The effects of exercise training in the cold on cerebral blood flow and cerebrovascular function in young healthy individuals.

Exercise elicits acute increases in cerebral blood flow velocity (CBFv) and provokes long-term beneficial effects on CBFv, thereby reducing cerebrovascular risk. Acute exposure to a cold stimulus also increases CBFv. We compared the impact of exercise training in cold and thermoneutral environments on CFBv, cerebrovascular function and peripheral endothelial function. Twenty-one (16 males, 22 ± 5 years) individuals were randomly allocated to either a cold (5 °C) or thermoneutral (15 °C) exercise intervention. Exercise consisted of 50-min cycling at 70% heart rate max, three times per week for eight weeks. Transcranial Doppler was used to determine pre and post intervention CBFv, dynamic cerebral autoregulation (dCA) and cerebrovascular reactivity (CVRCO2). Conduit endothelial function, microvascular function and cardiorespiratory fitness were also assessed. Cardiorespiratory fitness improved (2.91 ml.min.kg-1, 95%CI 0.49, 5.3; P = 0.02), regardless of exercise setting. Neither intervention had an impact on CBFv, CVRCO2, FMD or microvascular function (P > 0.05). There was a significant interaction between time and condition for dCA normalised gain with evidence of a decrease by 0.192%cm.s-1.%mmHg-1 (95%CI -0.318, -0.065) following training in the cold and increase (0.129%cm.s-1.%mmHg-1, 95%CI 0.011, 0.248) following training in the thermoneutral environment (P = 0.001). This was also evident for dCA phase with evidence of an increase by 0.072 rad (95%CI -0.007, 0.152) following training in the cold and decrease by 0.065 (95%CI -0.144, 0.014) radians following training in the thermoneutral environment (P = 0.02). Both training interventions improved fitness but CBFv, CVRCO2 and peripheral endothelial function were unaltered. Exercise training in the cold improved dCA whereas thermoneutral negated dCA.

The incidence and nature of injuries sustained on grass and 3rd generation artificial turf: a pilot study in elite Saudi National Team footballers.

PURPOSE OF THE STUDY: To compare the incidence, severity and nature of injuries sustained by Saudi National Team footballers during match-play and training on natural grass and 3rd generation (3G) artificial turf. METHOD: Injury data was collected on all Saudi National Team players competing at the Gulf Cup (Yemen December 2010: 3G) and the Asian Cup (Qatar January 2011; grass). A total of 49 players were studied (mean ± SD; Age 27 ± 4 yr; body mass 71.4 ± 6.7 kg; height 176.8 ± 6.3 cm; professional playing experience 9 ± 3 yr) of which 31 competed at the Gulf Cup, 32 at the Asian Cup (14 at both). A prospective cohort design was used to investigate the incidence, nature and severity of injuries sustained with data collected using a standardised injury questionnaire. All data were collected by the team physiotherapist with the definition of injury set at any injury that required player and clinician contact. Injury and exposure data were collected and reported for games, training and all football activity. RESULTS: A total of 82 injuries [incidence - 56.1 per 1000 h total game and training exposure] were recorded at the Asian Cup (grass) and 72 injuries [incidence - 37.9 per 1000 h total game and training exposure] were recorded at the Gulf Cup (3G). Incidence data for training, game and all football exposure injury rates were higher when playing on grass. The vast majority of injuries on both surfaces were very minor that, whilst requiring medical attention, did not result in loss of match/training exposure. Injuries that resulted in 1-3 days absence from training or game play had similar incidence rates (Grass: 7.4 vs. 3G: 7.4 injuries per 1000 h exposure). More severe injuries were less frequent but with a higher incidence when playing on grass. Lower limb injuries were the most common in both tournaments with a higher incidence on grass (Grass: 14.2 vs. 3G: 7.9 injuries per 1000 h exposure). Muscle injuries were the most frequent of all injuries with similar incidence rates on both surfaces (Grass: 5.4 vs. 3G: 4.7 injuries per 1000 h exposure). Injuries that involved player contact were also more common on grass (Grass: 11.5 vs. 3G: 3.2 injuries per 1000 h exposure). CONCLUSION: Whether reporting all injuries or just those that prevented players from taking part in training or match play, injury incidence rates were generally higher when Saudi National Team footballers played on grass than on 3G artificial surface. Although this is a small study, the unique quasi-repeated measures study design with elite Saudi National Team footballers, adds to the current belief that 3G artificial turf does not increase injury risk in football.

