Background: Sedentary activity and sitting for at least 10 hours per day can increase the risk for cardiovascular disease by more than 60%. Use of standing desks may decrease sedentary time and improve cardiovascular health. Acute standing lowers pulse wave velocity (PWV), but chronic effects remain unknown. The purpose of this study was to determine the effect of chronic standing desk use on arterial stiffness versus seated controls. Methods: A total of 48 adults participated in this study. Twenty-four participants qualified as seated desk users (age 41 [10] y, body mass index 25 [4] kg/m2) and 24 as standing desk users (age 45 [12] y, body mass index 25 [5] kg/m2). Arterial stiffness was assessed as PWV within the aorta, arm, and leg. Results: Carotid–femoral PWV (cfPWV) was not different between seated (6.6 [1.3] m/s) and standing (6.9 [1.3] m/s) groups (P = .47). Similarly, there were no differences in arm or leg PWV between groups (P = .13 and P = .66, respectively). A secondary analysis of traditional factors of age and aerobic fitness revealed significant differences in cfPWV in seated and standing desk participants. Age also significantly influenced cfPWV across conditions. Conclusions: Standing for >50% of a workday did not affect PWV. Consistent with previous research, fitness and age are important modulators of arterial stiffness.

Sedentary behavior is an epidemic that plagues the daily lives of many American citizens. Sedentary behavior or sitting is often referred as the “new smoking.”1 For example, older cigarette smokers are nearly 3 times more likely to die from a cardiovascular disease (CVD) than age-matched nonsmokers.2 In comparison, a meta-analysis by Wilmot et al3 demonstrated that individuals who reported long bouts of sedentary activity had a 147% increased risk of CVD and 90% increase in cardiovascular mortality. Another study in women revealed a 63% increased CVD risk when average sitting time was 10 or more hours per day compared with 5 or less hours per day.4

The relation between sedentary behavior and CVD is complex. Sedentary behavior is shown to increase arterial stiffness and is a known contributor to hypertension and CVD.5,6 Clearly, a reduction in sedentary time and replacement with an aerobic and/or resistance exercise intervention can help to reduce arterial stiffness.7,8 However, there is a large cohort of individuals who may be exercise intolerant, have a limiting medical condition, or lack sufficient time to engage in proper daily exercise. For these reasons, and many others, office workers may consider a standing desk to sit less and potentially reduce health risks. In particular, there is evidence to suggest that standing workstations can provide cardiovascular benefits ranging from improved cardiometabolic risk factors9 to lower ambulatory blood pressure.10 Importantly, there is very little literature on the use of standing desks and arterial stiffness.

To our knowledge, only one study has examined the effect of standing desks on arterial stiffness. Specifically, Gibbs et al11 had participants alternate between sitting and standing throughout the day, and demonstrated acute decreases in carotid–ankle pulse wave velocity (PWV) compared with the seated controls, indicative of decreased arterial stiffness. In addition, there was a trend to decrease carotid–radial PWV (crPWV), an indicator of arm arterial stiffness. No changes were observed in carotid–femoral PWV (cfPWV),11 often considered the gold standard assessment of arterial health with applanation tonometry.12 To date, no published studies have reported the chronic effects of standing desk use on PWV. Therefore, the purpose of this study was to determine the chronic effect of standing desk use on arterial stiffness versus seated controls. We hypothesized that university office staff/faculty individuals who chronically stand at work would demonstrate lower arterial stiffness (ie, cfPWV, crPWV, and leg PWV [lPWV]) than those who chronically sit at work.

Methods

Participant Information

Healthy adult office workers between 18 and 65 years of age were recruited from Michigan Technological University and the local surrounding community. Potential participants were included in the study if they (1) performed light office work at a seated or standing workstation for >4 hours per day, (2) were free of diagnosed cardiovascular and metabolic diseases, (3) had a body mass index (BMI) < 40 kg/m2, (4) were not hypertensive (systolic arterial pressure [SAP] < 140 mm Hg, diastolic arterial pressure [DAP] < 90 mm Hg), and (5) had aortic pulse pressure below 50 mm Hg. A self-report questionnaire was administered to determine the number of hours spent sitting and standing throughout the workday. Office workers that used a standing desk >4 hours per day for a minimum of 8 weeks (desk use 2 [1] y) were classified as chronic standing desk users. Eight weeks is double the traditional 4 weeks minimum allotted to determine changes in endothelial function from interventional studies.13

Fifty-five participants were recruited, and 50 (42 females and 8 males) were enrolled in the study. Normality tests were conducted on the variables of age, predicted VO2peak, and trunk fat percentage. Two participant’s VO2peak values were classified as outliers and thus excluded from analyses. Thus, our final sample size consisted of 24 chronic seated desk users (19 females and 5 males) and 24 chronic standing desk users (21 females and 3 males). All participants were nonsmokers, did not take cardiovascular medications, and were free of signs of CVD such as hypertension, stroke, and diabetes. Demographic data between seated and standing classifications are presented in Table 1. All women were not pregnant and reported their menstrual cycle status/phase during the final testing session in an effort to have equal distribution of early follicular, mid-luteal, perimenopausal, and postmenopausal women within the seated and standing desk groups. This study was approved by the Michigan Technological University Institutional Review Board. All participants provided written informed consent prior to testing.

Table 1

Participant Demographics: Seated Versus Standing

VariableSeated (n = 24, 19 females)Standing (n = 24, 21 females)P value
Age, y41 (10)45 (12).24
Height, m1.67 (0.1)1.67 (0.1).96
Body mass, kg70 (12)71 (13).70
BMI, kg/m225 (4)25 (5).86
Fat, %28 (8)30 (8).36
Trunk fat, %26 (8)28 (8).26
VO2peak, mL·kg−1·min−139 (8)34 (10).12
Godin (score, a.u.)61 (63)47 (22).31
SAP, mm Hg113 (8)115 (11).53
DAP, mm Hg66 (5)71 (7)*.01
HR, beats/min59 (11)63 (9).21

Abbreviations: a.u., arbitrary units; BMI, body mass index; DAP, diastolic arterial pressure; Godin, Physical Activity Questionnaire activity score; HR, heart rate; n, number of participants; SAP, systolic arterial pressure. Note: Values are presented in mean (SD).

