title: The Impact of Training Quantity on Structure-Function Relationships of the Cyclist's Heart
Creators: name: Brown, B
Publisher: name: Liverpool John Moores University
Year: 2020

description: Structural and functional adaptations of the left ventricle (LV) in response to chronic exercise training termed the “athlete’s heart” (AH) are central to a road cyclist’s (RC) performance capacity. As a result, RC athletes complete very high training hours, which generate a stimulus for cardiac remodelling. In some cases, the profound adaptation observed in these athletes can mimic pathological processes, presenting a risk of false-positive identification of cardiomyopathy at pre-participation screening or during follow-up. Furthermore, emerging data suggest acute transient post-strenuous exercise reductions in LV systolic and diastolic function termed “exercise induced cardiac fatigue” (EICF) may be extended to short-term periods such as overload training where very high training hours and limited recovery exist (i.e. training camps and/or stage races). The magnitude and possible mechanism(s) responsible for persistent EICF in overload training, and implications for pre-participation screening/follow-up of RC are not fully understood. Based on this, the aims of this thesis were: 1) establish the impact of moderate and very high chronic training hours on structural, functional and mechanical remodelling of the road cyclist’s LV, 2) determine how the LV responds to variations in training hours across a competitive road cycling season, 3) assess the impact of short-term overload endurance training on LV structure-function-mechanical relationships of the road cyclist’s LV, and 4) evaluate the relationship between LV function and road cycling performance following short-term overload endurance training. Study 1 (Chapter 4) highlighted that LV eccentric hypertrophy is commonly presented by elite cyclists (EC) (35%), but not sub-elite cyclists (SEC) (3%). Increases in LV mass between non-athletes (NA) and SEC (133 ± 24 vs 163 ± 26 g, P&lt;0.001) were predominantly driven by chamber expansion, whereas increased chamber concentricity between SEC and EC (5.85 ± 0.98 vs 7.11 ± 1.08 g/ml2/3, P&lt;0.001) drove further LV mass development (133 ± 24 vs 210 ± 31 g, P&lt;0.001). Marked structural remodelling in EC was also associated with a high prevalence of reduced (&lt;52%) LV ejection fraction (LV EF) (12 %) and mildly reduced diastolic function. Study 2 (Chapter 5) established a progressive increase in LV mass between off-season and end-season in parallel with an accumulation of training hours in RC (143 ± 17 vs 162 ± 31, P&lt;0.05), which was eccentric in nature. Although RC presented mildly decreased early diastolic function during the most rapid increase in training hours, both resting and in-exercise mechanics remained unchanged across all timepoints. In study 3 (chapter 6), 3-weeks of overload (OL) training elicited acute fatigue in RC, which was associated with dilatation of the LV (50.8 ± 2.9 vs 51.8 ± 3.2 mm, P&lt;0.05), a decreased ability to augment LV EF (67 ± 5 vs 63 ± 3, P=0.056), and an increased atrial contribution to diastolic filling in-exercise (9 ± 3 vs 12 ± 2 cm/s, P&lt;0.05). Decreased LV twist (17.7 ± 4.5 vs 15.3 ± 3.3, P&lt;0.05) and global longitudinal strain (GL ɛ) (-20.2 ± 1.0 vs 19.2 ± 1.3, P= 0.063) are indicative of intrinsic contractile dysfunction and suggest similar mechanisms are involved in both acute and persistent EICF. The application of conventional and novel echocardiographic techniques have provided further understanding of normal physiological adaptation of the LV in response to short-, medium- and long-term high training hours in RC. These insights may lead to improvements in pre-participation screening and influence the training practices of this athlete group.