894 Physiology & Biochemistry

Effect of a Single Bout of Resistance Exercise on Arterial Stiffness Following a High-Fat Meal

Affiliations

Key words

▶ vascular function ● ▶ arterial stiffness ● ▶ high-fat meal ● ▶ resistance exercise ●

accepted after revision November 19, 2013 Bibliography DOI http://dx.doi.org/ 10.1055/s-0033-1363266 Published online: June 2, 2014 Int J Sports Med 2014; 35: 894–899 © Georg Thieme Verlag KG Stuttgart · New York ISSN 0172-4622 Correspondence Dr. Kevin Scott Heffernan Department of Exercise Science Syracuse University Human Performance Lab Syracuse 13244 United States Tel.: + 1/315/443 9801 Fax: + 1/315/443 9375 ksheff[email protected]

J. Augustine1, B. Tarzia1, A. Kasprowicz1, K. S. Heffernan2 1 2

Exercise Science, Syracuse University, Syracuse, United States Department of Exercise Science, Syracuse University, Syracuse, United States

Abstract Consumption of a high-fat meal (HFM) causes postprandial lipemia and vascular dysfunction. Acute resistance exercise (RE) alone may also have a negative effect on vascular function. The purpose of this study was to measure arterial stiffness and postprandial lipemia after a HFM with or without acute RE. 9 recreationally active men (age 24 ± 5 years, BMI 25 ± 3 kg/m2) completed both: (1) HFM alone and (2) HFM + RE in a randomized order. Pulse wave velocity (PWV) from carotid to femoral artery and carotid to radial artery were used as measures of central/ aortic and peripheral arterial stiffness, respec-

tively. Circulating triglycerides (TRG) were obtained from finger stick samples as a marker of lipemia. There was a significant conditionby-time interaction for TRG (p < 0.05). TRG levels increased significantly following both conditions with a significantly attenuated increase following HFM + RE (p < 0.05). There was a significant condition-by-time interaction for peripheral PWV as this parameter increased following HFM, but decreased following HFM + RE (p = 0.021). Central PWV did not change with HFM or HFM + RE (p > 0.05). Following a HFM, acute RE attenuates postprandial lipemia and improves peripheral arterial stiffness without having a negative effect on central arterial stiffness.

Post-prandial lipemia contributes to the development of atherosclerotic cardiovascular disease (CVD) and is predictive of future CVD events [25]. This metabolic state induced most notably by consumption of a high-fat meal (HFM) is characterized by augmented plasma triglycerides (TRG). Consumption of a single HFM causes vascular dysfunction manifesting as an increase in both central and peripheral arterial stiffness [3, 21, 24]. This vascular dysfunction can be detected within an hour of HFM consumption and lasts upwards of 6 h post ingestion [40]. Interestingly, eating a second HFM leads to further vascular derangement [38]. Thus it has been suggested that vascular dysfunction occurring with each successive HFM exposure will lead to aggregate vascular damage, hastening the atherosclerotic process [40]. Although avoiding HFM would reduce CVD risk, modifying diet remains a dubious task. Another equally effective strategy for reducing CVD risk may reside in preventing the detrimental vascular cascade following consumption of HFM. Acute aerobic exercise has a favorable effect on vasculature by improving endothelial dependent vasodilation [12] and reducing arterial stiffness [15, 18]. More importantly, a single bout of acute

aerobic exercise performed after a HFM attenuates the negative effects of the fat load on vasculature [6, 22, 26]. It has been suggested that the mechanism behind the favorable effects of exercise on vasculature in the postprandial state may be related to noted reductions in triglycerides [11]. In other words, prevention of postprandial lipemia with acute aerobic exercise may prevent subsequent vascular damage. There is currently a void in the literature regarding the acute postprandial vascular response to another popular form of exercise, resistance exercise (RE). Acute RE has been shown to have no effect or possibly exacerbate postprandial lipemia [5]. Similar to acute aerobic exercise, acute RE reduces peripheral arterial stiffness [9]. However acute RE is known to transiently increase central artery stiffness [15] and cause peripheral endothelial dysfunction [17], suggesting that RE may not afford the same cardio-protective effect as aerobic exercise. The heterogeneous vascular sequela produced by acute RE coupled with potential augmentation of postprandial lipemia raises the intriguing possibility that acute RE could aggravate the detrimental vascular response to HFM thus fostering an atherogenic milieu. There-



Augustine J et al. Resistance Exercise and Postprandial Arterial Stiffness… Int J Sports Med 2014; 35: 894–899

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Authors

Physiology & Biochemistry

fore, the purpose of this study was to examine changes in triglycerides and arterial stiffness after the consumption of a HFM with and without the addition of acute RE. It was hypothesized that acute RE performed after eating a HFM would lead to augmented vascular damage compared to HFM alone, manifesting as a greater increase in central and peripheral arterial stiffness.