Significance of deep T-wave inversions in asymptomatic athletes with normal cardiovascular examinations: practical solutions for managing the diagnostic conundrum.

Preparticipation screening programmes for underlying cardiac pathologies are now commonplace for many international sporting organisations. However, providing medical clearance for an asymptomatic athlete without a family history of sudden cardiac death (SCD) is especially challenging when the athlete demonstrates particularly abnormal repolarisation patterns, highly suggestive of an inherited cardiomyopathy or channelopathy. Deep T-wave inversions of ≥ 2 contiguous anterior or lateral leads (but not aVR, and III) are of major concern for sports cardiologists who advise referring team physicians, as these ECG alterations are a recognised manifestation of hypertrophic cardiomyopathy (HCM) and arrhythmogenic right ventricular cardiomyopathy (ARVC). Subsequently, inverted T-waves may represent the first and only sign of an inherited heart muscle disease, in the absence of any other features and before structural changes in the heart can be detected. However, to date, there remains little evidence that deep T-wave inversions are always pathognomonic of either a cardiomyopathy or an ion channel disorder in an asymptomatic athlete following long-term follow-up. This paper aims to provide a systematic review of the prevalence of T-wave inversion in athletes and examine T-wave inversion and its relationship to structural heart disease, notably HCM and ARVC with a view to identify young athletes at risk of SCD during sport. Finally, the review proposes clinical management pathways (including genetic testing) for asymptomatic athletes demonstrating significant T-wave inversion with structurally normal hearts.

The influence of a half-marathon race upon cardiac troponin T release in adolescent runners.

OBJECTIVES: Post-exercise cardiac troponin T (cTnT) release has been widely reported in adult athletes but limited data is available for adolescents. The aim of this study was to determine the incidence and magnitude of cTnT appearance in a large group of adolescent runners, and to determine any association between cTnT release and personal characteristics of adolescents. METHODS: We recruited 63 adolescent runners (mean±SD: age 16.4±1.5 years; 10 females) who all completed a simulated half-marathon race (an all-out 21-km run) during routine training. Personal data collected included age, training history, 21-km run performance as well as pre-post exercise serum cTnT levels. Serum cTnT was assayed using a 3rd generation assay. RESULTS: At pre-exercise, cTnT concentrations were below the 0.01 µg/L cTnT detection limit of assay in 58/63 runners. The post-exercise cTnT level (range: <0.01-1.36 µg/L) was significantly (p<0.001) greater than that of the pre-exercise (range: <0.01-0.02 µg/L). After the exercise, 57 (90%) and 44 (70%) subjects had cTnT concentrations above the detection: 0.01, and clinical thresholds: 0.05 µg/L, respectively. Post-exercise cTnT was inversely correlated with training years (r=-0.25, p<0.05) and age (r=-0.31, p<0.05). Compared with runners who had trained for ≥ 3 years, runners with less training experience demonstrated increased post-race cTnT levels (p<0.01). CONCLUSION: cTnT increases are virtually universal among adolescent runners following a 21-km run during routine training and can reach levels typically diagnostic for acute myocardial infarction potentially initiating diagnostic dilemmas. Adolescents with less training experience had higher post-exercise cTnT.

The carotid baroreflex is reset following prolonged exercise in humans.

