Blood pressure (BP) is a commonly measured vital sign and important for clinical decision making (1). BP is a modifiable risk factor for cardiovascular disease (CVD) and an important consideration when developing safe and effective exercise prescriptions. BP should be measured in both arms upon initial assessment by a health care professional, and the higher of the two arms should be utilized for further measures if there is a consistent difference (2). Although the clinical value of resting bilateral BP measurement has been known by physicians for decades, only approximately 23% participate in this practice (3). However, recognizing an interarm difference (IAD) in BP allows for better patient classification, which is especially important in certain populations (e.g., diabetic patients) and may improve diagnosis and treatment of hypertension (4), which is necessary for effective care (5).
A large IAD in systolic BP (IAD+; ≥10 mm Hg difference between arms) has been reported in normotensive (6,7) and hypertensive individuals (8,9) at rest. A range of 4%–39% of the population has been estimated to express IAD+ at rest, with a conservative prevalence of 10% frequently quantified (10). Furthermore, IAD+ is linked to peripheral vascular disease (11), arterial stiffness (12,13), and premature morbidity and mortality (8,10,14). However, a comprehensive understanding of the mechanisms that elicit IAD+ has yet to be elucidated.
Interarm BP difference has been extensively studied at rest, but to the authors’ knowledge, only one published study has examined systolic exercise IAD (eIAD). In IAD− individuals (<10 mm Hg difference between arms), the investigators observed increased eIAD during a short moderate-intensity bout of aerobic exercise (15). Furthermore, an interarm systolic BP difference of 4 mm Hg was observed in IAD+ individuals during an active recovery (AR) from the moderate-intensity aerobic exercise bout when compared with baseline (15). Acute aerobic exercise affected eIAD differentially based on resting IAD status. In addition, only two published studies regarding the effect of unilateral arm exercise on bilateral postexercise diastolic BP response between arms have been completed (16,17). Although systolic eIAD was assessed in these studies, it was not reported as a variable of interest.
Exercise can reveal underlying CVD risk factors that are absent during rest. This understanding provides the logic behind graded exercise stress tests for determining the presence and severity of CVD based on the patient’s physiological response to the stress of exercise (18). As previously noted, exercise as a perturbation may elicit a large eIAD when not otherwise present at rest (15). Expanding this understanding to a guideline recommended bout of aerobic exercise may provide plausibility for eIAD as a diagnostic/prognostic tool, and for the use of exercise as a therapeutic intervention to alter IAD or reduce IAD+.
Therefore, the purpose of the study was threefold: 1) to determine if there is a relationship between eIAD and IAD, 2) to observe the pattern of eIAD during a prolonged steady-state bout of aerobic exercise in IAD− and IAD+ individuals, and 3) to determine if current recommendations (i.e., using the arm with the higher SBP measured at rest) provide adequate reasoning for performing unilateral BP measurement during aerobic exercise.
Individuals 18 to 45 yr of age were recruited from Slippery Rock University and the surrounding area. Exclusion criteria included diagnosed hypertension, CVD, or metabolic disease or being on any medication that affected BP. Furthermore, anyone who needed medical clearance as determined by risk stratification practices outlined by the American College of Sports Medicine (18) was excluded from the study. Before data collection, procedures were approved by the Slippery Rock University Institutional Review Board. All participants completed an informed consent and health history documents before completing the study, and researchers adhered to all ethical regulations.
Before testing for both visits, participants were asked to refrain from exercise, alcohol, and caffeine for 24 h, and calorie consumption and smoking for 3 h. All visits were scheduled at a similar time of the day (i.e., within a 2-h window) to account for potential variation in measurements at different times of the day. At least 48 h transpired between visits 1 and 2. Female participants scheduled visits during the early follicular phase of their menstrual cycle to minimize the effect of estrogen on measured variables. These instructions were implemented to contribute to a consistent physiological state with each visit.
Height (cm) and weight (kg) were measured using a digital scale-stadiometer (Seca 769, Chino, CA). Body mass index (kg·m−2) was determined from height and weight. Waist circumference (cm) was measured at the narrowest point between the xiphoid process of the sternum and the umbilicus. Using standard procedures, percent body fat was estimated utilizing skinfold calipers (%; Lange, Santa Cruz, CA) (18).
A lipid/glucose profile was obtained via the fingerstick method for each participant (Alere Cholestech LDX® Analyzer, Freehold, NJ). The lipid/glucose variables consisted of total cholesterol (mg·dL−1), LDL (mg·dL−1), HDL (mg·dL−1), triglycerides (mg·dL−1), and whole blood glucose (GLU; mg·dL−1).