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High fat meal The HFM consisted of sausage, egg and cheese on a croissant from Dunkin Donuts (710 calories, 49 g fat, 20 g saturated fat, 0.5 g trans-fat, 245 mg cholesterol, 1 370 mg sodium, 41 g carbohydrate, 2 g fiber, 6 g sugar, and 25 g protein). Fluid intake was limited to water ad libitum. The amount of fat in this meal has previously been used in other studies to induce changes in vascular function [26].



Exercise protocol

10 recreationally active men were recruited for this study. All subjects were free of cardiovascular, metabolic, renal or respiratory disease as determined from a health history questionnaire. Subjects neither smoked nor were taking medications known to affect cardiovascular function. All subjects were required to give written consent, and the University Institutional Review Board approved this study. This study complies with all ethical standards put forth by the International Journal of Sports Medicine [14].

Subjects participated in a randomized, counterbalanced experimental study and reported to the research facility on 3 separate occasions. The first visit consisted of a familiarization phase in which subjects were introduced to the tests that were used during the protocol. During the first visit subjects filled out the consent form, health history and physical activity questionnaire. The subject’s 5-Repetition Maximum (5-RM) on the bench press and 10-Repetition Maximum (10-RM) on the biceps curl was determined (described below). Subjects were then randomized to undergo RE + HFM or HFM alone. Visits 2 and 3 were completed no less than 3 and no more than 7 days apart. Subjects reported to the laboratory following an overnight fast. Once in the laboratory, subjects were required to lie in the supine position for a minimum of 10 min, after which time blood lipids, blood pressure and vascular measures were conducted. All subjects were instructed to refrain from exercise, alcohol or caffeine for 24 h prior to testing. Following baseline measures, subjects consumed a HFM. Two hours and fifteen minutes after HFM consumption, subjects engaged in an acute RE bout or an inactive control condition (quiet seated rest). Post-prandial vascular measurements were taken 3 h following ingestion of the HFM, as peak vascular response has been shown to occur within 1 h of RE [7, 15, 42] and within 4 h after HFM [6, 22]. Measurement at this time ensured that we captured the most robust change in vascular response to both RE and HFM.

The maximum amount of weight lifted with proper form through a full range of motion for 5 repetitions for the bench press and 10 repetitions for the biceps curl was determined to be the participants’ 5-RM and 10-RM, respectively. This was determined using guidelines set forth by the National Strength and Conditioning Association [1]. Biceps curl was performed using a 2-arm E-Z curl bar. For both exercises, participants first completed a brief warm-up consisting of 10 repetitions of a submaximal load. With the help of a prediction table that can estimate maximal work from submaximal loads [1], weight was added in 5–10 kg increments until participants could no longer successfully complete the 5 or 10 repetitions (could not complete the concentric portion of the contraction without assistance). The heaviest weight lifted with proper form and no assistance for the 5 or 10 repetitions was recorded as the subject’s 5-RM or 10-RM maximum weight, respectively. Participants were allowed 3–5 min of rest between sets to ensure that a maximal effort was exerted with each attempt. Maximal values were attained for all participants in less than 5 attempts. A spotter was present at all testing sessions to ensure the participant’s safety during testing. The RE bout consisted of a warm-up comprised of 10 bench press repetitions of a submaximal weight. This was followed by 5 sets of the subject’s 5-RM on the bench press. After bench press, 5 sets of 10 repetitions of the subject’s 10-RM for biceps curl was completed using a 2-arm E-Z curl bar. Cadence was set at an approximate 2-1-2 duty cycle (2 s concentric, 1 s pause, 2 s eccentric). Exactly 90 s of rest was afforded between each set. The subject completed their 5-RM and 10-RM to its entirety. If the participant could not complete the allotted repetitions, a drop set was instigated whereby weight was taken off incrementally (5–10 kg) until the participant could complete a set of 5 or 10 repetitions with proper form. A spotter was present during all exercise to ensure proper form and to assist the participant if fatigue occurred. This protocol has previously been used to successfully induce acute vascular changes [9].

