Non-technical summary This is the first study, to our knowledge, to use cardiac MRI before and after intensive and closely supervised resistance and endurance exercise training in humans. There is a long held belief that these different forms of training induce 'concentric' and 'eccentric' adaptation of the heart, but this concept is based on echocardiographic assessments and cross-sectional comparison of different types of elite athletes. Our findings, using highly sensitive MRI methodology, suggest that concept may need to be reconsidered. This study is of fundamental importance to the understanding of the impact of exercise on human cardiac morphology and physiology.Abstract The principle that 'concentric' cardiac hypertrophy occurs in response to strength training, whilst 'eccentric' hypertrophy results from endurance exercise has been a fundamental tenet of exercise science. This notion is largely based on cross-sectional comparisons of athletes using echocardiography. In this study, young (27.4 ± 1.1 years) untrained subjects were randomly assigned to supervised, intensive, endurance (END, n = 10) or resistance (RES, n = 13) exercise and cardiac MRI scans and myocardial speckle tracking echocardiography were performed at baseline, after 6 months of training and after a subsequent 6 weeks of detraining. Aerobic fitness increased significantly in END (3.5 to 3.8 l min −1 , P < 0.05) but was unchanged in RES. Muscular strength significantly improved compared to baseline in both RES and END ( = 53.0 ± 1.1 versus 36.4 ± 4.5 kg, both P < 0.001) as did lean body mass (2.3 ± 0.4 kg, P < 0.001 versus 1.4 ± 0.6 kg P < 0.05). MRI derived left ventricular (LV) mass increased significantly following END (112.5 ± 7.3 to 121.8 ± 6.6 g, P < 0.01) but not RES, whilst training increased end-diastolic volume ( LVEDV, END: +9.0 ± 5.0 versus RES +3.1 ± 3.6 ml, P = 0.05). Interventricular wall thickness significantly increased with training in END (1.06 ± 0.0 to 1.14 ± 0.06, P < 0.05) but not RES. Longitudinal strain and strain rates did not change following exercise training. Detraining reduced aerobic fitness, LV mass and wall thickness in END (P < 0.05), whereas LVEDV remained elevated. This study is the first to use MRI to compare LV adaptation in response to intensive supervised endurance and resistance training. Our findings provide some support for the 'Morganroth hypothesis' , as it pertains to LV remodelling in response to endurance training, but cast some doubt over the proposal that remodelling occurs in response to resistance training.

Whilst the existence of a specific phenotype characterized as 'athlete's heart' is generally acknowledged, the question of whether athletes exhibit characteristic vascular adaptations has not been specifically addressed. To do so in this symposium, studies which have assessed the size, wall thickness and function of elastic, large muscular and smaller resistance arteries in athletes have been reviewed. Notwithstanding the caveats pertaining to cross-sectional comparisons between athletes and 'matched' control subjects, these studies reveal increased conduit artery size, including enlargement of epicardial arteries and those supplying skeletal muscle. Evidence that peak limb blood flow responses are enhanced in athletes further suggests that resistance arteries undergo increases in total cross-sectional area. Such increases can be localized to those arteries supplying active muscle leading to speculation, supported by exercise training studies in humans and animal and cellular data, that arterial enlargement is associated with repetitive episodic increases in arterial shear stress which elicit endothelium-mediated remodelling. Such structural remodelling at conduit and resistance artery level may play a role in accommodating the substantial increase in cardiac output apparent in endurance athletes; arterial pressure is not increased at rest or during exercise in athletes (versus control subjects). Arterial wall remodelling also occurs in athletes but, in contrast to the impact of shear stress on remodelling of arterial lumenal dimensions, the impact of endurance athletic status on wall thickness may be a systemic, rather than localized, phenomenon. Finally, the question of whether the arteries of athletes exhibit enhanced function is moot. Somewhat paradoxically, measures of conduit and resistance artery endothelial function may not be enhanced, compared with healthy control subjects. This may relate to the inherent difficulty of improving arterial function which is already normal, or the time course and transient nature of functional change. It may also relate to the impact of compensatory structural remodelling, as arterial lumen size and wall thickness both affect functional responsiveness. In summary, there is clear evidence for an impact of athletic status on arterial structure and function, at least with respect to the impact of endurance training. Arterial adaptation may, to some extent, emulate that evident in the hearts of endurance athletes, and it is tempting to speculate that similar mechanisms may be at play.

The contribution of endothelium-derived nitric oxide (NO) to exercise hyperaemia remains controversial. Disparate findings may, in part, be explained by different shear stress stimuli as a result of different types of exercise. We have directly compared forearm blood flow (FBF) responses to incremental handgrip and cycle ergometer exercise in 14 subjects (age ± S.E.M.) using a novel software system which calculates conduit artery blood flow continuously across the cardiac cycle by synchronising automated edge-detection and wall tracking of high resolution B-mode arterial ultrasound images and Doppler waveform envelope analysis. Monomethyl arginine (L-NMMA) was infused during repeat bouts of each incremental exercise test to assess the contribution of NO to hyperaemic responses. During handgrip, mean FBF increased with workload (P < 0.01) whereas FBF decreased at lower cycle workloads (P < 0.05), before increasing at 120 W (P < 0.001). Differences in these patterns of mean FBF response to different exercise modalities were due to the influence of retrograde diastolic flow during cycling, which had a relatively larger impact on mean flows at lower workloads. Retrograde diastolic flow was negligible during handgrip. Although mean FBF was lower in response to cycling than handgrip exercise, the impact of L-NMMA was significant during the cycle modality only (P < 0.05), possibly reflecting the importance of an oscillatory antegrade/retrograde flow pattern on shear stress-mediated release of NO from the endothelium. In conclusion, different types of exercise present different haemodynamic stimuli to the endothelium, which may result in differential effects of shear stress on the vasculature.

