BackgroundThe cardiac consequences of undertaking endurance exercise are the topic of recent debate. The purpose of this review is to provide an update on a growing body of literature, focusing on left ventricular (LV) function following prolonged endurance exercise over 2 h in duration which have employed novel techniques, including myocardial speckle tracking, to provide a more comprehensive global and regional assessment of LV mechanics.MethodsProspective studies were filtered independently following a pre-set criteria, resulting in the inclusion of 27 studies in the analyses. A random-effects meta-analysis was used to determine the weighted mean difference and 95% confidence intervals (CI) of LV functional and mechanical data from pre-to-post-exercise. Narrative commentary was also provided where volume of available evidence precluded meta-analysis.ResultsA significant overall reduction in LV longitudinal strain (Ɛ) n = 22 (− 18 ± 1 to − 17 ± 1%; effect size (d) − 9: − 1 to − 0.5%), strain rate n = 10 (SR; d − 0.9: − 0.1.3 to − 0.5 l/s) and twist n = 5 (11.9 ± 2.2 to 8.7 ± 2.2°, d − 1: − 1.6 to − 0.3°) was observed following strenuous endurance exercise (range 120–1740 min) (P < 0.01). A smaller number of studies (n = 4) also reported a non-significant reduction in global circumferential and radial Ɛ (P > 0.05).ConclusionThe meta-analysis and narrative commentary demonstrated that a reduction in LV function and mechanics is evident following prolonged endurance exercise. The mechanism(s) responsible for these changes are complex and likely multi-factorial in nature and may be linked to right and left ventricular interaction.

This study focused on the influence of habitual endurance exercise training (i.e., committed runner or nonrunner) on the regulation of muscle sympathetic nerve activity (MSNA) and arterial pressure in middle-aged (50 to 63 yr, n = 23) and younger (19 to 30 yr; n = 23) normotensive men. Hemodynamic and neurophysiological assessments were performed at rest. Indices of vascular sympathetic baroreflex function were determined from the relationship between spontaneous changes in diastolic blood pressure (DBP) and MSNA. Large vessel arterial stiffness and left ventricular stroke volume also were measured. Paired comparisons were performed within each age category. Mean arterial pressure and basal MSNA bursts/min were not different between age-matched runners and nonrunners. However, MSNA bursts/100 heartbeats, an index of baroreflex regulation of MSNA (vascular sympathetic baroreflex operating point), was higher for middle-aged runners ( P = 0.006), whereas this was not different between young runners and nonrunners. The slope of the DBP-MSNA relationship (vascular sympathetic baroreflex gain) was not different between groups in either age category. Aortic pulse wave velocity was lower for runners of both age categories ( P < 0.03), although carotid β-stiffness was lower only for middle-aged runners ( P = 0.04). For runners of both age categories, stroke volume was larger, whereas heart rate was lower (both P < 0.01). In conclusion, we suggest that neural remodeling and upward setting of the vascular sympathetic baroreflex compensates for cardiovascular adaptations after many years committed to endurance exercise training, presumably to maintain arterial blood pressure stability. NEW & NOTEWORTHY Exercise training reduces muscle sympathetic burst activity in disease; this is often extrapolated to infer a similar effect in health. We demonstrate that burst frequency of middle-aged and younger men committed to endurance training is not different compared with age-matched casual exercisers. Notably, well-trained, middle-aged runners display similar arterial pressure but higher sympathetic burst occurrence than untrained peers. We suggest that homeostatic plasticity and upward setting of the vascular sympathetic baroreflex maintains arterial pressure stability following years of training.