AIM: Alterations in the carotid baroreflex (CBR) control of arterial pressure may explain the reduction in arterial pressure and left ventricular (LV) function after prolonged exercise. We examined the CBR control of heart rate (HR) and mean arterial pressure (MAP), in addition to changes in LV function, pre- to post-exercise. METHODS: Seven males (age, mean ± SEM; 29 ± 4 years) completed 4 h of ergometer rowing at a workload of 10-15% below the lactate threshold. The CBR control of HR and MAP was assessed via the rapid neck-suction/pressure protocol. LV systolic function was measured by echocardiography, where ejection fraction (EF), the ratio of systolic blood pressure to end systolic volume (SBP/ESV) and stroke volume (SV) were estimated. RESULTS: Following exercise MAP was reduced (12 ± 3%) and HR was elevated (35 ± 5%; P < 0.05). Furthermore, CBR control of MAP was relocated to the left on the stimulus-response curve (P < 0.05) demonstrating that the CBR operated around a lower arterial pressure. Concomitantly, LV systolic function was reduced, indicated by a decrease in EF (22 ± 2%), SBP/ESV (32 ± 14%) and SV (25 ± 5%, P < 0.05). The reduced EF and SBP/ESV were associated with the decreased MAP operating point (r² = 0.71 and r² = 0.47, respectively, P < 0.05). CONCLUSION: The CBR is reset after prolonged exercise to a lower prevailing arterial pressure. This resetting of the CBR may contribute to the reduction arterial pressure and LV function after exercise.

Blood pressure status and post-exercise hypotension: an example of a spurious correlation in hypertension research?

A single bout of exercise lowers blood pressure (BP) for up to 24 h afterwards. The magnitude of this post-exercise hypotension (PEH) has been reported to be correlated most strongly to pre-exercise BP, and this apparent relationship has influenced position statements about the value of exercise in arterial hypertension. Nevertheless, this correlation could be adversely affected by mathematical coupling and regression-to-the-mean artefacts. Therefore, we aimed to examine the degree to which BP status moderates PEH while, for the first time, controlling for these statistical artefacts. A total of 32 participants, with pre-exercise mean arterial pressures of 65-110 mm Hg, cycled for 30 min at 70% peak oxygen uptake. Systolic BP and diastolic BP were measured (Portapres) before exercise and for 20 min after exercise. Changes in BP were regressed against pre-exercise values, and against the mean of pre- and post-exercise BP, among other indices that are also known not to be prone to artefacts. Correlations between pre-exercise BP and the exercise-mediated reductions were typical of those previously reported (r=0.37-0.62, P<0.05), but not large enough to rule out spuriousness (P>0.05). Artefact-free indices of BP status (pre- and post-exercise mean as well as an earlier independent measurement) did not correlate with reductions in BP (P>0.05), which were moderated more by peak oxygen uptake and time of day (P<0.05). These data indicate that, if statistical artefacts are not controlled for, the influence of BP status on the degree of PEH can be spuriously exaggerated to the extent that other more important moderators of BP change are masked.

The effect of prolonged endurance exercise upon blood pressure regulation during a postexercise orthostatic challenge.

OBJECTIVE: To investigate the regulation of blood pressure in response to an orthostatic challenge in athletes running a marathon. METHODS: 10 experienced male runners (mean (SD) age 29 (4) years) were tested on the day prior to the 2004 London Marathon, and again immediately postrace (race time 210 (36) min). In addition, 6 of the subjects were retested 24 h postrace. During each examination, beat-to-beat systolic arterial blood pressure (SBP) and heart rate (HR) were measured, and stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) were estimated via arterial transmural pressure waveforms during 3 min in a supine position and then during 3 min of upright, unsupported standing. Data were averaged over 20 s epochs, and the final 20 s of each posture were compared prerace and postrace via repeated measures 2-way ANOVA. RESULTS: Prerace SBP in standing increased only moderately when compared with supine values (2 (9) mm Hg, NS). This was accompanied by an increase in HR (13 (7) beats/min, p<0.05), as well as a decrease in SV (16 (9) ml, p<0.05). However, there was little change in CO (-0.13 (0.97) litres/min, NS) or TPR (0.047 (0.280) medical units (MU), NS). Postrace SBP significantly decreased from supine to standing (-15 (20) mm Hg, p<0.05). The change in SBP was accompanied by an increase in HR (19 (6) beats/min, p<0.05) and a reduction in SV (26 (14) ml, p<0.05) and CO (-1.02 (1.39) litres/min, p = 0.05). Postrace there was no change in TPR (0.366 (0.607) MU, NS) upon standing. The orthostatic adjustments in SBP, HR and CO were greater than at prerace (p<0.05). The postrace orthostatic challenge resulted in only one subject experiencing presyncopal symptoms. At 24 h postrace, cardiovascular responses to an orthostatic challenge mirrored those at prerace. CONCLUSIONS: Following prolonged exercise, a fall in systolic blood pressure during orthostasis results from an inadequately compensated decrease in SV and resultant CO during standing.

