Importance of prudent antibiotic use on dairy farms in South Carolina: a pilot project on farmers' knowledge, attitudes and practices.

Inappropriate use of antibiotics in humans and animals contributes to decreased antimicrobial susceptibility in bacteria of medical importance. Resistant bacteria being transferred from animals to humans are causing public health concern. In-person interviews were conducted with 20 dairy farmers in rural counties of South Carolina to determine farmers' knowledge and attitudes about prudent antibiotic use among livestock. Four focus groups (n = 22) were also conducted to ascertain farmers' specific information needs about proper antibiotic use. Survey results showed that participants (100%) typically determined a need for antibiotic treatment using symptom assessment and reported following some form of operating procedures regarding administration of antibiotics. Few farmers (32%) had actual written antibiotic protocols. Preferred information sources about antibiotics were veterinarians (100%) and other dairy farmers (50%). Most farmers (86%) were not concerned that overuse of antibiotics in animals could result in antibiotic resistance among farm workers. Qualitative analysis of focus groups revealed significant barriers to following proper antibiotic procedures including limited finances and lack of time. The need for bilingual educational resources for Hispanic/Latino dairy workers was expressed. Desired formats for educational materials were posters, flowcharts, videos, and seminars. Education of South Carolina dairy farmers by veterinarians and public health professionals on the appropriate use of antibiotics in dairy cattle is needed to ensure antibiotic effectiveness in both animals and humans.

Health literacy and the World Wide Web: comparing the readability of leading incident cancers on the Internet.

PRIMARY OBJECTIVE: to assess the readability level of Web-based information on leading incident cancers. RESEARCH DESIGN: websites on breast, prostate, and colorectal cancers were selected for analysis by comparing the first 100 hits across 10 popular search engines. A total of 100 websites on breast (n=33), prostate (n=34), and colorectal (n=33) cancers were included in the final analysis. METHODS: readability was assessed using SMOG, Flesch-Kincaid (F - K), and Flesch Reading Ease (FRE) measures. SMOG was hand-calculated on 10 - 30 lines of continuous text. Identical text was entered into Microsoft Word 2002 where F - K and FRE scores were determined automatically by the word processor. RESULTS: the mean readability score of the cancer websites was Grade 12.9 using SMOG and Grade 10.7 according to F - K. The mean FRE score was 45.3, a score considered 'difficult'. Colorectal cancer websites were most difficult to read compared to breast and prostate cancer websites. All measures indicated that prostate cancer websites were written at the lowest readability. Significantly higher reading levels were required for concluding paragraphs of Web articles compared to introduction paragraphs. CONCLUSIONS: findings suggest the need for readable cancer information on the Web. Health promoters, health informaticians, medical journalists, and web page editors must collaborate to ensure the use of plain language to match the literacy skills of consumers.

Yeast Mps1p phosphorylates the spindle pole component Spc110p in the N-terminal domain.

The yeast spindle pole body (SPB) component Spc110p (Nuf1p) undergoes specific serine/threonine phosphorylation as the mitotic spindle apparatus forms, and this phosphorylation persists until cells enter anaphase. We demonstrate that the dual-specificity kinase Mps1p is essential for the mitosis-specific phosphorylation of Spc110p in vivo and that Mps1p phosphorylates Spc110p in vitro. Phosphopeptides generated by proteolytic cleavage were identified and sequenced by mass spectrometry. Ser(60), Thr(64), and Thr(68) are the major sites in Spc110p phosphorylated by Mps1p in vitro, and alanine substitution at these sites abolishes the mitosis-specific isoform in vivo. This is the first time that phosphorylation sites of an SPB component have been determined, and these are the first sites of Mps1p phosphorylation identified. Alanine substitution for any one of these phosphorylated residues, in conjunction with an alanine substitution at residue Ser(36), is lethal in combination with alleles of SPC97, which encodes a component of the Tub4p complex. Consistent with a specific dysfunction for the alanine substitution mutations, simultaneous mutation of all four serine/threonine residues to aspartate does not confer any defect. Sites of Mps1p phosphorylation and Ser(36) are located within the N-terminal globular domain of Spc110p, which resides at the inner plaque of the SPB and binds the Tub4p complex.

