Faculty Bibliography

The effect sodium citrate ingestion had on 3,000-m running performance was examined. Nine elite multidisciplinary athletes (7 men and 2 women, age 27.8 +/- 4.7 years, height 176 +/- 11 cm, mass 70.9 +/- 8.7 kg) completed two 3,000-m trials. The trials were double-blind and randomly assigned for sodium citrate (0.5 g x kg(-1) body mass) and for sodium (NaCl, 0.1 g x kg(-1) body mass). Split times, heart rate (HR), and 3,000-m completion times were measured. Blood samples were collected preingestion, pre-exercise, postexercise, and 10 minutes postexercise and analyzed for lactate concentration. Blood lactate (LA) was significantly higher (p < 0.05) for the sodium citrate trial, both postexercise and 10 minutes postexercise. No significant differences (p > 0.05) in HR were observed between trials. Performance time was significantly faster (p < 0.05) for the sodium citrate trial (610.9 +/- 36.6 seconds) compared with the placebo trial (621.6 +/- 31.4 seconds). Sodium citrate ingestion improved 3,000-m running performance in elite multidisciplinary athletes; however, the high potential for gastrointestinal distress likely precludes the use of sodium citrate as an ergogenic aid among athletes.

In 1999, Wilson and Batterham proposed a new approach to assessing the test-retest stability of psychometric questionnaires. They recommended assessing the proportion of agreement - that is, the proportion of participants that record the same response to an item - using a test-retest design. They went on to use a bootstrapping technique to estimate the uncertainty of the proportion of agreement. The aims of this short communication are (1) to demonstrate that the sampling distribution of the proportion of agreement is well known (the binomial distribution), making the technique of 'bootstrapping' redundant, and (2) to suggest a much simpler, more sensitive method of assessing the stability of a psychometric questionnaire, based on the test-retest differences (within-individuals) for each item. Adopting methods similar to Wilson and Batterham, 97 sport students completed the Social Physique Anxiety Scale on two occasions. Test-retest differences were calculated for each item. Our results show that the proportion of agreement ignores the nature of disagreement. Items 4 and 11 showed similar agreement (44.3% and 43.3% respectively), but 89 of the participants (91.8%) differed by just +/-1 point when responding to item 4, indicating a relatively stable item. In contrast, only 78 of the participants (80.4%) recorded a difference within +/- 1 point when responding to item 11, suggesting quite contrasting stability for the two items. We recommend that, when assessing the stability of self-report questionnaires using a 5-point scale, most participants (90%) should record test-retest differences within a reference value of +/- 1.

Empirically derived relationships between body size variables and cardiac dimensions have not been published previously for a large sample of male and female athletes. This process would inform scaling practice and facilitate intra- and inter-group comparisons of cardiac data. Therefore we investigated the relationships of body mass (BM), height and body surface area (BS) with a range of cardiac dimensions derived by echocardiography in 464 male and female elite junior athletes (age range 14-18 years; sporting allocation included rowers, cyclists, footballers, tennis players, swimmers and a miscellaneous group). Initial linearity checks suggested that most of the relationships between the body size variables and cardiac dimensions were non-linear, thus precluding the simple ratio standard approach to scaling. Multiple log-log least-squares linear regression confirmed commonality of slopes (between males and females, across the age range and between sporting groups) for all relationships involving BM and BS. Subsequent analyses of the slope exponent (b) for left ventricular dimensions supported previous data and were dimensionally consistent (LVM-BM, b=0.91+/-0.11; LVM-BS, b=1.44+/-0.19; where LVM is left ventricular mass), except for left ventricular internal dimension in diastole (LVIDd) (LVIDd-BM, b=0.25+/-0.04). Data for the left atria internal dimension (LA) were also dimensionally consistent (LA-BM, b=0.29+/-0.09); however, this was not the case for the right ventricular internal dimension in diastole (RVIDd) (RVIDd-BM, b=0.76+/-0.14). It is possible that these results were due to a study-specific limitation in the data range (LVIDd) and the geometric peculiarities of RVIDd compared with LVIDd. The gender/age/sporting groupxbody size interaction factor for virtually all relationships between height and cardiac dimensions was significant (P<0.05), and thus whole-group b exponents could not be generated. Generally these data support previous small-sample research with athletes, and suggest that allometric scaling, as opposed to simple ratio scaling, should be adopted in studies of cardiac dimensions in athletes. This should allow, with minimal mathematical difficulty, the production of body-size-independent cardiac indices to be evaluated in laboratory or clinical work. Further research is required to develop normative 'allometrically derived' cardiac indices, and care should be taken to determine relationships in specific population groups as well as to confirm commonality of slopes in multiple group comparisons. Caution is expressed regarding the use of height as a scaling variable in future research.

OBJECTIVES/OBJECTIVE:This study evaluated the role of metabolic (cardiopulmonary gas exchange) exercise testing in differentiating physiologic LVH in athletes from HCM. BACKGROUND:Regular intensive training may cause mild increases in left ventricular wall thickness (LVWT). Although the degree of left ventricular hypertrophy (LVH) is typically less than that seen in hypertrophic cardiomyopathy (HCM), genetic studies have shown that a substantial minority of patients with HCM have an LVWT in the same range. The differentiation of physiologic and pathologic LVH in this "gray zone" can be problematic using echocardiography and electrocardiography alone. METHODS:Eight athletic men with genetically proven HCM and mild LVH (13.9 +/- 1.1 mm) and eight elite male athletes matched for age, size and LVWT (13.4 +/- 0.9 mm) underwent symptom limited metabolic exercise stress testing. Peak oxygen consumption (pVO2), anaerobic threshold, oxygen pulse and respiratory exchange ratios were measured in both groups and compared with those observed in 12 elite and 12 recreational age- and size-matched athletes without LVH. RESULTS:Elite athletes with LVH had significantly greater pVO2 (66.2 +/- 4.1 ml/kg/min vs. 34.3 +/- 4.1 ml/kg/min; p < 0.0001), anaerobic threshold (61.6 +/- 1.8% of the predicted maximum VO2 vs. 41.4 +/- 4.9% of the predicted maximum VO2; p < 0.001) and oxygen pulse (27.1 +/- 3.2 ml/beat vs. 14.3 +/- 1.8 ml/beat; p < 0.0001) than individuals with HCM. A pVO2 >50 ml/kg/min or >20% above the predicted maximum VO2 differentiated athlete's heart from HCM. CONCLUSIONS:Metabolic exercise testing facilitates the differentiation between physiologic LVH and HCM in individuals in the "gray zone."

