Greg Whyte

Physiologic limits of left ventricular hypertrophy in elite junior athletes : Relevance to differential diagnosis of athlete's heart and hypertrophic cardiomyopathy

OBJECTIVES The present study was undertaken to define physiologic limits of left ventricular hypertrophy in elite adolescent athletes. BACKGROUND Systematic sports training may cause increased left ventricular wall thickness (LVWT), creating uncertainty regarding the differential diagnosis of athletes heart from hypertrophic cardiomyopathy (HCM). This distinction is crucial because HCM is responsible for about one-third of all sudden deaths in young athletes. Echocardiographic data defining athletes heart are limited largely to adults, with little information specifically in adolescent athletes (14 to 18 years old), for whom the risk of sudden death from HCM is highest. METHODS Seven hundred and twenty elite adolescent athletes (75% male) aged 15.7 +/- 1.4 years participating in ball, racket, and endurance sports and 250 healthy sedentary controls of similar age, gender, and body surface area underwent echocardiography. RESULTS Compared with controls, athletes had greater absolute LVWT (9.5 +/- 1.7 mm vs. 8.4 +/- 1.4 mm; p < 0.0001). Maximal LVWT exceeded predicted upper limits in 38 athletes (5%); however, no female athlete had a LVWT >11 mm and only three trained male athletes had absolute LVWT >12 mm (0.4%). Each of the 38 athletes with a LVWT exceeding predicted limits also showed enlarged left ventricular cavity dimension (54.4 +/- 2.1 mm; range 52 to 60 mm). CONCLUSIONS Trained adolescent athletes demonstrated greater absolute LVWT compared with nonathletes. Only a small proportion of athletes exhibited a LVWT exceeding upper limits, very rarely >12 mm, and then always with chamber enlargement. Hypertrophic cardiomyopathy should be considered strongly in any trained adolescent male athlete with LVWT >12 mm (females >11 mm) and nondilated left ventricle.

Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes

This study examined the cardiac structure and function of a unique cohort of documented lifelong, competitive endurance veteran athletes (>50 yr). Twelve lifelong veteran male endurance athletes [mean ± SD (range) age: 56 ± 6 yr (50-67)], 20 age-matched veteran controls [60 ± 5 yr; (52-69)], and 17 younger male endurance athletes [31 ± 5 yr (26-40)] without significant comorbidities underwent cardiac magnetic resonance (CMR) imaging to assess cardiac morphology and function, as well as CMR imaging with late gadolinium enhancement (LGE) to assess myocardial fibrosis. Lifelong veteran athletes had smaller left (LV) and right ventricular (RV) end-diastolic and end-systolic volumes (P < 0.05), but maintained LV and RV systolic function compared with young athletes. However, veteran athletes had a significantly larger absolute and indexed LV and RV end-diastolic and systolic volumes, intraventricular septum thickness during diastole, posterior wall thickness during diastole, and LV and RV stroke volumes (P < 0.05), together with significantly reduced LV and RV ejection fractions (P < 0.05), compared with veteran controls. In six (50%) of the veteran athletes, LGE of CMR indicated the presence of myocardial fibrosis (4 veteran athletes with LGE of nonspecific cause, 1 probable previous myocarditis, and 1 probable previous silent myocardial infarction). There was no LGE in the age-matched veteran controls or young athletes. The prevalence of LGE in veteran athletes was not associated with age, height, weight, or body surface area (P > 0.05), but was significantly associated with the number of years spent training (P < 0.001), number of competitive marathons (P < 0.001), and ultraendurance (>50 miles) marathons (P < 0.007) completed. An unexpectedly high prevalence of myocardial fibrosis (50%) was observed in healthy, asymptomatic, lifelong veteran male athletes, compared with zero cases in age-matched veteran controls and young athletes. These data suggest a link between lifelong endurance exercise and myocardial fibrosis that requires further investigation.

Cardiac Troponin T Release Is Stimulated by Endurance Exercise in Healthy Humans

To the Editor: Post-exercise release of cardiac troponin (cTn)T and cTnI has been previously reported after prolonged bouts of exercise ([1][1]). However, this release has only been observed in a limited number of subjects ([2][2]). It is unclear whether post-exercise release of cTn represents

Changes in vascular and cardiac function after prolonged strenuous exercise in humans

Prolonged exercise has been shown to result in an acute depression in cardiac function. However, little is known about the effect of this type of exercise on vascular function. Therefore, the purpose of the present study was to investigate the impact of an acute bout of prolonged strenuous exercise on vascular and cardiac function and the appearance of biomarkers of cardiomyocyte damage in 15 male (32 +/- 10 yr) nonelite runners. The subjects were tested on two occasions, the day before and within an hour of finishing the London marathon (229 +/- 38 min). Function of the brachial and femoral arteries was determined using flow-mediated dilatation (FMD). Echocardiographic assessment of cardiac strain, strain rate, tissue velocities, and flow velocities during diastole and systole were also obtained. Venous blood samples were taken for later assessment of cardiac troponin I (cTnI), a biomarker of cardiomyocyte damage. Completion of the marathon resulted in a depression in femoral (P = 0.04), but not brachial (P = 0.96), artery FMD. There was no change, pre- vs. postmarathon, in vascular shear, indicating that the impaired femoral artery function was not related to hemodynamic changes. The ratio of peak early to atrial radial strain rate, a measure of left ventricular diastolic function, was reduced postmarathon (P = 0.006). Postrace cTnI was elevated in 12 of 13 runners, with levels above the recognized clinical threshold for damage in 7 of these. In conclusion, when taken together, these data suggest a transient depression in cardiac and leg vascular function following prolonged intensive exercise.

