Influences of two high intensity interval exercise protocols on the main determinants of blood fluidity in overweight men

Abstract

BACKGROUND: Acute effects of continuous exercise on the markers of blood fluidity have been addressed in different populations and the changes are intensity related. However, the effect of different high intensity interval exercise (HIIE) on these variables is unclear.

OBJECTIVE: This study is designed to determine the effects of two different HIIE with different work/rest ratios but the same energy expenditure on the main determinants of blood fluidity.

METHODS: Ten overweight men (age, 26.3±1.7 yrs) completed two HIIE protocols on two separate occasions with one week intervening. The two HIIE encompassed performing: 1) 6 intervals of 2 min activity at 85% of VO_2max interspersed by 2 min active recovery at 30% of VO_2max (ratio 1 to 1, HIIE_1/1), and 2) 6 intervals of 30 s activity at 110% of VO_2max interspersed by 4 min active recovery at 40% of VO_2max (ratio 1 to 8, HIIE_1/8). Each exercise trial was followed by 30 min rest. Venous blood samples were obtained before exercise, immediately after exercise and after recovery and analyzed for blood and plasma viscosity, fibrinogen and red blood cell indices.

RESULTS: The HIIE_1/1 protocol led to higher reduction (P < 0.01) in plasma volume changes compared to HIIE_1/8 (9.9% vs 5.7%). Moreover, increases in blood viscosity, plasma viscosity, hematocrit, RBC count and mean arterial blood pressure observed following HIIE_1/1 were significantly (P < 0.05) higher than HIIE_1/8 ; whereas, the changes in fibrinogen concentration neither were significant in response to both trials nor were significantly different between two protocols (P > 0.05). However, the changes in all variables during exercise were transient and returned to the baseline levels after 30 min recovery.

CONCLUSIONS: It is concluded that the HIIE protocol with lower intensity and shorter rest intervals (higher work to rest ratio) clearly results in more physiological strain than HIIE with higher intensity but longer rest intervals (lower work to rest ratio) in overweight individuals, and that the work to rest ratio could be as important as exercise intensity when considering the hemorheological variables during HIIE.

Keywords

Interval exercise exercise intensity blood viscosity fibrinogen

1 Introduction

Despite scientific progresses in recognizing the cellular and molecular aspects of all types of diseases and their treatments, events related to cardiovascular diseases (CVDs) remain the biggest cause of deaths worldwide with more than 17 million death from CVDs in 2008 [27]. Associations between hemorheological variables including blood and plasma viscosity, fibrinogen and hematocrit with cardiovascular risk factors, incident cardiovascular disease and vascular and nonvascular mortality has been shown [23 , 37]. Although, exercise-induced increases in shear stress upregulates the production of endothelium-derived nitric oxide (NO), strenuous exercise by stimulating the oxidative stress and catecholamine release leads to blood cell activation and consequently acute coronary syndrome [13, 21]. In addition, heavy exercise leads to plasma volume reduction and in tandem with hemoconcentration by shifting plasma from intracellular space to muscle tissue [2]. Exercise related sudden deaths (during exercise or early after exercise) has been reported in both athletes and sedentary individuals and are attributed to cardiovascular and microcirculatory problems [4].

Acute effects of continuous exercise on the markers of blood fluidity has been addressed in different populations, and based on the subjects’ characteristics, measurement methods, exercise type, exercise duration and exercise intensity different results are concluded [3 , 38]. Intensity of exercise is one of the main training variables that its effect on the responses of hemorheological variables to acute exercise has been confirmed [12 , 38]. On the other hand, exercise modality is another important factor that has always been used to justify the discrepancies on the effects of exercise on hemorheological variables.

High intensity interval training (HIIT) is an exercise modality that include intermittent burst of vigorous activity, interspersed by periods of passive or active rests [17]. High-intensity interval training is one of the most effective means of improving, endothelial function, inflammatory markers, cardiorespiratory and metabolic function [1 , 34–36] as well as physical performance in athletes [17]. High intensity interval exercise (HIIE) involves repeated short-to-long bouts of rather high-intensity exercise interspersed with rest periods. Prescription for HIIE consists of the manipulation of up to nine variables, with the most important being the work and recovery intensity and duration (work to rest ratio) and the manipulation of any of these variables can affect the acute physiological responses to HIIE [9, 10]. Based on VO_2max, the range of exercise intensity in HIIE is between 85% to 120% [10], though, there is no agreement on optimal intensity, duration or work to rest ratio for HIIE and no superior protocol or single regimen has been recommended yet. Most researchers believe that HIIE is superior than moderate continuous exercise (MCE), because of increasing the subjects’ adherence to physical training and consuming the same energy expenditure in a shorter time period [28]; whereas, others have argued that HIIE is not safe, because of the excessive shear stress [19] produced by peak workloads. The latter has been confirmed recently by two studies that showed increases in blood viscosity [5] and IL-6 [15] following HIIE compared to MCE.

