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Gregory Whyte

Publications and source records attributed to Gregory Whyte.

13 recordsLinked to original sources

Altered left ventricular diastolic filling following a marathon is a reproducible phenomenon.

The present study examined the reproducibility of alterations in left ventricular function and cardiac biomarkers in a cohort of athletes following two marathons, one year apart. Eight participants in the 2004 and 2005 London Marathons were tested pre- and post-race via echocardiography and humoral analysis. Reductions in diastolic filling, unrelated to loading or heart rate, following both marathons were reproducible within individuals, which may be a function of exercise duration. In contrast, exercise-induced cardiac troponin release was inconsistent.

Adult↗

Impact of repeated prolonged exercise bouts on cardiac function and biomarkers.

PURPOSE: The present study examined the impact of repeated bouts of prolonged (< 60 min) exercise on left ventricular function and cardiac biomarkers. METHODS: Ten athletes completed a 15.3-mile hill run on three consecutive days and were assessed before, immediately after, 1 h after, and 20 h after each bout. Six of the athletes completed a fourth bout. Left ventricular (LV) function was examined echocardiographically using two-dimensional M-mode, Doppler, and flow propagation velocity (Vp). Venous blood samples were analyzed for cardiac biomarkers including cardiac troponin T (cTnT). RESULTS: Ejection fraction (EF) significantly decreased (P = 0.027) after the third exercise bout compared with baseline (mean +/- SD: 56.3 +/- 4.4 vs 51.3 +/- 5.9%), accompanied by a nonsignificant decrease in systolic blood pressure/end systolic volume (SBP/ESV) ratio. A sustained depression in systolic function 20 h after bout 3 also persisted in the subset who completed a fourth bout, yet this did not reach clinical levels. Significant (P < 0.01) reductions in early to late diastolic filling (E:A) ratio pre-to post-bout 1 (mean +/- SD: 1.9 +/- 0.5 vs 1.4 +/- 0.3) and pre- to post-bout 3(2.0 +/- 0.5 vs 1.3 +/- 0.4) normalized after each 20-h recovery period. A similar pattern of change was observed in Vp. Cardiac troponin T was elevated in four individuals 1 h after bout 1 (range: 0.013-0.125 microg.L(-1)) but was undetectable thereafter except in one athlete. CONCLUSION: Repeated bouts of prolonged exercise induce short-term reductions in diastolic filling and a cumulative decrease in systolic function, yet these alterations seem to have minimal clinical or functional impact. Elevated cTnT after the initial bout, but not thereafter, may represent an adaptive response to prolonged exercise.

Adult↗

Angiotensin-converting enzyme genotype predicts cardiac and autonomic responses to prolonged exercise.

OBJECTIVES: The purpose of this study was to investigate the phenomenon of left ventricular (LV) dysfunction after ultraendurance exercise. BACKGROUND: Subclinical LV dysfunction in response to endurance exercise up to 24 h duration has been described, but its mechanism remains elusive. METHODS: We tested 86 athletes before and after the Adrenalin Rush Adventure Race using echocardiography, impedance cardiography, and plasma immunoassay. RESULTS: At baseline, athletes demonstrated physiology characteristic of extreme endurance training. After 90 to 120 h of almost-continuous exercise, LV systolic and diastolic function declined (fractional shortening before the race, 39.6 +/- 0.65%; after, 32.2 +/- 0.84%, p < 0.001; mitral inflow E-wave deceleration time before the race, 133 +/- 5 ms; after, 160 +/- 5 ms, n = 48, p < 0.001) without change in loading conditions as defined by LV end-diastolic dimension and total peripheral resistance estimated by thoracic impedance. There was a compensatory increase in heart rate (before, 55 +/- 1.3 beats/min; after, 59 +/- 1.5 beats/min, p = 0.05), which left cardiac output unchanged, as well as significant-but-subclinical increases in brain natriuretic peptide and troponin I. In addition, we found that athletes who were homozygous for the intron-16 insertion polymorphism of the angiotensin-converting enzyme (ACE) gene exhibited a significantly greater decrease in fractional shortening than athletes who were homozygous for the deletion allele. Heterozygotes showed an intermediate phenotype. In addition, the deletion group manifest an enhanced sympathovagal balance after the race, as evidenced by greater power in the low-frequency component of blood pressure variability. CONCLUSIONS: The ACE genotype predicts the extent of reversible subclinical LV dysfunction after prolonged exercise and is associated with a differential postactivity augmentation of sympathetic nervous system function that may explain it.