The purpose of this study was to determine whether the critical swimming velocity (Vcrit) corresponds to the velocity at lactate threshold (V-LT) in elite triathletes. Eight elite triathletes (5 male, 3 female; age 26 +/- 4 years; height 1.7 +/- 0.1 m and body mass 75 +/- 4 kg) participated in the study. Vcrit, defined as the speed that could theoretically be maintained indefinitely without exhaustion, was expressed as the slope of a regression line between swimming distance covered and the corresponding times of five time trials over 100, 200, 400, 800 and 1500m and all combinations of these. Lactate threshold (LT) was determined by visual inspection as the point of first inflection of the lactate-work rate curve following 5 x 300 m swims of increasing velocity which were paced using the Aquapacer (Challenge and Response, Inverurie, Scotland). Velocities of the 300 m swims were -10, -5, 0, +5 and +10% of the average 100m pace from a 1500 m time trial. Vcrit was similar regardless of the combination or number of time trials used in the linear regression. For all subjects Vcrit was significantly faster (p <0.05) than V-LT (1.23 +/- 0.11 m x s(-1) and 1.15 +/- 0.10 m x s(-1) respectively). Blood lactate concentrations were also significantly higher (p < 0.05) at Vcrit (3.0 +/- 1.0 mM) than at LT (1.9 +/- 0.4 mM). Results from the present study demonstrate that Vcrit can be calculated from any two time trials in triathletes, however Vcrit did not represent V-LT in triathletes. Since Vcrit is faster than V-LT it is unlikely to be sustained indefinitely and consequently the notion of Vcrit should be re-evaluated in light of these findings.

BACKGROUND:To report physiological profiles, and investigate the relationship between selected physiological variables and cycling performance in ultra-endurance triathletes. METHODS: PARTICIPANTS/METHODS:ten male (mean+/-SD, age; 32+/-5 years) ultra-endurance triathletes participated in the study. Physiological profiles were compared with 10 male age-matched control subjects. MEASURES/METHODS:left ventricular structure (wall thickness [LVPWd], internal diameter [LVIDd], and mass [LVM]) and function (diastolic filling, fractional shortening, and stroke volume [SV]) were assessed using standard M-Mode, 2D, and Doppler echocardiography. Maximal and sub-maximal exercise gas exchange responses were measured on-line during a maximal ramping cycle-ergometer exercise test. RESULTS:Ultra-endurance triathletes demonstrated significantly larger LVPWd, LVIDd, LVM, SV, VO2max anaerobic threshold (AT), and power to body-mass ratio compared with controls. Cycling performance for both Ironman and half Ironman were significantly correlated with LVPWd, LVM, and SV. LVIDd was significantly correlated Ironman cycle time alone. Oxygen consumption (VO2) at AT, percentage of VO2max at AT, and peak power to bodymass ratio were significantly correlated to bike finish time in the half Ironman, but not Ironman. CONCLUSIONS:The correlation between cycling performance, LVM and SV suggests that the more conditioned athletes may be better able to maintain a high cardiac output during prolonged cycling. Sub-maximal gas exchange responses are predictors of cycling performance for the half-Ironman but not the Ironman. These results suggest that other factors including the longer duration swim prior to the cycling component, may impact upon cycle performance.

PURPOSE/OBJECTIVE:Recent echocardiographic studies have reported cardiac dysfunction following ultra-endurance exercise in trained individuals. The duration of exercise required to elicit cardiac dysfunction and the mechanisms underlying this phenomenon have not been fully elucidated. The aim of the present study was to examine the presence of cardiac dysfunction following a half-Ironman and Ironman triathlon in trained individuals. METHODS:14 male triathletes (age: 32 +/- 5 yr; height: 180 +/- 8 cm; body mass: 75 +/- 9 kg) completed a half-Ironman triathlon. Following a 4-wk period, 10 of the original 14 triathletes completed an Ironman triathlon. All triathletes were assessed using ECG, echocardiography, and blood analysis pre-, immediately post-, and 48 h postrace for both distances. RESULTS:Echocardiographic results indicated diastolic and systolic left ventricular dysfunction, for both race distances, which were associated with altered relaxation characteristics and a reduced inotropic contractility, respectively. Following 48-h recovery, all echocardiographic measures were similar to resting values. Creatine kinase MB (CKMB) was significantly elevated immediately postrace for both distances; however, it accounted for less than 5% of the total CK value and in the presence of an elevated total CK and CKMM implied that the elevated CKMB was noncardiac in origin. Troponin-T, however, was significantly elevated immediately postrace for both distances and returned to normal following 48-h recovery indicating myocardial damage. CONCLUSIONS:Ironman and half-Ironman competition resulted in reversible abnormalities in resting left ventricular diastolic and systolic function. Results suggest that myocardial damage may be, in part, responsible for cardiac dysfunction, although the mechanisms responsible for this cardiac damage remain to be fully elucidated.