ABSTRACT:Mounting evidence has firmly established that low levels of cardiorespiratory fitness (CRF) are associated with a high risk of cardiovascular disease, all-cause mortality, and mortality rates attributable to various cancers. A growing body of epidemiological and clinical evidence demonstrates not only that CRF is a potentially stronger predictor of mortality than established risk factors such as smoking, hypertension, high cholesterol, and type 2 diabetes mellitus, but that the addition of CRF to traditional risk factors significantly improves the reclassification of risk for adverse outcomes. The purpose of this statement is to review current knowledge related to the association between CRF and health outcomes, increase awareness of the added value of CRF to improve risk prediction, and suggest future directions in research. Although the statement is not intended to be a comprehensive review, critical references that address important advances in the field are highlighted. The underlying premise of this statement is that the addition of CRF for risk classification presents health professionals with unique opportunities to improve patient management and to encourage lifestyle-based strategies designed to reduce cardiovascular risk. These opportunities must be realized to optimize the prevention and treatment of cardiovascular disease and hence meet the American Heart Association's 2020 goals.M ounting evidence over the past 3 decades has firmly established that low levels of cardiorespiratory fitness (CRF) are associated with a high risk of cardiovascular disease (CVD) and all-cause mortality, as well as mortality rates attributable to various cancers, especially of the breast and colon/digestive tract. [1][2][3][4] Importantly, improvements in CRF are associated with reduced mortality risk.5 Although CRF is now recognized as an important marker of cardiovascular health, it is currently the only major risk factor not routinely assessed in clinical practice.In 2013, the American Heart Association and the American College of Cardiology jointly released new guidelines for the prevention and treatment of coronary artery disease.6 Although CRF is the fourth-leading risk factor for CVD and has long been established as a significant prognostic marker, 7 it was excluded from the risk calculator. The authors of the guidelines noted that the evidence that CRF would enhance risk classification was inconclusive, and thus, the added contribution of CRF to determine CVD risk was uncertain. There is, however, a large body of epidemiological and clinical evidence demonstrating not only that CRF is a potentially stronger predictor of mortality than established risk factors such as smoking, hypertension, high cholesterol, and type 2 diabetes mellitus (T2DM), but that the addition of CRF to traditional risk factors significantly improves the reclassification of risk for adverse outcomes.

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Background Obesity (OB) is a serious epidemic in the United States. Methods We examined OB patterns and time trends across socio-economic and geographic parameters and projected the future situation. Large national databases were used. Overweight (OW), OB and severe obesity (SOB) were defined using body mass index cut-points/percentiles; central obesity (CO), waist circumference cut-point in adults and waist:height ratio cutoff in youth. Various meta-regression analysis models were fit for projection analyses. Results OB prevalence had consistently risen since 1999 and considerable differences existed across groups and regions. Among adults, men’s OB (33.7%) and OW (71.6%) levelled off in 2009–2012, resuming the increase to 38.0 and 74.7% in 2015–2016, respectively. Women showed an uninterrupted increase in OB/OW prevalence since 1999, reaching 41.5% (OB) and 68.9% (OW) in 2015–2016. SOB levelled off in 2013–2016 (men: 5.5–5.6%; women: 9.7–9.5%), after annual increases of 0.2% between 1999 and 2012. Non-Hispanic Blacks had the highest prevalence in women’s OB/SOB and men’s SOB. OB prevalence in boys rose continuously to 20.6% and SOB to 7.5% in 2015–2016, but not in girls. By 2030, most Americans will be OB/OW and nearly 50% of adults OB, whereas ∼33% of children aged 6–11 and ∼50% of adolescents aged 12–19 will be OB/OW. Since 1999, CO has risen steadily, and by 2030 is projected to reach 55.6% in men, 80.0% in women, 47.6% among girls and 38.9% among boys. Regional differences exist in adult OB prevalence (2011–2016) and across ethnicities; South (32.0%) and Midwest (31.4%) had the highest rates. Conclusions US obesity prevalence has been rising, despite a temporary pause in 2009–2012. Wide disparities across groups and geographical regions persist. Effective, sustainable, culturally-tailored interventions are needed.