Adult↗

Novel application of flow propagation velocity and ischaemia-modified albumin in analysis of postexercise cardiac function in man.

The present study employed novel echocardiographic tools and cardiac markers to obtain a greater understanding of the aetiology and time course of altered cardiac function and cardiac damage following prolonged exercise and, in particular, the possible role of transient ischaemia within these phenomena. Fourteen runners in the 2004 London Marathon were assessed pre-, immediately post-, 1 h post- and 24 h postcompletion of the race. Left ventricular function was examined echocardiographically using 2-D, M-mode, tissue Doppler imaging and flow propagation velocity (Vp). Venous blood samples were analysed for N-terminal pro-B-type natriuretic peptide (proBNP), cardiac troponin T (cTnT) and ischaemia-modified albumin (IMA). Left ventricular (LV) diastolic filling was altered on completion of the race, as indicated by significant decreases in mean early to late diastolic myocardial wave (E':A') ratio and Vp (from 1.82 +/- 0.9 to 1.32 +/- 0.32, and from 67.5 +/- 9.3 to 60.2 +/- 8.2 cm s(-1), respectively, P < 0.05), accompanied by an increase in proBNP (from 21.6 +/- 11 to 47.08 +/- 19.5 pg l(-1), P < 0.05). The observed reduction in LV diastolic filling following completion of a marathon, unrelated to changes in heart rate or loading parameters, indicates an intrinsically mediated change in diastolic filling. Exercise-induced elevations in cTnT in nine individuals (range, 0.023-0.37 microg l(-1)) were indicative of minor cardiac damage. A significant reduction in IMA was observed after the marathon (from 63.68 +/- 9.83 to 44.94 +/- 16.13 Um l(-1), P < 0.05), unrelated to the alterations in cardiac function, proBNP or cTnT. The absence of an elevation in IMA suggests that exercise-induced myocardial ischaemia did not occur and therefore could not explain the changes in cardiac function or biomarkers. Future studies in this area should investigate alternative diagnostic tools for the detection of transient ischaemia, and other potential mechanisms, in order to extend the understanding of this phenomenon.

Adult↗

The impact of marathon running upon ventricular function as assessed by 2D, Doppler, and tissue-Doppler echocardiography.

The impact of prolonged exercise upon right ventricular (RV) function is poorly understood and to date no studies have utilized tissue-Doppler imaging (TDI). Thirty-five marathon runners (age range 18-50 years) volunteered for the study. Two-dimensional, pulsed Doppler, and TDI studies were performed one day before and immediately following race completion. Right and left ventricular (LV) longitudinal TDI myocardial velocities were acquired from the tricuspid annulus and mitral annulus, providing velocity data during systole (S'), early diastole (E'), and late diastole (A'). Transtricuspid and transmitral, early diastolic (E), and late diastolic (A) velocities and ratios were assessed using conventional pulsed-wave Doppler. RV and LV fractional area changes (FAC) were calculated from RV and LV end-diastolic and end-systolic areas recorded from 2D scans in a subsample (n = 23). RV myocardial velocities were unchanged pre-post race in S' (21.1 +/- 2.7 to 21.7 +/- 4.5 cm s(-1), P > 0.05), reduced in E' (23.3 +/- 3.5 to 19.9 +/- 5.3 cm s(-1), P < 0.05), increased in A' (19.1 +/- 3.6 to 23.7 +/- 6.8 cm s(-1), P < 0.05) with a resultant decline in E'/A' (1.28 +/- 0.36 to 0.94 +/- 0.45, P < 0.05). This pattern of data was mirrored in the LV. Similarly both pulsed-Doppler tricuspid and mitral E/A ratios decreased from pre- to postrace (P < 0.05). FAC for the RV and LV were unaltered postrace (P > 0.05). The impact of differing age, finishing time (173-330 min), hemodynamic loading and heart rate upon RV and LV function pre- to postrace was negligible. In conclusion, TDI and 2D data, for both the RV and LV demonstrated little change in systolic function after a marathon race. Conversely, a reduction in diastolic function was observed in both ventricles for which a mechanism has yet to be deduced.

Adolescent↗

Left ventricular function immediately following prolonged exercise: A meta-analysis.