Investigators then screened each participant for peripheral artery disease using a standard ankle-brachial index (ABI) protocol. Briefly, similar to the measurement of BP, a cuff was inflated to ~220 mm Hg on the upper arm (on the side of the body with the higher BP) and a probe (MD6 Doppler; D.E. Hokanson, Inc., Bellevue, WA) was placed on the brachial artery. Cuff pressure was gently released (~2–3 mm Hg·s−1) until the first sound from the probe was heard and pressure recorded. An identical procedure was then performed at the ipsilateral posterior tibial (PT), ipsilateral dorsalis pedis (DP), contralateral DP, contralateral PT, and contralateral brachial arteries, respectively. The ratio of the ankle/brachial pressures on each side (i.e., higher PT or DP (per side)/higher brachial (right or left arm)) was calculated based on standard procedures. The lower number (i.e., right or left side) was recorded as the participant’s ABI. Ratios ≥0.90 were considered normal, and ratios <0.90 were considered abnormal.
Upon being fitted for proper seat height, participants performed a maximal graded exercise test on a Monark cycle ergometer (Ergomedic 828 E; Monark Exercise AB, Vansbro, Sweden). Oxygen consumption was measured continually utilizing a metabolic cart (ParvoMedics TrueOne®2400, Sandy Lake, UT). Heart rate (HR) was monitored throughout (Polar Electro Inc., Lake Success, NY). The cadence was held constant at 60-rpm throughout testing. The peak test began with unloaded cycling for 2 min. Thereafter, workload increased by 0.5 kp every 2 min until the participant reached volitional fatigue, or the cadence was not able to be maintained (i.e., dropped below 55 rpm). Peak aerobic capacity (V˙O2peak) was recorded as the highest oxygen consumption achieved during the test.
After a 10-min supine rest, IAD status was determined using sequential bilateral BP measurement with a sphygmomanometer and a stethoscope. The initial arm measured (right or left) was alternated between participants. Proper BP cuff sizes were identified through the “80% rule” (i.e., arm circumference is ≥80% of the BP cuff bladder length) (18). Arm circumference was measured at the halfway point between the acromion process of the scapula and the olecranon process of the ulna. Then, the brachial artery was palpated, and the midline of the bladder was placed directly over the artery line. BP was measured utilizing standard auscultation (mercury sphygmomanometer, Baumanometer; W. A. Baum Co. Inc.; stethoscope, Master Classic II; 3 M Littmann, St Paul, MN) by investigators who were experienced in BP measurement and trained repeatedly according to the recommendations of the American Heart Association. During BP measurement participants’ arms were supported, and they were instructed not to talk. BP was measured in the first arm, and then immediately measured in the other arm with an approximately 30-s interval between measures. Interarm SBP difference was recorded as the absolute difference between right and left arms (mm Hg).
Participants then completed an acute 30-min bout of steady-state aerobic exercise. Participants cycled on the Monark cycle ergometer at a workload equivalent to 50% of the V˙O2peak value obtained during visit 1. Participants were asked to maintain a 60-rpm cadence for the duration of the exercise bout. Bilateral BP and HR were measured at 5, 10, 20, and 30 min. After 30 min, all resistances were released from the cycle ergometer, and participants continued pedaling for an AR. Two minutes into AR, final measures of bilateral BP and HR were measured. The initial arm (right or left) measured was alternated with each time point. eIAD was recorded as the absolute difference in systolic BP between the right and left arms at each exercise time point (mm Hg). Rate pressure product (RPP; HR × SBP) was calculated during rest and submaximal exercise.
Descriptive characteristics were generated for all variables and reported as mean and SEM. Multiple linear regression modeling was used to determine the relationship of eIAD and resting IAD. Participants were classified as either IAD− (<10 mm Hg difference in resting SBP between arms) or IAD+ (≥10 mm Hg difference in resting SBP between arms). An independent samples t-test was used to compare demographic and resting/exercise cardiovascular variables (i.e., eIAD, SBP, HR, RPP) between IAD− and IAD+ individuals. To determine a relative response for eIAD, SBP, and HR, percent change was calculated using the following formula: (time point − rest)/rest × 100. Absolute values for eIAD and percent change in eIAD, SBP (left and right arms), and HR across the exercise bout were compared between IAD− and IAD+ individuals using a repeated-measures ANOVA. The proportion of participants with a higher right or left arm SBP was recorded, and the lower arm SBP was compared with SBP in the higher arm during exercise and AR. Instances of a higher SBP in the contralateral arm were noted, and a χ2 analysis was used to compare the prevalence of a “masked” higher BP during exercise and AR between IAD status (IAD− and IAD+) and higher arm (right or left at rest). An a priori α significance level of 0.05 was used across all analyses.