Flow-mediated dilation and intima-media thickness of the brachial and axillary arteries in individuals with and without inducible axillary artery compression.

The presence of axillary artery aneurysm and/or thrombus in overhead throwing athletes has been linked, theoretically, with the finding of compression by the humeral head induced by a diagnostic arm maneuver. However, whether this intermittent compression is incidental or of pathological significance has yet to be determined. Flow-mediated vasodilation (FMD), intima-media thickness (IMT) and maximum vasodilatory capacity were measured locally (3rd portion of the axillary artery) and downstream (brachial artery) in individuals previously tested for inducible axillary artery compression (compressor group [COMP]: n=8, mean (SD) age: 23 (4) y; "noncompressor" control group [NONCOMP]: n=8, 26 (4) y). A high-resolution ultrasound machine recorded arterial diameter and blood flow velocity. A rapid inflation/deflation pneumatic cuff placed distal to the site of measurement induced reactive hyperemia. Custom-designed wall tracking software with synchronized Doppler waveform analysis detected changes in arterial diameter, blood flow velocity and shear rate from baseline to 3min after cuff deflation. Glyceryl trinitrate and/or ischemic hand grip exercises were administered to induce maximum vasodilation. No significant differences in FMD, IMT or maximum vasodilator capacity were observed between groups at the axillary artery. However, the downstream brachial FMD response was significantly diminished in the COMP group (6.38 [3.28]%) compared with the NONCOMP group (10.38 [2.74]%; p=0.006) despite a comparable shear rate between groups (COMP: 81.92 (44.55) s(-1); NONCOMP: 83.18 (40.02) s(-1); p=0.961). Pooled data revealed a significant negative relationship (r=-0.52, p=0.038) between the FMD response and degree of arterial compression. These results suggest a chronic change in downstream vascular function in individuals demonstrating clinically significant inducible axillary artery compression.

Preload maintenance and the left ventricular response to prolonged exercise in men.

This study examined whether left ventricular function was reduced during 3 h of semi-recumbent ergometer cycling at 70% of maximal oxygen uptake while preload to the heart was maintained via saline infusion. Indices of left ventricular systolic function (end-systolic blood pressure-volume relationship, SBP/ESV) and diastolic filling (ratio of early to late peak filling velocities into the left ventricle, E:A) were calculated during recovery and compared with baseline resting data. During exercise in seven healthy, trained male subjects, an arterial catheter allowed continuous assessment of arterial pressure, stroke volume (SV), cardiac output ( ) and an index of contractility (dP/dt(max)). A venous catheter assessed that central venous pressure (CVP) was maintained throughout rest, exercise and 10 min into recovery. Both systolic blood pressure and heart rate (HR) increased with the onset of exercise (from 132 +/- 5 to 185 +/- 19 mmHg and from 66 +/- 9 to 135 +/- 23 beats min(-1); increases from rest to the end of the first 5 min of exercise in SBP and HR, respectively) but systolic blood pressure did not change from 30 to 180 min of exercise ( approximately 150 mmHg), while heart rate only increased by 8 +/- 9 beats min(-1) (means +/- s.d.; P > 0.05). The attenuated increase in HR compared with other studies suggests that the maintained CVP ( approximately 5 mmHg) helped to prevent cardiovascular drift in this protocol. Stroke volume, and dP/dt(max) were all increased with the onset of exercise (from 85 +/- 8 to 120 +/- 18 ml, from 5.4 +/- 1.3 to 16.5 +/- 3.3 l min(-1) and from 14.4 +/- 4 to 28 +/- 8 mmHg s(-1); values from rest to the end of the first 5 min of exercise for SV, and dP/dt(max), respectively) and were maintained during exercise. There was no difference in the SBP/ESV ratio from pre- to postexercise. Conversely, E:A was reduced from 2.0 +/- 0.4 to 1.6 +/- 0.5 postexercise (P < 0.05), returning to normal values at 24 h postexercise. This change in diastolic filling could not be fully explained (r(2) = 0.39) by an increased heart rate and, with CVP unchanged, it is likely to represent some depression of intrinsic relaxation properties of left ventricular myocytes. Three hours of semi-supine cycling resulted in no evidence of a depression in left ventricular systolic function, while left ventricular diastolic function declined postexercise.