PURPOSE: Evidence supporting cardiac fatigue following prolonged endurance exercise remains equivocal. The purpose of this meta-analysis was to quantify all data fulfilling the specified inclusion criteria, examining the short-term effect of prolonged endurance exercise on left ventricular function. METHODS: A random effects meta-analysis of the weighted mean change in ejection fraction (EF), systolic blood pressure/end systolic volume (SBP/ESV) ratio, and early-to-late diastolic filling (E/A) was conducted on 23 studies using the SE of the between-subjects SD. HR, SBP, and left ventricular internal diameter during diastole (LVIDd) were also analyzed. Studies were coded according to exercise duration and training status: moderate duration trained (MDt) and untrained (MDu), 60-150 min; long duration (LD), 166-430 min; and ultra duration (UD), 640-1440 min. Relationships were assessed via Pearson's product-moment correlation. RESULTS: A significant (P < 0.05) overall decrease in EF (mean, confidence interval (CI): -1.95%, -1.03 to -2.88%), SBP/ESV (mean, CI: -0.8, -0.63 to -0.97), and E/A (mean, CI: -0.45, -0.39 to -0.51) was observed. Only UD and MDu subgroups demonstrated a reduction in EF. All subgroups demonstrated significant (P < 0.05) decreases in E/A. Alterations in LVIDd and SBP were related to respective decreases in EF and SBP/ESV, but not to E/A. CONCLUSION: The decrease in EF and SBP/ESV observed in UD and MDu indicates a reduction in systolic function, partially explained by altered cardiac loading. A decrease in E/A in all subgroups, unrelated to changes in loading, suggests an intrinsic impairment of left ventricular relaxation. Future investigators should employ load-independent indices of cardiac function and attempt to uncover the mechanisms of this phenomenon.

Echocardiography↗

Impact of marathon running on cardiac structure and function in recreational runners.

The present study examined the relationship between LV (left ventricular) function, markers of cardiac-specific damage and markers of oxidative stress in recreational runners following a marathon. Runners (n=52; 43 male and nine female; age, 35+/-10 years; height, 1.74+/-0.08 m; body mass, 75.9+/-8.9 kg) were assessed pre- and immediately post-marathon. LV function was assessed using standard M-mode two-dimensional Doppler echocardiography and TDI (tissue-Doppler imaging) echocardiography. Serum was analysed for cTnT (cardiac troponin-T), TEAC (Trolox equivalent antioxidant capacity; a measure of total antioxidant capacity), MDA (malondealdehyde) and 4-HNE (4-hydroxynonenal). A strong relationship was observed between standard and TDI echocardiography for all functional measures. Diastolic function was altered post-marathon characterized by a reduction in E (peak early diastolic filling: 0.79+/-0.11 compared with 0.64+/-0.16 cm/s; P<0.001), an increase in A (peak late diastolic filling: 0.48+/-0.11 compared with 0.60+/-0.12 cm/s; P<0.001) and a resultant decrease in E/A (ratio of E to A; 1.71+/-0.48 compared with 1.10+/-0.31; P<0.001). Ejection fraction remained unchanged post-marathon. Thirty-two runners presented with cTnT values above the lower limit of detection for the assay (0.01 microg/l), and 20 runners presented post-marathon with cTnT values above the acute myocardial infarction cut-off value (0.05 microg/l). No significant correlations were observed between cTnT and any functional measurements. MDA (2.90+/-1.58 compared with 3.59+/-1.47 micromol/l) and TEAC (1.80+/-0.12 compared with 1.89+/-0.21 mmol/l) were significantly increased post-marathon, but were unrelated to changes in function or cTnT. In conclusion, the present study demonstrated a reduction in diastolic function and widespread evidence of minimal cardiac damage following a marathon in recreational runners. The mechanism(s) underpinning the altered function and appearance of cTnT appear unrelated to reactive oxygen species.

Adolescent↗

Are there limits to running world records?

PURPOSE: Previous researchers have adopted linear models to predict athletic running world records, based on records recorded throughout the 20th century. These linear models imply that there is no limit to human performance and that, based on projected estimates, women will eventually run faster than men. The purpose of this article is to assess whether a more biologically sound, flattened "S-shaped" curve could provide a better and more interpretable fit to the data, suggesting that running world records could reach their asymptotic limits some time in the future. METHODS: Middle- and long-distance running world record speeds recorded during the 20th century were modeled using a flattened S-shaped logistic curve. RESULTS: The logistic curves produce significantly better fits to these world records than linear models (assessed by separating/partitioning the explained variance from the logistic and linear models using ANOVA). The models identify a slow rise in world-record speeds during the early year of the century, followed by a period of "acceleration" in the middle of the century (due to the professionalization of sport and advances in technology and science), and a subsequent reduction in the prevalence of record-breaking performances towards the end of the century. The model predicts that men's world records are nearing their asymptotic limits (within 1-3%). Indeed, the current women's 1500-m world record speed of 6.51 m x s(-1) may well have reached its limit (time 3:50.46). CONCLUSIONS: Many of the established men's and women's endurance running world records are nearing their limits and, consequently, women's world records are unlikely to ever reach those achieved by men.