Utility of cardiopulmonary exercise in the assessment of clinical determinants of functional capacity in hypertrophic cardiomyopathy.

The utility of metabolic gas exchange measurements in evaluating the severity and determinants of exercise limitation was studied during upright symptom-limited cardiopulmonary exercise in 135 consecutive patients with hypertrophic cardiomyopathy (HC) and 50 healthy age- and gender-matched volunteers. Peak oxygen consumption (VO(2)) was less than predicted (age, gender, and size) in 99% patients. Peak VO(2) was significantly associated with New York Heart Association functional class; however, there was considerable overlap of peak VO(2) between classes I and III (70 +/- 15%, 56 +/- 15%, 35 +/- 11%, respectively). Patients with abnormal blood pressure responses and patients with chronotropic incompetence during exercise had lower percent-predicted peak VO(2) than patients with normal blood pressure and heart rate responses during exercise (p = 0.0001 and p <0.001, respectively). Percent-predicted peak VO(2) was similar in patients with and without resting left ventricular outflow obstruction. Of those patients with resting gradients, however, there was a strong inverse correlation between the magnitude of the gradient and peak VO(2) (r = 0.5; p <0.001). In conclusion, peak VO(2) is significantly related to New York Heart Association functional class in this group of patients with HC, but peak VO(2) is a superior measure of cardiovascular performance in individual patients. Our peak VO(2) data indicate that mechanical obstruction has an adverse pathophysiologic effect on functional capacity and provide the rationale to support treatments aimed at gradient reduction. Low peak VO(2) characteristics including those with normal or near-normal left ventricular wall thickness suggests that measurement of peak VO(2) may aid in the differential diagnosis between HC and athletes heart.

The specificity of training prescription and physiological assessment: A review

Abstract The aims in this review are: (1) to identify physiological determinants of performance; (2) to consider training specificity by examining aerobic, team and racket sports, strength and power activities, and cross-training and concurrent training methods; and (3) to evaluate the role of specificity in the physiological assessment of performance determinants. Assessment of the physiological determinants of performance is an integral part of sports science support for elite athletes. Laboratory and field-based physiological assessments are fundamental elements in profiling athletes, assessing training adaptations, and interrogating programme efficacy. The relatively small and highly specific adaptations associated with high-performance training call for valid, reliable, and sensitive methods of assessment. Recent advances in the physiological assessment of athletes have led to the development of a plethora of laboratory and field-based procedures. In the assessment of the athlete, there is a tension between the high reliability and low ecological validity of laboratory assessments and the low reliability and high validity of field-based methods. In an attempt to enhance ecological validity of training and physiological assessment, various sports-specific ergometers have been designed. This development has helped to match fitness assessment procedures to the demands of the sport concerned.

Senescent T-lymphocytes are mobilised into the peripheral blood compartment in young and older humans after exhaustive exercise.

Senescent T-lymphocytes are antigen-experienced cells that express the killer-cell lectin-like receptor G1 (KLRG1) and/or CD57; fail to clonally expand following further antigenic stimulation and prevail in the resting blood of older adults compared to the young. Physical exercise mobilises T-lymphocytes into the bloodstream and is therefore a model with which to compare age-related phenotypes of blood-resident T-cells with those T-cells entering the blood from peripheral lymphoid compartments. Eight young (Y; Age: 21+/-3 years) and 8 older (O; Age: 56+/-3 years) healthy males completed a maximal treadmill exercise protocol. Blood lymphocytes isolated before, immediately after and 1h after exercise were assessed for cell surface expression of KLRG1, CD57, CD28, CD45RA, CD45RO, CD62L and lymphocyte subset markers using three-colour flow cytometry. Lymphocyte subset numbers (CD3+, CD3+/CD4+, CD3+/CD8 and CD3-/CD56+) increased with exercise (p<0.05) but were not different between Y and O. At rest and immediately after exercise, the percentage of CD3+/CD8+ T-lymphocytes expressing KLRG1 and CD45RO was greater in O than Y, whereas Y had a greater expression of CD45RA and CD62L than O. The percentage of all CD3+/CD8+ and CD3+/CD4+ T-lymphocytes expressing KLRG1 and CD57 increased after exercise, but the magnitude of change was not age-dependent. In conclusion, there is a greater proportion of senescent CD3+/CD8+ T-lymphocytes in the blood of older adults compared to young at rest and immediately after exhaustive exercise, indicating that the greater frequency of KLRG1+/CD8+ T-lymphocytes in older humans is ubiquitous and not localised to the peripheral blood.

