Natalie Middleton

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

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.

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 μg 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.

Postexercise Changes in Left Ventricular Function: The Evidence So Far

Whether prolonged exercise results in a transient depression in left ventricular (LV) function has been the focus of numerous studies since the 1960s. This review attempts to summarize the findings of this growing body of research. Understanding in this area has followed the advances in imaging techniques and specifically in echocardiographic technology. As such, the review focuses on evidence from the traditional echocardiographic technology (two-dimensional and Doppler measures), the more advanced technique of tissue Doppler imaging (TDI), and finally the assessment of myocardial strain and strain rate. Although many of the studies have adopted a similar cross-sectional pre- to postexercise design, there are often significant differences in terms of subject characteristics, exercise duration, and exercise modality. Accordingly, we draw together the common findings from this growing body of research in an attempt to reach a consensus regarding the influence of prolonged exercise on LV function.

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.

Changes in respiratory muscle and lung function following marathon running in man

Abstract Respiratory muscle fatigue has been reported following short bouts of high-intensity exercise, and prolonged, moderate-intensity exercise, as evidenced by decrements in inspiratory and expiratory mouth pressures. However, links to functionally relevant outcomes such as breathing effort have been lacking. The present study examined dyspnoea and leg fatigue during a treadmill marathon in nine experienced runners. Maximal inspiratory and expiratory pressure, peak inspiratory and expiratory flow, forced vital capacity, and forced expiratory volume in one second were assessed before, immediately after, and four and 24 hours after a marathon. During the run, leg effort was rated higher than respiratory effort from 18 through 42 km (P < 0.05). Immediately after the marathon, there were significant decreases in maximal inspiratory pressure and peak inspiratory flow (from 118 ± 20 cm H2O and 6.3 ± 1.4 litres · s−1 to 100 ± 22 cm H2O and 4.9 ± 1.5 litres · s−1 respectively; P < 0.01), while expiratory function remained unchanged. Leg maximum voluntary contraction force was significantly lower post-marathon. Breathing effort correlated significantly with leg fatigue (r = 0.69), but not inspiratory muscle fatigue. Our results confirm that prolonged moderate-intensity exercise induces inspiratory muscle fatigue. Furthermore, they suggest that the relative intensity of inspiratory muscle work during exercise makes some contribution to leg fatigue.

The effect of prolonged endurance exercise upon blood pressure regulation during a postexercise orthostatic challenge

Objective To investigate the regulation of blood pressure in response to an orthostatic challenge in athletes running a marathon. Methods 10 experienced male runners (mean (SD) age 29 (4) years) were tested on the day prior to the 2004 London Marathon, and again immediately postrace (race time 210 (36) min). In addition, 6 of the subjects were retested 24 h postrace. During each examination, beat-to-beat systolic arterial blood pressure (SBP) and heart rate (HR) were measured, and stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) were estimated via arterial transmural pressure waveforms during 3 min in a supine position and then during 3 min of upright, unsupported standing. Data were averaged over 20 s epochs, and the final 20 s of each posture were compared prerace and postrace via repeated measures 2-way ANOVA. Results Prerace SBP in standing increased only moderately when compared with supine values (2 (9) mm Hg, NS). This was accompanied by an increase in HR (13 (7) beats/min, p<0.05), as well as a decrease in SV (16 (9) ml, p<0.05). However, there was little change in CO (−0.13 (0.97) litres/min, NS) or TPR (0.047 (0.280) medical units (MU), NS). Postrace SBP significantly decreased from supine to standing (−15 (20) mm Hg, p<0.05). The change in SBP was accompanied by an increase in HR (19 (6) beats/min, p<0.05) and a reduction in SV (26 (14) ml, p<0.05) and CO (−1.02 (1.39) litres/min, p = 0.05). Postrace there was no change in TPR (0.366 (0.607) MU, NS) upon standing. The orthostatic adjustments in SBP, HR and CO were greater than at prerace (p<0.05). The postrace orthostatic challenge resulted in only one subject experiencing presyncopal symptoms. At 24 h postrace, cardiovascular responses to an orthostatic challenge mirrored those at prerace. Conclusions Following prolonged exercise, a fall in systolic blood pressure during orthostasis results from an inadequately compensated decrease in SV and resultant CO during standing.

Echocardiograph-determined Left Ventricular Function Immediately After Prolonged Exercise: a Meta-analysis

Exercise-induced acute cardiac fatigue (EACF) is characterised by a reduction in left ventricular function immediately following prolonged athletic events. Individual studies on EACF have involved small sample sizes (n<20) and have differed in the selected exercise duration and the training statu