*Significantly different from corresponding seated value, P < .05.

Procedures

Participants arrived to the Clinical and Applied Human Physiology Laboratory following a fast for a minimum of 3 hours and abstaining from exercise, alcohol, and caffeine for at least 12 hours prior to the scheduled orientation and testing sessions. During the orientation session, participants completed an informed consent form, participant information sheet, and a Godin Leisure-Time Questionnaire (ie, quantify physical activity habits outside of normal workday). Height and body mass were recorded. In addition, body fat percentage was estimated with a bioelectrical impedance scale (BC-418 Segmental Body Composition Analyzer; Tanita, Tokyo, Japan).14 Participants were positioned supine on an examination table, and following quiet rest, 3 brachial blood pressure recordings were taken using an automated sphygmomanometer. Preliminary arterial stiffness measures were taken via pulse wave analysis recordings of the radial artery to screen for aortic pulse pressure.15 Aerobic fitness was estimated via a Rockport Walk test16 on a treadmill at 1% grade within the laboratory following completion of a Physical Activity Readiness Questionnaire (Canadian Society for Exercise Physiology).

Following the orientation session, participants reported to the laboratory approximately 2 weeks later for their scheduled testing session. Following instrumentation, participants were asked to refrain from talking for 5 minutes, while laying supine, on a cushioned examination table prior to blood pressure measurements. Using an automated sphygmomanometer, 3 brachial blood pressures were obtained, with each measurement separated by 1 minute. Duplicate pulse wave analysis recordings were then collected from the radial pulse site for 10 cardiac cycles, with operator indices above 80%. Estimates of aortic systolic arterial pressure (aSAP) and aortic diastolic arterial pressure (aDAP) were recorded in addition to aortic augmentation index (AIx) and AIx normalized to 75 heart beats per minute (AIx @75). Three regional PWV measures (carotid–femoral, carotid–radial, and femoral–dorsalis pedis) were performed to assess arterial stiffness within the aorta, arm, and leg via duplicate recordings at each site. Measures of distance (measured in millimeter) were taken from the suprasternal notch (landmark for aorta) to the pulse site of interest (carotid, radial, femoral, or dorsalis pedis). Successful recordings were obtained at carotid, radial, and femoral arteries for all participants. However, 2 dorsalis pedis recordings lacked quality in the seated group. Hence, n = 22 and 24 in the seated and standing groups for lPWV, respectively.

Measurements

Blood Pressure

Following 5 minutes of supine rest, brachial blood pressure recordings were taken with an automated sphygmomanometer (Omron HEM-907XL; Omron Health Care, Kyoto, Japan). Blood pressure recordings were performed in triplicate during the testing session with 1 minute between consecutive recordings.

Pulse Wave Analysis

The average brachial blood pressure was entered in the SphygmoCor data collection software (SphygmoCor; CPVH, Sydney, Australia) for calibration purposes. The tonometer probe was placed over the radial artery to gently press it against the carpals of the wrist. Following probe adjustment to find a strong reading and eliminate systolic and diastolic variation, the probe was kept still for approximately 10 to 12 seconds to capture 10 radial pulse waves. This technique was done in duplicate to ensure consistent quality recordings. The software analyzed the radial pulse wave via a generalized transfer function to generate an aortic pulse wave and aortic blood pressure values.

Pulse Wave Velocity

Measurements of straight-line distance (measured in mm) were recorded from the suprasternal notch to pulse sites of interest to examine cfPWV and crPWV. Likewise, a straight-line distance from the suprasternal notch to the femoral and dorsalis pedis (ie, top of the foot) and pulse sites were recorded for lPWV. Each pulse wave reading was gated to the R waves from lead II of the ECG to calculate the time delay between pulse creation at the heart and arrival at the pulse site. The change in the distance (proximal–distal in reference to aorta) was divided by the change in time delay (proximal–distal) to provide a speed in meters per second. Duplicate readings with an SD ≤10% were used for data analysis.

Data and Statistical Analyses

Data were exported from the SphygmoCor system to a Microsoft Excel file and then to SPSS. The duplicate pulse wave velocities were averaged in preparation for statistical analysis using a commercial software (SPSS version 25.0; SPSS, Chicago, IL). Normality analyses were performed for all major variables including age, estimated VO2peak, body mass index, trunk fat percentage, blood pressure (SAP and DAP), heart rate, and arterial stiffness values, and these were compared between seated and standing groups via independent sample t tests. We used a median analysis to classify participants by age, aerobic fitness (VO2peak), and trunk fat percentage (ie, younger vs older, higher fitness vs lower fitness, and higher trunk fat vs lower trunk fat) for additional secondary analysis of cfPWV. Univariate analysis of variance analysis was used to detect condition (ie, seated or standing) interaction with the variables of age, aerobic fitness, and trunk fat percentage (ie, traditional factors). If a significant condition × traditional factor interaction was detected, post hoc unpaired t tests were used to compare group means. Results are expressed as mean (SD). Means were considered significantly different when P < .05 (ie, 2-tailed test).

Power Analysis

Power analysis was performed to ensure an adequate sample size for a clinically relevant 1 m/s difference in cfPWV, as such a reduction can reportedly reduce CVD risk and mortality by 15%.12 Power analysis software (G*Power version 3.1.9.2; Kiel, Germany) was used to determine proper effect size for total sample power of 0.8, alpha of .05, and equal allocation ratio. Effect size was determined via group mean and group SD. A difference of 1 was selected between group means from Vlachopoulos et al12 and an SD of 1.2 was selected from The Reference Values for Arterial Stiffness Collaboration via cfPWV reference value of 40- to 49-year-old individuals with normal blood pressure (n = 562).17 Adequate statistical power of β = 0.8333 was achieved with a sample size of n = 48 (n = 24 in each group).