This study aimed to determine the importance of repeated increases in blood flow to conduit artery adaptation, using an exercise-independent repeated episodic stimulus. Recent studies suggest that exercise training improves vasodilator function of conduit arteries via shear stress-mediated mechanisms. However, exercise is a complex stimulus that may induce shear-independent adaptations. Nine healthy men immersed their forearms in water at 42°C for three 30-min sessions/wk across 8 wk. During each session, a pneumatic pressure cuff was inflated around one forearm to unilaterally modulate heating-induced increases in shear. Forearm heating was associated with an increase in brachial artery blood flow (P Ͻ 0.001) and shear rate (P Ͻ 0.001) in the uncuffed forearm; this response was attenuated in the cuffed limb (P Ͻ 0.005). Repeated episodic exposure to bilateral heating induced an increase in endothelium-dependent vasodilation in response to 5-min ischemic (P Ͻ 0.05) and ischemic handgrip exercise (P Ͻ 0.005) stimuli in the uncuffed forearm, whereas the 8-wk heating intervention did not influence dilation to either stimulus in the cuffed limb. Endothelium-independent glyceryl trinitrate responses were not altered in either limb. Repeated heating increases blood flow to levels that enhance endothelium-mediated vasodilator function in humans. These findings reinforce the importance of the direct impacts of shear stress on the vascular endothelium in humans.

The endothelium, a single layer of cells lining the entire circulatory system, plays a key role in maintaining vascular health. Endothelial dysfunction independently predicts cardiovascular events and improvement in endothelial function is associated with decreased vascular risk. Previous studies have suggested that exercise training improves endothelial function in macrovessels, a benefit mediated via repeated episodic increases in shear stress. However, less is known of the effects of shear stress modulation in microvessels. In the present study we examined the hypothesis that repeated skin heating improves cutaneous microvascular vasodilator function via a shear stress-dependent mechanism. We recruited 10 recreationally active males who underwent bilateral forearm immersion in warm water (42 • C), 3 times per week for 30 min. During these immersion sessions, shear stress was manipulated in one arm by inflating a pneumatic cuff to 100 mmHg, whilst the other arm remained uncuffed. Vasodilatation to local heating, a NO-dependent response assessed using laser Doppler, improved across the 8 week intervention period in the uncuffed arm (cutaneous vascular conductance week 0 vs. week 4 at 41• C: 1.37 ± 0.45 vs. 2.0 ± 0.91 units, P = 0.04; 42 • C: 2.06 ± 0.45 vs. 2.68 ± 0.83 units; P = 0.04), whereas no significant changes were evident in the cuffed arm. We conclude that increased blood flow, and the likely attendant increase in shear stress, is a key physiological stimulus for enhancing microvascular vasodilator function in humans.

The objectives of our study were to examine 1) the proportion of responders and nonresponders to exercise training in terms of vascular function; 2) a priori factors related to exercise training-induced changes in conduit artery function, and 3) the contribution of traditional cardiovascular risk factors to exercise-induced changes in artery function. We pooled data from our laboratories involving 182 subjects who underwent supervised, large-muscle group, endurance-type exercise training interventions with pre-/posttraining measures of flow-mediated dilation (FMD%) to assess artery function. All studies adopted an identical FMD protocol (5-min ischemia, distal cuff inflation), contemporary echo-Doppler methodology, and observer-independent automated analysis. Linear regression analysis was used to identify factors contributing to changes in FMD%. We found that cardiopulmonary fitness improved, and weight, body mass index (BMI), cholesterol, and mean arterial pressure (MAP) decreased after training, while FMD% increased in 76% of subjects (P < 0.001). Training-induced increase in FMD% was predicted by lower body weight (β = -0.212), lower baseline FMD% (β = -0.469), lower training frequency (β = -0.256), and longer training duration (β = 0.367) (combined: P < 0.001, r = 0.63). With the exception of a modest correlation with total cholesterol (r = -0.243, P < 0.01), changes in traditional cardiovascular risk factors were not significantly related to changes in FMD% (P > 0.05). In conclusion, we found that, while some subjects do not demonstrate increases following exercise training, improvement in FMD% is present in those with lower pretraining body weight and endothelial function. Moreover, exercise training-induced change in FMD% did not correlate with changes in traditional cardiovascular risk factors, indicating that some cardioprotective effects of exercise training are independent of improvement in risk factors.

The purpose of this study was to establish valid indexes of conduit and resistance vessel structure in humans by using edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, to calculate conduit artery blood flow and diameter continuously across the cardiac cycle. Nine subjects aged 36.7 (9.2) yr underwent, on separate days, assessment of brachial artery blood flow and diameter response to 5-, 10-, and 15-min periods of forearm ischemia in the presence and absence of combined sublingual glyceryl trinitrate (GTN) administration. Two further sessions examined responses to ischemic exercise, one in combination with GTN. The peak brachial artery diameter was observed in response to the combination of ischemic exercise and GTN; a significant difference existed between resting brachial artery diameter and peak brachial artery diameter, indicating that resting diameter may be a poor measure of conduit vessel structure in vivo. Peak brachial artery flow was also observed in response to a combination of forearm ischemia exercise and GTN administration, the response being greater than that induced by periods of ischemia, GTN, or ischemic exercise alone. These data indicate that noninvasive indexes of conduit and resistance vessel structure can be simultaneously determined in vivo in response to a single, brief, stimulus and that caution should be applied in using resting arterial diameter as a surrogate measure of conduit artery structure in vivo.

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