Blood lipid profile

Brachial blood pressure

Total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides (TRG) and glucose levels (GLU) were measured using an automated Cholestech LDX blood lipid analysis device. Blood samples were taken at baseline and 3 h post ingestion of the HFM. Small samples of blood were obtained via finger lancet on the non-dominant hand of the participant with his arm in a supine position. After immediate blood collection in small heparin-coated capillary tubes, the blood was transferred to Cholestech cartridges and loaded in the device to be analyzed. This technique has previously been established to be valid and reliable [31].

Resting systolic and diastolic blood pressures (SBP and DBP, respectively) were measured in the supine position using an automated oscillometric cuff (Panasonic). Blood pressure measurements were made in duplicate. The average of the 2 values was recorded and used for subsequent analysis. If the 2 recorded values were not within 5 mmHg of one another, values were taken continuously until 2 consecutive readings were obtained that were within 5 mmHg of one another.

Experimental design

Body composition Body composition was assessed using air displacement plethysmography (BodPod) to estimate lean body mass and fat mass.

Arterial stiffness measurements Pulse wave velocity (PWV) was measured at 2 time points: baseline and 3 h after the ingestion of a HFM. A single high-fidelity pressure transducer (SpyghmoCor, AtCor Medical) was used to consecutively measure pressure waveforms between (1) the left common carotid artery and the left radial artery to represent

Augustine J et al. Resistance Exercise and Postprandial Arterial Stiffness… Int J Sports Med 2014; 35: 894–899

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Methods

896 Physiology & Biochemistry

Table 1 Lipid and hemodynamic measures before and after conditions. n=9 SBP (mmHg) DBP (mmHg)† Total Cholesterol (mg/dl) HDL-C (mg/dl) Glucose (mg/dl) Triglycerides (mg/dl)† Peripheral PWV (m/s)† Aortic PWV (m/s)

Pre HFM + RE

Post HFM + RE

Pre HFM

122 ± 7 78 ± 5 152 ± 30 48 ± 12 89 ± 5 67 ± 23 6.9 ± 0.8 5.4 ± 0.5

123 ± 3 67 ± 4* 154 ± 29 49 ± 11 89 ± 13 102 ± 37* 5.7 ± 0.8* 5.6 ± 0.5

121 ± 6 75 ± 5 155 ± 23 47 ± 17 88 ± 7 79 ± 44 6.8 ± 0.9 5.6 ± 0.7

Post HFM 123 ± 10 75 ± 4# 157 ± 21 45 ± 17 87 ± 6 153 ± 61*# 7.6 ± 1.3# 5.5 ± 0.6

Partial η2

Observed Power

0.044 0.78 0.01 0.06 0.01 0.41 0.51 0.15

0.08 0.98 0.050 0.10 0.051 0.53 0.71 0.19

† Significant group-by-time interaction, p < 0.05 * Significant time effect (p < 0.05)

Statistical analysis Statistical analyses were performed using SPSS version 20.0 (IBM). Data is expressed as mean ± standard deviation. Data were analyzed using a 2 × 2 analysis of variance (ANOVA) with repeated measures [(HFM vs. HFM + RE) × (pre vs. post)]. If a condition by time interaction was detected, appropriate post hoc comparisons were made using t-tests with a Bonferroni correction for multiple comparisons. Change scores were computed as post values – pre values. Correlations of interest were performed using Pearson correlation coefficients. Statistical significance was set a prior at p < 0.05.

Results



One participant was excluded from data analysis as resting lipids could not be assessed by the point-of-care device. Complete data were obtained in the remaining 9 men (age: 24 ± 6 years; body mass index: 25 ± 3 kg/m2, body fat 12 ± 8 %, LDL-C 93 ± 26 mg/dL). There were no differences in baseline/fasting total cholesterol, HDL-cholesterol, triglycerides (HFM: 79 ± 44 mg/dl vs. HFM + RE: 67 ± 22 mg/dl, p = 0.37), glucose, blood pressure, peripheral PWV (HFM: 6.8 ± 0.9 m/s vs. HFM + RE: 6.9 ± 0.8 m/s, p = 0.76) or aortic ▶ Table 1, p > 0.05). A significant PWV between testing days (● ▶ Table 1, group-by-time interaction was found for DBP (● p < 0.05). DBP decreased following HFM + RE (p < 0.05) with no change seen following HFM (p > 0.05). A significant group-bytime interaction was found for triglycerides (p < 0.05). While there were significant increases in values following both condi-

a

2

*

Absolute ∆ Peripheral PWV (m/s)