Results

Participant Demographics

Table 1 compares demographic data between seated and standing desk participants. No differences were detected in age, height, body mass, body mass index, body fat percentage, trunk fat percentage, estimated VO2peak, Godin activity score, SAP, and heart rate. However, standing desk participants exhibited a higher DAP (71 [7] mm Hg) compared with seated desk participants (66 [5] mm Hg, P = .01).

Central Hemodynamics and Augmentation Index

Table 2 compares aortic blood pressure and AIx values between seated and standing desk participants. No differences were detected in aSAP, AIx, or Alx normalized to 75 heart beats per minute (AIx @75). Similar to brachial DAP, aDAP was higher in standing desk participants (72 [7] mm Hg) compared with seated desk participants (67 [5] mm Hg, P = .01).

Table 2

Central Hemodynamics and Augmentation Index: Seated Versus Standing

VariableSeated (n = 24, 19 females)Standing (n = 24, 21 females)P value
aSAP101 (7)104 (12).20
aDAP67 (5)72 (7)*.01
AIx19 (11)19 (15).88
AIx @7510 (11)13 (14).50

Abbreviations: aDAP, aortic diastolic arterial pressure; AIx @75, aortic augmentation index normalized to 75 cardiac cycles; AIx, aortic augmentation index; aSAP, aortic systolic arterial pressure; n, number of participants. Note: Values are presented in mean (SD).

*Significantly different from corresponding seated value, P < .05.

Standing Desks and PWV

Figure 1 compares cfPWV, or arterial stiffness in the aorta, when categorized by seated and standing. No differences were detected between seated and standing groups (Panel A, P = .47) or when normalized to aortic mean arterial pressure (Panel B, P = .54). Figure 2 represents crPWV (Panel A) and lPWV (Panel B). The recordings represent arterial stiffness in the arm and leg, respectively, where there was no significant difference between seated and standing groups (P = .13 and .66, respectively).

Figure 1
Figure 1

—cfPWV (Panel A) and cfPWV normalized to aMAP (Panel B), when classified by seated versus standing (P = .47 and .54). Results are presented as mean (SD). aMAP indicates aortic mean arterial pressure; cfPWV, carotid–femoral pulse wave velocity.

Citation: Journal of Physical Activity and Health 16, 11; 10.1123/jpah.2018-0668

Figure 2
Figure 2

—crPWV in Panel A and LPWV in Panel B, when classified by seated versus standing (P = .13 and .66). Results are presented as means (SD). cfPWV indicates carotid–femoral pulse wave velocity; LPWV, leg pulse wave velocity.

Citation: Journal of Physical Activity and Health 16, 11; 10.1123/jpah.2018-0668

Traditional Factors and cfPWV

Based on median analysis of age, aerobic fitness, and trunk fat percentage, Figure 3 shows participants separated into seated and standing categories (ie, condition), further classified by traditional categories of older versus younger, lower fitness versus higher fitness, and higher trunk fat versus lower trunk fat. A significant condition × age (P = .02) and condition × aerobic fitness (P = .01) interaction was detected, but not trunk fat percentage. Panel A of Figure 3 demonstrates that younger and older seated desk participants (median = 41.5 y) had similar cfPWV. However, there was a trend for younger standing desk participants to have lower cfPWV compared with older standing desk participants (median = 44.5 y; P = .05). Panel B of Figure 3 demonstrates that cfPWV in seated higher and lower aerobic fitness participants (median = 37.1 mL·kg−1·min−1) did not differ. However, cfPWV in higher aerobic fitness standing desk participants was significantly lower compared with lower aerobic fitness standing desk participants (6.2 [1.0] m/s vs 7.5 [1.2] m/s; median = 33.9 mL·kg−1·min−1; P = .03). In addition, higher aerobic fitness seated participants had lower cfPWV when compared with lower aerobic fitness standing desk participants (6.1 [0.6] m/s vs 7.5 [1.2] m/s; P = .02). Finally, Panel C of Figure 3 shows no significant interaction of trunk fat percentage on the seated versus standing classifications and cfPWV (P = .17).

Figure 3
Figure 3

—Carotid–femoral pulse wave velocity (cfPWV) classified as seated versus standing and traditional factors such as age (Panel A; seated median = 41.5 y, standing median = 44.5 y), fitness (Panel B; seated median = 37.1 mL·kg−1·min−1, standing median = 33.9 mL·kg−1·min−1), and trunk fat (Panel C; seated median = 24.4%, standing median = 28.7%). Results are presented as means (SD). *Significantly different cfPWV between standing higher and lower fitness, P = .03. Significantly different cfPWV between seated higher fitness and standing lower fitness, P = .02.

Citation: Journal of Physical Activity and Health 16, 11; 10.1123/jpah.2018-0668

Discussion

Main Findings

To our knowledge, this is the first study to examine chronic use of a standing desk in the workplace on arterial function. Traditional factors including age and aerobic fitness significantly influenced cfPWV. By contrast, cfPWV, crPWV, and lPWV were not different between chronic seated and standing desk workers. The results of this study did not support our hypothesis, as cfPWV of individuals who used a standing desk for at least 50% of the day was not lower compared with seated desk controls. However, our results reinforce the importance of age and aerobic fitness as key modulators of arterial stiffness.

Standing Desk and cfPWV

As outlined previously, cfPWV is considered to be the gold standard of assessing arterial stiffness, where a 1 m/s decrease is associated with a 15% reduction in CVD risk.12 The comparison between seated and standing groups revealed no significant difference of cfPWV. This is supported by findings by Kruse et al,18 which suggest that acute standing does not improve the endothelial dysfunction induced by prolonged sitting. Altogether, this could be due to lack of achieving light physical activity while working at a standing desk. The relationship between light physical activity and cfPWV has been demonstrated in older (ie, 65–85 y) adults,19 but not in younger individuals.20 There is some evidence to suggest that only vigorous activity is correlated with improved arterial stiffness in younger adults, rather than habitual light to moderate physical activity.20 Importantly, this study examined primarily “mid-life” adults, which remains an understudied population. These findings are strengthened by fact that the standing and seated group participants reported similar activity levels via the Godin Leisure-Time Exercise Questionnaire, in addition to similar estimated VO2peak.