Risks of endoscopy in hospitalized pediatric patients with collagen vascular diseases.

BACKGROUND: The gastrointestinal manifestations of the collagen vascular diseases have been well described in the pediatric population. These patients frequently have symptoms that constitute indications for endoscopy. However, the risks and benefits of endoscopy in this population have not been examined. METHODS: A retrospective review of all patients with collagen vascular diseases hospitalized during a 7-year period was undertaken, and those patients who underwent endoscopy were identified. RESULTS: Nine patients (5%) underwent endoscopic procedures (eight upper and three lower endoscopy). Complications and outcomes were analyzed. Indications for endoscopy included abdominal pain, gastrointestinal (GI) bleeding, and/or vomiting and diarrhea. Two patients had complications that required surgery within 1 day of the endoscopic procedure. One of these patients subsequently died with GI bleeding. Five of the nine patients had changes in their management after endoscopy. Helicobacter pylori infection was identified and treated in two patients. Three patients had esophagitis or gastritis and acid suppression treatment was started or optimized. Vasculopathy was present in the patients who had complications. CONCLUSIONS: This series suggests that endoscopy can provide useful information for the management of the pediatric patient with GI symptoms and collagen vascular diseases. However, because serious and potentially life-threatening complications can occur, great care is needed in evaluating the risk/benefit ratio of endoscopy in these patients.

DNA-binding activities of Hop1 protein, a synaptonemal complex component from Saccharomyces cerevisiae.

The meiosis-specific HOP1 gene is important both for crossing over between homologs and for production of viable spores. hop1 diploids fail to assemble synaptonemal complex (SC), which normally provides the framework for meiotic synapsis. Immunochemical methods have shown that the 70-kDa HOP1 product is a component of the SC. To assess its molecular function, we have purified Hop1 protein to homogeneity and shown that it forms dimers and higher oligomers in solution. Consistent with the zinc-finger motif in its sequence, the purified protein contained about 1 mol equivalent of zinc whereas mutant protein lacking a conserved cysteine within this motif did not. Electrophoretic gel mobility shift assays with different forms of M13 DNA showed that Hop1 binds more readily to linear duplex DNA and negatively superhelical DNA than to nicked circular duplex DNA and even more weakly to single-stranded DNA. Linear duplex DNA binding was enhanced by the addition of Zn2+, was stronger for longer DNA fragments, and was saturable to about 55 bp/protein monomer. Competitive inhibition of this binding by added oligonucleotides suggests preferential affinity for G-rich sequences and weaker binding to poly(dA-dT). Nuclear extracts of meiotic cells caused exonucleolytic degradation of linear duplex DNA if the extracts were prepared from hop1 mutants; addition of purified Hop1 conferred protection against this degradation. These findings suggest that Hop1 acts in meiotic synapsis by binding to sites of double-strand break formation and helping to mediate their processing in the pathway to meiotic recombination.

Compliance and efficacy of cardiac rehabilitation and risk factor modification in the medically indigent.

To compare the compliance and efficacy of cardiac rehabilitation in medically indigent patients with more affluent patients, we evaluated the first 65 patients referred to a new cardiac rehabilitation program of whom 36 were medically indigent (i.e., dependent on Medicaid for health care reimbursement) and 29 were funded by private medical insurance. Attendance during 12 weeks of monitored, supervised, phase II cardiac rehabilitation was examined retrospectively. In addition, training history, cardiovascular response to submaximal exercise, dietary fat intake, and smoking incidence were studied at baseline and repeated prospectively between 6 months and 1 year (8.2 +/- 1.1 months) after program completion. Both the indigent and private patients attended >90% of scheduled sessions and achieved a significant improvement in submaximal work capacity which was well maintained at the time of follow-up. Also, both groups continued to eat a diet low in saturated and total fat. The indigent patients smoked more before the program but were equally successful at quitting cigarette smoking as the private patients. We conclude that in the appropriate setting, indigent patients can successfully complete and maintain excellent compliance with a program of coronary risk factor modification including exercise training, dietary modification, and cessation of cigarette smoking, to a degree equivalent to more affluent and educated patients. Compliance may be enhanced by employing a small program emphasizing extensive personal contact with rehabilitation staff.

