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Biomedical subjects

Keith George

Publications and source records attributed to Keith George.

At least 19 recordsLinked to original sources
PubMed2007

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↗
PubMed2007

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↗
PubMed2006

Corticomotor excitability contributes to neuromuscular fatigue following marathon running in man.

It is unknown whether changes in corticomotor excitability follow prolonged exercise in healthy humans. Furthermore, the role of supraspinal fatigue in decrements of force production and voluntary activation following prolonged exercise has not been established. This study investigated peripheral and central fatigue after a marathon (42.2 km) on a treadmill. Isometric ankle dorsiflexion force and electromyographic responses of the tibialis anterior in response to magnetic stimulation of the peroneal nerve (PNMS) and the motor cortex (TMS) were measured before, immediately after, 4 and 24 h post-marathon (MAR) in nine volunteers (mean +/- s.d. completion time, 208 +/- 22 min). Maximal voluntary contraction decreased by 18 +/- 7% immediately after MAR (P = 0.009) and remained significantly decreased after 4 h. The amplitude of the evoked response to TMS, but not to PNMS, was depressed immediately post-MAR by 57 +/- 25% (P = 0.04). Potentiated resting twitch force was reduced in response to both TMS and PNMS post-MAR (71 +/- 8 and 35 +/- 2% decrease, P = 0.035 and 0.037, respectively), and voluntary activation was reduced to 61.9 +/- 18% immediately post-MAR (P < 0.05). All measures had returned to baseline values after 24 h. These results suggest that fatigue was attributable to both a disturbance of the contractile apparatus within the muscle and submaximal output from the motor cortex.

Ankle Joint↗
PubMed2006

The effects of marathon running on expression of the complement regulatory proteins CD55 (DAF) and CD59 (MACIF) on red blood cells.

Exercise is known to result in the haemolysis of red blood cells (RBCs). Although mechanical stressors such as footstrike and an increased velocity of blood flow may be involved, the biological mechanisms that underpin RBC haemolysis remain elusive. RBCs are potentially susceptible to lysis by autologous complement activation. RBCs are protected from the lytic effects of complement by regulatory proteins (CRPs) bound to the cell membrane via glycosylphosphatidylinositol (GPI) anchors. This study aimed to determine if marathon running would result in RBC haemolysis through a loss of membrane expression of the CRPs CD55 (decay accelerating factor) and CD59 (membrane attack complex inhibitory factor). Blood samples were obtained from 14 male runners before, within 30 min after, and 24 h after completion of the 2004 London Marathon. RBCs were assessed for cell surface CD55 and CD59 expression using indirect immunofluorescence assays and flow cytometry. No significant changes in the total RBC count, haematocrit or haemoglobin concentrations were found in response to running the marathon (P > 0.05). Blood bilirubin concentrations after the marathon were significantly greater than the pre-race values (P < 0.01). The relative fluorescent intensity (arbitrary units) of CD55 and CD59 expression on RBC membranes did not change in response to the marathon race (P > 0.05). In conclusion, marathon running did not alter the expression of CD55 or CD59 on RBCs, despite concomitant elevations in blood bilirubin concentrations. Consequently, any haemolysis of RBCs that occurred in response to the marathon was not likely due to a loss of membrane bound CRPs and subsequent cell lysis by autologous complement.

Adult↗
PubMed2006

Beta-adrenergic receptor desensitization in man: insight into post-exercise attenuation of cardiac function.