Standing Desk and DAP

Our results indicate that brachial and aDAP was elevated among participants in the standing desk group. This group of participants stood for at least 50% of a normal workday on average, which could increase baseline vascular tone or change vessel lumen diameter.21 The simple act of standing activates the sympathetic nervous system to mitigate blood pooling in the lower extremities and prevent presyncopal symptoms.22 Quiet standing can elicit a sympathoexcitatory response during a postprandial period, which is applicable to individuals working at a standing desk,23 potentially affecting blood pressure. Alternatively, chronic standing may lead to decreased vessel lumen diameter via remodeling, which can lead to increased DAP. Much of the literature reports acute lowering of blood pressure upon standing for extended periods, under both acute11 and chronic conditions.10,11 However, at least one other study reported an acute increase.24 The elevation of DAP in our healthy population is likely a minor concern as the standing group’s mean value was well below 80 mm Hg.

Median Analysis of Age, Aerobic Fitness, and Trunk Fat Percentage

A wide body of literature exists regarding the influence of age, aerobic fitness, and body fat on arterial stiffness.25,26 Our sample is in agreement with the literature where arterial stiffness is lower, or tends to be lower, in younger, high fit and low trunk fat individuals. However, standing did not have any additional influence on cfPWV when considering age, aerobic fitness, and trunk fat as shown in Figure 3. This again highlights that the act of prolonged standing may not activate mechanisms associated with arterial health or vessel elasticity independent of age, aerobic fitness, and trunk fat. Panel B of Figure 3 further highlights that fitness may be one of the most important regulators of arterial stiffness, given both seated and standing higher aerobic fitness participants exhibited lower cfPWV compared with standing lower aerobic fitness participants. We provide additional support that maintenance of aerobic fitness throughout the lifespan can help to keep cfPWV within a healthy range.27

Peripheral Arterial Stiffness and Standing Desks

Previous work on the acute effects of standing desk use shows significant reductions in carotid–ankle PWV.11 Inherently, the nature of PWV recordings in the periphery (ie, arm and leg) provides an indication of the stiffness of the muscular arteries. Muscular arteries aid in filtering excess pulsatility throughout the cardiovascular system to various end organs such as the brain or kidneys.28 Gibbs et al11 noted a trend for a change in crPWV, thus future work warrants investigation of how sit to stand transitions and/or intermittent walking may affect lPWV and crPWV.

Potential Energy Expenditure Influence on Arterial Stiffness

It is widely acknowledged that excess sitting is detrimental to health, often stemming from lack of energy expenditure and excess caloric intake.29 In principle, the concept of a standing desk is to attenuate sedentary time and increase energy expenditure. Numerous studies found standing increases energy expenditure above seated values.30,31 However, the amount of additional energy expended is somewhat trivial when comparing standing and seated values.32 With maintenance of current lifestyle and replacing sitting with standing, it would take many months to lose even 1 kg.33 With little differences in energy expenditure, this may be one of the contributing factors why the standing desk individuals did not exhibit differences in arterial stiffness compared with seated controls. Indirect calorimetry shows that standing increases oxygen consumption, but the increase does not achieve a level associated with light physical activity (ie, ≥2.5 METs).32 This is an important threshold, as lower cfPWV has been associated with increased light physical activity minutes in older adults.19 Replacing seated intervals with small walking periods at break or on lunch can significantly increase energy expenditure,31 and improve various risk factors for CVD.34 As previously mentioned, one acute study showed alternating sitting and standing through a workday (ie, alternating every 30 min) decreased carotid–ankle PWV, but only at the midday measures. Notably, cfPWV was not affected by intermittent standing.11 This finding, coupled with our findings, provide further evidence that standing may not be enough to prevent or improve arterial stiffness. It appears that intermittent activity at work and maintenance of aerobic fitness are more important for preventing age-related arterial stiffness than chronic standing.

Future Directions

Opportunities remain in the realm of arterial stiffness and standing desk, or alternative work stations. Cross-sectional designs have inherent limitations. Future work might initiate a standing desk intervention for 8 weeks or more to examine if/when arterial stiffness is affected from standing for most of the day after controlling for physical activity minutes outside of work. In addition, longitudinal studies should consider building upon initial cross-sectional designs to determine if chronic standing desk use can significantly attenuate arterial stiffness during the aging process compared with the seated desk controls.

Limitations

One potential limitation in this study is the small number of men, and that women were not studied in one phase of the menstrual cycle. Menstrual cycle status is reported to influence arterial stiffness. PWV measures are at the lowest during the mid-luteal phase35 and higher during early follicular.36 In addition, the onset of menopause appears to accelerate the age-related increases of arterial stiffness when compared with age-matched women who still possess their menstrual cycle.37 We recorded menstrual cycle status and this potential limitation should be minimized by the similar distribution of women in each phase/status (ie, early follicular, mid-luteal, perimenopause, and postmenopause). Distributions were 37%, 26%, 5%, and 26% in seated participants, and 24%, 24%, 5%, and 38%, respectively in standing participants. About 5% chose not to report menstrual status in the seated group, and 10% did not report in the standing group. Another potential limitation associated with this study is the variable time the standing desk participants had their workstation. However, we believe that this limitation is minimized as there was no significant relationship between length of standing desk use and cfPWV. Finally, we acknowledge the large SD of physical activity quantification via the Godin leisure-time survey among seated desk participants as a limitation. We believe that 3 participants over estimated their physical activity habits. This limitation is minimized by the fact that their estimated VO2peak scores were not abnormally high, and the distribution of the Godin scores was also normal.