1.5 1 0.5 0 –0.5 –1 –1.5

b

–2 140

*

120 Absolute ∆ Triglycerides (mg/dl)

peripheral stiffness and (2) the left common carotid artery and the left femoral artery to represent central (aortic) stiffness. Distances from the carotid artery to the radial and femoral arteries were measured as the distance from the suprasternal notch to the radial artery, suprasternal notch to the femoral artery and suprasternal notch to the carotid artery using a standard tape measurer. The distance from the suprasternal notch to the carotid artery was then subtracted from the suprasternal notchradial distance and suprasternal notch-femoral distance to account for differences in direction of pulse wave propagation. PWV was calculated from the distances between measurement points and the measured time delay (Δt) between proximal and distal waveforms. Simultaneous 3-lead ECG was assessed to obtain heart rate. The peak of the in-phase R wave was attained from sequential ECG monitoring that was used as a timing marker. The intra-class correlation coefficient for carotid-femoral and carotid-radial PWV obtained from the resting data in our participants was 0.85 and 0.79, respectively.

100 80 60 40 20 0

HFM + RE

HFM

Fig. 1 a Absolute change in triglycerides (TRG) measured before and after a high-fat meal (HFM) vs. HFM combined with resistance exercise (HFM + RE). Values are means ± standard deviations. A significant condition-by-time interaction was detected (p < 0.05). *Significantly different change (p < 0.05). b Absolute change in peripheral pulse wave velocity (PWV) measured from the carotid to radial artery before and after HFM vs. HFM + RE. A significant condition by time interaction was detected (p < 0.05) *Significantly different change (p < 0.05)

tions, increases were greater following HFM compared to ▶ Fig. 1a, p < 0.05). Peripheral PWV showed a signifiHFM + RE (● cant condition by time interaction (p < 0.05). While values increased following HFM, values decreased following HFM + RE ▶ Fig. 1b, p < 0.05). There was no change in aortic PWV with (● ▶ Table 1, p > 0.05). Change in peripheral PWV either condition (● was moderately associated with change in TRG across conditions (r = 0.44, p = 0.035).

Augustine J et al. Resistance Exercise and Postprandial Arterial Stiffness… Int J Sports Med 2014; 35: 894–899

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# Significantly different from post HFM + RE (p < 0.05)

Discussion



The primary findings from this study suggest that a single RE session attenuated the increase in TRG observed 3 h following the ingestion of a HFM. Moreover, when performed after HFM, acute RE still produces favorable changes in peripheral arterial stiffness. Interestingly, there was no change in central arterial stiffness when acute RE was performed after a HFM. Overall, RE may have a positive effect on cardiovascular health in the postprandial state owing to its ability to favorably alter lipemia coupled with its ability to acutely prevent peripheral vascular dysfunction. A single session of aerobic exercise can reduce the postprandial rise in TRG by upwards of 20–25 % [40]. The effect of acute RE on the TRG response to HFM appears disparate with some studies noting increases in the TRG and others reporting reductions or no change [28, 32, 34, 43]. We noted an attenuated increase in TRG when HFM was followed by acute RE. Discrepancies in findings likely reside in the timing of the exercise relative to the timing of meal consumption (before vs. after) combined with different acute RE protocols varying in volume and intensity. The mechanisms through which a HFM could lead to an increase in peripheral PWV may be multidimensional. Evidence suggests that elevated serum TRG levels may lead to oxidative stress and impaired endothelial function through acute reductions in NO [6]. Changes in peripheral PWV with exercise are largely related to endothelial function [23, 36]: 1) reductions in nitric oxide (NO) have been shown to increase peripheral arterial stiffness [19]; 2) flow-mediated increases in NO result in reduction in PWV which can be prevented with NO-inhibition [2]. In support of this, increases in peripheral PWV with HFM were associated with changes in TRG (i. e. those with the largest increase in TRG following HFM alone had the largest increase in PWV), which is consistent with previous findings. Another potential link between HFM and vascular function could be related to insulin activity. Studies using insulinemic clamp methodology have shown that insulin might be an important factor moderating arterial stiffness in the postprandial state [41]. Insulin may have a vasodilatory effect on the peripheral vessels by increasing NO release [35]. However, high fat intake is accompanied with acute insulin resistance [29] that may attenuate the vasodilatory properties of insulin. The increased TRG content and increased insulin resistance accompanying a HFM both lead to acute reductions in NO and may play a role in the arterial stiffness associated with a HFM. The mechanism behind insulin and arterial stiffness is not entirely understood, and future studies should examine this association. A single session of aerobic exercise has been shown to improve postprandial vascular function by decreasing the TRG concentrations after a HFM [40]. Present findings revealed that reductions in peripheral arterial stiffness following acute RE are somewhat preserved in the postprandial state (although attenuated compared to previous reports conducted in the fasted state) [9] and associated with changes in TRG (i. e. those with no change/the smallest increase in TRG following HFM + RE had the largest reduction in PWV). Thus, acute RE may prevent peripheral vascular damage induced by HFM possibly via its ability to attenuate increases in TRG after HFM. It is plausible that acute RE acts through a blood flow-mediated mechanism to increase shear stress and stimulate the release of nitric oxide (NO). Subsequent reductions in vascular smooth muscle tone (smooth

