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116


Prevalence and significance of T-wave inversions on the 12-lead ECG in 1400 junior elite athletes participating in ball, racket, and endurance sports [Meeting Abstract]

Makan, J; Sharma, S; Whyte, G; Jackson, PG; McKenna, WJ
ISI:000224783503814
ISSN: 0009-7322
CID: 3852532

Exercise and the environment [Editorial]

Whyte, G; Reilly, T
ISI:000225966500001
ISSN: 0264-0414
CID: 3852542

The validity of capillary blood sampling in the determination of human growth hormone concentration during exercise in men

Godfrey, R J; Whyte, G; McCarthy, J; Nevill, A; Head, A
BACKGROUND:Studies measuring human growth hormone (hGH) in blood during exercise have mainly used venous sampling. The invasive nature of this procedure makes evaluation of hGH impossible in various exercise environments. OBJECTIVE:To determine whether capillary sampling could offer an alternative sampling method. METHODS:Capillary and venous blood samples were collected for determination of hGH at the end of each exercise stage during an incremental exercise test in 16 male club level competitive cyclists (mean (SD) age 30.8 (8.0) years, body mass 72.2 (7.1) kg, body fat 12.9 (3.5)%, peak oxygen consumption 4.18 (0.46) l x min(-1)). Linear regression, from a plot of venous v capillary blood hGH concentration, showed a correlation coefficient of r = 0.986 (p<0.001). When geometric means and log transformations were used, a coefficient of variation of 14.2% was demonstrated between venous and capillary flow for hGH concentration. The mean ratio limits of agreement were 0.62 (1.72)-that is, 95% of the ratios were contained between 0.36 and 1.07, with a mean of 0.62. CONCLUSIONS:Capillary blood sampling is an acceptable alternative to venous sampling for determining hGH concentration during rest and exercise. Sample sites should not be used interchangeably: one site should be chosen and its use standardised.
PMCID:1724910
PMID: 15388571
ISSN: 1473-0480
CID: 3851452

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

George, K P; Dawson, E; Shave, R E; Whyte, G; Jones, M; Hare, E; Gaze, D; Collinson, P
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/OBJECTIVE: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.
PMCID:1724883
PMID: 15273183
ISSN: 1473-0480
CID: 3851422

The upper limit of physiological cardiac hypertrophy in elite male and female athletes: the British experience

Whyte, G P; George, K; Sharma, S; Firoozi, S; Stephens, N; Senior, R; McKenna, W J
Establishment of upper normal limits of physiological hypertrophy in response to physical training is important in the differentiation of physiological and pathological left ventricular hypertrophy. The genetic differences that exist in the adaptive response of the heart to physical training and the causes of sudden cardiac death in young athletes indicate the need for population-specific normal values. Between September 1994 and December 2001, 442 (306 male, 136 female) elite British athletes from 13 sports were profiled. Standard two-dimensional guided M-mode and Doppler echocardiography were employed to evaluate left ventricular morphology and function. Eleven (2.5%) athletes, competing in a range of sports including judo, skiing, cycling, triathlon, rugby and tennis, presented with a wall thickness >13 mm, commensurate with a diagnosis of hypertrophic cardiomyopathy. Eighteen (5.8%) male athletes presented with a left ventricular internal diameter during diastole (LVIDd) >60 mm, with an upper limit of 65 mm. Of the 136 female athletes, none where found to have a maximum wall thickness >11 mm. Left ventricular internal diameter was <60 mm in all female athletes. Systolic and diastolic function were within normal limits for all athletes. Upper normal limits for left ventricular wall thickness and LVIDd are 14 mm and 65 mm for elite male British athletes, and 11 mm and 60 mm for elite female British athletes. Values in excess of these should be viewed with caution and should prompt further investigation to identify the underlying mechanism.
PMID: 15054661
ISSN: 1439-6319
CID: 3850332