The influence of body size on measurements of overall cardiac function.

The purpose of this study was to determine the best scaling method to account for the effects of body size on measurements of overall cardiac function and subsequently the interpretation of data based on cardiac power output (CPO). CPO was measured at rest (CPO(rest)) and at maximal exercise (CPO(max)) on 88 and 103 healthy but untrained men and women, respectively, over the age range of 20-70 yr. Cardiac reserve (CR) was calculated as CPO(max) - CPO(rest). CPO(rest), CPO(max), and CR were all significantly related to body mass (BM), body surface area (BSA), and lean body mass (LBM). The linear regression model failed to completely normalize these measurements. In contrast, the allometric model produced size-independent values of CPO. Furthermore, all the assumptions associated with the allometric model were achieved. For CPO(rest), mean body size exponents were BM(0.33), BSA(0.60), and LBM(0.47). For CPO(max), the exponents were BM(0.41), BSA(0.81), and LBM(0.71). For CR, mean body size exponents were BM(0.44), BSA(0.87), and LBM(0.79). LBM was identified (from the root-mean-squares errors of the separate regression models) as the best physiological variable (based on its high metabolic activity) to be scaled in the allometric model. Scaling of CPO to LBM(b) (where b is the scaling exponent) dramatically reduced the between-gender differences with only a 7% difference in CPO(rest) and CPO(max) values. In addition, the gender difference in CR was completely removed. To avoid erroneous interpretations and conclusions being made when comparing data between men and women of different ages, the allometric scaling of CPO to LBM(b) would seem crucial.

A survey of flexibility training protocols and hamstring strains in professional football clubs in England.

OBJECTIVES: To investigate the relation between current flexibility training protocols, including stretching, and hamstring strain rates (HSRs) in English professional football clubs. METHOD: Questionnaire based data on flexibility training methods and HSRs were collected from 30 English professional football clubs in the four divisions during the 1998/99 season. Data were coded and analysed using cross tabulation, correlation, and multiple regression. RESULTS: Flexibility training protocols were characterised by wide variability, with static stretching the most popular stretching technique used. Hamstring strains represented 11% of all injuries and one third of all muscle strains. About 14% of hamstring strains were reinjuries. HSRs were highest in the Premiership (13.3 (9.4)/1000 hours) with the lowest rates in Division 2 (7.8 (2.9)/1000 hours); values are mean (SD). Most (97%) hamstring strains were grade I and II, two thirds of which occurred late during training/matches. Forwards were injured most often. Use of the standard stretching protocol (SSP) was the only factor significantly related to HSR (r = -0.45, p = 0.031) in the correlation analysis, suggesting that the more SSP is used, the lower the HSR. About 80% of HSR variability was accounted for by stretching holding time (SHT), SSP, and stretching technique (STE) in the multiple regression equation: HSR = 37.79 - (0.33SHT + [corrected] 10.05SSP + 2.24STE) +/- 2.34. SHT (negatively correlated with HSR) was the single highest predictor, and accounted for 30% of HSR variability, and an additional 40% in combination with SSP. CONCLUSIONS: Flexibility training protocols in the professional clubs were variable and appeared to depend on staffing expertise. Hamstring stretching was the most important training factor associated with HSR. The use of SSP, STE, and SHT are probably involved in a complex synergism which may reduce hamstring strains. Modification of current training patterns, especially stretching protocols, may reduce HSRs in professional footballers.

