The ‘Morganroth Hypothesis’: Prolonged Resistance Training & Cardiac Hypertrophy

Updated: Mar 4, 2020

Regular and prolonged exercise stimuli are associated with central and peripheral cardiovascular adaptations as well as a haemodynamic overload on the left ventricle (LV), which is deemed a key stimulus for cardiac adaptation (D’Ascenzi et al., 2015). Hypertrophy of the myocardium is a principle feature of the ‘athlete’s heart’ and allows for increased stroke volume and cardiac output (Naylor et al., 2008). It is general consensus that left ventricular mass (LVM) is enhanced in athletic populations (Pluim et al., 2000) and is calculated using geometrical assumptions for volume which can vary between scans (Myerson et al., 2002). Adaptation to the LV following prolonged exercise has been predominantly underpinned by the concept of sport-specificity within the ‘Morganroth hypothesis’ (1975). Morganroth et al. (1975) observed increased LV end-diastolic volume (LVEDV), increased LVM and normal LV thickness in endurance athletes compared to sedentary controls. In contrast, resistance athletes demonstrated increased LV wall thickness and LVM with no change in LVEDV compared to sedentary controls. These physiological adaptations were later defined as eccentric hypertrophy in endurance athletes in response to increased preload, and concentric hypertrophy in resistance athletes in response to increased afterload (Naylor et al., 2008; Spence et al., 2011). It was found that resistance training caused LV hypertrophy without increased cavity size, which explains the lack of stroke volume increase (Naylor et al., 2008). However, the ‘Morganroth hypothesis’ was proposed 40 years ago. Therefore, this review poses the question ‘is the Morganroth hypothesis valid?’ specifically in terms of resistance training and cardiac hypertrophy.

Endurance or ‘dynamic’ exercise has been typically defined as changes in muscle length and joint movement with rhythmic contractions resulting in minimal force development. Resistance or ‘static’ training has been defined as development of relatively large intramuscular force with minimal change in muscle length or joint movement (Mitchell et al., 2005). These definitions describe two ends of a spectrum, whereas there are sports and training modalities that create haemodynamic stimuli that do not fit purely into either one definition alone (Naylor et al., 2008). A haemodynamic overload of the LV is believed to be the primary mechanism to elicit cardiac morphological changes (Morganroth et al., 1975). The ‘Morganroth hypothesis’ implies wall thickness adapts to changes in wall stress accrued from repetitive exercise bouts. Ventricular wall stress has been defined as the product of LV geometry and transmural pressure (Naylor et al., 2008).

It has been well understood for some time that cardiac adaptation, in particular increased LVM, is enhanced in athletic populations (Pellicia et al., 1999; Pluim et al., 2000). This has posed the problem of differential diagnosis between athletic and pathological hypertrophy. However, the effect of different training modalities on cardiac adaptation is not fully understood. Investigations regarding cardiovascular adaptation in endurance-trained athletes are generally in agreement with the ‘Morganroth hypothesis’. Scharhag et al. (2002) compared endurance athletes to matched non-athletic controls and observed enlarged ventricular mass (200 vs. 148g) and volumes (167 vs. 125 ml) in the athletic population. Wernstedt et al. (2002) compared endurance and strength athletes with a control. They reported higher LV mass (210g) and volume in the endurance group, compared to both the resistance (163g) and control groups (144g). These endurance exercise adaptations may be explained by prolonged haemodynamic stress, which may increase protein synthesis and facilitate hypertrophy of the myocardium (Ruwhof & Van der Laars, 2000).

In contrast, evidence regarding resistance training is somewhat equivocal. A number of studies have tried to distinguish differences between training modalities by comparing resistance- and endurance-trained athletes. Although somewhat dated, Longhurst et al. (1980) highlighted enhanced LVM in long distance runners compared with weightlifters. In contrast, significantly increased LVM has been documented in resistance (power lifters) compared to endurance (swimmers) athletes, although both groups represented enhanced LVM compared with controls (Colan et al., 1985). Increased body surface area (BSA) was documented in the strength athletes compared with both endurance and control groups. Left ventricular cavity size, determined as the internal cavity dimension during diastole (LVIDd), was similar in both athletic groups. The increased LVM in the resistance athletes was therefore deemed to have accrued from enlarged LV wall thickness.