muscle relaxation) result in reductions in arterial stiffness. Overall, our findings suggest that this process is not altered in the postprandial state following acute RE due to favorable changes in TRG. There was no change in central PWV with HFM, and this is consistent with previous reports [10]. Moreover, central arterial stiffness did not change following a HFM-RE and this was surprising. Previous studies suggest that the increase in central stiffness observed after an acute bout of RE is primarily due to increases in BP [7, 16]. Postprandial lipemia induced by a HFM blunts the increase in BP typically observed during exercise [30]. Therefore, a lower BP response to RE combined with HFM may abrogate the typical increase in central stiffness previously reported in the literature [7, 15, 42]. It is also possible that alterations in mesenteric blood flow following a high-fat meal have a favorable effect on overall aortic stiffness [8]. The superior mesenteric artery branches off the abdominal aorta and supplies the intestine and pancreas. In the postprandial state, superior mesenteric blood flow is substantially increased particularly following HFM, resulting in shear-stress mediated vasodilation [33]. Superior mesenteric vasodilation following HFM is not affected by acute static [39] or dynamic [27] exercise, suggesting that blood flow to digesting splanchnic organs maintains high priority in the postprandial state independent of competing effects from active skeletal muscle. Regional changes in downstream abdominal aortic function stemming from superior mesenteric NO release may offset increases in ascending/transverse aortic stiffness from acute RE, resulting in no net change in aortic PWV. More research is needed to examine the vascular response to acute RE in the postprandial state. We wish to underscore the practical implications of present findings. We are not advocating that athletes consume a high-fat meal prior to acute RE in order to prevent increases in arterial stiffness that may occur following this exercise modality. Firstly, it is presently unknown if acute increases in aortic PWV following acute RE are in fact detrimental. Secondly, chronic consumption of a high fat (coupled with highly processed carbohydrates) diet has numerous established negative effects on cardiovascular function and overall cardiovascular health. Additional research is needed to examine other pre-exercise meals that may augment skeletal muscle myogenic pathways (i. e. whey protein) while concomitantly attenuating potentially “detrimental” vascular effects. We recognize that our study is limited to the examination of young healthy men. Therefore, our results and conclusions cannot be applied to women. Previous studies report sex differences in the vascular response to a HFM [4, 13, 20, 37]. Following a HFM vascular function is preserved in women compared to men [13]. Women have also been reported to have lower postprandial lipemic oxidative stress [4] and lower triglycerides following acute RE + HFM [32]. The effect of acute RE on arterial stiffness in women remains unknown. This study also has a small sample size, thereby producing moderate effect sizes. As such, interpretation of results/conclusions should be viewed not as definitive but as hypothesis-generating. In conclusion, an acute bout of RE attenuates the increase in postprandial TRG levels that occur when consuming a HFM. Moreover, peripheral PWV is reduced following acute RE + HFM, suggesting that this combination is not detrimental to the vascular wall. Finally, central PWV is not altered when acute RE is performed after eating a HFM. Overall, findings suggest that acute RE does

Augustine J et al. Resistance Exercise and Postprandial Arterial Stiffness… Int J Sports Med 2014; 35: 894–899

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not negatively impact the vascular response to HFM. Conversely, acute RE performed in the postprandial state may be protective.

Author Contributions



Each author contributed to all aspects of the study (conceptualization, study design, data collection, analyses, interpretation) and final manuscript preparation. The authors declare that they have no conflict of interest.

Acknowledgements



The present study was funded by support from the Joan N. Burstyn Endowed Fund for Collaborative Research in Education at Syracuse University.

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Effect of a single bout of resistance exercise on arterial stiffness following a high-fat meal.

Consumption of a high-fat meal (HFM) causes postprandial lipemia and vascular dysfunction. Acute resistance exercise (RE) alone may also have a negati...
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