Desensitization of the beta-adrenoreceptors (beta-AR) may contribute to a post-exercise reduction in left ventricular (LV) function. However, attenuation of the chronotropic and inotropic responses to a beta-AR agonist may depend upon alterations in parasympathetic tone. Furthermore, changes in cardiac output and LV diastolic function in response to a beta-AR agonist, pre- to post-prolonged exercise, remain unclear. Seven trained males (mean+/-s.d., age 27+/-6 years) performed 4 h of ergometer rowing. Peak heart rate (HR) and LV systolic and diastolic functional responses to incremental isoproterenol (isoprenaline) infusion (2, 4 and 6 microg kg min-1) were assessed after vagal blockade (glycopyrrolate, 1.2 mg). LV systolic function was assessed by the pressure/volume ratio (systolic blood pressure/end systolic volume) and , whilst diastolic function was evaluated as peak early and late transmitral filling velocities. Following exercise, the pressure/volume ratio decreased by 25% (P<0.05), whereas was unchanged (P>0.05). The early/late filling ratio was reduced by 36% after exercise, due to an elevation in late LV filling (P<0.01). The increase in HR response to isoproterenol infusion was blunted post-exercise at both 4 and 6 microg kg min-1 (127+/-7 and 132+/-6 beats min-1) compared with pre-exercise (138+/-8 and 141+/-12 beats min-1, P<0.05). Additionally, the pressure/volume ratio and were blunted post-exercise in response to isoproterenol (P<0.05). In contrast, diastolic function was similar before and after exercise during isoproterenol infusion (P>0.05). Desensitization of the beta-AR contributes to an attenuated left ventricular systolic but not diastolic function following prolonged exercise.

Adrenergic beta-Agonists↗
PubMed2006

Reactivity of ambulatory blood pressure to physical activity varies with time of day.

Blood pressure (BP) fluctuates over a 24-hour period, but it is unclear to what extent this variation is governed completely by changes in physical activity. Our aim was to use a BP "reactivity index" to investigate whether the BP response to a given level of physical activity changes during a normal sleep-wake cycle. Hypertensive patients (n=440) underwent simultaneous 24-hour ambulatory BP, heart rate (HR), and activity monitoring. BP and HR were measured every 20 minutes. Actigraphy data were averaged over the 15 minutes that preceded a BP measurement. Individual BP and HR reactivity indices were calculated using least-squares regression for twelve 2-hour periods. These indices were then analyzed for time-of-day differences using a general linear model. Systolic BP and HR were generally more reactive to physical activity than diastolic BP. The highest reactivity of systolic BP (mean+/-SE=4+/-1 mm Hg per logged unit change in activity) was observed between 8:00 AM and 10:00 AM (P=0.014). Between 10:00 AM and 12:00 PM, BP reactivity then decreased (P=0.048) and showed a secondary rise in the early afternoon. These 24-hour changes in BP reactivity did not differ significantly between groups formed on the basis of early and late wake times (P=0.485), medication use, age, and sex (P>0.350). In conclusion, under conditions of normal living, the reactivity of BP and HR to a given unit change in activity is highest in the morning and shows a secondary rise in the afternoon.

Adult↗
PubMed2006

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↗
PubMed2006

Cardiac and vascular adaptations to exercise.

PURPOSE OF REVIEW: To briefly review some recent studies of cardiac and vascular adaptation to acute exercise and exercise training. RECENT FINDINGS: Recent studies have suggested that prolonged strenuous bouts of exercise may be associated with transient impairment in systolic and diastolic function, referred to as 'cardiac fatigue'. Furthermore, some studies have reported increased circulating concentrations of cardiac troponins and brain natriuretic peptide following prolonged endurance exercise, suggestive of possible myocyte damage or impairment. Meanwhile, emerging studies of the effects of exercise training on diastolic function are somewhat conflicting; the discrepancies may relate to variability in study designs, indices selected to represent diastolic function or timing of measurements around training cycles. Finally, recent studies of vascular structure and function confirm established evidence for remodelling of large and small arteries and improvement in vascular function with exercise training. SUMMARY: Emerging evidence suggests that prolonged strenuous exercise may be associated with 'cardiac fatigue' or 'cardiac damage', although the clinical implications remain obscure. Vascular adaptations to training improve vasomotor function and induce arterial enlargement, favouring decreased atherothrombotic risk.

Adaptation, Physiological↗
PubMed2006

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↗
PubMed2006

Longitudinal and radial systolic myocardial tissue velocities after prolonged exercise.