A key issue with most studies including that of Morganroth et al. (1975) and their hypothesis is the use of 2-dimensional (2D) and M-mode echocardiography which estimate LVM and volumes through geometric assumptions (Naylor et al., 2008). Athletes generally display 15-20% increased wall thickness and 10% enhanced cavity size compared to non-athletes (Sharma et al., 2002). It is interesting that the error associated with motion and M-mode echocardiography is greater than these physiological differences (Pollick et al., 1983). Therefore, early findings using these methods need to be taken with consideration as some findings may be due to measurement error rather than physiological adaptation. In contrast, magnetic resonance imagining (MRI) has been considered the ’gold standard’ for cardiovascular assessments due to its accuracy, sensitivity and reproducibility in identifying cardiac morphological changes in comparison with echocardiography (Myerson et al., 2002). Using radiofrequency waves and a magnetic field, MRI can assess the 3D structure and function of the heart without the error of geometric assumptions associated with echocardiography (Jenkins et al., 2007). However, due to the limited access and cost of MRI, echocardiography has been described as the only cost-effective, validated imaging modality that is widely available and capable of analysing cardiac morphology (Paterick et al., 2014). Relatively novel, 3D echocardiography has been found to be a more reliable and accurate method than 2D and M-mode echocardiographic analysis of LVM, although correlation with ‘gold standard’ MRI was moderate (r = 0.36–0.57; Jenkins et al., 2007).

There are major limitations with cross-sectional studies, which have been widely used to describe the ‘athlete’s heart’ as well as support the ‘Morganroth hypothesis’ (Fagard et al., 1984; Colan et al., 1985; Haykowsky et al., 1999; Baggish et al., 2008). A key assumption is that differences between groups are due to training adaptation and not between-group differences. An example of a between-group difference is body size and composition, which independently influence cardiac morphology, in particular LVM (Riding et al., 2012). There are also variations of techniques (2D, M-mode and 3D echocardiography) as well as cardiac measurement variation between studies, which makes comparison somewhat limited. Longitudinal, repeated within-subject designs eliminate many of the limitations found in cross-sectional investigations as well as providing a better approach for echocardiographic investigations (Naylor et al., 2008). In comparison to the number of cross-sectional studies, longitudinal studies are limited and especially sparse for resistance exercise (Spence et al., 2011).

Spence et al. (2011) was the first known randomised, longitudinal study to utilise MRI pre- and post-intensive, supervised resistance and endurance training programmes. Their major finding was that LVM and wall thickness significantly increased following six months of endurance training, whereas no significant change was evident in resistance-trained subjects. A greater increase in LVEDV was found in endurance compared with resistance athletes. The ratio of LVM: LVEDV was unchanged, which indicated an eccentric hypertrophy pattern in the endurance group as a result of proportionate increases in both LVM and LVEDV. This study therefore supports the notion of eccentric hypertrophy following endurance training, whereas resistance training was not associated with any significant LV morphological changes despite gains in strength and LBM (Spence et al., 2011). Conversely, a recent longitudinal study examining team athletes reported findings consistent with the ‘Morganroth hypothesis’ (Baggish et al., 2008). Isolated LV hypertrophy (12%) and reduced diastolic function was evident in strength-trained athletes, whereas developed bi-ventricular dilation (LV hypertrophy: 11%) and enhanced diastolic function was found in endurance athletes after 90 days of training. It is however, important to consider possible limitations of the study. The use of rowers (endurance) and American footballers (resistance) represent mixed sports (involving a combination of resistance and endurance training) and therefore generate unique haemodynamic loads (Naylor et al., 2008). The duration of training was not controlled; however, they stated that this was intentional in order to reveal the adaptation of specific sport-populations. Although they found strength training to elicit LV hypertrophy comparable to that of endurance training, it may be of note that the resistance-trained athletes were not tested for steroid use. The mean increase recorded was ∼30 grams (g), which was markedly higher than ∼9g exhibited from intensive endurance training using MRI (Spence et al., 2011). Another limitation is the lack of normalisation; the study indexed LVM to BSA and monitored changes in mass, but did not monitor changes in lean body mass (LBM). Normalisation is important for comparison due to the fact LVM has been associated with body size and composition (Naylor et al., 2008). Salton et al. (2002) stated that height was simple to determine and strongly correlated with LBM, which may best reflect metabolic effects on the heart. Other studies have reported a strong linear relationship between BSA and LV dimensions (Riding et al., 2011). However, George et al. (2009) utilising MRI, concluded that height, weight and BSA in particular were poorly correlated with LVM and LV dimensions due to non-linear relationships. As BSA is the most commonly used scaling index in ‘athlete’s heart’ studies, its widespread use must be questioned (George et al., 2009). It has been suggested that the LV adapts concurrently with metabolically active tissue induced by training (LBM; D’Ascenzi et al., 2015). Therefore, LBM may be a reasonably accurate variable for indexing LVM, although, simple scaling is questionable and other methods need consideration (Naylor et al., 2008). This supports earlier findings that LBM was the only scaling index to LVM that was geometrically consistent with a linear relationship and narrow confidence intervals (Batterham et al., 1997).