A sustained-release formulation of a potent gonadotropin-releasing hormone (GnRH) agonist, Zoladex (D-Ser(But),6 Aza Gly10-GnRH; ICI 118,630; goserelin), was administered subcutaneously (3.6 mg/depot) to male rats once every 28 days for 2-24 wk to determine the extent to which pituitary-testis function could be suppressed and whether suppression was maintained throughout the period of treatment. Administration of Zoladex resulted in sustained decreases in weight of the testis, epididymis, seminal vesicles and prostate gland. The decreases were apparent within 2 wk of initiating treatment. Patchy degeneration of the seminiferous tubules and atrophy of the Leydig cells were observed, but did not progress beyond the degree observed after 1 month of treatment. Serum and testis testosterone were markedly depressed after 2 wk of treatment, as was testis [125I]hCG binding. Serum gonadotropins were also reduced by treatment. Serum androgen binding protein (ABP) was elevated, testis ABP content remained unchanged, and epididymal ABP content was reduced. The changes are consistent with the hypothesis that this compound affects both the anterior pituitary gland and the testis. These findings indicate that depot delivery systems are a convenient way to administer GnRH analogs for sustained treatment schedules.

Changes in the arterial baroreflex arc contribute to elevated sympathetic outflow and altered reflex control of blood pressure with human ageing. Utilizing ultrasound and sympathetic microneurography (muscle sympathetic nerve activity; MSNA)we investigated the relationships between aortic and carotid artery wall tension (indices of baroreceptor activation) andthe vascular sympathetic baroreflex operating point (OP; MSNA burst incidence) in healthy, normotensive young (n = 27, 23 ± 3 years) and middle-aged men (n = 22, 55 ± 4 years).In young men, the OP was positively related to the magnitude and rate of unloading and time spent unloaded in the aortic artery (r = 0.56, 0.65 and 0.51, P= 0.02, 0.003 and 0.03), but not related to the magnitude or rate of unloading or time spent unloaded in the carotid artery (r = -0.32, -0.07 and 0.06, P= 0.25, 0.81 and 0.85). In contrast, in middle-aged men, the OP was not related to either the magnitude or rate of unloading or time spent unloaded in the aortic (r = 0.22, 0.21 and 0.27, P= 0.41, 0.43 and 031) or carotid artery (r = 0.48, 0.28 and -0.01, P= 0.06, 0.25 and 0.98). In conclusion, in young men, aortic unloading mechanics may play a role in determining the vascular sympathetic baroreflex OP. In contrast, in middle-aged men, barosensory vessel unloading mechanics do not appear to determine the vascular sympathetic baroreflex OP, and therefore do not contribute to age-related arterial baroreflex resetting and increased resting MSNA.

Background: Structural remodeling of the right ventricle (RV) is widely documented in athletes. However, functional adaptation, including RV pressure generation and systolic free-wall longitudinal mechanics, remains equivocal. This meta-analysis compared RV pressure and function in athletes and controls. Methods: A systematic review of online databases was conducted up to June 4, 2020. Meta-analyses were performed on RV systolic pressures, at rest and during exercise, tricuspid annular plane systolic displacement, myocardial velocity (S’), and global and regional longitudinal strain. Bias was assessed using Egger regression for asymmetry. Data were analyzed using random-effects models with weighted mean difference and 95% CI. Results: Fifty-three studies were eligible for inclusion. RV systolic pressure was obtained from 21 studies at rest ( n =1043:1651; controls:athletes) and 8 studies during exercise ( n =240:495) and was significantly greater in athletes at rest (weighted mean difference, 2.9 mmHg [CI, 1.3–4.5 mmHg]; P =0.0005) and during exercise (11.0 [6.5–15.6 mm Hg]; P <0.0001) versus controls. Resting tricuspid annular plane systolic displacement ( P <0.0001) and S’ ( P =0.001) were greater in athletes. In contrast, athletes had similar RV free-wall longitudinal strain (17 studies; n =450:605), compared with controls but showed greater longitudinal apical strain (16 studies; n =455:669; 0.9%, 0.1%–1.8%; P =0.03) and lower basal strain (−2.5% [−1.4 to −3.5%]; P <0.0001). Conclusions: Functional RV adaptation, characterized by increased tricuspid annular displacement and velocity and a greater base-to-apex strain gradient, is a normal feature of the athlete’s heart, together with a slightly elevated RV systolic pressure. These findings contribute to our understanding of RV in athletes and highlight the importance of considering RV function in combination with structure in the clinical interpretation of the athlete’s heart.