Left ventricular systolic function and diastolic filling after intermittent high intensity team sports.

BACKGROUND: Prolonged steady state exercise can lead to a decrease in left ventricular (LV) function as well as promote the release of cardiac troponin T (cTnT). There is limited information on the effect of intermittent high intensity exercise of moderate duration. OBJECTIVES: To determine the effect of intermittent high intensity exercise of moderate duration on LV function. METHODS: Nineteen male rugby and football players (mean (SD) age 21 (2) years) volunteered. Assessments, before, immediately after, and 24 hours after competitive games, included body mass, heart rate (HR), and systolic blood pressure (sBP) as well as echocardiography to assess stroke volume (SV), ejection fraction (EF), systolic blood pressure/end systolic volume ratio (sBP/ESV), and global diastolic filling (E:A) as well as to indirectly quantify preload (LV internal dimension at end diastole (LVIDd)). Serum cTnT was analysed using a 3rd generation assay. Changes in LV function were analysed by repeated measures analysis of variance. cTnT data are presented descriptively. RESULTS: SV (91 (26) v 91 (36) v 90 (35) ml before, after, and 24 hours after the game respectively), EF (71 (8) v 70 (9) v 71 (7)%), and sBP/ESV (4.2 (1.8) v 3.8 (1.9) v 4.1 (1.6) mm Hg/ml) were not significantly altered (p>0.05). Interestingly, whereas LVIDd was maintained after the game (50 (5) v 50 (6) mm), sBP was transiently but significantly reduced (131 (3) v 122 (3) mm Hg; p<0.05). E:A was moderately (p<0.05) reduced after the game (2.0 (0.4) v 1.5 (0.4)) but returned to baseline within 24 hours. No blood sample contained detectable levels of cTnT. CONCLUSIONS: In this cohort, LV systolic function was not significantly altered after intermittent activity. A transient depression in global diastolic filling was partially attributable to a raised HR and could not be explained by myocyte disruption as represented by cTnT release.

Ankle to brachial pressure index in normal subjects and trained cyclists with exercise-induced leg pain.

PURPOSE: This study compared ankle to brachial pressure indices (ABPI) before and after maximal exercise in three groups in order to investigate maximal exercise testing and ABPI as a useful procedure for the differential diagnosis of exercise-induced leg pain (EILP) in athletes. METHODS: ABPI measurements were taken before and after cycle ergometer exercise to volitional exhaustion or reproduction of symptoms in three groups: 1) untrained individuals (N = 10, 3 female, 7 male; age 35 +/- 5 yr (mean +/- SD)); 2) trained cyclists (N = 10, 3 female, 7 male; age, 30 +/- 5 yr); and 3) symptomatic group of trained cyclists, complaining of EILP (N = 12, 2 female, 10 male; age, 35 +/- 9 yr). RESULTS: Resting blood pressure indices were similar in all groups. ABPI were reduced (P < 0.05) in all groups after exercise. No differences between left and right legs were noted in the elite and untrained groups; however, a significant difference (P < 0.05) was noted between the nonsymptomatic (0.79 +/- 0.10) and symptomatic (0.61 +/- 0.20) legs in the subjects with EILP. Despite these group results, only three subjects in the symptomatic group met the published criteria (index of < 0.5) for endofibrosis of the external iliac artery. All positive ABPI tests were subsequently confirmed via arteriogram. CONCLUSION: Maximal exercise testing combined with ABPI measurement is a simple noninvasive procedure that may be useful for the examination of EILP. The results of this study suggest that, in cases with unilateral symptoms, a between-leg ABPI difference of 0.18 (at the first minute of recovery) may be considered as a useful additional diagnostic criterion.

