concluded that inactivity-associated changes in exercise performance capacity and skeletal muscle occurring in SCI individuals after injury are reversible, even up to over 20 years after the injury. It follows that electrically induced exercise training of the paralysed limbs is an effective rehabilitation tool that should be offered to SCI individuals in the future.

Adaptation, Physiological↗

In vivo cell-mediated immunity and vaccination response following prolonged, intense exercise.

Epidemiological and experimental studies have shown increased frequency and severity of infections after intense, long-term exercise. This study examines whether an in vivo impairment of the cell-mediated immunity and antibody production can be demonstrated after intense, long-term exercise. Twenty-two male triathletes performed one-half an ironman (group A). Vaccinations with tetanus and diphtheritis toxoid and purified pneumococcal polysaccharide were given after the exercise. Furthermore, a skin test with seven different antigens was applied on the forearm. Antibody titers were measured before and 2 wk after the exercise. The skin test was read 48 h after the application. Eleven non-exercising triathletes (group B) and 22 moderately trained men (group C) were used as control groups. Group A revealed a significantly lower skin test response to the tetanus antigen than both groups B and C. In group A, a smaller cumulative response (sum of the diameters of indurations and number of positive skin test spots) was found than in both groups B and C. No differences in antibody titers were found among the three groups. Thus, the in vivo cell-mediated immunity was impaired in the first days after prolonged, high intensity exercise, whereas there was no impairment of the in vivo antibody production measured 2 wk after vaccination.

Adult↗

Myosin heavy chain isoform transformation in single fibres from m. vastus lateralis in spinal cord injured individuals: effects of long-term functional electrical stimulation (FES).

The myosin heavy chain (MHC) composition of single fibres from m. vastus lateralis of five spinal- cord-injured (SCI) individuals was analysed by Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) before, and after 6 and 12 months of functional electrical stimulation (FES)-training, administrated for 30 min three times per week. Prior to FES training 37.2% of the fibres contained only MHC IIB, 21.2% only MHC IIA, and 40.7% co-expressed MHC IIA and MHC IIB. After 6 months of FES-training the number of fibres containing only MHC IIB was reduced to 2.6% (P < 0.05), the number of fibres containing only MHC IIA was increased to 44.3% (P < 0.05), and the number of fibres co-expressing MHC IIA and MHC IIB was 50.9% (ns). After 12 months almost all fibres (91.2%, P < 0.05) contained only MHC IIA. The number of fibres containing only MHC IIB was 2.3% and the fibres co-expressing MHC IIA and IIB had decreased to 4.6% (P < 0.05). The amount of fibres containing only MHC I never exceeded 0.5%. Likewise, the number of fibres co-expressing MHC I and MHC IIA was below 2% throughout the study period. In total, the MHC composition of 1596 single fibres was determined. This study shows that FES-training of paralysed human skeletal muscle administrated over a prolonged period of time, can lead to a marked switch in MHC expression from about equal amounts of MHC IIA and MHC IIB to an almost total dominance of MHC IIA.

Adult↗

Assessing individual differences in constructive versus destructive responses to anger across the lifespan.

Scenario-based, self-report measures were developed to assess how people characteristically experience and manage anger from middle childhood through adulthood. The Anger Response Inventories (ARIs) for children, adolescents, and adults each assess (a) anger arousal, (b) intentions, (c) cognitive and behavioral responses, and (d) Long-term consequences. Several independent studies provide support for the reliability and validity of the ARIs. Theoretically consistent patterns of correlations were observed with (a) global self-report measures of hostility, aggression, and anger-management strategies (adult version); (b) teacher reports of behavioral and emotional adjustment (child and adolescent versions); and (c) self- and family-member reports of behaviors on specific anger episodes (adolescent and adult versions). Findings from additional personality and developmental studies are summarized, further supporting construct validity.

Adaptation, Psychological↗

Viscoelastic stress relaxation during static stretch in human skeletal muscle in the absence of EMG activity.