Sixty-two (N = 62) individuals completed all of the requirements of the study. All mean values for body composition and metabolic profiles were within normal limits (18). As expected, men (n = 32) were taller (179 ± 1 vs 169 ± 1 cm; P < 0.05), heavier (82 ± 2 vs 68 ± 2 kg; P < 0.05), leaner (14 ± 1% vs 26% ± 1%; P < 0.05), and more aerobically fit (41 ± 1 vs 33 ± 1 mL·kg−1 ·min−1; P < 0.05) than their female counterparts (n = 30). Men also had lower HDL cholesterol (55 ± 2 vs 64 ± 3 mg·dL−1; P < 0.05) and larger waist circumferences (85 ± 2 vs 76 ± 2 cm; P < 0.05).
Relationship of eIAD and Resting IAD
A positive relationship exists between eIAD and resting IAD (P < 0.05). When using the following time points (5, 10, 20, 30, and AR), the proportion of shared variance between eIAD and IAD was 25% (r2 = 0.25; P < 0.05). The model for predicting resting IAD from eIAD was as follows: y = 2.320 + 0.1102(5) + 0.1040(10) + 0.2515(20) − 0.04886 (30) + 0.09589 (AR).
Based on sequential bilateral BP measurement at rest, 19% (12/62 participants) were observed as IAD+, with an absolute difference of 13 ± 1 mm Hg (Fig. 1; P < 0.05). Therefore, 81% (50/62 participants) did not demonstrate IAD+ (i.e., IAD−), and this group presented with an absolute difference of 4 ± 1 mm Hg (Fig. 1). IAD+ individuals had lower fasting triglyceride (P < 0.05) and higher fasting GLU (P < 0.05) compared with their IAD− counterparts (Table 1).
Acute Bout of Steady-State Exercise
HR responded as expected during the 30-min bout of aerobic exercise and AR (Table 2), with no differences noted at any time point between IAD− and IAD+. Similarly, RPP increased with exercise (P < 0.05), with no observable differences between IAD− and IAD+ (Table 2). Collectively, these observations suggest that the intensity of aerobic exercise experienced at 50% of V̇O2peak was similar between IAD− and IAD+ participants. As expected, SBP increased in both the IAD− and IAD+ groups with exercise (Table 2; P < 0.05). IAD− had differences in SBP at all exercise time points (Table 2; P < 0.05). No differences in SBP between arms existed in IAD+ during exercise (Table 2; NSD).
A significant main effect of IAD status (i.e., IAD− and IAD+) on the absolute eIAD response was observed (Fig. 1; P < 0.05), with IAD+ expressing a higher eIAD than IAD−. However, when determining the relative response using the percent change in eIAD (with IAD status as baseline), IAD− was associated with a greater % increase in eIAD at all exercise time points and during AR (Fig. 2; P < 0.05). Similarly, when SBP was compared between the right and left arms, a clear distinction was noted between IAD− and IAD+, with right arm pressures higher at the 5-, 10-, and 30-min time points (Fig. 3A; P < 0.05) in IAD− individuals, and no differences were noted in the left arm between groups (Fig. 3B).
In the present cohort, there were three individuals (3/62; 5%) who had identical SBP measures in their right and left arms. It follows that 60 individuals (60/62; 95%) in the cohort had a different measured SBP in the right and left arms. If a participant had a higher measured SBP in their right arm at rest (IAD−, n = 23 (49%); IAD+, n = 10 (83%)), then unilateral BP measurement of the right arm during aerobic exercise would have masked a higher SBP in 22–35% of IAD− and 30%–50% of IAD+ measurements, respectively (Table 3). Likewise, in participants with a higher measured SBP in the left arm at rest, unilateral BP measurement in the left arm during aerobic exercise would have masked a higher SBP in 50%–79% of IAD− and 50% of IAD+ of exercise and AR stages (Table 3). In IAD−, a higher left arm SBP at rest resulted in a significantly greater odds of missing a higher BP in the right arm compared with IAD− individuals with a higher right arm SBP at rest (P < 0.05; Table 3).
The current study examined the pattern of eIAD during prolonged steady-state aerobic exercise in IAD− and IAD+ individuals. Nineteen percent of the sample presented as IAD+, which falls in line with the 4%–39% prevalence range in the current literature (10), particularly when sequential measurement is considered. The primary findings include the following: 1) eIAD is related to resting IAD, 2) absolute and relative eIAD were different based on IAD status, and 3) regardless of IAD status, observed bilateral differences in SBP provided insight into the limitations of unilateral BP measurement during aerobic exercise testing.
