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      Impaired popliteal artery flow-mediated dilation caused by reduced daily physical activity is prevented by increased shear stress

      1 , 2 , 1
      Journal of Applied Physiology
      American Physiological Society

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          Abstract

          <p class="first" id="d9650849e182">We found that the impairment in popliteal artery flow-mediated dilation caused by physical inactivity can be prevented by increased shear stress. These findings indicate that reduced leg blood flow-induced shear stress during physical inactivity may be a key underlying mechanism mediating the detrimental leg vascular effects of physical inactivity. Heating the foot area may be used as a nonpharmacological therapy to combat inactivity-induced leg vascular dysfunction, especially in people who are unable or unwilling to be active. </p><p class="first" id="d9650849e185">We recently showed that 5 days of reduced daily physical activity impair popliteal artery, but not brachial artery, flow-mediated dilation (FMD). However, the mechanisms by which physical inactivity causes leg vascular dysfunction are unclear. We reason that a reduction in leg blood flow-induced shear stress is a primary underlying mechanism by which reduced daily physical activity impairs popliteal artery FMD. Thus the purpose of this study was to determine whether increased leg blood flow and shear stress during inactivity prevent the reduction in popliteal artery FMD. Bilateral popliteal artery FMD measures were performed at baseline and after 5 days of a transition from high (&gt;10,000 steps/day) to low levels (&lt;5,000 steps/day) of physical activity in 13 healthy and physically active men [20 ± 2 (SD) yr]. During the inactive period, one foot was submerged in ~42°C water (i.e., heated leg) three times a day for 30 min each period, to increase blood flow and thus shear stress, whereas the contralateral leg remained dry and served as internal control (i.e., nonheated leg). During heating, popliteal artery mean shear rate was increased in the heated leg (change of 119.3 ± 26.4%, <i>P</i> &lt; 0.01) but slightly decreased in the nonheated leg (change of −21.8 ± 7.5%, <i>P</i> = 0.03). Popliteal artery FMD was impaired after 5 days of reduced daily physical activity in the control nonheated leg ( <i>P</i> &lt; 0.01) but was unchanged in the heated leg ( <i>P</i> = 0.34). These results support the hypothesis that reduced leg blood flow-induced shear stress during physical inactivity is a key underlying mechanism mediating leg vascular dysfunction. </p><p id="d9650849e199"> <b>NEW &amp; NOTEWORTHY</b> We found that the impairment in popliteal artery flow-mediated dilation caused by physical inactivity can be prevented by increased shear stress. These findings indicate that reduced leg blood flow-induced shear stress during physical inactivity may be a key underlying mechanism mediating the detrimental leg vascular effects of physical inactivity. Heating the foot area may be used as a nonpharmacological therapy to combat inactivity-induced leg vascular dysfunction, especially in people who are unable or unwilling to be active. </p>

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          Lack of exercise is a major cause of chronic diseases.

          Chronic diseases are major killers in the modern era. Physical inactivity is a primary cause of most chronic diseases. The initial third of the article considers: activity and prevention definitions; historical evidence showing physical inactivity is detrimental to health and normal organ functional capacities; cause versus treatment; physical activity and inactivity mechanisms differ; gene-environment interaction (including aerobic training adaptations, personalized medicine, and co-twin physical activity); and specificity of adaptations to type of training. Next, physical activity/exercise is examined as primary prevention against 35 chronic conditions [accelerated biological aging/premature death, low cardiorespiratory fitness (VO2max), sarcopenia, metabolic syndrome, obesity, insulin resistance, prediabetes, type 2 diabetes, nonalcoholic fatty liver disease, coronary heart disease, peripheral artery disease, hypertension, stroke, congestive heart failure, endothelial dysfunction, arterial dyslipidemia, hemostasis, deep vein thrombosis, cognitive dysfunction, depression and anxiety, osteoporosis, osteoarthritis, balance, bone fracture/falls, rheumatoid arthritis, colon cancer, breast cancer, endometrial cancer, gestational diabetes, pre-eclampsia, polycystic ovary syndrome, erectile dysfunction, pain, diverticulitis, constipation, and gallbladder diseases]. The article ends with consideration of deterioration of risk factors in longer-term sedentary groups; clinical consequences of inactive childhood/adolescence; and public policy. In summary, the body rapidly maladapts to insufficient physical activity, and if continued, results in substantial decreases in both total and quality years of life. Taken together, conclusive evidence exists that physical inactivity is one important cause of most chronic diseases. In addition, physical activity primarily prevents, or delays, chronic diseases, implying that chronic disease need not be an inevitable outcome during life. © 2012 American Physiological Society. Compr Physiol 2:1143-1211, 2012.
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            Influences of cardiorespiratory fitness and other precursors on cardiovascular disease and all-cause mortality in men and women.

