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Despite major efforts to reduce atherosclerotic cardiovascular disease (ASCVD) burden with conventional risk factor control, significant residual risk remains. Recent evidence on non-traditional determinants of cardiometabolic health has advanced our understanding of lifestyle-disease interactions. Chronic exposure to environmental stressors like poor diet quality, sedentarism, ambient air pollution and noise, sleep deprivation and psychosocial stress affect numerous traditional and non-traditional intermediary pathways related to ASCVD. These include body composition, cardiorespiratory fitness, muscle strength and functionality and the intestinal microbiome, which are increasingly recognized as major determinants of cardiovascular health. Evidence points to partially overlapping mechanisms, including effects on inflammatory and nutrient sensing pathways, endocrine signalling, autonomic function and autophagy. Of particular relevance is the potential of low-risk lifestyle factors to impact on plaque vulnerability through altered adipose tissue and skeletal muscle phenotype and secretome. Collectively, low-risk lifestyle factors cause a set of phenotypic adaptations shifting tissue cross-talk from a proinflammatory milieu conducive for high-risk atherosclerosis to an anti-atherogenic milieu. The ketone body ß-hydroxybutyrate, through inhibition of the NLRP-3 inflammasome, is likely to be an intermediary for many of these observed benefits. Adhering to low-risk lifestyle factors adds to the prognostic value of optimal risk factor management, and benefit occurs even when the impact on conventional risk markers is discouragingly minimal or not present. The aims of this review are (a) to discuss novel lifestyle risk factors and their underlying biochemical principles and (b) to provide new perspectives on potentially more feasible recommendations to improve long-term adherence to low-risk lifestyle factors.

Objective Carotid intima-media thickness (IMT) is used to assess cardiovascular risk and progression of atherosclerosis. It is known that regular physical activity of moderate intensity has beneficial effects on the vasculature. However, it is still discussed controversially whether prolonged exercise, including participation in exhaustive competitive sports such as long-distance races, has also beneficial effects or might even be harmful regarding the cardiovascular system. Patients and methods Thirty-eight male marathon runners (45.8 ± 7.3 years) were investigated twice (2009 and 2013) for their carotid IMT (using ultrasound techniques), anthropometrics and clinical chemistry. Additionally, training volume (running kilometres per year) and competition participation (half marathon, marathon and ultramarathon) within this follow-up period were assessed. Results During 3.8 ± 0.4 years of follow-up, runners performed 1587 (850-2500) training kilometres per year and participated in a total of 7 (4-12) long distance competitions. IMT increased in total by 0.05 ± 0.09 mm or annually by 0.013 ± 0.023 mm, respectively. Higher increase in IMT over that period was associated with higher fasting blood glucose (beta = .355, p = .045) at baseline examination. Effects of training volume and number of competitions on the progression of IMT could not be demonstrated in our longitudinal analysis. Conclusions Higher blood glucose levels are associated with detrimental effects on vasculature in otherwise healthy male marathon runners. Regular marathon training, including competition participation over at least several years, was not associated with detrimental effects on IMT or, vice versa, seems not to provide beneficial effects on vasculature.

Background In contrast to the well-accepted benefits of moderate exercise, recent research has suggested potential deleterious effects of repeated marathon running on the cardiovascular system. We thus performed a comprehensive analysis of markers of subclinical vascular damage in a cohort of runners having finished multiple marathon races successfully. Design This was a prospective, observational study. Methods A total of 97 healthy male Munich marathon participants (mean age 44 ± 10 years) underwent detailed training history, cardiopulmonary exercise testing for assessment of peak oxygen uptake, ultrasound for assessment of intima-media-thickness as well as non-invasive assessments of ankle-brachial index, augmentation index, pulse wave velocity and reactive hyperaemia index. Results Runners had previously completed a median of eight (range 1-500) half marathons, six (1-100) full marathons and three (1-40) ultramarathons; mean weekly and annual training volumes were 59 ± 23 and 1639 ± 979 km. Mean peak oxygen uptake was 50 ± 8 ml/min/kg, and the Munich marathon was finished in 3:45 ± 0:32 h. Runners showed normal mean values for intima-media-thickness (0.60 ± 0.14 mm), ankle-brachial index (1.2 ± 0.1), augmentation index (17 ± 13%), pulse wave velocity (8.7 ± 1.4 cm/s) and reactive hyperaemia index (1.96 ± 0.50). Age was significantly and independently associated with intima-media-thickness ( r = 0.531; p < 0.001), augmentation index ( r = 0.593; p < 0.001) and pulse wave velocity ( r = 0.357; p < 0.001). However, no independent associations of peak oxygen uptake, marathon finishing time, number of completed races or weekly and annual training km with any of the vascular parameters were observed. Conclusions In this cohort of healthy male runners, running multiple marathon races did not pose an additional risk factor for premature subclinical vascular impairment beyond age.

Background: Correction for body composition is recommended for appropriate interpretation of equivocally altered cardiac dimensions. We sought to investigate the impact of body composition on athletes' heart., Methods: Left ventricular mass (LVM), septal wall thickness (SWT) and end-diastolic diameter (LVEDD) were measured by echocardiography in 1051 elite athletes (26% female, aged 18-40 years) and in 338 sedentary controls matched for age, gender and body size. Body fat was determined by skinfold thickness measurements., Results: Normative ranges are provided for LVM, LVEDD and SWT scaled to body surface area (BSA), height, height(2.7) and fat-free mass (FFM). The strongest correlation was found for FFM (r = 0.70; 0.64; 0.49; p < 0.001 each). LVM, LVEDD and SWT differed significantly (p < 0.05) between athletes of low, moderate and high dynamic disciplines. Correcting LVEDD for height(2.7) eliminated these differences (p > 0.05), whereas LVM and SWT remained significantly increased in high dynamic athletes despite correction for body size. Gender differences were consistently eliminated by scaling LVEDD to FFM(0.33) and SWT to BSA, but scaled LVM remained significantly increased in male athletes. Compared to sedentary controls, significant differences in LVEDD and SWT disappeared after correction for height(2.7) and FFM, but LVM again remained significantly higher in athletes., Conclusions: Adaptation of left ventricular dimensions to exercise training is closely related to body composition, in particular to FFM. The normative ranges for LVEDD, SWT and LVM scaled to body size aid interpretation of equivocal alterations in elite athletes. However, the increase of LVM in particular reveals exercise-induced adaptations beyond these associations.