The present study sought to investigate the role of EMG activity during passive static stretch. EMG and passive resistance were measured during static stretching of human skeletal muscle in eight neurologically intact control subjects and six spinal cord-injured (SCI) subjects with complete motor loss. Resistance to stretch offered by the hamstring muscles during passive knee extension was defined as passive torque (Nm). The knee was passively extended at 5 degrees/s to a predetermined final position, where it remained stationary for 90 s (static phase) while force and integrated EMG of the hamstring muscle were recorded. EMG was sampled for frequency domain analysis in a second stretch maneuver in five control and three SCI subjects. There was a decline in passive torque in the 90-s static phase for both control and SCI subjects, P < 0.05. Although peak passive torque was greater in control subjects, P < 0.05, there was no difference in time-dependent passive torque response between control (33%) and SCI (38%) subjects. Initial and final 5-s IEMG ranged from 1.8 to 3.4 microV.s and did not change during a stretch or differ between control and SCI subjects. Frequency domain analysis yielded similar results in both groups, with an equal energy distribution in all harmonics, indicative of 'white noise'. The present data demonstrate that no measurable EMG activity was detected in either group during the static stretch maneuver. Therefore, the decline in resistance to static stretch was a viscoelastic stress relaxation response.

Adolescent↗

Regulation of glucose turnover and hormonal responses during electrical cycling in tetraplegic humans.

To examine the importance of blood-borne vs. neural mechanisms for hormonal responses and substrate mobilization during exercise, six spinal cord-injured tetraplegic (C5-T1) males (mean age: 35 yr, range: 24-55 yr) were recruited to perform involuntary, electrically induced cycling [functional electrical stimulation (FES)] to fatigue for 24.6 +/- 2.3 min (mean and SE), and heart rate rose from 67 +/- 7 (rest) to 107 +/- 5 (exercise) beats/min. Voluntary arm cranking in tetraplegics (ARM) and voluntary leg cycling in six matched, long-term immobilized (2-12 mo) males (Vol) served as control experiments. In FES, peripheral glucose uptake increased [12.4 +/- 1.1 (rest) to 19.5 +/- 4.3 (exercise) mumol.min-1.kg-1; P < 0.05], whereas hepatic glucose production did not change from basal values [12.4 +/- 1.4 (rest) vs. 13.0 +/- 3.4 (exercise) mumol.min-1.kg-1]. Accordingly, plasma glucose decreased [from 5.4 +/- 0.3 (rest) to 4.7 +/- 0.3 (exercise) mmol/l; P < 0.05]. Plasma glucose did not change in response to ARM or Vol. Plasma free fatty acids and beta-hydroxybutyrate decreased only in FES experiments (P < 0.05). During FES, increases in growth hormone (GH) and epinephrine and decreases in insulin concentrations were abolished. Although subnormal throughout the exercise period, norepinephrine concentrations increased during FES, and responses of heart rate, adrenocorticotropic hormone, beta-endorphin, renin, lactate, and potassium were marked. In conclusion, during exercise, activity in motor centers and afferent muscle nerves is important for normal responses of GH, catecholamines, insulin, glucose production, and lipolysis. Humoral feedback and spinal or simple autonomic nervous reflex mechanisms are not sufficient. However, such mechanisms are involved in redundant control of heart rate and neuroendocrine activity in exercise.

Adult↗

Acute effects of caffeine ingestion at rest in humans with impaired epinephrine responses.

Caffeine ingestion has been demonstrated to increase circulating epinephrine (Epi) and norepinephrine (NE), elevate free fatty acids (FFAs), and alter heart rate, blood pressure (BP), and ventilation in humans. Whether these physiological responses are a result of caffeine acting through direct stimulation of specific tissues via adenosine receptors or secondary to Epi increases is not known. In the present experiment, six tetraplegics (level of spinal cord lesions C4-C6) were tested at rest for 3 h to investigate the effects of 6 mg/kg caffeine in capsule form on subjects with impaired Epi responses. Ventilatory, cardiovascular, metabolic, and hormonal data were collected every 15-20 min after caffeine ingestion. There were no significant (P > 0.05) increases in plasma Epi after caffeine ingestion [0.19 +/- 0.04 (SE) nM (preingestion); 0.20 +/- 0.04 nM (80 min postingestion)] or in plasma NE [0.53 +/- 0.16 nM (preingestion); 0.49 +/- 0.09 nM (80 min postingestion; P > 0.05)]. However, significant increases were found in serum FFAs [0.53 +/- 0.08 nM (preingestion); 1.03 +/- 0.20 mM (40 min postingestion; P < 0.05] and in glycerol. These concentrations remained elevated throughout the experiment. BP increased in the first hour postingestion. These data demonstrate that caffeine in physiological doses directly stimulates specific tissues, i.e., adipose and peripheral vascular tissue, and these effects are not secondary to increases in Epi after caffeine ingestion.

Adult↗

Hormonal and metabolic responses to electrically induced cycling during epidural anesthesia in humans.