Mechanisms regulating regional cerebral activation during dynamic handgrip in humans.

Dynamic hand movement increases regional cerebral blood flow (rCBF) of the contralateral motor sensory cortex (MS1). This increase is eliminated by regional anesthesia of the working arm, indicating the importance of afferent neural input. The purpose of this study was to determine the specific type of afferent input required for this cerebral activation. The rCBF was measured at +5.0 and +9.0 cm above the orbitomeatal (OM) plane in 13 subjects during 1) rest; 2) dynamic left-hand contractions; 3) postcontraction ischemia (metaboreceptor afferents); and 4) biceps brachii tendon vibration (muscle spindles). The rCBF increased only during dynamic hand contraction; contralateral MS1 (OM +9) by 15% to 64 +/- 8.6 ml.100 g-1.min-1 (P < 0.05); supplementary motor area (OM +9) by 11% to 69 +/- 9.8 ml.100 g-1.min-1 (P < 0.05); and there were also bilateral increases at MS2 (OM +5) [by 16% to 64 +/- 8.6 ml.100 g-1.min-1 (P < 0.05)]. These findings suggest that the rCBF increase during dynamic hand contraction does not require neural input from muscle spindles or metabolically sensitive nerve fibers, although the involvement of mechanoreceptors (group III or Ib) cannot be excluded.

The 110-kD spindle pole body component of Saccharomyces cerevisiae is a phosphoprotein that is modified in a cell cycle-dependent manner.

Spc110p (Nuf1p) is an essential component of the yeast microtubule organizing center, or spindle pole body (SPB). Asynchronous wild-type cultures contain two electrophoretically distinct isoforms of Spc110p as detected by Western blot analysis, suggesting that Spc110p is modified in vivo. Both isoforms incorporate 32Pi in vivo, suggesting that Spc110p is post-translationally modified by phosphorylation. The slower-migrating 120-kD Spc110p isoform after incubation is converted to the faster-migrating 112-kD isoform after incubation with protein phosphatase PP2A, and specific PP2A inhibitors block this conversion. Thus, additional phosphorylation of Spc110p at serine and/or threonine residues gives rise to the slower-migrating 120-kD isoform. The 120-kD isoform predominates in cells arrested in mitosis by the addition of nocodazole. However, the 120-kD isoform is not detectable in cells grown to stationary phase (G0) or in cells arrested in G1 by the addition of alpha-factor. Temperature-sensitive cell division cycle (cdc) mutations demonstrate that the presence of the 120-kD isoform correlates with mitotic spindle formation but not with SPB duplication. In a synchronous wild-type population, the additional serine/threonine phosphorylation that gives rise to the 120-kD isoform appears as cells are forming the mitotic spindle and diminishes as cells enter anaphase. None of several sequences similar to the consensus for phosphorylation by the Cdc28p (cdc2p34) kinase is important for these mitosis-specific phosphorylations or for function. Carboxy-terminal Spc110p truncations lacking the calmodulin binding site can support growth and are also phosphorylated in a cell cycle-specific manner. Further truncation of the Spc110p carboxy terminus results in mutant proteins that are unable to support growth and now migrate as single species. Collectively, these results provide the first evidence of a structural component of the SPB that is phosphorylated during spindle formation and dephosphorylated as cells enter anaphase.

Cardiovascular responses at the onset of static exercise in patients with dual-chamber pacemakers.

