Biomedical subjects

Rob Shave

Publications and source records attributed to Rob Shave.

9 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↗

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

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

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↗

PubMed2003

Does the human heart fatigue subsequent to prolonged exercise?

A reduction in left ventricular systolic and diastolic function subsequent to prolonged exercise in healthy humans, often called exercise-induced cardiac fatigue (EICF), has recently been reported in the literature. However, our current understanding of the exact nature and magnitude of EICF is limited. To date, there is no consensus as to the clinical relevance of such findings and whether such alterations in function are likely to impact upon performance. Much of the existing literature has employed field-based competitions. Whilst ecologically valid, this approach has made it difficult to control many factors such as the duration and intensity of effort, fitness and training status of subjects and environmental conditions. The impact of such variables on EICF has not been fully evaluated and is worthy of further research. To date, most EICF studies have been descriptive, with limited success in elucidating mechanisms. To this end, the assessment of humoral markers of cardiac myocyte or membrane disruption has produced contradictory findings partially due to controversy over the validity of specific assays. It is, therefore, important that future research utilises reliable and valid biochemical techniques to address these aetiological factors as well as develop work on other potential contributors to EICF such as elevated free fatty acid concentrations, free radicals and beta-adrenoceptor down-regulation. In summary, whilst some descriptive evidence of EICF is available, there are large gaps in our knowledge of what specific factors related to exercise might facilitate functional changes. These topics present interesting but complex challenges to future research in this field.

Cardiomyopathies↗

PubMedDate not supplied

Effect of weightlifting upon left ventricular function and markers of cardiomyocyte damage.

The purpose of this study was to assess left ventricular (LV) function and biochemical markers of myocyte after prolonged weightlifting activity. Seventeen male subjects (age range 20-34 years) performed a 90-min bout of weightlifting exercise consisting of three sets of 8-10 repetitions at 70% one-repetition maximum. Body mass, heart rate, systolic blood pressure (SBP) and echocardiographically determined indices of LV loading (LV internal diameter during diastole, LV meridonial wall stress), systolic function (stroke volume (SV), ejection fraction (EF), end-systolic pressure volume relationship; SBP/ESV) and diastolic filling (ratio of early to late; E:A) were obtained pre-exercise, immediately after and 24 h post-exercise. A 5-ml venous blood sample was obtained for the assessment of cardiac troponin T (cTnT) via third generation electrochemiluminescence assay. Data were assessed via one-way ANOVA and Pearson's correlation. Although SV declined (80.9 +/- 18.3 vs. 66.9 +/- 17.2, p < 0.05) there was no alteration in LV contractility (EF 62 +/- 6 vs. 59 +/- 7; SBP/ESV 3.51 +/- 1.4 vs. 3.51 +/- 1.4, p > 0.05). The E:A ratio was significantly decreased following exercise (1.78 +/- 0.41 vs. 1.33 +/- 0.37, p < 0.05). This decrease was not fully explained by loading conditions (r2 = 0.05 to 0.24). All values returned to baseline 24 h post-exercise. No cTnT was reported in any of the blood samples. In conclusion, there was no significant evidence of any LV contractile depression and no cTnT was observed post exercise. The small reduction in diastolic filling could not be explained by changes in haemodynamic loading or the post-exercise elevation in heart rate.

Adult↗