Competitive Behavior↗

Acute sleep responses in a normobaric hypoxic tent.

PURPOSE: Sleeping in a hypoxic environment is becoming increasingly popular among athletes attempting to simulate a "live high, train low" training regime. The purpose of this study was to investigate the acute effects (one night) of sleeping in a normobaric hypoxic tent (NH) (PO(2) = 110 mm Hg approximately 2500 m) upon markers of sleep physiology and quality, compared with sleep in a normal ambient environment (BL) (PO(2) = 159 mm Hg approximately sea level) and sleep in a normobaric normoxic tent (NN) (PO(2) = 159 mm Hg). METHODS: Eight male recreational athletes (age 34.5 +/- 6.9 yr; stature 169.1 +/- 8.7 cm; mass 69.3 +/- 8.2 kg; VO(2max) 56.4 +/- 8.3 mL.kg(-1).min(-1)) participated in the study using a randomized, double-blind crossover design. Polysomnographic studies were undertaken to measure sleep stages, arterial oxygen saturation (SpO(2)), heart rate (HR), and the Respiratory Disturbance Index (RDI). The Leeds Sleep Evaluation Questionnaire (LSEQ) was used to measure subjective sleep quality. RESULTS: NH (89.9 +/- 4.8%) resulted in a significantly lower (P < 0.05) SpO(2) compared with both BL (95.7 +/- 1.5%) and NN (93.5 +/- 4.0%). Heart rate was significantly higher (P < 0.05) in NH (51.5 +/- 7.6 beats.min(-1)) compared with NN (48.3 +/- 6.9 beats.min(-1)) but was similar versus BL (50.3 +/- 4.3 beats.min(-1)). RDI (counts.h) and RDI (total counts) were lowest in BL (3.5 +/- 2.5; 18.1 +/- 7.9) and highest in NH (36.8 +/- 42.7; 221.9 +/- 254.5). The difference in RDI (counts.h(-1) and total counts) between NH and BL was significant (P < 0.05). The LSEQ revealed that subjects' "behavior following waking" score was significantly (P < 0.05) lower in NH (40.9 +/- 9.2) compared with BL (52.3 +/- 8.3). CONCLUSION: This study presents evidence that sleep in a normobaric hypoxic tent at a simulated altitude of 2500 m may affect sleep parameters in some individuals. This type of analysis may be useful in the early identification of poorly responding individuals to simulated altitude environments.

Adult↗

Altered cardiac function and minimal cardiac damage during prolonged exercise.

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 MB(mass) (CK-MB(mass)), 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-MB(mass) 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.

Adult↗

The impact of prolonged exercise in a cold environment upon cardiac function.

PURPOSE: The purpose of the present study was to examine the impact of cold exposure coupled with prolonged exercise upon postexercise left ventricular (LV) function and markers of myocardial damage. METHODS: colon; Eight highly trained male athletes (mean +/- SD; age: 28.2 +/- 8.8 yr; height: 1.78 +/- 0.07 m; body mass: 74.9 +/- 7.6 kg; VO2max: 65.6 +/- 7.0 mL x kg(-1) x min(-1)) performed two 100-mile cycle trials, the first in an ambient temperature of 0 degrees C, the second in an ambient temperature of 19 degrees C. Echocardiographic assessment was completed and blood samples drawn before, immediately postexercise, and 24-h postexercise. Left ventricular systolic (stroke volume [SV], ejection fraction [EF], and systolic blood pressure/end systolic volume ratio [SBP/ESV]) and diastolic (early [E] to late [A] filling ratio [E:A]) parameters were calculated. Serum was analyzed for creatine kinase isoenzyme MB (CK-MBmass) and cardiac troponin T (cTnT). cTnT was analyzed descriptively whereas other variables were assessed using two-way repeated-measures ANOVA. RESULTS: No significant change was observed in systolic function across time or between trials. A significant difference between trials was observed in E:A immediately after exercise (1.4 +/- 0.4 [19 degrees C] vs 1.8 +/- 0.3 [0 degrees C]) (P < 0.05). CK-MBmass was significantly elevated immediately after exercise in both trials (P < 0.05). Positive cTnT concentrations were observed in two subjects immediately after the 19 degrees C trial (0.012 microg x L(-1) and 0.034 microg x L(-1)). CONCLUSIONS: Cycling 100 miles in an ambient temperature of 19 degrees C is associated with an acute change in diastolic filling that is not observed after prolonged exercise at 0 degrees C. Prolonged exercise is associated with minimal cardiac damage in some individuals; it appears that this is a separate phenomenon to the change in diastolic filling.