Summary

Workplace standing desks and active workstations are in popular demand in the office, whereas their effects on human health are largely unknown. This study comparing chronic standing desk users and chronic seated desk users did not identify any differences in cfPWV, crPWV, or lPWV. In addition, secondary analysis of traditional factors of age and aerobic fitness revealed significant differences in cfPWV in seated and standing desk participants. Chronic standing for >4 hours per day does not appear to affect arterial stiffness. Thus, we suggest that aerobic fitness can be gained or maintained via a structured exercise protocol38 and/or intermittent physical activity at work such as taking the stairs or getting up and moving at least every hour.39

Acknowledgments

The authors would like to thank the participants from Michigan Technological University and local community for agreeing to participate in this study. In addition, the authors would like to thank undergraduate students Malina Felten and Katie Heikkinen for their assistance during the data collection portion of this study. Finally, we extend our appreciation to graduate student Travis Wakeham for his assistance with the data collection process. There were no funding sources associated with this study.

References

  • 1.

    Baddeley B, Sornalingam S, Cooper M. Sitting is the new smoking: where do we stand? Br J Gen Pract. 2016;66(646):258. PubMed ID: 27127279 doi:10.3399/bjgp16X685009

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 2.

    Taghizadeh N, Vonk JM, Boezen HM. Lifetime smoking history and cause-specific mortality in a cohort study with 43 years of follow-up. PLoS ONE. 2016;11(4):e0153310. PubMed ID: 27055053 doi:10.1371/journal.pone.0153310

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3.

    Wilmot EG, Edwardson CL, Achana FA, et al. Sedentary time in adults and the association with diabetes, cardiovascular disease and death: systematic review and meta-analysis. Diabetologia. 2012;55(11):2895–2905. PubMed ID: 22890825 doi:10.1007/s00125-012-2677-z

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 4.

    Chomistek AK, Manson JE, Stefanick ML, et al. Relationship of sedentary behavior and physical activity to incident cardiovascular disease: results from the Women’s Health Initiative. J Am Coll Cardiol. 2013;61(23):2346–2354. PubMed ID: 23583242 doi:10.1016/j.jacc.2013.03.031

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5.

    Horta BL, Schaan BD, Bielemann RM, et al. Objectively measured physical activity and sedentary-time are associated with arterial stiffness in Brazilian young adults. Atherosclerosis. 2015;243(1):148–154. PubMed ID: 26386211 doi:10.1016/j.atherosclerosis.2015.09.005

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6.

    Niiranen TJ, Kalesan B, Hamburg NM, Benjamin EJ, Mitchell GF, Vasan RS. Relative contributions of arterial stiffness and hypertension to cardiovascular disease: the framingham heart study. J Am Heart Assoc. 2016;5(11):pii: e004271. doi:10.1161/JAHA.116.004271

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Donley DA, Fournier SB, Reger BL, et al. Aerobic exercise training reduces arterial stiffness in metabolic syndrome. J Appl Physiol. 2014;116(11):1396–1404. doi:10.1152/japplphysiol.00151.2014

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8.

    Son WM, Sung KD, Cho JM, Park SY. Combined exercise reduces arterial stiffness, blood pressure, and blood markers for cardiovascular risk in postmenopausal women with hypertension. Menopause. 2017;24(3):262–268. PubMed ID: 27779565 doi:10.1097/GME.0000000000000765

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 9.

    Winkler EAH, Chastin S, Eakin EG, et al. Cardiometabolic impact of changing sitting, standing, and stepping in the workplace. Med Sci Sport Exer. 2018;50(3):516–524. doi:10.1249/MSS.0000000000001453

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10.

    Zeigler ZS, Mullane SL, Crespo NC, Buman MP, Gaesser GA. Effects of standing and light-intensity activity on ambulatory blood pressure. Med Sci Sport Exer. 2016;48(2):175–181. doi:10.1249/MSS.0000000000000754

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Gibbs BB, Kowalsky RJ, Perdomo SJ, Taormina JM, Balzer JR, Jakicic JM. Effect of alternating standing and sitting on blood pressure and pulse wave velocity during a simulated workday in adults with overweight/obesity. J Hypertens. 2017;35(12):2411–2418. doi:10.1097/HJH.0000000000001463

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Vlachopoulos C, Aznaouridis K, Stefanadis C. Prediction of cardiovascular events and all-cause mortality with arterial stiffness: a systematic review and meta-analysis. J Am Coll Cardiol. 2010;55(13):1318–1327. PubMed ID: 20338492 doi:10.1016/j.jacc.2009.10.061

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13.

    Kingwell BA, Sherrard B, Jennings GL, Dart AM. Four weeks of cycle training increases basal production of nitric oxide from the forearm. Am J Physiol. 1997;272(3 Pt 2):H1070–1077. PubMed ID: 9087577

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 14.

    Ward LC. Segmental bioelectrical impedance analysis: an update. Curr Opin Clin Nutr Metab Care. 2012;15(5):424–429. PubMed ID: 22814626 doi:10.1097/MCO.0b013e328356b944

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 15.

    Roman MJ, Devereux RB, Kizer JR, et al. High central pulse pressure is independently associated with adverse cardiovascular outcome the strong heart study. J Am Coll Cardiol. 2009;54(18):1730–1734. PubMed ID: 19850215 doi:10.1016/j.jacc.2009.05.070

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16.

    Kline GM, Porcari JP, Hintermeister R, et al. Estimation of VO2max from a one-mile track walk, gender, age, and body weight. Med Sci Sport Exer. 1987;19(3):253–259. doi:10.1249/00005768-198706000-00012

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Reference Values for Arterial Stiffness’ Collaboration. Determinants of pulse wave velocity in healthy people and in the presence of cardiovascular risk factors: “establishing normal and reference values.” Eur Heart J. 2010;31(19):2338–2350. doi:10.1093/eurheartj/ehq165

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 18.