Hormonal and metabolic responses to electrically induced dynamic exercise were investigated in eight healthy young men with afferent neural influence from the legs blocked by epidural anesthesia (25 ml of 2% lidocaine) at L3-L4. This caused cutaneous sensory anesthesia below T8-T9 and complete paralysis of the legs. Cycling increased oxygen uptake to 1.90 +/- 0.13 (SE) l/min, and fatigue developed after 22.7 +/- 2.7 min. Compared with voluntary exercise at the same oxygen uptake and heart rate, concentrations of blood and muscle lactate (musculus vastus lateralis) as well as plasma potassium increased more while muscle glycogen decreased more during electrically induced exercise. Hepatic glucose production always rose during exercise. However, during involuntary exercise with sensory blockade, it did not match the rise in peripheral glucose uptake and plasma glucose decreased (P < 0.05). Plasma glycerol increased less in electrically induced vs. voluntary exercise, and free fatty acids and beta-hydroxybutyrate decreased only during electrically induced exercise. Epinephrine, growth hormone, adrenocorticotropic hormone, and cortisol levels were higher during involuntary vs. voluntary exercise (P < 0.05). In conclusion, neural and humoral mechanisms exert redundant control with regard to responses of catecholamines and pituitary hormones (growth hormone and adrenocorticotropic hormone). In contrast, neural input from motor centers and feedback from working muscle are important for glucose production and lipolysis during exercise in humans. Humoral feedback is apparently not sufficient to trigger normal mobilization of extramuscular fuel stores.

Adult↗

Radical outcome method. A new approach to critical pathways in congenital heart disease.

BACKGROUND: Treatment of congenital heart disease has entered a new era of healthcare delivery and cost containment. Critical pathway method (CPM) has been previously demonstrated by us to produce a significant reduction in average length of stay (ALOS) in hospital of -44%. A new approach, radical outcome method (ROM), has produced comparable results that appear to improve over time. The dynamic nature is examined. METHODS AND RESULTS: Two hundred consecutive patients with congenital heart disease were treated by a single surgeon at a single health maintenance organization (HMO) facility. ROM was used in all patients. This method uses seven critical moments at which shortening rather than confirmation of the ALOS is possible. This process is completed by the second post-operative day. Overall mortality was 1%. The 200 patients were divided into two consecutive groups of 100 patients to determine the effectiveness of ROM over time. Fifty sets were matched. ALOS hospital decreased by 29 days (mean, 0.6 d/set), P < .003. Thirty sets who underwent cardiopulmonary bypass had a 16% decrease (P < .03), and 20 sets in whom nonbypass procedures were performed had a decrease of 16% (P < .02). ALOS in hospital for the 50 sets decreased from 3.7 to 3.1 days (-16%, P < .003). Outcome data demonstrated no significant difference. CONCLUSIONS: ROM, a proactive approach to hospital stay, is a dynamic process that reduces ALOS in hospital. This is achieved by both reducing negative variation in the standard CPM and allowing for positive variation. Outcome data confirm that this approach can reduce ALOS in hospital while providing optimal patient care and family satisfaction, a standard for the new era of healthcare delivery.

Cardiopulmonary Bypass↗

Stimulation of reactive oxygen species production and cytotoxicity in human neutrophils in vitro and after oral administration of a polyenzyme preparation.

Polymorphonuclear neutrophils (PMN) can be primed for enhanced release of reactive oxygen species (ROS) by exposure to cytokines and biological response modifiers. ROS are considered to possess tumoricidal activity. The polyenzyme preparation Wobenzym (WE) contains pancreatin, papain, bromelain trypsin and chymotrypsin and is used in adjuvant tumor therapy. We investigated killing of WE-exposed PMN against tumor cells and analyzed WE influence on ROS production in a chemiluminescence assay in PMN in vitro and in vivo. Depending on dose WE stimulates the cytotoxic capacity of PMN in vitro against tumor cells (50 micrograms/ml:p < 0.01). Exposure of PMN to Wobenzym caused a time-dependent significant (p < 0.02) increase in release of ROS. Similarly, oral administration of Wobenzym to healthy volunteers (n = 28) resulted in significant increases (p < 0.01) in ROS production, depending on dose (peak with 20 tablets) and time (peak 4 hours after Wobenzym administration). In contrast, ROS production was not elevated in the PMN of healthy volunteers receiving placebo (n = 8) or no treatment (n = 16). These findings point to an immunomodulatory capacity of WE in adjuvant tumor therapy.

Administration, Oral↗

Cardiovascular and ventilatory responses to electrically induced cycling with complete epidural anaesthesia in humans.