Cardiac output (CO) responses to exercise can be altered by ventricular pacing in pacemaker-dependent patients. The relative contributions of CO and peripheral vascular resistance (PVR) toward the initial increase in blood pressure with the initiation of static exercise were investigated in eight otherwise healthy pacemaker-dependent subjects [age 24 +/- 2 yr (range 17-37 yr)]. Beat-by-beat measures of heart rate (HR; electrocardiography), mean arterial pressure (MAP), and CO derived from stroke volume (SV) (CO = HR.SV; 2-D echocardiography) were determined during the first 20 s of a one-legged static knee extension performed at 20% maximal voluntary effort by using three pacing modalities: dual pacing and sensing mode (DDD, i.e., normal physiological HR response), fixed at resting HR (DOO-R), and fixed at peak exercise HR (DOO-E), as previously achieved during 5 min of sustained contraction in the DDD mode. There were no differences in MAP, CO, or PVR (PVR = MAP/CO) between modes at rest (P > 0.05). With DOO-E pacing, SV was lower at rest compared with the other modes and increased with exercise (P < 0.05). Although there were no significant increase in MAP or CO during DOO-R pacing, both variables were elevated by leg contraction during DDD and DOO-E pacing (P < 0.05), with no significant change in PVR. Additionally, the CO and MAP increases were significantly greater with DOO-E pacing (P < 0.05). Thus the magnitude of the initial increase in arterial pressure at the onset of mild one-legged static exercise was dictated by the changes in CO as PVR remained unchanged.

Reduced arterial diameter during static exercise in humans.

In eight subjects luminal diameter of the resting limb radial and dorsalis pedis arteries was determined by high-resolution ultrasound (20 MHz). This measurement was followed during rest and during 2 min of static handgrip or of one-leg knee extension at 30% of maximal voluntary contraction of another limb. Static exercise increased heart rate and mean arterial pressure, which were largest during one-leg knee extension. After exercise heart rate and mean arterial pressure returned to the resting level. No changes were recorded in arterial carbon dioxide tension, and the rate of perceived exertion was approximately 15 units after both types of exercise. The dorsalis pedis arterial diameter was 1.50 +/- 0.20 mm (mean and SE) and the radial AD 2.45 +/- 0.12 mm. During both types of contractions the luminal diameters decreased approximately 3.5% within the first 30 s (P < 0.05), and during one-leg knee extension they continued to decrease to a final exercise value 7.6 +/- 1.1% lower than at rest (P < 0.05). Thus, they became smaller than during the handgrip. After exercise resting values were reestablished. When the arterial diameter was expressed in relation to mean arterial pressure for the radial and dorsalis pedis artery was 22 +/- 3 and 28 +/- 3% lower during handgrip than the relation during rest, respectively. After one-leg knee extension both arteries reached 30 +/- 4% lower values. This study demonstrated arterial constriction in the resting limbs within the first 30 s of static exercise, and continued constriction during one-leg knee extension.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory nuclei share synaptic connectivity with pontine reticular regions regulating REM sleep.

Injection of cholinomimetics into the medial pontine reticular formation (mPRF) of intact, unanesthetized cat causes a rapid eye movement (REM) sleep-like state and respiratory depression. The mPRF contains no concentrations of respiratory neurons, and this study examined the hypothesis that respiratory depression evoked from the mPRF is synaptically mediated. The mPRF of conscious cats was injected with bethanechol to define an mPRF zone causing state-dependent respiratory depression. Bethanechol caused a 361% increase in the REM sleep-like state and a 37% decrease in minute ventilation. Additional cats were injected with the retrograde fluorescent tracers True Blue and either Fluoro-Gold or Diamidino Yellow aimed for the cholinoceptive mPRF or for the pontine respiratory group (PRG). After mPRF dye injection, 1) labeling was observed in the PRG, dorsal respiratory group (DRG), and ventral respiratory group (VRG); and 2) double-labeled cells were observed in the VRG and PRG. Dye injections into the PRG produced contralateral and ipsilateral fluorescent labeling of the mPRF, DRG, and VRG. Thus cholinoceptive regions of the mPRF involved in REM sleep generation have reciprocal monosynaptic connections with the PRG and receive monosynaptic projections from the DRG and VRG.

Relation of thrombus in the left atrial appendage by transesophageal echocardiography to clinical risk factors for thrombus formation.