Since, the workload in HIIE during active part of exercise is high, the acute physiological responses and the potential risks, particularly in respect to hemorheological variables, may be increased. In addition, based on this notion that the changes in hemorheological variables in response to acute continuous exercise are intensity related, we hypothesized that responses of the main determinants of blood fluidity to HIIE modality would be intensity related. Therefore, we designed the present study to 1) determine the effects of two HIIE with different work/rest ratios but the same energy expenditure (investigate the safety of this exercise modality), and 2) determine whether the changes associated with HIIE are intensity related.

2 Methods

2.1 Subject

Ten healthy male overweight subjects (mean±SD: age, 26.3±1.7 yrs; body weight, 82.7±5.3 kg, height, 176±5 cm) who were non-smokers and free of medication volunteered to participate in the study (Table 1). The university’s ethics committee initially approved the experimental procedures and study protocols, which were fully explained to all subjects, and a written consent form was signed after having read and understood the details of the experiments. This article is written in accordance to the ethical guidelines of the Clinical Hemorheology and Microcirculation [6].

2.2 Study design and experimental protocols

Two familiarization sessions were designed to habituate subjects with the testing procedures and laboratory environment. All basic measurements including body mass, height, and body fat percent were performed in this session. Body mass was measured to the nearest 0.1 kg using calibrated balance scales and the height was measured to the nearest 0.5 cm without shoes. Body mass index (BMI) was calculated as body weight (kg) divided by height (m²). The skinfolds were obtained using Harpenden skinfold caliper (Slim Guioe, US) on the right side of the body at the following sites: triceps, abdominal, and thigh. All measurements were taken in triplicate and average values at each point were used to estimate body fat percent using Jackson-Pollack equation [22]. In the second session, for the determination of VO_2max subjects performed an incremental cycling test to volitional fatigue. The incremental test started with 3 minutes warm up at 25 W on a cycle ergometer, thereafter, the power output was increased by 50 W every 2 minutes until the subjects were unable to maintain a pedaling cadence above 60 rev.min^-1. Expired gas analysis was acquired with a Metalyzer 3B analyser (Cortex: biophysik, GMbH, Germany), and VO_2max was calculated as the highest oxygen consumed over a 1 min period. For the duration of the test, heart rate was measured continuously using a heart rate monitor (PE3000, Polar Electro, Kemple, Finland). VO_2max was confirmed using established physiological criteria from the British Association of Sport and Exercise Science [8]. To calculate the power output equivalent to the designated intensity for both main exercise trials, at the end of each stage power output and VO₂ were recorded and a curve was extrapolated.

After familiarization and basal measurements, subjects attended the physiology laboratory to perform two HIIE protocols in two separate sessions with one week intervening. They were asked to not perform any kind of exercise 48 h prior to these sessions. All subjects attended the laboratory between 08:00–09:00, one hour after having a small standard breakfast. After changing the attire, subjects remained seated for 30 min before exercise, which was followed by measuring heart rate and blood pressure and taking the baseline blood sample (8 ml). Thereafter, subjects performed 3 minutes warm-up at 30% of VO_2max, which was followed by HIIE trial included 6 intervals of 2 min work at 85% of VO_2max interspersed by 2 min active recovery at 30% of VO_2max (ratio 1/1, Fig. 1A). Immediately after exercise (duration, 24 minutes) the second blood sample was taken and subjects had 30 minutes recovery. The third blood sample was taken after this period. The second HIIE protocol involved 30 s work at 110% of VO_2max interspersed by 4 min active recovery at 40% of VO_2max (ratio 1/8, Fig. 1B) until the point that subjects reached the same energy expenditure as the first protocol. To control for possible effects of time of day, all exercise trials were performed at the same time of day (08:00–09:00). Care was taken to ensure that the environmental conditions (ambient temperature 25±2°C and relative humidity 34±2%) were identical during all exercise sessions.

