Pressure overload – using echocardiography to investigate left ventricular responses to resistance exercise

Abstract

Previous research has highlighted significant cardiac alterations in individuals engaged in chronic physical training (Barbier et al., 2006b; Pluim et al., 2000) – a phenomenon known as the 'Athlete's Heart'. Whilst it has been hypothesised that these alterations may be training dependent specifically when examining the pattern of left ventricular (LV) hypertrophy displayed (Morganroth et al., 1975), there is currently no clear consensus regarding cardiac alterations in individuals engaged in chronic resistance training. Therefore, the purpose of this thesis was to investigate differences in cardiac structure and function in resistance-trained (RT) athletes and untrained (UT) individuals. Furthermore, as resistance exercise has been found to cause significant elevations in blood pressure (MacDougall et al., 1985; Lentini et al. 1993), it has been suggested that observed differences in cardiac structure between these individuals are a result of exposure to a significant 'pressure overload' like that experienced in pathological cardiac conditions (Grossman, Jones, and McLaurin, 1975; Haykowsky et al., 2001). With the use of echocardiography, continuous blood pressure monitoring and mouth pressure (MP) measurements, acute LV responses to resistance exercise – specifically left ventricular systolic wall stress (LV σ) were examined at various submaximal intensities to explore this possible explanation for the observed cardiac alterations previously seen in RT athletes.This thesis found significant differences in cardiac structure between RT athletes and UT individuals (Study 1-3). Specifically, RT athletes displayed significantly greater left ventricular mass (LVM) and interventricular septum (IVS), and posterior wall (PW) thickness compared to both the UT individuals and published upper normal limits (Lang et al., 2015). Additionally, despite evident structural adaptations, no significant impairments in cardiac function were found in the RT athletes (Studies 1-3). During submaximal lower-body resistance exercise systolic blood pressure (SBP) was found to significantly increase - indicative of a pressure overload (Study 3). Consequently, LV σ was significantly higher during resistance exercise compared to rest (Study 3) – in contrast to previous research (Haykowsky et al., 2001), with differing acute responses between the RT and UT individuals with regards to MP noted. Significant differences in MP at 80% one-repetition max (1RM) suggested that whilst UT individuals involuntarily performed a breath holding technique known as a Valsalva Manoeuvre (VM) at high intensities, RT athletes did not. To examine these differences further, Study 4 investigated LV response to resistance exercise under different breathing conditions (No instruction, Instructed Steady Breathing, and a Modified VM). Performing a VM caused significant elevations in SBP and MP, although in contrast to previous research this manoeuvre was found to be avoidable during high intensities (Blazek et al., 2019). These elevations in SBP and MP did, however, cause a reduction in transmural pressure (TMP) and consequent LV σ. Overall this thesis indicates that whilst lower-body resistance exercise causes a significant pressure overload, only when a VM is avoided and LV σ is subsequently high, may this explain the significant wall thickening that is observed in RT athletes.

Date of Award	May 2024
Original language	English
Awarding Institution	University of Bedfordshire
Supervisor	Jo Richards (Supervisor), Rebecca Jones (Second supervisor) & Andrew Mitchell (Third supervisor)