Transesophageal echocardiography provides excellent visualization of the left atrial appendage (LAA). This study was conducted to determine whether specific clinical risk factors could predict the presence of LAA thrombus as demonstrated by transesophageal echocardiography. The most recent 860 transesophageal echocardiographic studies performed at our institution were retrospectively reviewed. The LAA was adequately visualized in 778 patients (90%). For each study, the presence or absence of 5 specific clinical risk factors (mitral stenosis, severe left ventricular dysfunction, left atrial dilatation, atrial fibrillation, or a prosthetic mitral valve) and the presence or absence of LAA thrombi were assessed. One or more clinical risk factors were present in 149 patients, whereas no defined risk factors were noted in 629. Left atrial appendage thrombi were found in 20 of 149 patients with versus 6 of 629 patients without a clinical risk factor (13% vs 1%, p = 0.0001). By logistic regression analysis, mitral stenosis, severe left ventricular dysfunction, and left atrial dilatation were independent risk factors for LAA thrombus formation. Neither atrial fibrillation nor the presence of a mitral prosthetic valve achieved statistical significance as independent risk factors for LAA thrombus. Thus, LAA thrombi occur most often in patients with risk factors for thrombus formation that can be determined by clinical evaluation and transthoracic echocardiography. Transesophageal echocardiography rarely identifies LAA thrombi in patients without such clinical risk factors.

Cardiovascular responses to active and passive cycling movements.

Ten healthy subjects were evaluated at rest and at 5 min of unloaded active (AC) and passive (PC) cycling. Passive limb movements were accomplished using a tandem bicycle with a second rider performing the movements. We measured heart rate (HR), mean arterial pressure (MAP), cardiac output (CO), oxygen uptake (VO2), rating of perceived exertion (RPE), and electrical activity (EMG) of lower limbs muscles. Values for stroke volume (SV) and peripheral vascular resistance (PVR) were calculated. EMG, RPE, and VO2 were higher during AC than during PC (P < 0.001). CO increased during both modes of cycling, but during AC it resulted from a HR acceleration (73 +/- 2 at rest to 82 +/- 2 beats.min-1 at 60 rpm; P < 0.001) with no change in SV whereas during PC, SV increased from rest (65 +/- 4 at rest to 71 +/- 3 ml at 60 rpm; P = 0.003) along with no change in HR. PVR remained constant during PC, but decreased by 13% during AC (P < 0.001) and MAP increased only during PC (93 +/- 2 at rest to 107 +/- 2 mm Hg at 60 rpm). These results supports the concept that central command determines the HR response to dynamic exercise. The increase in SV and consequently in MAP during PC was probably due to increased venous return and/or to muscle mechanoreceptor-evoked increased myocardial contractility.

Cardiovascular responses during static exercise. Studies in patients with complete heart block and dual chamber pacemakers.

BACKGROUND: During static exercise in normal subjects, the mean arterial pressure increases as a result of an increase in heart rate and thereby cardiac output with no significant change in stroke volume or systemic vascular resistance. We hypothesized that if one component of the blood pressure response to static exercise, ie, heart rate, were fixed, plasticity of the neural control mechanisms during exercise would allow for preservation of the blood pressure response by alternative mechanisms. METHODS AND RESULTS: Thirteen patients 20 to 68 years old with structurally normal hearts, complete heart block, and dual chamber pacemakers performed static exercise during three conditions: (1) normal dual chamber sensing and pacing mode, (2) heart rate fixed at the resting value obtained in the DDD mode of 78 +/- 4 beats per minute, and (3) heart rate fixed at the peak value obtained during exercise in the DDD mode of 94 +/- 4 beats per minute. Heart rate, blood pressure, and cardiac output were measured and stroke volume and systemic vascular resistance were calculated at rest and at 1 and 5 minutes during static one-leg extension at 20% of maximal voluntary contraction. The mean arterial pressures at rest and at 5 minutes were higher when the heart rate was fixed at the faster peak exercise heart rate. In the DDD mode, heart rate increased by 16 beats per minute and cardiac output by 1.1 L/min, with a resultant 25 mm Hg increase in mean arterial pressure at 5 minutes with no change in the stroke volume or systemic vascular resistance. In both fixed heart rate pacing modes, mean arterial pressure increased by 24 mm Hg when the heart rate was fixed at the resting heart rate and by 25 mm Hg when the heart rate was fixed at the faster peak exercise heart rate pacing modes associated with an increase in stroke volume, with similar increases in cardiac output. During static exercise there was no change in systemic vascular resistance from the resting value in any pacing mode. CONCLUSIONS: When heart rate is fixed in the presence of normal left ventricular function, the mean arterial pressure increases normally during static exercise because of an increase in stroke volume with no change in the systemic vascular resistance.