Altered cardiac function and minimal cardiac damage during: Prolonged exercise

Shave, R; Dawson, E; Whyte, G; George, K; Gaze, D; Collinson, P
SHAVE, R., E. DAWSON, G. WHYTE, K. GEORGE, D. GAZE, and P. COLLINSON. Altered Cardiac Function and Minimal Cardiac Damage during Prolonged Exercise. Med. Sci. Sports Exerc., Vol. 36, No. 7, pp. 1098-1103, 2004. Purpose: The purpose of the present study was to examine markers of cardiac function and cardiac damage during a simulated half-ironman triathlon in highly trained athletes. Methods: Nine highly trained male triathletes volunteered for the study (mean +/- SD; age: 33 +/- 3 yr; height: 1.8 +/- 0.1 m; body mass: 77.7 +/- 3.2 kg). The subjects completed a half-ironman triathlon; 1.9-km swim in an indoor 20-m pool, followed by a laboratory-based 90-km cycle and 21.1-km run. Venous blood samples were drawn and echocardiographic assessment completed before the start of exercise, immediately after each stage, and 24 h postexercise. Serum was analyzed for total creatine kinase activity (CK), creatine kinase isoenzyme MBmass (CK-MBmass), and cardiac troponin T (cTnT). Left ventricular systolic (stroke volume, and systolic blood pressure/end systolic volume ratio (SBP/ESV)) and diastolic (ratio of early [E] to late [A], ventricular filling E:A) measurements were derived from echocardiographic assessment. Results: The mean completion time of the half-ironman triathlon was 301 +/- 28 min. Left ventricular contractility (SBP/ESV) was significantly reduced after the half-ironman triathlon (P < 0.05). A significant reduction in E:A was observed after the run phase of the half-ironman triathlon (P < 0.05). Significant increases in CK and CK-MBmass, were observed during and after the half-ironman triathlon (P < 0.05), and cTnT was elevated in four subjects over the course of the half-ironman triathlon. Conclusions: The physiologic stress imposed by the half-ironman triathlon resulted in a reduced left ventricular contractility and altered diastolic filling, coupled with minimal cardiac damage in a number of highly trained male triathletes. The mechanisms behind such altered cardiac function and cardiac damage after prolonged exercise are yet to be elucidated.
ISI:000222585700002
ISSN: 0195-9131
CID: 3852502

Left ventricular morphology and function in female athletes: a meta-analysis

Whyte, G P; George, K; Nevill, A; Shave, R; Sharma, S; McKenna, W J
The purpose of the present study was to examine the impact of physical training upon cardiac structure and function, and identify physiologic upper limits in female athletes. Meta-analytical techniques were applied to 13 published echocardiographic studies examining cardiac structure and function in female athletes. The study group included 890 athletes and 333 controls. For comparison of sporting discipline, studies were partitioned into 3 categories (endurance, strength/sprint, team). Significant (p < 0.05) effect sizes were observed for all structural measures between athletes and controls. Significant effect size differences existed between sporting groups for LVIDd and LVM only, with endurance and team game athletes demonstrating the largest effect sizes compared to strength trained athletes. No significant effect of training was observed for left ventricular diastolic or systolic function, with the exception of stroke volume where a significant effect size difference was observed between athletes and controls with no observed difference between sporting groups. Maximum reported upper limits for LV wall thickness and LVIDd in female athletes were 12 mm and 66 mm respectively. Chronic exercise training results in cardiac enlargement in female athletes. The nature of physiologic adaptation is similar to that observed in male athletes. LV wall thickness values greater than 12 mm in female athletes should be viewed with caution and indicate a more comprehensive evaluation to establish a physiological or pathological basis for the observed left ventricular enlargement.
PMID: 15241719
ISSN: 0172-4622
CID: 3850342

Spontaneous atrial fibrillation in a freestyle skier [Case Report]

Whyte, G; Stephens, N; Sharma, S; Shave, R; Budgett, R; McKenna, W J
A male freestyle skier was found to have atrial fibrillation during a routine physiological assessment. This was found to be associated with the consumption of an unusually large amount of alcohol. Athletes should be counselled about the potential dangers of alcohol consumption before exhaustive exercise.
PMCID:1724760
PMID: 15039268
ISSN: 0306-3674
CID: 3851392

Effect of prolonged exercise in a hypoxic environment on cardiac function and cardiac troponin T

Shave, R E; Dawson, E; Whyte, G; George, K; Gaze, D; Collinson, P
BACKGROUND:Exercise induced cardiac fatigue has recently been observed after prolonged exercise. A moderate to high altitude has been suggested as a possible stimulus in the genesis of such cardiac fatigue. OBJECTIVE:To investigate if exercise induced cardiac fatigue and or cardiac damage occurs after prolonged exercise in a hypoxic environment. METHODS:Eight trained male triathletes volunteered for the study. Each completed two 50 mile cycle trials, randomly assigned from normobaric normoxia and normobaric hypoxia (15% FIO(2)). Echocardiographic assessment and whole blood collection was completed before, immediately after, and 24 hours after exercise. Left ventricular systolic and diastolic functional variables were calculated, and serum was analysed for cardiac troponin T. Results were analysed using a two way repeated measures analysis of variance, with alpha set at 0.05. RESULTS:No significant differences were observed in either systolic or diastolic function across time or between trials. Cardiac troponin T was detected in one subject immediately after exercise in the normobaric hypoxic trial. CONCLUSIONS:A 50 mile cycle trial in either normobaric normoxia or normobaric hypoxia does not induce exercise induced cardiac fatigue. Some people, however, may exhibit minimal cardiac damage after exercise in normobaric hypoxia. The clinical significance of this is yet to be elucidated.
PMCID:1724732
PMID: 14751955
ISSN: 0306-3674
CID: 3851382

Exercise induced neurally mediated syncope in an elite rower: a treatment dilemma [Case Report]

Whyte, G; Stephens, N; Budgett, R; Sharma, S; Shave, R E; McKenna, W J
PMCID:1724729
PMID: 14751954
ISSN: 0306-3674
CID: 3851372