Cardiovascular and ventilatory responses to electrically induced dynamic exercise were investigated in eight healthy young males with afferent neural influence from the legs blocked by epidural anaesthesia (25 ml 2% lidocaine) at L3-L4. This caused cutaneous sensory anaesthesia below T8-T9 and complete paralysis of the legs. Cycling was performed for 22.7 +/- 2.7 min (mean, SE) (fatigue) and oxygen uptake (VO2) increased to 1.90 +/- 0.13 1 min-1. Compared with voluntary exercise at the same VO2, increases in heart rate (HR) (135 +/- 7 vs. 130 +/- 9 beats min-1) and cardiac output (16.9 +/- 1.1 vs. 17.3 +/- 0.91 min-1) were similar, and ventilation (54 +/- 5 vs. 45 +/- 41 min-1) was higher (P < 0.05). In contrast, the rise in mean arterial blood pressure during voluntary exercise (93 +/- 4 (rest) to 119 +/- 4 mmHg (exercise)) was not manifest during electrically induced exercise with epidural anaesthesia [93 +/- 3 (rest) to 95 +/- 5 mmHg (exercise)]. As there is ample evidence for similar cardiovascular and ventilatory responses to electrically induced and voluntary exercise (Strange et al. 1993), the present results support the fact that the neural input from working muscle is crucial for the normal blood pressure response to exercise. Other haemodynamic and/or humoral mechanisms must operate in a decisive manner in the control of HR, CO and VE during dynamic exercise with large muscle groups.

Adult↗

Exercise-induced fall in insulin: mechanism of action at the liver and effects on muscle glucose metabolism.

To determine the importance of the fall in insulin on whole body glucose fluxes and muscle glucose metabolism during exercise, dogs ran on a motorized treadmill for 90 min at a moderate work rate with somatostatin (SRIF) infused to suppress insulin and glucagon and basal (B-INS; n = 6 dogs) or exercise-stimulated (S-INS; n = 8 dogs) insulin replacement. The fall in insulin during exercise potently stimulates glucose production at least in part by potentiating the actions of glucagon. To assess the hepatic effects of insulin in the absence of its potentiating effect on glucagon action, glucagon levels were not restored during SRIF infusion. At least 17 days before experimentation, dogs underwent surgery for chronic placement of sampling (carotid artery and femoral vein) and infusion (inferior vena cava and portal vein) catheters. Hindlimb blood flow was assessed by placement of a Doppler flow cuff on the external iliac artery. Whole body glucose production (Ra) and disappearance (Rd) were assessed with [3-3H]glucose, and hindlimb glucose uptake and metabolism were assessed with arterial-venous differences and [U-14C]glucose. Insulin levels were 69 +/- 6 and 61 +/- 7 pM at rest in B-INS and S-INS and 62 +/- 10 and 41 +/- 6 pM at 30 min of exercise. Glucose levels were clamped at euglycemic levels with an exogenous glucose infusion during rest and exercise in both groups. Exercise-induced increases in Ra, Rd, hindlimb glucose uptake, and hindlimb oxidative and nonoxidative glucose metabolism were not affected by maintenance of basil insulin levels during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗

Impact of insulin deficiency on glucose fluxes and muscle glucose metabolism during exercise.