Adult↗

Postexercise left ventricular function and cTnT in recreational marathon runners.

PURPOSE: To assess the impact of prolonged exercise on left ventricular (LV) function and the appearance of cardiac troponin T (cTnT) in older and recreational athletes. METHODS: Heart rate (HR), blood pressures, and cTnT were recorded in 35 subjects (age range 22-57 yr, finishing time 157-341 min) pre- and postrace. Echocardiograms (N = 26) assessed stroke volume (SV), ejection fraction (EF), sBP/LV end-systolic volume (sBP/ESV), diastolic filling (E:A ratio) as well as preload (LV internal dimension at end-diastole [LVIDd]) and afterload (LV wall stress). HR and core temperature were recorded in-event. Prepost changes in LV function were analyzed by repeated measures t-test. Delta scores for LV function and cTnT data were correlated with each other, age, finishing time, alterations in loading, and in-event data. RESULTS: SV was significantly decreased postrace (109 +/- 31 vs 85 +/- 25 mL, P < 0.05) likely due to a significant decrease in LVIDd (5.3 +/- 0.4 vs 4.9 +/- 0.5 cm, P < 0.05; r = 0.80, P < 0.05). LV wall stress was unchanged postrace (90 +/- 25 vs 89 +/- 27 g x cm(-2), P > 0.05). EF (70 +/- 12 vs.70 +/- 10%, P > 0.05) and sBP/ESV (3.7 +/- 2.9 vs 4.0 +/- 2.0, P > 0.05) did not change prepost race and were not related to age or finishing time (P > 0.05). E:A ratio was significantly reduced postrace (1.73 +/- 0.38 vs 1.41 +/- 0.25, P < 0.05) and could not be explained by an increased HR (56 +/- 9 vs 84 +/- 10, P < 0.05; r = 0.08, P > 0.05), a reduced LVIDd (r = 0.11, P > 0.05), age, finishing time, or in-event data. Postrace 26/33 subjects presented cTnT values in the range 0.024-0.080 microg x L(-1) that were not related to changes in LV function, loading, age, finishing time, or in-event data. CONCLUSION: No evidence of load-independent depression in LV systolic function was reported. Changes in cTnT and E:A were not related, and their etiology is uncertain.

Adult↗

The cardiospecificity of the third-generation cTnT assay after exercise-induced muscle damage.

PURPOSE: The purpose of the present study was to examine the cardiospecificity of cTnI and the new third-generation cTnT assay, in the presence of exercise-induced muscle damage in highly trained individuals, and to examine the impact of a maximal-ramping treadmill test on cardiac function. METHODS: Eight highly trained male triathletes (mean +/- SD; age: 29 +/- 9 yr; height: 1.79 +/- 0.10 m; body mass: 77 +/- 10 kg; .VO(2max): 67.4 +/- 6.3 mL.kg(-1).min(-1)) completed two bouts of exercise. On the first occasion, subjects completed a maximal-ramping treadmill test. On a separate occasion, the subjects completed 30 min of downhill running (15% gradient) at a speed equivalent to 70% of maximal running velocity attained during the maximal-ramping treadmill test. All subjects were assessed using ECG, echocardiography, and blood analysis. Measurements were taken at rest, immediately after, and 48 h postexercise for each bout of exercise. Echocardiographic analysis was used to determine left ventricular systolic and diastolic function. Blood samples were analyzed for markers of myocyte damage. RESULTS: Echocardiographic results indicated normal left ventricular function before and after both exercise bouts. Total CK and CKMB were significantly elevated 48 h after the downhill run. cTnT and cTnI were not elevated at any stage of the study. CONCLUSIONS: Neither the maximal-ramping treadmill test nor the 30-min downhill run produced cardiac dysfunction or myocardial damage in young, healthy trained subjects. The elevated total CK and CKMB within the downhill study are noncardiac in origin as demonstrated by the lack of cTnT and cTnI. The cTnI and new third-generation cTnT assays may be used to detect cardiac damage in the presence of elevated total CK and CKMB associated with exercise-induced skeletal muscle damage.

Adult↗