The influence of recovery posture on post-exercise hypotension in normotensive men.

PURPOSE: Postexercise hypotension may be the result of an impaired vasoconstrictor response. This hypothesis was investigated by examining the central and peripheral hemodynamic responses during supine and seated recovery after maximal upright exercise. METHODS: After supine or seated baseline measurements, seven normotensive male volunteers completed a graded upright cycling protocol to volitional exhaustion. This was immediately followed by either supine or seated recovery. Measurements of pulsatile arterial blood pressure and central and peripheral hemodynamic variables recorded 30 min before exercise were compared with those taken throughout 60 min of recovery. RESULTS: Compared with baseline, mean arterial pressure (MAP) was reduced after exercise (P < 0.05) although the degree of change was not different between the supine (-9 +/- 4 mm Hg) and seated positions (-6 +/- 2 mm Hg). This change in MAP was associated with a reduction in diastolic blood pressure (DBP) (P < 0.05) and arterial pulse pressure (APP) (P < 0.01) for the supine and seated positions, respectively. The reduction in APP during seated recovery was accompanied by a decline in stroke volume (SV) (P < 0.05), not seen in the supine position, that limited the contribution of cardiac output (CO) to the maintenance of MAP. This effect of seated recovery was compensated by greater systemic (SVR) and regional vascular resistances in the forearm (FVR) and the forearm skin (SkVRA). There was also evidence of an augmented return of FVR and SkVRA to resting levels in the seated position after exercise. CONCLUSION: The lower peripheral resistance in the supine compared with seated recovery position suggests there is potential for greater vasoconstriction, although this is not evoked to increase blood pressure. This further suggests that the arterial baroreceptor reflex is reset to a lower operating pressure after exercise.

Cortical language lateralization in right handed normal subjects using functional magnetic resonance imaging.

In 95% of right handed individuals the left hemisphere is dominant for speech and language function. The evidence for this is accumulated primarily from clinical populations. We investigated cortical topography of language function and lateralization in a sample of the right handed population using functional magnetic resonance imaging and two lexical-semantic paradigms. Activated cortical language networks were assessed topographically and quantitatively by using a lateralization index. As a group, we observed left hemispheric language dominance. Individually, the lateralization index varied continuously from left hemisphere dominant to bilateral representation. In males, language primarily lateralized to left, and in females, approximately half had left lateralization and the other half had bilateral representation. Our data indicate that a previous view of female bilateral hemispheric dominance for language (McGlone, 1980. Sex differences in human brain asymmetry: a critical survey. Behav Brain Sci 3:215-263; Shaywitz et al., 1995. Sex differences in the functional organization of the brain for language. Nature 373:607-609) simplifies the complexity of cortical language distribution in this population. Analysis of the distribution of the lateralization index in our study allowed us to make this difference in females apparent.

Estrogen variation and resting left ventricular structure and function in young healthy females.

PURPOSE: A potential confounding factor in the interpretation of left ventricular (LV) structural and functional data in female subjects could be menstrual phase or contraceptive use upon assessment. To date no study has addressed this issue. METHODS: Seventeen eumenorrheic (EU; mean +/- SD age = 21 +/- 3 yr) and 14 combined-oral contraceptive pill-using (COC: mean +/- SD age = 21 +/- 3 yr) females volunteered to participate. The EU had stable menstrual cycles and the COC had all been using the same pill preparation for a minimum of 6 months. Echocardiographic examinations occurred during the mid-follicular phase and mid-luteal phases in the EU and during mid-consumption and mid-end of withdrawal in the COC. LV structure and function were assessed using M-mode and pulsed-wave Doppler echocardiography. Data were compared via Student t-tests and limits of agreement (LoA) were calculated. RESULTS: Structure and function did not significantly differ between phases of the menstrual cycle or between consumption and withdrawal of oral contraception (P > 0.05). However, there was considerable variance in the LoA between variables. Smaller LoA were reported for those variables directly measured from echocardiograms compared with those from derived data. For example, in a measured variable such as LV internal dimension in diastole, the LoA data represented a variation of +/- 0.4 mm (+/- 1%) between phases. Conversely, data for LV mass, a derived variable, reported LoA values of +/- 15 g (10%) between phases. The LoA were consistent between EU and COC. Variation in both measured and derived variables were within, or close to, accepted limits of measurement or biological error. CONCLUSION: It would seem that in studies assessing LV structure and function in women the influence of menstrual phase or oral contraceptive use is of minor significance.