Insertional mutations in the yeast HOP1 gene: evidence for multimeric assembly in meiosis.

The HOP1 gene of Saccharomyces cerevisiae has been shown to play an important role in meiotic synapsis. In this study we analyzed the mechanism of this function by phenotypic characterization of novel in-frame linker-insertion mutations located at various sites throughout the HOP1 coding sequence. Among 12 mutations found to cause defects in meiotic recombination and spore viability, three were temperature-sensitive for the spore viability defect. Although substantial meiotic recombination was found for these conditional alleles at the restrictive temperature, the level of exchange measured in spo13 meiosis was reduced in some of the monitored intervals, indicating that nondisjunction resulting from a deficit in crossing over could account for SPO13 spore inviability. Intragenic complementation between linker-insertion alleles was assessed by testing the viability of spores generated from heteroallelic diploids after SPO13 meiosis. Complex patterns of complementation and enhancement of the spore-inviability phenotype indicate that HOP1 functions in a multimeric complex. In addition, the ability of alleles which map near the carboxyl terminus to complement several other alleles provides evidence for a functional domain in this region of the protein. Two previously identified multicopy suppressors of the conditional hop1-628ts allele were tested for their effects in cells bearing the linker-insertion hop1 alleles. Overexpression of REC104 from a 2 mu plasmid was shown to enhance the spore viability of every allele tested, including a hop1 disruption allele. On the other hand, suppression by overexpression of RED1 from a 2 mu plasmid was found only for allele hop1-628ts. Surprisingly, similar overexpression of RED1 in strains bearing several other conditional hop1 linker-insertion alleles caused enhanced spore lethality. This finding, in conjunction with the evidence for a carboxy-terminal domain, provides new insight into the nature of interactions between the HOP1 and RED1 products in meiosis.

Hypoxia and training-induced adaptation of hormonal responses to exercise in humans.

To establish whether or not hypoxia influences the training-induced adaptation of hormonal responses to exercise, 21 healthy, untrained subjects (2) years, mean (SE)] were studied in three groups before and after 5 weeks' training (cycle ergometer, 45 min.day-1, 5 days.week-1). Group 1 trained at sea level at 70% maximal oxygen uptake (VO2max), group 2 in a hypobaric chamber at a simulated altitude of 2500 m at 70% of altitude VO2max, and group 3 at a simulated altitude of 2500 m at the same absolute work rate as group 1. Arterial blood was sampled before, during and at the end of exhaustive cycling at sea level (85% of pretraining VO2max). VO2max increased by 12 (2)% with no significant difference between groups, whereas endurance improved most in group 1 (P < 0.05). Training-induced changes in response to exercise of noradrenaline, adrenaline, growth hormone, beta-endorphin, glucagon, and insulin were similar in the three groups. Concentrations of erythropoietin and 2,3-diphosphoglycerate at rest did not change over the training period. In conclusion, within 5 weeks of training, no further adaptation of hormonal exercise responses takes place if intensity is increased above 70% VO2max. Furthermore, hypoxia per se does not add to the training-induced hormonal responses to exercise.

Heart rate and blood pressure responses at the onset of dynamic exercise: effect of Valsalva manoeuvre.

The influence of respiration on the mean blood pressure (Pa) and R-R interval responses at the onset of dynamic exercise was studied in 15 healthy subjects who performed 4 s of unloaded cycling at 1.5-2.0 Hz, 4 s of Valsalva manoeuvre at 5.3 kPa, and a combination of both, each during a 12-s long apnoea at total lung capacity. The R-R intervals were obtained from the electrocardiogram, Pa was measured continuously by finger plethysmography, and intra-oral pressure was used to estimate the changes in intrapleural pressure. There was an immediate and significant shortening of the R-R intervals during exercise [mean (SE): 790 (20) to 642 (20) ms] that was not modified when Valsalva manoeuvre was added [783 (28) to 654 (21) ms]. Although 4 s of exercise alone did not alter Pa [13.8 (0.5) to 13.7 (0.7) kPa], this may indicate a pressor response, since Pa decreased during apnoea alone. When exercise was performed simultaneously with Valsalva manoeuvre, Pa increased significantly [13.6 (0.4) to 15.8 (0.5) kPa] and of similar magnitude during Valsalva alone [13.2 (0.4) to 15.3 (0.7) kPa]. In conclusion, 4 s of unloaded cycling elicited a fast R-R shortening with no change in Pa from rest. A concomitant Valsalva manoeuvre had no effect on the R-R interval response but caused a marked increase in Pa. From these findings, it is suggested that respiratory influences should be controlled in studies concerned with the cardiovascular responses at the onset of dynamic exercise.