    Kruse NT, Hughes WE, Benzo RM, Carr LJ, Casey DP. Workplace strategies to prevent sitting-induced endothelial dysfunction. Med Sci Sport Exer. 2018;50(4):801–808. doi:10.1249/MSS.0000000000001484

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Gando Y, Yamamoto K, Murakami H, et al. Longer time spent in light physical activity is associated with reduced arterial stiffness in older adults. Hypertension. 2010;56(3):540–546. PubMed ID: 20606102 doi:10.1161/HYPERTENSIONAHA.110.156331

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20.

    van de Laar RJ, Ferreira I, van Mechelen W, Prins MH, Twisk JW, Stehouwer CD. Lifetime vigorous but not light-to-moderate habitual physical activity impacts favorably on carotid stiffness in young adults: the Amsterdam growth and health longitudinal study. Hypertension. 2010;55(1):33–39. PubMed ID: 19996070 doi:10.1161/HYPERTENSIONAHA.109.138289

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Mulvany MJ, Baumbach GL, Aalkjaer C, et al. Vascular remodeling. Hypertension. 1996;28(3):505–506. PubMed ID: 8794840

  • 22.

    Amberson WR. Physiologic adjustments to the standing posture. Uni Md Sch Med Bull 1943;27:127–145.

  • 23.

    Cao L, Pilowsky PM. Quiet standing after carbohydrate ingestion induces sympathoexcitatory and pressor responses in young healthy males. Auton Neurosci. 2014;185:112–119. PubMed ID: 25129222 doi:10.1016/j.autneu.2014.07.007

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 24.

    Cox RH, Guth J, Siekemeyer L, Kellems B, Brehm SB, Ohlinger CM. Metabolic cost and speech quality while using an active workstation. J Phys Act Health. 2011;8(3):332–339. PubMed ID: 21487132 doi:10.1123/jpah.8.3.332

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 25.

    Vaitkevicius PV, Fleg JL, Engel JH, et al. Effects of age and aerobic capacity on arterial stiffness in healthy adults. Circulation. 1993;88(4 Pt 1):1456–1462. PubMed ID: 8403292 doi:10.1161/01.CIR.88.4.1456

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 26.

    Ferreira I, Snijder MB, Twisk JW, et al. Central fat mass versus peripheral fat and lean mass: opposite (adverse versus favorable) associations with arterial stiffness? The Amsterdam Growth and Health Longitudinal Study. J Clin Endocrinol Metab. 2004;89(6):2632–2639. PubMed ID: 15181034 doi:10.1210/jc.2003-031619

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 27.

    Tomoto T, Maeda S, Sugawara J. Relation between arterial stiffness and aerobic capacity: importance of proximal aortic stiffness. Eur J Sport Sci. 2017;17(5):571–575. PubMed ID: 28100164 doi:10.1080/17461391.2016.1277787

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 28.

    Zarrinkoob L, Ambarki K, Wahlin A, et al. Aging alters the dampening of pulsatile blood flow in cerebral arteries. J Cereb Blood Flow Metab. 2016;36(9):1519–1527. PubMed ID: 26823470 doi:10.1177/0271678X16629486

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 29.

    Levine JA. Lethal sitting: homo sedentarius seeks answers. Physiology. 2014;29(5):300–301.

  • 30.

    Gibbs BB, Kowalsky RJ, Perdomo SJ, Grier M, Jakicic JM. Energy expenditure of deskwork when sitting, standing or alternating positions. Occup Med. 2017;67(2):121–127. doi:10.1093/occmed/kqw115

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Creasy SA, Rogers RJ, Byard TD, Kowalsky RJ, Jakicic JM. Energy expenditure during acute periods of sitting, standing, and walking. J Phys Act Health. 2016;13(6):573–578. PubMed ID: 26693809 doi:10.1123/jpah.2015-0419

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 32.

    Reiff C, Marlatt K, Dengel DR. Difference in caloric expenditure in sitting versus standing desks. J Phys Act Health. 2012;9(7):1009–1011. PubMed ID: 22971879 doi:10.1123/jpah.9.7.1009

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 33.

    Saeidifard F, Medina-Inojosa JR, Supervia M, et al. Differences of energy expenditure while sitting versus standing: a systematic review and meta-analysis. Eur J Prev Cardiol. 2018;25(5):522–538. PubMed ID: 29385357 doi:10.1177/2047487317752186

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 34.

    Altenburg TM, Rotteveel J, Dunstan DW, Salmon J, Chinapaw MJ. The effect of interrupting prolonged sitting time with short, hourly, moderate-intensity cycling bouts on cardiometabolic risk factors in healthy, young adults. J Appl Physiol. 2013;115(12):1751–1756. doi:10.1152/japplphysiol.00662.2013

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 35.

    Madhura M, Sandhya T. Effect of different phases of menstrual cycle on reflection index, stiffness index and pulse wave velocity in healthy subjects. JCDR. 2014;8(9):BC01.

    • Search Google Scholar
    • Export Citation
  • 36.

    Ounis-Skali N, Mitchell GF, Solomon CG, Solomon SD, Seely EW. Changes in central arterial pressure waveforms during the normal menstrual cycle. J Investig Med. 2006;54(6):321–326. PubMed ID: 17134615 doi:10.2310/6650.2006.05055

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 37.

    Moreau KL, Hildreth KL. Vascular aging across the menopause transition in healthy women. Adv Vasc Med. 2014;2014:pii: 204390.

  • 38.

    Xu D, Wang H, Chen S, et al. Aerobic exercise training improves orthostatic tolerance in aging humans. Med Sci Sport Exer. 2017;49(4):728–735. doi:10.1249/MSS.0000000000001153

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 39.

    Yu J, Abraham JM, Dowd B, Higuera LF, Nyman JA. Impact of a workplace physical activity tracking program on biometric health outcomes. Prev Med. 2017;105:135–141. PubMed ID: 28890355 doi:10.1016/j.ypmed.2017.09.002

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation

If the inline PDF is not rendering correctly, you can download the PDF file here.

Greenlund, Elmer, and Carter are with the Department of Kinesiology & Integrative Physiology, Michigan Technological University, Houghton, MI. Greenlund, Suriano, and Durocher are with the Department of Biological Sciences, Michigan Technological University, Houghton, MI.

Durocher (jjduroch@mtu.edu) is corresponding author.
  • View in gallery

    —cfPWV (Panel A) and cfPWV normalized to aMAP (Panel B), when classified by seated versus standing (P = .47 and .54). Results are presented as mean (SD). aMAP indicates aortic mean arterial pressure; cfPWV, carotid–femoral pulse wave velocity.