We assessed segmental and global left ventricular (LV) systolic function using tissue Doppler imaging (TDI) in 30 subjects (age: 18-62 y) before and after a marathon race. Longitudinal plane systolic (S') TDI velocities were assessed at 5 sites on the mitral annulus and radial plane S' velocities were assessed at the LV septal and free wall in a subsample (n = 9). Heart rate (HR) and LV diastolic internal dimension were also assessed before (pre) and immediately after (post) the race. Pre-post changes in all variables were analysed by repeated measures analysis of variance (ANOVA). Delta scores for TDI data were correlated with alterations in indices of LV loading, as well as with age and finishing time. Segmental longitudinal and radial TDI velocities were not significantly different pre to post race (p > 0.05), which resulted in no change in mean S' velocities (longitudinal: pre 17.0 +/- 3.4 cm x s(-1), post 17.4 +/- 4.0 cm x s(-)1; radial: pre 13.0 +/- 5.4 cm x s(-1), post 14.2 +/- 7.1 cm x s(-1); p > 0.05). Any pre-post changes in TDI data were not related to an elevated post race HR (r = 0.15, p > 0.05), a decreased post race LV internal dimension in diastole (r = 0.10, p > 0.05), age (r = -0.25, p > 0.05), or finishing time (r = -0.13, p > 0.05). Our data suggest that marathon running does not induce any segmental or global depression in LV systolic function.

Adolescent↗
PubMed2006

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↗
PubMed2006

Chronobiological considerations for exercise and heart disease.

Although regular physical activity is beneficial for many clinical conditions, an acute bout of exercise might increase the risk of an adverse clinical event, such as sudden cardiac death or myocardial infarction, particularly in vulnerable individuals. Since it is also known that the incidence of these events peaks in the morning and that some cardiac patients prefer to schedule leisure-time physical activity before lunch, the question arises as to whether morning exercise is 'inherently' more risky than physical activity performed at other times of day. We attempt to answer this question by reviewing the relevant epidemiological data as well as the results of chronobiological and exercise-related studies that have concentrated on the pathophysiological mechanisms for sudden cardiac events. We also consider generally how chronobiology might impact on exercise prescription in heart disease. We performed a structured literature search in the PubMed and WEBofSCIENCE databases for relevant studies published between 1981 and 2004. The limited amount of published epidemiological data did not allow us to conclude that a bout of vigorous exercise in the morning increases the relative risk of either primary cardiac events in apparently healthy individuals, or secondary events in cardiac patients enrolled in supervised exercise programmes. Nevertheless, these data are not directly relevant to individuals who have a history of heart disease and perform uncontrolled habitual activities. It appears as though the influence of time of day on the cardiovascular safety of this type of exercise has not been examined in this population. There is evidence that several pathophysiological variables (e.g. blood pressure, endothelial function, fibrinolysis) vary in parallel with typical diurnal changes in freely chosen activity. Nevertheless, few studies have been designed to examine specifically whether such variables respond differently to a 'set' level of exercise in the morning compared with the afternoon or evening. Even fewer researchers have adequately separated the influences of waking from sleep, adopting an upright posture and physical exertion per se on these pathophysiological responses at different times of day. In healthy individuals, exercise is generally perceived as more difficult and functional performance is decreased in the morning hours. These observations have been confirmed for patients with heart disease in only one small study. It has also not been confirmed, using an adequately powered study involving cardiac patients, that the responses of heart rate and oxygen consumption (VO(2)) to a set bout of exercise show the highest reactivity in the afternoon and evening, which is the case with healthy individuals. Confirmation of this circadian variation would be important, since it would mean that exercise might be prescribed at too high an intensity in the morning if heart rate or VO(2) responses are employed as markers of exercise load. We conclude that there is some parallelism between the diurnal changes in physical activity and those in the pathophysiological mechanisms associated with acute cardiac events. Nevertheless, more studies are needed to ascertain whether the responses of endothelial function, fibrinolysis and blood pressure to a set exercise regimen differ according to time of day. The results of epidemiological studies suggest that morning exercise is just as safe as afternoon exercise for cardiac patients enrolled in a supervised rehabilitation programme. Nevertheless, it is unclear whether time of day alters the risk of a cardiac event occurring during spontaneous physical activity performed by individuals with established risk factors for heart disease.