Exercise in the insulin-deficient diabetic state is characterized by a further increase in elevated circulating glucose and NEFA levels and by excessive counterregulatory hormone levels. The aim of this study was to distinguish the direct glucoregulatory effects of insulinopenia during exercise from the indirect effects that result from the metabolic and hormonal environment that accompanies insulin deficiency. For this purpose, dogs underwent 90 min of treadmill exercise during SRIF infusion with (SRIF + INS, n = 8) or without (SRIF - INS, n = 6) intraportal insulin replacement. Glucagon was not replaced, thus allowing assessment of the direct effect of insulinopenia at the liver independent of the potentiation of glucagon action. Glucose was infused to maintain euglycemia. Hepatic glucose production (Ra); glucose utilization (Rd); and LGlcU, LGlcE, and LGlcO were assessed with tracers ([3H]glucose, [14C]glucose) and arteriovenous differences. With exercise, insulin fell from 66 +/- 6 to 42 +/- 6 pM in the SRIF + INS group, and was undetectable in the SRIF - INS group. Plasma glucose was 6.33 +/- 0.38 and 6.26 +/- 0.30 mM at rest in the SRIF + INS and SRIF - INS groups, respectively, and was unchanged with exercise. Ra rose from 7.5 +/- 2.3 to 16.5 +/- 2.2 mumol.kg-1.min-1 and 9.1 +/- 2.0 to 31.4 +/- 3.9 mumol.kg-1.min-1 with exercise in the SRIF + INS and SRIF - INS groups, whereas Rd rose from 19.5 +/- 2.0 to 46.8 +/- 3.9 mumol.kg-1.min-1 and 15.1 +/- 1.8 to 29.9 +/- 3.3 mumol.kg-1.min-1. LGlcU rose from 36 +/- 9 to 112 +/- 25 mumol/min and 15 +/- 4 to 59 +/- 13 mumol/min and LGlcO rose from 5 +/- 2 to 61 +/- 12 mumol/min and 5 +/- 3 to 32 +/- 9 mumol/min with exercise in the SRIF+INS and SRIF-INS groups, respectively. Arterial levels and limb balances of NEFAs and glycerol were similar in the two groups. In summary, during exercise: 1) marked insulinopenia attenuates the increases in muscle glucose uptake and oxidation by approximately 50%, independent of changes in circulating metabolic substrate levels; 2) substantial increases in muscle glucose uptake and oxidation are, however, still present even in the absence of detectable insulin levels; and 3) insulinopenia facilitates the increase in Ra, independent of the potentiation of basal glucagon action. In conclusion, marked insulinopenia contributes directly to the exacerbation of glucoregulation during exercise in the diabetic state by limiting the rises in glucose uptake and metabolism and by enhancing hepatic glucose production.

Analysis of Variance↗

Maximal oxygen uptake and erythropoietic responses after training at moderate altitude.

Six well-trained male cross-county skiers trained for 7 days at 2700 m above sea level, their accommodation being at 1695 m. Blood samples for haemoglobin concentration [Hb], erythropoietin concentration [EPO] and reticulocyte count were collected before, during and after altitude exposure. Packed cell volume (PCV), red blood cell count (RBC), transferrin-iron saturation, mean red cell volume (MCV), mean corpuscular haemoglobin concentration (MCHC), maximal oxygen uptake, maximal achieved ventilation and heart rate were determined pre- and postaltitude exposure. The [EPO] increased significantly from pre-altitude (mean 36 mU.ml-1, SD 5) to maximal altitude values (mean 47 mU.ml-1, SD 3). The [Hb] had increased significantly above pre-altitude values (mean 8.8 mmol.l-1, SD 0.5) on day 2 (mean 9.1 mmol.l-1, SD 0.4) and day 7 (mean 9.4 mmol.l-1, SD 0.4) at altitude and on day 4 postaltitutde (mean 9.2 mmol.l-1, SD 0.4). The reticulocyte counts had increased significantly above pre-altitude values (mean 6%, SD 3%) on day 3 at altitude (mean 12%, SD 8%) and day 4 postaltitude (mean 10%, SD 5%). The RBC counts had increased on the 4th postaltitude day. The transferrin-iron saturation had decreased below pre-altitude values (mean 23%, SD 4%) on day 4 postaltitude (mean 14%, SD 5%) and had increased on day 11 postaltitude (mean 22%, SD 7%). There were no significant changes in MCV, MCHC, PCV, maximal oxygen uptake and maximal achieved ventilation, and heart rate pre- to postaltitude. These observations demonstrated an erythropoietic response to the altitude training which was not sufficient to increase the postaltitude maximal oxygen uptake.

Adolescent↗

[Epidemiological studies of the frequency of the abuse of analgesics].

To assess the epidemiology of habitual use of analgesics in South-West Germany (i) urine specimens of employees of a factory, of patients seen by a general practitioner (GP) and of patients attending a renal clinic were examined for paracetamol; (ii) mucosa of the left renal pelvis was examined for the presence of capillary sclerosis as an index of habitual use of phenacetin or paracetamol in 258 consecutive autopsies; (iii) in a regional renal clinic, the frequency of analgesic nephropathy was determined amongst outpatients and amongst patients on hemodialysis. Paracetamol was found in the urine of 4.1% of factory employees, in 3.5% of patients seen by a GP and in 2% of patients seen in the renal clinic. Capillary sclerosis was found in only one of 258 autopsies, in a patient dialysed for analgesic nephropathy. During the past two years, analgesic nephropathy was diagnosed in 3% of all patients seen for nephrological examination. Analgesic nephropathy was the cause of terminal renal failure in 15 of 166 patients (9.4%) on dialysis. The present study documents that habitual use of paracetamol-type analgesics continues in the general population despite the ban of phenacetin.

Acetaminophen↗