IAD has been extensively examined at rest in individuals with normal (6,7) and high BP (8,9) and is associated with peripheral vascular disease (11), arterial stiffness (12,13), type 2 diabetes mellitus (4), and premature morbidity and mortality (8,10,14). However, research is lacking regarding the eIAD response. Notably, our investigation is the first to determine that IAD observed at rest is related to eIAD. Considering the established relationships between resting IAD and CVD, and knowing that eIAD can explain 25% of the variance in IAD suggest that eIAD may have clinical value. An additional marker of interest, which may be low at rest (19) and during submaximal exercise (20,21) even in apparently healthy subjects, is RPP. Although our participants had a reasonable RPP response to exercise (19), it does not appear that resting IAD status or eIAD was related to RPP.
This investigation confirmed that IAD− and IAD+ individuals experienced different eIAD responses to aerobic exercise even when adjusted for the corresponding baseline SBP. In the observed cohort, IAD− individuals had an increased absolute (4 mm Hg at 30 min, 2 mm Hg at AR) and relative (150% at 30 min, 100% at AR) eIAD. Although vascular function measures were not obtained during exercise, it is possible that bilateral differences in function exist. To our knowledge, bilateral differences in arterial stiffness and endothelial function have not been characterized in relation to IAD or eIAD. However, it has been suggested that one of the main etiological factors responsible for IAD may be arterial stiffness (12,13). IAD+ individuals responded with a decreased absolute eIAD (−3 mm Hg at 30 min, −6 mm Hg during AR) and relative eIAD (−25% at 30 min, −50% during AR). These observations are congruent with prior findings by our laboratory. However, IAD+ individuals had an absolute eIAD approximately 3 mm Hg lower than reported by Holmstrup et al. (15). Some of these subtle observed differences may be explained simply by methodological differences. Despite the same modality, differences existed between the intensity and duration for the acute exercise bout. Specifically, in the current investigation, the exercise duration was approximately fourfold to fivefold, and the intensity was one metabolic equivalent greater and relative to the participant’s fitness level. Our observation of a decrease in eIAD in the IAD+ group may be linked to the phenomenon of postexercise hypotension where not only a decrease in SBP is observed after aerobic exercise, but also the absolute difference between arms may subsequently decrease.
Information provided by resting BP measurement is used for the determination of prescription medication and diagnosis of CVD. Current recommendations suggest that resting BP should be measured in both arms at an initial patient visit, with the higher arm used for future decision making (22,23). However, BP is widely utilized in diseased populations before partaking in daily exercise. In addition, the BP measures acquired during exercise are responsible for providing the clinician necessary information for stress test monitoring and termination. The current findings demonstrate the importance of measuring BP bilaterally during exercise. Considering the response in our apparently healthy cohort, this may be even more imperative in diseased populations. Furthermore, the demonstrated changes in SBP in right and left arms and incidence of masked higher BPs in the lower resting arm suggests that incorrectly quantifying one’s exercise BP through unilateral measurement could lead to inappropriate stress test monitoring and termination.
Single-incidence measures of resting, exercise, and recovery BP were utilized in this study, whereas the most topical recommendations call for repeated measures to ensure the reproducibility of IAD status. In addition, bilateral BP can be measured either simultaneously through an automatic device or sequentially through standard auscultation. In the current investigation, it was not possible to accurately measure simultaneous BP during exercise because of the oscillometric nature of automated simultaneous devices. Therefore, eIAD and IAD status were identified from sequential bilateral BP measurement. We controlled for the use of sequential measurement to the best of our ability using identical cuffs and cuff placement, a consistent investigator measuring the bilateral BP for each participant, and only a brief delay between measures on each arm (~30 s).
The current study provides novel evidence of disparate eIAD responses in individuals with and without significant IAD at rest. These data contribute to a diminutive body of evidence, suggesting that exercise affects IAD, and BP responses may be expressed differentially when subjected to prolonged steady-state aerobic exercise based on resting IAD. Characterizing these responses may be an important step in establishing the utility of aerobic exercise to reduce IAD+, although the effects of chronic exercise on IAD are unkown. As BP is a commonly measured vital sign, screening, monitoring, diagnostic, and prognostic tool during exercise, it is important that bilateral measurement is considered.
The authors thank Dr. Kevin Heffernan, Dr. Wesley Lefferts, and Mr. Jacob DeBlois for their contributions to the development of the project.
Funding sources included the Pennsylvania State System of Higher Education Faculty Professional Development Council and Slippery Rock University Faculty/Student Research Grant. The authors report no conflict of interest.
Results of the present study do not constitute endorsement by the American College of Sports Medicine.
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