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.

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.

Shear-Mediated Dilation of the Internal Carotid Artery Occurs Independent of Hypercapnia.http://researchonline.ljmu.ac.uk/6418/ Article LJMU has developed LJMU Research Online for users to access the research output of the University more effectively. Copyright © and Moral Rights for the papers on this site are retained by the individual authors and/or other copyright owners. Users may download and/or print one copy of any article(s) in LJMU Research Online to facilitate their private study or for non-commercial research. You may not engage in further distribution of the material or use it for any profit-making activities or any commercial gain.The version presented here may differ from the published version or from the version of the record. Please see the repository URL above for details on accessing the published version and note that access may require a subscription.

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.

S mall cerebral arteries and arterioles (eg, pial vessels) respond rapidly to changes in their metabolic milieu and are highly sensitive to the partial pressure of arterial carbon dioxide (PaCO 2 ).1 Vasomotor responsiveness to PaCO 2 , termed CO 2 reactivity, is integral to stabilizing blood pH levels, and previous studies have associated lower CO 2 reactivity to increased cardiovascular and all-cause mortality.2 Recent magnetic resonance imaging studies in humans have revealed that vasomotor changes also occur in the middle cerebral artery (MCA) 3-5 and basilar artery 6 across the hypo-and hypercapnic range. These studies demonstrate the involvement of larger cerebral arteries in the PaCO 2 reactivity response, 7 findings consistent with well-controlled, animal studies. 8 Other recent studies using Duplex ultrasound have investigated extracranial artery responses during hypo-and hypercapnia.9,10 These studies provide direct evidence that changes in end-tidal CO 2 (PETCO 2 ) are associated with directionally similar, and dosedependent, changes in internal carotid artery (ICA) diameter. The mechanism(s), however, mediating these changes in extracranial ICA diameter remain unclear.Significant and rapid changes in extracranial artery blood flow occur across the hypo-and hypercapnic range. [9][10][11] In peripheral conduits such as the radial and brachial arteries, such changes in flow and attendant arterial shear stress represent potent vasoactive stimuli.12,13 Although Pohl et al 14 and Rubanyi et al 15 were the first to identify that flow-mediated dilation (FMD) is endothelium dependent, it is now well established that this phenomenon occurs in humans and that NO plays a significant role. [16][17][18][19] The widely used FMD test 13 relies on dilation of small arteries and arterioles in the limbs, as a consequence of cuff-induced ischemia, to induce an increase in upstream conduit artery shear stress and dilation. In the context of these studies, it is conceivable that rapid and profound dilation of intracranial vessels in response to hypercapnia induces extracranial (ICA) dilation as a consequence of increased shear stress. The aim of this study was to identify whether hypercapnia induces shear-mediated dilation in the carotid arteries. Using high-resolution Duplex ultrasound combined with novel, edge-detection software, we assessed simultaneous common Abstract-Increases in arterial carbon dioxide tension (hypercapnia) elicit potent vasodilation of cerebral arterioles. Recent studies have also reported vasodilation of the internal carotid artery during hypercapnia, but the mechanism(s) mediating this extracranial vasoreactivity are unknown. Hypercapnia increases carotid shear stress, a known stimulus to vasodilation in other conduit arteries. To explore the hypothesis that shear stress contributes to hypercapnic internal carotid dilation in humans, temporal changes in internal and common carotid shear rate and diameter, along with changes in middle cerebral artery velocity, were simultaneously assessed in 18 su...

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Episodic increases in cerebrovascular perfusion and shear stress may have beneficial impacts on endothelial function that improve brain health. We hypothesized that water immersion to the level of the right atrium in humans would increase cerebral perfusion. We continuously measured, in 9 young (means ± SD, 24.6 ± 2.0 yr) healthy men, systemic hemodynamic variables along with blood flows in the common carotid and middle and posterior cerebral arteries during controlled filling and emptying of a water tank to the level of the right atrium. Mean arterial pressure (80 ± 9 vs. 91 ± 12 mmHg, P < 0.05), cardiac output (4.8 ± 0.7 vs. 5.1 ± 0.6 l/min, P < 0.05) and end-tidal carbon dioxide (PetCO2, 39.5 ± 2.0 vs. 44.4 ± 3.5 mmHg, P < 0.05) increased with water immersion, along with middle (59 ± 6 vs. 64 ± 6 cm/s, P < 0.05) and posterior cerebral artery blood flow velocities (41 ± 9 vs. 44 ± 10 cm/s, P < 0.05). These changes were reversed when the tank was emptied. Water immersion is associated with hemodynamic and PetCO2 changes, which increase cerebral blood velocities in humans. This study provides an evidence base for future studies to examine the potential additive effect of exercise in water on improving cerebrovascular health.

Key points• We compared the effects of 6 months of randomly allocated endurance or resistance training on arterial dimensions.• Previous research suggests that arterial size increases with exercise, but this is based on cross-sectional comparisons or interventions that rarely exceeded 12 weeks.• Using high-resolution ultrasound, we demonstrated arterial size adaptations that are specific to the exercise mode. Resistance exercise increased diameter and function in the brachial artery. Femoral diameter and function increased after endurance exercise. Carotid arterial wall thickness decreased with training, while conduit arterial wall thicknesses remained unchanged.• This study directly addressed the question of differential impacts of exercise modality on vascular adaptations of conduit arteries in humans in response to a relatively prolonged training intervention period. We conclude that both endurance and resistance modalities have impacts on arterial size, function and wall thickness in vivo, which would be expected to translate to decreased cardiovascular risk.Abstract This randomized trial evaluated the impact of different exercise training modalities on the function and size of conduit arteries in healthy volunteers. Young (27 ± 5 years) healthy male subjects were randomized to undertake 6 months of either endurance training (ET; n = 10) or resistance training (RT; n = 13). High-resolution ultrasound was used to determine brachial, femoral and carotid artery diameter and wall thickness (IMT) and femoral and brachial flow-mediated dilatation (FMD) and glyceryl trinitrate (GTN)-mediated dilatation. Improvements in peak oxygen uptake occurred with ET (from 3.6 ± 0.7 to 3.8 ± 0.6 l min −1 , P = 0.024) but not RT. Upper body muscular strength increased following RT (from 57.8 ± 17.7 to 69.0 ± 19.5 kg, P < 0.001), but not ET. Both groups exhibited increases in lean body mass ( ET, 1.4 ± 1.8 kg and RT, 2.3 ± 1.3 kg, P < 0.05). Resistance training increased brachial artery resting diameter (from 3.8 ± 0.5 to 4.1 ± 0.4 mm, P < 0.05), peak FMD diameter (+0.2 ± 0.2 mm, P < 0.05) and GTN-mediated diameter (+0.3 ± 0.3 mm, P < 0.01), as well as brachial FMD (from 5.1 ± 2.2 to 7.0 ± 3.9%, P < 0.05). No improvements in any brachial parameters were observed following ET. Conversely, ET increased femoral artery resting diameter (from 6.2 ± 0.7 to 6.4 ± 0.6 mm, P < 0.05), peak FMD diameter (+0.4 ± 0.4 mm, P < 0.05) and GTN-induced diameter (+0.3 ± 0.3 mm, P < 0.05), as well as femoral FMD-to-GTN ratio (from 0.6 ± 0.3 to 1.1 ± 0.8, P < 0.05). Resistance training did not induce changes in femoral artery parameters. Carotid artery IMT decreased in response to both forms of training. These findings indicate that 6 months of supervised exercise training induced changes in brachial and femoral artery size and function and decreased carotid artery IMT. These impacts of both RT and ET would be expected to translate to decreased cardiovascular risk.