Haykowsky et al. (2000a) found no change in LV morphology or function in elite junior and master strength trained athletes. This highlights that short- and long-term resistance training does not elicit LV morphological adaptations and supports the notion that duration of resistance training does not impact on LV adaptation (Yeater et al., 1996). This expands on one of the largest known studies in relation to cardiac adaptation associated with ‘athlete’s heart’ (Pelliccia et al., 1991). Pelliccia et al. (1991) assessed 947 national and international standard Italian athletes from 25 different sports. Rowers and endurance athletes in general were associated with greater LVM than resistance athletes. In further support of lack of LV adaptation to resistance exercise, Haykowsky et al. (2000b) reported no change in LV wall thickness or cavity dimension in older, healthy subjects following 16 weeks of resistance training. Correspondingly, resistance training and a combination of resistance and endurance training both failed to elicit cardiac morphological adaptation in older women following 12 weeks of training (Haykowsky et al., 2005). Whilst it is considered increased arterial pressure associated with increased ventricle pressure is a key stimulus for LV adaptation; transmural pressure may not increase during resistance exercise if intra-thoracic pressure simultaneously increases with arterial pressure (Haykowsky et al., 2000a). It is therefore questionable as to whether concentric hypertrophy occurs from resistance training due to its limited effect on LV wall stress, particularly due to the effect of a Valsalva manoeuvre, which is a natural response during submaximal and maximal resistance exercise (Haykowsky et al., 2001).

There is strong evidence for endurance training and eccentric hypertrophy in agreement with the ‘Morganroth hypothesis’ (Utomi et al., 2013). However, the focus of this review has been resistance exercise and concentric hypertrophy; current literature is far too equivocal for validation of the hypothesis. These ambiguous findings may be due to principle issues of study type, normalisation and variety of techniques which have a significant impact on the interpretation of ‘athlete’s heart’ data (Utomi et al., 2013). Most of the data supporting the hypothesis is cross-sectional in nature and therefore may be reporting between-group differences rather than physiological adaptation. There are varying methods of scaling for normalisation; worryingly, the most frequently used is BSA and is associated with a poor relationship with LVM (George et al., 2009). Cross-sectional studies have almost completely utilised echocardiography with modest sample sizes, which as previously discussed, is associated with levels of error that is greater than most cardiac morphological adaptations (Jenkins et al., 2007). The physiological mechanism for LV adaptation also questions the ‘Morganroth hypothesis’ due to the notion that resistance training does not stress the LV wall (Haykowsky et al., 2001).

Recommendations for Practice and Future Research

‘Athlete’s heart’ research to-date has focussed on LV adaptation, whereas, right ventricle literature is sparse, due to its complexity and difficulty imaging (Spence et al., 2012). Right ventricular adaptation elicited from six months of intense endurance and resistance training was found to mirror that of LV adaptation (George et al., 2012). Whereas, Baggish et al. (2008) found only LV adaptation in resistance-trained individuals and bi-ventricular adaptation in endurance-trained individuals. It is therefore recommended that future research should focus on other cardiac features such as the right ventricle and atria in both healthy and diseased populations. The issue of scaling approaches within cardiac morphological analysis also warrants further consideration, LBM providing the strongest relationship with LVM. Further longitudinal investigations utilising MRI are required to better depict the sport-specific adaptations to exercise and to better differentiate between athletic and pathological hypertrophy.

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