Exercise and arterial adaptation in humans: uncoupling localized and systemic effects

Previous studies have established effects of exercise training on arterial wall thickness, remodeling, and function in humans, but the extent to which these changes are locally or systemically mediated is unclear. We examined the brachial arteries of the dominant (D) and nondominant (ND) upper limbs of elite racquet sportsmen and compared them to those of matched healthy inactive controls. Carotid and superficial femoral artery responses were also assessed in both groups. High-resolution duplex ultrasound was used to examine resting diameter, wall thickness, peak diameter, and blood flow. We found larger resting arterial diameter in the preferred arm of the athletes (4.9 ± 0.5 mm) relative to their nonpreferred arm (4.3 ± 0.4 mm, P < 0.05) and both arms of control subjects (D: 4.1 ± 0.4 mm; ND: 4.0 ± 0.4, P < 0.05). Similar limb-specific differences were also evident in brachial artery dilator capacity (5.5 ± 0.5 vs. 4.8 ± 0.4, 4.8 ± 0.6, and 4.8 ± 0.6 mm, respectively; P < 0.05) following glyceryl trinitrate administration and peak blood flow (1,118 ± 326 vs. 732 ± 320, 737 ± 219, and 698 ± 174 ml/min, respectively; P < 0.05) following ischemic handgrip exercise. In contrast, athletes demonstrated consistently lower wall thickness in carotid (509 ± 55 μm), brachial (D: 239 ± 100 μm; ND: 234 ± 133 μm), and femoral (D: 479 ± 38 μm; ND: 479 ± 42 μm) arteries compared with control subjects (carotid: 618 ± 74 μm; brachial D: 516 ± 100 μm; ND: 539 ± 129 μm; femoral D: 634 ± 155 μm; ND: 589 ± 112 μm; all P < 0.05 vs. athletes), with no differences between the limbs of either group. These data suggest that localized effects of exercise are evident in the remodeling of arterial size, whereas arterial wall thickness appears to be affected by systemic factors.

Screening elite winter athletes for exercise induced asthma: a comparison of three challenge methods

Background: The reported prevalence of exercise induced asthma (EIA) in elite winter athletes ranges from 9% to 50%. Many elite winter athletes do not report symptoms of EIA. At present there is no gold standard test for EIA. Objective: To establish the efficacy of screening for EIA and examine the role of the eucapnic voluntary hyperventilation (EVH) challenge and laboratory based and sport specific exercise challenges in the evaluation of elite winter athletes. Methods: 14 athletes (mean (SD) age 22.6 (5.7) years, height 177.2 (7.0) cm, body mass 68.9 (16.9) kg) from the Great Britain short-track speed skating (n = 10) and biathlon teams (n = 4) were studied. Each athlete completed a laboratory based and sport specific exercise challenge as well as an EVH challenge, in randomised order. Results: All 14 athletes completed each challenge. Two had a previous history of asthma. Ten (including the two with a previous history) had a positive test to at least one of the challenges. Ten athletes had a positive response to EVH; of these, only three also had a positive response to the sport specific challenge. No athletes had a positive response to the laboratory based challenge. Conclusions: Elite athletes should be screened for EIA. EVH is a more sensitive challenge in asymptomatic athletes than sport specific and laboratory based challenges. If sporting governing bodies were to implement screening programmes to test athletes for EIA, EVH is the challenge of choice.

Troponin release following endurance exercise: Is inflammation the cause? a cardiovascular magnetic resonance study

BackgroundThe aetiology and clinical significance of troponin release following endurance exercise is unclear but may be due to transient myocardial inflammation. Cardiovascular magnetic resonance (CMR) affords us the opportunity to evaluate the presence of myocardial inflammation and focal fibrosis and is the ideal imaging modality to study this hypothesis. We sought to correlate the relationship between acute bouts of ultra endurance exercise leading to cardiac biomarkers elevation and the presence of myocardial inflammation and fibrosis using CMR.Methods17 recreation athletes (33.5 +/- 6.5 years) were studied before and after a marathon run with troponin, NTproBNP, and CMR. Specific imaging parameters to look for inflammation included T2 weighted images, and T1 weighted spin-echo images before and after an intravenous gadolinium-DTPA to detect myocardial hyperemia secondary to inflammation. Late gadolinium imaging was performed (LGE) to detect any focal regions of replacement fibrosis.ResultsEleven of the 17 participant had elevations of TnI above levels of cut off for myocardial infarction 6 hrs after the marathon (0.075 +/- 0.02, p = 0.007). Left ventricular volumes were reduced post marathon and a small increase in ejection fraction was noted (64+/- 1% pre, 67+/- 1.2% post, P = 0.014). Right ventricular volumes, stroke volume, and ejection fraction were unchanged post marathon. No athlete fulfilled criteria for myocardial inflammation based on current criteria. No regions of focal fibrosis were seen in any of the participants.ConclusionExercise induced cardiac biomarker release is not associated with any functional changes by CMR or any detectable myocardial inflammation or fibrosis.