Scaling cardiac structural data by body dimensions: a review of theory, practice, and problems.

Robust estimates of the "true" bivariate relationship between body size (X) and heart size (Y) have seldom been determined empirically. The removal of the covariate influence of body size from cardiac dimension variables facilitates both correct inter- or intra-group comparisons, and the construction of reference standards for normality. In the literature to date this "scaling" or normalisation of cardiac dimensions has been performed typically via a per-ratio standards method, (Y/X), with body surface area chosen as the size denominator. This review demonstrates that the per-ratio standards approach may be theoretically, mathematically, and empirically flawed. The most appropriate scaling procedure appears to be a curvilinear, allometric model of the general form Y = aXb. The cardiac dimension variable (Y) may be regressed upon the body size variable (X) to derive a power function ratio (Y/Xb) that is allegedly size-independent. The current consensus is that an estimate of fat-free mass (FFM) provides the most appropriate body size variable. In the scaling literature allometric modelling procedures have generally yielded FFM exponents (b) consistent with the theory of geometric similarity. We suggest that cardiac dimension data should be scaled by appropriate powers of FFM, derived from allometric modelling. However, despite the potential superiority of FFM as a scaling denominator, reference standards for normality based on FFM have not been developed or proposed. Future research should examine the robustness of the FFM-cardiac dimension relationship in large samples.

Genetic monitoring of the human population from high-level natural radiation areas of Kerala on the southwest coast of India. II. Incidence of numerical and structural chromosomal aberrations in the lymphocytes of newborns.

Cytogenetic studies using cord blood samples from newborns from high-level natural radiation areas of the Kerala coast in Southwest India have been in progress since 1986. A total of 963,940 metaphases from 10,230 newborns have been screened for various types of chromosomal aberrations. Comparison of 8,493 newborns (804,212 cells) from high-level natural radiation areas (dose rate >1.5 mGy/year) and 1,737 newborns (159,728 cells) from normal-level natural radiation areas (

Cortical language activation in stroke patients recovering from aphasia with functional MRI.

BACKGROUND AND PURPOSE: Two mechanisms for recovery from aphasia, repair of damaged language networks and activation of compensatory areas, have been proposed. In this study, we investigated whether both mechanisms or one instead of the other take place in the brain of recovered aphasic patients. METHODS: Using blood oxygenation level-dependent functional MRI (fMRI), we studied cortical language networks during lexical-semantic processing tasks in 7 right-handed aphasic patients at least 5 months after the onset of left-hemisphere stroke and had regained substantial language functions since then. RESULTS: We found that in the recovered aphasic patient group, functional language activity significantly increased in the right hemisphere and nonsignificantly decreased in the left hemisphere compared with that in the normal group. Bilateral language networks resulted from partial restitution of damaged functions in the left hemisphere and activation of compensated (or recruited) areas in the right hemisphere. Failure to restore any language function in the left hemisphere led to predominantly right hemispheric networks in some individuals. However, better language recovery, at least for lexical-semantic processing, was observed in individuals who had bilateral rather than right hemisphere-predominant networks. CONCLUSIONS: The results indicate that the restoration of left-hemisphere language networks is associated with better recovery and inversely related to activity in the compensated or recruited areas of the right hemisphere.