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Harber MP, Konopka AR, Douglass MD, Minchev K, Kaminsky LA, Trappe TA, Trappe S. Aerobic exercise training improves whole muscle and single myofiber size and function in older women. Am J Physiol Regul Integr Comp Physiol 297: R1452-R1459, 2009. First published August 19, 2009 doi:10.1152/ajpregu.00354.2009.-To comprehensively assess the influence of aerobic training on muscle size and function, we examined seven older women (71 Ϯ 2 yr) before and after 12 wk of cycle ergometer training. The training program increased (P Ͻ 0.05) aerobic capacity by 30 Ϯ 6%. Quadriceps muscle volume, determined by magnetic resonance imaging (MRI), was 12 Ϯ 2% greater (P Ͻ 0.05) after training and knee extensor power increased 55 Ϯ 7% (P Ͻ 0.05). Muscle biopsies were obtained from the vastus lateralis to determine size and contractile properties of individual slow (MHC I) and fast (MHC IIa) myofibers, myosin light chain (MLC) composition, and muscle protein concentration. Aerobic training increased (P Ͻ 0.05) MHC I fiber size 16 Ϯ 5%, while MHC IIa fiber size was unchanged. MHC I peak power was elevated 21 Ϯ 8% (P Ͻ 0.05) after training, while MHC IIa peak power was unaltered. Peak force (Po) was unchanged in both fiber types, while normalized force (Po/cross-sectional area) was 10% lower (P Ͻ 0.05) for both MHC I and MHC IIa fibers after training. The decrease in normalized force was likely related to a reduction (P Ͻ 0.05) in myofibrillar protein concentration after training. In the absence of an increase in Po, the increase in MHC I peak power was mediated through an increased (P Ͻ 0.05) maximum contraction velocity (Vo) of MHC I fibers only. The relative proportion of MLC1s (Pre: 0.62 Ϯ 0.01; Post: 0.58 Ϯ 0.01) was lower (P Ͻ 0.05) in MHC I myofibers after training, while no differences were present for MLC 2s and MLC 3f isoforms. These data indicate that aerobic exercise training improves muscle function through remodeling the contractile properties at the myofiber level, in addition to pronounced muscle hypertrophy. Progressive aerobic exercise training should be considered a viable exercise modality to combat sarcopenia in the elderly population.

To examine potential age-specific adaptations in skeletal muscle size and myofiber contractile physiology in response to aerobic exercise, seven young (YM; 20 ± 1 yr) and six older men (OM; 74 ± 3 yr) performed 12 wk of cycle ergometer training. Muscle biopsies were obtained from the vastus lateralis to determine size and contractile properties of isolated slow [myosin heavy chain (MHC) I] and fast (MHC IIa) myofibers, MHC composition, and muscle protein concentration. Aerobic capacity was higher (P < 0.05) after training in both YM (16 ± 2%) and OM (13 ± 3%). Quadriceps muscle volume, determined via MRI, was 5 ± 1 and 6 ± 1% greater (P < 0.05) after training for YM and OM, respectively, which was associated with an increase in MHC I myofiber cross-sectional area (CSA), independent of age. MHC I peak power was higher (P < 0.05) after training for both YM and OM, while MHC IIa peak power was increased (P < 0.05) with training in OM only. MHC I and MHC IIa myofiber peak and normalized (peak force/CSA) force were preserved with training in OM, while MHC I peak force/CSA and MHC IIa peak force were lower (P < 0.05) after training in YM. The age-dependent adaptations in myofiber function were not due to changes in protein content, as total muscle protein and myofibrillar protein concentration were unchanged (P > 0.05) with training. Training reduced (P < 0.05) the proportion of MHC IIx isoform, independent of age, whereas no other changes in MHC composition were observed. These data suggest relative improvements in muscle size and aerobic capacity are similar between YM and OM, while adaptations in myofiber contractile function showed a general improvement in OM. Training-related increases in MHC I and MHC IIa peak power reveal that skeletal muscle of OM is responsive to aerobic exercise training and further support the use of aerobic exercise for improving cardiovascular and skeletal muscle health in older individuals.