Maximal inspiratory pressure following endurance training at altitude.

Effects of endurance training on maximal inspiratory pressure and fatigue were evaluated after 5 weeks. Twelve male and 9 female untrained subjects were matched in the three groups for sex and maximal oxygen uptake (VO2 max). Training was performed at 70% VO2max; 45 min day-1; 5 days week-1 (n = 7); and at the same relative (n = 7) and absolute (n = 7) work loads in a pressure chamber corresponding to 2500 m (560 mmHg). Work load was increased every week to maintain the training heart rate. Maximal respiratory pressure was measured at the mouth before and 30, 60 and 120 s after maximal exercise. With no significant difference between the three groups of subjects, VO2max increased from 2.96 (1.98-4.47) (median and range for 21 subjects) to 3.33 (2.50-4.72) 1 min-1 (p < 0.001) and ventilation (VE max) from 109 (57-147) to 123 (73-148) 1 min-1 (p < 0.001), while maximal heart rate decreased from 193 (180-211) to 192 (169-207) beats min-1 (p < 0.01). Maximal inspiratory pressure (87 (56-115) mmHg), inspiratory muscle fatigue (18 (-2-43)%, p < 0.001), and arterial oxygen tension during exercise (12.4 (9.9-15.6)kPa) were similar before and after training. The results demonstrate that training at simulated altitude at 2500 m does not increase VE max or VO2 max above the increases obtained from training at sea level. Furthermore, VEmax and VO2 max increased approximately 13% despite unchanged maximal inspiratory pressure and inspiratory muscle fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of epidural anaesthesia with 1% lidocaine on the pressor response to dynamic exercise in man.

1. In order to examine the sensitivity to local anaesthetics of afferent neural feedback from working muscle during dynamic exercise, sixteen subjects cycled for 12 min before and after epidural anaesthesia using 1% lidocaine. The presence of afferent neural blockade was verified by elimination of the blood pressure response to a cold pressor test, laser-induced evoked potentials and increases in pain detection and tolerance thresholds of the foot. Conversely, epidural anaesthesia had no effect on these variables in the unblocked skin areas or on electrically evoked potentials in blocked or unblocked skin. 2. During dynamic exercise, heart rate increased as did mean arterial pressure and cardiac output. Mean arterial pressure remained at the exercise level during post-exercise ischaemia, but heart rate and cardiac output decreased while total peripheral resistance increased. Epidural anaesthesia did not significantly affect these variables during rest, dynamic exercise, post-exercise ischaemia or recovery. 3. The results of this study show that, in order to affect blood pressure during dynamic exercise, epidural anaesthesia must block the pressor response to post-exercise ischaemia. The implication of these data is that complete or almost complete block of group III and/or group IV muscle afferents is necessary to inhibit the pressor response to dynamic exercise in man.

Traumatic myocardial infarction during competitive volleyball: a case report.

A previously asymptomatic physically active 41-yr-old Caucasian male was hit in the chest by a spiked volleyball. Following the impact of the ball he developed substernal chest pain, which persisted during and after the game. Despite the administration of thrombolytic therapy, he suffered an extensive anteroapical myocardial infarction; subsequent cardiac catheterization revealed the presence of a 70% occlusion in his mid left anterior descending coronary artery. We hypothesize that this patient sustained a traumatic coronary artery thrombosis resulting in acute myocardial infarction. The presence of underlying coronary artery disease may predispose an individual to traumatic myocardial infarction.