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      Association between resting heart rate, metabolic syndrome and cardiorespiratory fitness in Korean male adults

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          Abstract

          Background/Objective

          The present study aimed to investigate the association between metabolic syndrome and cardiorespiratory fitness according to resting heart rate of Korean male adults.

          Methods

          A total of 11,876 male adults aged 20–65 years who underwent health examinations from 2010 to 2015 at a National Fitness Centre in South Korea were included. Subjects' resting heart rate, cardiorespiratory fitness (VO 2max), and metabolic syndrome parameters were collected. The subjects were divided into 5 categories (<60 bpm, 60–69 bpm, 70–79 bpm, 80–89 bpm, and ≥90 bpm) of resting heart rate for further analysis.

          Results

          We found that elevated resting heart rate was positively associated with body mass index, systolic blood pressure, diastolic blood pressure, triglycerides, and fasting blood glucose levels ( p < 0.001, respectively); in contrast, elevated resting heart rate was inversely associated with VO 2max ( p < 0.001). When resting heart rate of subjects was categorized into quintiles and analysed, the results showed that the relative risk of metabolic syndrome was 1.53-fold higher (95% CI, 1.34 to 1.82) in the range of 60–69 beats per minute (bpm), 2.08-fold higher (95% CI, 1.77 to 2.45) in the range of 70–79 bpm, 2.28-fold higher (95% CI, 1.73 to 3.00) in the range of 80–89 bpm, and 2.61-fold higher (95% CI, 1.62 to 4.20) in the range of ≥90 bpm, compared to those <60 bpm; this indicated that as resting heart rate increased, the relative risk of metabolic syndrome also increased.

          Conclusion

          Resting heart rate of male adults was found to be associated with cardiorespiratory fitness; the risk factors for metabolic syndrome and relative risk of metabolic syndrome increased as resting heart rate increased.

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          Most cited references26

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          Banting lecture 1988. Role of insulin resistance in human disease.

          G M Reaven (1988)
          Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Physical fitness and all-cause mortality. A prospective study of healthy men and women.

            We studied physical fitness and risk of all-cause and cause-specific mortality in 10,224 men and 3120 women who were given a preventive medical examination. Physical fitness was measured by a maximal treadmill exercise test. Average follow-up was slightly more than 8 years, for a total of 110,482 person-years of observation. There were 240 deaths in men and 43 deaths in women. Age-adjusted all-cause mortality rates declined across physical fitness quintiles from 64.0 per 10,000 person-years in the least-fit men to 18.6 per 10,000 person-years in the most-fit men (slope, -4.5). Corresponding values for women were 39.5 per 10,000 person-years to 8.5 per 10,000 person-years (slope, -5.5). These trends remained after statistical adjustment for age, smoking habit, cholesterol level, systolic blood pressure, fasting blood glucose level, parental history of coronary heart disease, and follow-up interval. Lower mortality rates in higher fitness categories also were seen for cardiovascular disease and cancer of combined sites. Attributable risk estimates for all-cause mortality indicated that low physical fitness was an important risk factor in both men and women. Higher levels of physical fitness appear to delay all-cause mortality primarily due to lowered rates of cardiovascular disease and cancer.
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              Effective arterial elastance as index of arterial vascular load in humans.

              This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (Ea), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [Ea(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [Ea(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of Ea(PV), both Ea(Z) and Ea(PV) were virtually identical over a broad range of altered conditions: Ea(PV) = 0.97.Ea(Z) + 0.17; n = 33, r2 = 0.98, SEE = 0.09, p less than 0.0001. Whereas Ea(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate Ea (PV) from routine arterial pressures were tested and validated. Ea(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by Ea.
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                Author and article information

                Contributors
                Journal
                J Exerc Sci Fit
                J Exerc Sci Fit
                Journal of Exercise Science and Fitness
                The Society of Chinese Scholars on Exercise Physiology and Fitness
                1728-869X
                2226-5104
                20 June 2017
                June 2017
                20 June 2017
                : 15
                : 1
                : 27-31
                Affiliations
                [a ]Department of Physical Education, Changwon National University, Republic of Korea
                [b ]Department of Sports Medicine, National Health Fitness Center, Republic of Korea
                Author notes
                []Corresponding author. Department of Sports Medicine, National Fitness Center, Olympic-ro 424, Songpa-gu, Seoul, 05540, Republic of Korea.Department of Sports MedicineNational Fitness CenterOlympic-ro 424Songpa-guSeoul05540Republic of Korea tigerkor80@ 123456naver.com
                Article
                S1728-869X(17)30028-X
                10.1016/j.jesf.2017.06.001
                5812868
                29541128
                20a6e69f-ccca-4ba7-80e8-5c8b33726448
                © 2017 The Society of Chinese Scholars on Exercise Physiology and Fitness. Published by Elsevier (Singapore) Pte Ltd.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 24 February 2017
                : 2 June 2017
                : 8 June 2017
                Categories
                Original Article

                cardiorespiratory fitness,metabolic syndrome,resting heart rate

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