  • View in gallery

    —crPWV in Panel A and LPWV in Panel B, when classified by seated versus standing (P = .13 and .66). Results are presented as means (SD). cfPWV indicates carotid–femoral pulse wave velocity; LPWV, leg pulse wave velocity.

  • View in gallery

    —Carotid–femoral pulse wave velocity (cfPWV) classified as seated versus standing and traditional factors such as age (Panel A; seated median = 41.5 y, standing median = 44.5 y), fitness (Panel B; seated median = 37.1 mL·kg−1·min−1, standing median = 33.9 mL·kg−1·min−1), and trunk fat (Panel C; seated median = 24.4%, standing median = 28.7%). Results are presented as means (SD). *Significantly different cfPWV between standing higher and lower fitness, P = .03. Significantly different cfPWV between seated higher fitness and standing lower fitness, P = .02.

  • 1.

    Baddeley B, Sornalingam S, Cooper M. Sitting is the new smoking: where do we stand? Br J Gen Pract. 2016;66(646):258. PubMed ID: 27127279 doi:10.3399/bjgp16X685009

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 2.

    Taghizadeh N, Vonk JM, Boezen HM. Lifetime smoking history and cause-specific mortality in a cohort study with 43 years of follow-up. PLoS ONE. 2016;11(4):e0153310. PubMed ID: 27055053 doi:10.1371/journal.pone.0153310

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 3.

    Wilmot EG, Edwardson CL, Achana FA, et al. Sedentary time in adults and the association with diabetes, cardiovascular disease and death: systematic review and meta-analysis. Diabetologia. 2012;55(11):2895–2905. PubMed ID: 22890825 doi:10.1007/s00125-012-2677-z

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 4.

    Chomistek AK, Manson JE, Stefanick ML, et al. Relationship of sedentary behavior and physical activity to incident cardiovascular disease: results from the Women’s Health Initiative. J Am Coll Cardiol. 2013;61(23):2346–2354. PubMed ID: 23583242 doi:10.1016/j.jacc.2013.03.031

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5.

    Horta BL, Schaan BD, Bielemann RM, et al. Objectively measured physical activity and sedentary-time are associated with arterial stiffness in Brazilian young adults. Atherosclerosis. 2015;243(1):148–154. PubMed ID: 26386211 doi:10.1016/j.atherosclerosis.2015.09.005

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 6.

    Niiranen TJ, Kalesan B, Hamburg NM, Benjamin EJ, Mitchell GF, Vasan RS. Relative contributions of arterial stiffness and hypertension to cardiovascular disease: the framingham heart study. J Am Heart Assoc. 2016;5(11):pii: e004271. doi:10.1161/JAHA.116.004271

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Donley DA, Fournier SB, Reger BL, et al. Aerobic exercise training reduces arterial stiffness in metabolic syndrome. J Appl Physiol. 2014;116(11):1396–1404. doi:10.1152/japplphysiol.00151.2014

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 8.

    Son WM, Sung KD, Cho JM, Park SY. Combined exercise reduces arterial stiffness, blood pressure, and blood markers for cardiovascular risk in postmenopausal women with hypertension. Menopause. 2017;24(3):262–268. PubMed ID: 27779565 doi:10.1097/GME.0000000000000765

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 9.

    Winkler EAH, Chastin S, Eakin EG, et al. Cardiometabolic impact of changing sitting, standing, and stepping in the workplace. Med Sci Sport Exer. 2018;50(3):516–524. doi:10.1249/MSS.0000000000001453

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 10.

    Zeigler ZS, Mullane SL, Crespo NC, Buman MP, Gaesser GA. Effects of standing and light-intensity activity on ambulatory blood pressure. Med Sci Sport Exer. 2016;48(2):175–181. doi:10.1249/MSS.0000000000000754

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Gibbs BB, Kowalsky RJ, Perdomo SJ, Taormina JM, Balzer JR, Jakicic JM. Effect of alternating standing and sitting on blood pressure and pulse wave velocity during a simulated workday in adults with overweight/obesity. J Hypertens. 2017;35(12):2411–2418. doi:10.1097/HJH.0000000000001463

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 12.

    Vlachopoulos C, Aznaouridis K, Stefanadis C. Prediction of cardiovascular events and all-cause mortality with arterial stiffness: a systematic review and meta-analysis. J Am Coll Cardiol. 2010;55(13):1318–1327. PubMed ID: 20338492 doi:10.1016/j.jacc.2009.10.061

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 13.

    Kingwell BA, Sherrard B, Jennings GL, Dart AM. Four weeks of cycle training increases basal production of nitric oxide from the forearm. Am J Physiol. 1997;272(3 Pt 2):H1070–1077. PubMed ID: 9087577

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 14.

    Ward LC. Segmental bioelectrical impedance analysis: an update. Curr Opin Clin Nutr Metab Care. 2012;15(5):424–429. PubMed ID: 22814626 doi:10.1097/MCO.0b013e328356b944

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 15.

    Roman MJ, Devereux RB, Kizer JR, et al. High central pulse pressure is independently associated with adverse cardiovascular outcome the strong heart study. J Am Coll Cardiol. 2009;54(18):1730–1734. PubMed ID: 19850215 doi:10.1016/j.jacc.2009.05.070

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 16.

    Kline GM, Porcari JP, Hintermeister R, et al. Estimation of VO2max from a one-mile track walk, gender, age, and body weight. Med Sci Sport Exer. 1987;19(3):253–259. doi:10.1249/00005768-198706000-00012

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Reference Values for Arterial Stiffness’ Collaboration. Determinants of pulse wave velocity in healthy people and in the presence of cardiovascular risk factors: “establishing normal and reference values.” Eur Heart J. 2010;31(19):2338–2350. doi:10.1093/eurheartj/ehq165

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 18.