            To quantify the relation of cardiorespiratory fitness to cardiovascular disease (CVD) mortality and to all-cause mortality within strata of other personal characteristics that predispose to early mortality. DESIGN--Observational cohort study. We calculated CVD and all-cause death rates for low (least fit 20%), moderate (next 40%), and high (most fit 40%) fitness categories by strata of smoking habit, cholesterol level, blood pressure, and health status. Preventive medicine clinic. Participants were 25341 men and 7080 women who completed preventive medical examinations, including a maximal exercise test. Cardiovascular disease and all-cause mortality. There were 601 deaths during 211996 man-years of follow-up, and 89 deaths during 52982 woman-years of follow-up. Independent predictors of mortality among men, with adjusted relative risks (RRs) and 95% confidence intervals (CIs), were low fitness (RR, 1.52;95% CI, 1.28-1.82), smoking (RR, 1.65; 95% CI, 1.39-1.97), abnormal electrocardiogram (RR, 1.64;95% CI, 1.34-2.01), chronic illness (RR, 1.63;95% CI, 1.37-1.95), increased cholesterol level (RR, 1.34; 95% CI, 1.13-1.59), and elevated systolic blood pressure (RR, 1.34; 95% CI, 1.13-1.59). The only statistically significant independent predictors of mortality in women were low fitness (RR, 2.10; 95% Cl, 1.36-3.21) and smoking (RR, 1.99; 95% Cl, 1.25-3.17). Inverse gradients were seen for mortality across fitness categories within strata of other mortality predictors for both sexes. Fit persons with any combination of smoking, elevated blood pressure, or elevated cholesterol level had lower adjusted death rates than low-fit persons with none of these characteristics. Low fitness is an important precursor of mortality. The protective effect of fitness held for smokers and nonsmokers, those with and without elevated cholesterol levels or elevated blood pressure, and unhealthy and healthy persons. Moderate fitness seems to protect against the influence of these other predictors on mortality. Physicians should encourage sedentary patients to become physically active and thereby reduce the risk of premature mortality.
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              A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.

              This report is the continuation of two earlier reports that defined human arterial intima and precursors of advanced atherosclerotic lesions in humans. This report describes the characteristic components and pathogenic mechanisms of the various advanced atherosclerotic lesions. These, with the earlier definitions of precursor lesions, led to the histological classification of human atherosclerotic lesions found in the second part of this report. The Committee on Vascular Lesions also attempted to correlate the appearance of lesions noted in clinical imaging studies with histological lesion types and corresponding clinical syndromes. In the histological classification, lesions are designated by Roman numerals, which indicate the usual sequence of lesion progression. The initial (type 1) lesion contains enough atherogenic lipoprotein to elicit an increase in macrophages and formation of scattered macrophage foam cells. As in subsequent lesion types, the changes are more marked in locations of arteries with adaptive intimal thickening. (Adaptive thickenings, which are present at constant locations in everyone from birth, do not obstruct the lumen and represent adaptations to local mechanical forces). Type II lesions consist primarily of layers of macrophage foam cells and lipid-laden smooth muscle cells and include lesions grossly designated as fatty streaks. Type III is the intermediate stage between type II and type IV (atheroma, a lesion that is potentially symptom-producing). In addition to the lipid-laden cells of type II, type III lesions contain scattered collections of extracellular lipid droplets and particles that disrupt the coherence of some intimal smooth muscle cells. This extracellular lipid is the immediate precursor of the larger, confluent, and more disruptive core of extracellular lipid that characterizes type IV lesions. Beginning around the fourth decade of life, lesions that usually have a lipid core may also contain thick layers of fibrous connective tissue (type V lesion) and/or fissure, hematoma, and thrombus (type VI lesion). Some type V lesions are largely calcified (type Vb), and some consist mainly of fibrous connective tissue and little or no accumulated lipid or calcium (type Vc).
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                Author and article information

                Journal
                Journal of Applied Physiology
                Journal of Applied Physiology
                American Physiological Society
                8750-7587
                1522-1601
                July 2017
                July 2017
                : 123
                : 1
                : 49-54
                Affiliations
                [1 ]Faculty of Physical Education, University of Brasília, Brasília, Brazil; and
                [2 ]Department of Nutrition and Exercise Physiology, Dalton Cardiovascular Research Center, Department of Child Health, University of Missouri, Columbia, Missouri
                Article
                10.1152/japplphysiol.00001.2017
                5538818
                28450547
                43f35a38-9156-40fb-b839-96ec12f2f30b
                © 2017
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