Circadian Rhythm↗
PubMed2005

Mitral annular myocardial velocity assessment of segmental left ventricular diastolic function after prolonged exercise in humans.

We assessed segmental and global left ventricular (LV) diastolic function via tissue-Doppler imaging (TDI) as well as Doppler flow variables before and after a marathon race to extend our knowledge of exercise-induced changes in cardiac function. Twenty-nine subjects (age 18-62 year) volunteered to participate and were assessed pre- and post-race. Measurements of longitudinal plane TDI myocardial diastolic velocities at five sites on the mitral annulus included peak early myocardial tissue velocity (E'), peak late (or atrial) myocardial tissue velocity (A') and the ratio E'/A'. Standard pulsed-wave Doppler transmitral and pulmonary vein flow indices were also recorded along with measurements of body mass, heart rate, blood pressures and cardiac troponin T (cTnT), a biomarker of myocyte damage. Pre- to post-race changes in LV diastolic function were analysed by repeated measures ANOVA. Delta scores for LV diastolic function were correlated with each other and alterations in indices of LV loading. Diastolic longitudinal segmental and mean TDI data were altered post-race such that the mean E'/A' ratio was significantly depressed (1.51 +/- 0.34 to 1.16 +/- 0.35, P < 0.05). Changes in segmental and global TDI data were not related to an elevated post-race HR, a decreased post-race pre-load or an elevated cTnT. The pulsed wave Doppler ratio of peak early transmitral flow velocity (E)/peak late (or atrial) flow velocity (A) was also significantly reduced post-race (1.75 +/- 0.46 to 1.05 +/- 0.30, P < 0.05); however, it was significantly correlated with post-race changes in heart rate. The lack of change in E/E' from pre- to post-race (3.4 +/- 0.8 and 3.3 +/- 0.7, respectively) suggests that the depression in diastolic function is likely to be due to altered relaxation of the left ventricle; however, the exact aetiology of this change remains to be determined.

Adolescent↗
PubMed2005

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↗
PubMed2004

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↗
PubMed2004

Effects of massage on limb and skin blood flow after quadriceps exercise.

PURPOSE: At present, there is little scientific evidence that postexercise manual massage has any effect on the factors associated with the recovery process. The purpose of this study was to compare the effects of massage against a resting control condition upon femoral artery blood flow (FABF), skin blood flow (SKBF), skin (SKT), and muscle (MT) temperature after dynamic quadriceps exercise. METHODS: Thirteen male volunteers participated in 3 x 2-min bouts of concentric quadriceps exercise followed by 2 x 6-min bouts of deep effleurage and pétrissage massage or a control (rest) period of similar duration in a counterbalanced fashion. Measures of FABF, SKBF, SKT, MT, blood lactate concentration (BLa), heart rate (HR), and blood pressure (BP) were taken at baseline, immediately after exercise, as well as at the midpoint and end of the massage/rest periods. Data were analyzed by two-way ANOVA. RESULTS: Significant main effects were found for all variables over time due to effects of exercise. Massage to the quadriceps did not significantly elevate FABF (end-massage 760 +/- 256 vs end-control 733 +/- 161 mL x min(-1)), MT, BL, HR, and BP over control values (P < 0.05). SKBF (end-massage 150 +/- 49 vs end control 6 +/- 4 au) SKT (end-massage 32.2 +/- 0.9 vs end-control 31.1 +/- 1.3degreesC) were elevated after the application of massage compared with the control trial (P < 0.05). CONCLUSION: From these data it is proposed that without an increase in arterial blood flow, any increase in SKBF is potentially diverting flow away from recovering muscle. Such a response would question the efficacy of massage as an aid to recovery in postexercise settings.

Adult↗