    Kruse NT, Hughes WE, Benzo RM, Carr LJ, Casey DP. Workplace strategies to prevent sitting-induced endothelial dysfunction. Med Sci Sport Exer. 2018;50(4):801–808. doi:10.1249/MSS.0000000000001484

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Gando Y, Yamamoto K, Murakami H, et al. Longer time spent in light physical activity is associated with reduced arterial stiffness in older adults. Hypertension. 2010;56(3):540–546. PubMed ID: 20606102 doi:10.1161/HYPERTENSIONAHA.110.156331

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 20.

    van de Laar RJ, Ferreira I, van Mechelen W, Prins MH, Twisk JW, Stehouwer CD. Lifetime vigorous but not light-to-moderate habitual physical activity impacts favorably on carotid stiffness in young adults: the Amsterdam growth and health longitudinal study. Hypertension. 2010;55(1):33–39. PubMed ID: 19996070 doi:10.1161/HYPERTENSIONAHA.109.138289

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 21.

    Mulvany MJ, Baumbach GL, Aalkjaer C, et al. Vascular remodeling. Hypertension. 1996;28(3):505–506. PubMed ID: 8794840

  • 22.

    Amberson WR. Physiologic adjustments to the standing posture. Uni Md Sch Med Bull 1943;27:127–145.

  • 23.

    Cao L, Pilowsky PM. Quiet standing after carbohydrate ingestion induces sympathoexcitatory and pressor responses in young healthy males. Auton Neurosci. 2014;185:112–119. PubMed ID: 25129222 doi:10.1016/j.autneu.2014.07.007

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 24.

    Cox RH, Guth J, Siekemeyer L, Kellems B, Brehm SB, Ohlinger CM. Metabolic cost and speech quality while using an active workstation. J Phys Act Health. 2011;8(3):332–339. PubMed ID: 21487132 doi:10.1123/jpah.8.3.332

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 25.

    Vaitkevicius PV, Fleg JL, Engel JH, et al. Effects of age and aerobic capacity on arterial stiffness in healthy adults. Circulation. 1993;88(4 Pt 1):1456–1462. PubMed ID: 8403292 doi:10.1161/01.CIR.88.4.1456

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 26.

    Ferreira I, Snijder MB, Twisk JW, et al. Central fat mass versus peripheral fat and lean mass: opposite (adverse versus favorable) associations with arterial stiffness? The Amsterdam Growth and Health Longitudinal Study. J Clin Endocrinol Metab. 2004;89(6):2632–2639. PubMed ID: 15181034 doi:10.1210/jc.2003-031619

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 27.

    Tomoto T, Maeda S, Sugawara J. Relation between arterial stiffness and aerobic capacity: importance of proximal aortic stiffness. Eur J Sport Sci. 2017;17(5):571–575. PubMed ID: 28100164 doi:10.1080/17461391.2016.1277787

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 28.

    Zarrinkoob L, Ambarki K, Wahlin A, et al. Aging alters the dampening of pulsatile blood flow in cerebral arteries. J Cereb Blood Flow Metab. 2016;36(9):1519–1527. PubMed ID: 26823470 doi:10.1177/0271678X16629486

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 29.

    Levine JA. Lethal sitting: homo sedentarius seeks answers. Physiology. 2014;29(5):300–301.

  • 30.

    Gibbs BB, Kowalsky RJ, Perdomo SJ, Grier M, Jakicic JM. Energy expenditure of deskwork when sitting, standing or alternating positions. Occup Med. 2017;67(2):121–127. doi:10.1093/occmed/kqw115

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Creasy SA, Rogers RJ, Byard TD, Kowalsky RJ, Jakicic JM. Energy expenditure during acute periods of sitting, standing, and walking. J Phys Act Health. 2016;13(6):573–578. PubMed ID: 26693809 doi:10.1123/jpah.2015-0419

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 32.

    Reiff C, Marlatt K, Dengel DR. Difference in caloric expenditure in sitting versus standing desks. J Phys Act Health. 2012;9(7):1009–1011. PubMed ID: 22971879 doi:10.1123/jpah.9.7.1009

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 33.

    Saeidifard F, Medina-Inojosa JR, Supervia M, et al. Differences of energy expenditure while sitting versus standing: a systematic review and meta-analysis. Eur J Prev Cardiol. 2018;25(5):522–538. PubMed ID: 29385357 doi:10.1177/2047487317752186

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 34.

    Altenburg TM, Rotteveel J, Dunstan DW, Salmon J, Chinapaw MJ. The effect of interrupting prolonged sitting time with short, hourly, moderate-intensity cycling bouts on cardiometabolic risk factors in healthy, young adults. J Appl Physiol. 2013;115(12):1751–1756. doi:10.1152/japplphysiol.00662.2013

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 35.

    Madhura M, Sandhya T. Effect of different phases of menstrual cycle on reflection index, stiffness index and pulse wave velocity in healthy subjects. JCDR. 2014;8(9):BC01.

    • Search Google Scholar
    • Export Citation
  • 36.

    Ounis-Skali N, Mitchell GF, Solomon CG, Solomon SD, Seely EW. Changes in central arterial pressure waveforms during the normal menstrual cycle. J Investig Med. 2006;54(6):321–326. PubMed ID: 17134615 doi:10.2310/6650.2006.05055

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 37.

    Moreau KL, Hildreth KL. Vascular aging across the menopause transition in healthy women. Adv Vasc Med. 2014;2014:pii: 204390.

  • 38.

    Xu D, Wang H, Chen S, et al. Aerobic exercise training improves orthostatic tolerance in aging humans. Med Sci Sport Exer. 2017;49(4):728–735. doi:10.1249/MSS.0000000000001153

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 39.

    Yu J, Abraham JM, Dowd B, Higuera LF, Nyman JA. Impact of a workplace physical activity tracking program on biometric health outcomes. Prev Med. 2017;105:135–141. PubMed ID: 28890355 doi:10.1016/j.ypmed.2017.09.002

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
All Time Past Year Past 30 Days
Abstract Views 0 0 0
Full Text Views 364 365 229
PDF Downloads 76 76 33