2.3 Blood sampling and analysis

Blood sampling and measurements of hemorheological variables were performed according to the recent guidelines for hemorheological measurements [7]. To control for posture-induced plasmavolume changes, all blood samples were taken in seated position. Three venous blood samples were obtained, with minimum stasis, from an antecubital vein after 30-min rest in seated position, immediately after exercise and after 30-min recovery. Whole blood anticoagulated with EDTA was used to measure whole blood viscosity at shear rate of 222.5 s^–1 using a cone-plate viscometer (Brookfield cone-plate viscometer, Brookfield, US) at 37°C. Whole EDTA blood was centrifuged at 3000 g for 5 minutes at 25°C and the plasma was used to measure plasma viscosity at 37°C by using a cone-plate viscometer. Hematocrit, hemoglobin and RBCs count were measured from EDTA blood using a cell counter (Cell counter Sysmex, KX21, Japan). Hematocrit and hemoglobin values were used to estimate plasma volume changes using the equation described by Dill and Costill [14].

Nine parts of whole blood were added to one part of tri-sodium citrate dehydrate, which was immediately centrifuged at 2500 g for 10 min at 4°C. The citrated plasma was separated and immediately stored at 70°C for subsequent determination of fibrinogen concentration. Frozen TCD plasma was thawed rapidly at 37 using a water bath to prevent denaturation of fibrinogen. Then, plasma samples were analyzed by using a fibrinogen kit (Stago, France) and a fibrinogen analyzer (Biosystems A.S, Spain).

2.4 Statistical analysis

All statistical analyses were performed using the software statistical package SPSS version 22. Distributions of all variables were assessed for normality using Shapiro-Wilk normality test. A two-way ANOVA with repeated measures (2×3) across protocol (1/1 and 1/8) and condition (rest, exercise and recovery) was employed to examine differences in mean values for all variables, except for plasma volume changes. When ANOVA indicated the presence of a significant difference, Bonferroni’s post-hoc test was used to identify which mean differences were statistically significant. Changes in plasma volume during two protocols were compared using paired t-test. Data are presented as mean (±SD) unless otherwise stated. The level of statistical significance was set at P < 0.05.

3 Results

Mean arterial blood pressure (MAP) increased in response to both HIIE protocols and returned to pre exercise level at the end of recovery (P > 0.01). MAP responses to HIIE with work/rest ratio of 1/1 was significantly (P = 0.007) higher than the protocol with 1/8 ratio (Table 2).

Similarly, HR, RBCs count, hemoglobin and hematocrit increased following both HIIE and returned to pre exercise levels at the end of recovery (P < 0.01), though, the responses to exercise and recovery for HIIE_1/1 protocol were significantly (P < 0.05) higher than HIIE_1/8 protocol.

Plasma volume decreased in response to HIIE_1/1 by 11.8% and in response to HIIE_1/8 by 7.8% (Fig. 2). Plasma volume increased by 9.94 and 5.7% at the end of recovery for HIIE_1/1 and HIIE_1/8, respectively. Plasma volume changes following two trials were significantly different (P = 0.005 for exercise, and P = 0.031 for recovery).

Repeated measures of ANOVA revealed significant interactions between protocol and condition for whole blood viscosity (P < 0.05) and plasma viscosity (P < 0.01) (Figs. 3 and 4). Post-hoc analyses showed that whole blood viscosity (P = 0.042) and plasma viscosity (P = 0.014) after exercise were significantly higher in HIIE1/1 than what observed for HIIE_1/8.

Plasma fibrinogen did not change in response to HIIE and no significant difference was detected between two protocols (Fig. 5).

4 Discussion

The main findings of the present study were that the markers of blood fluidity including blood viscosity, plasma viscosity and hematocrit increased in the exercise trial with lower intensity and higher duration more than the trial with higher intensity and lower duration. Based on these findings our hypothesis was rejected.

In the present study, plasma volume reduced by 11.8% and 7.8% following HIIE_1/1 and HIIE_1/8, respectively. These findings are in line with the results of previous studies that showed nearly 10 to 13% reductions in plasma volume after endurance exercise [3, 5]. In our previous study we reported 10 to 13.1% reductions in plasma volume following 30 minutes of continuous cycling at 70–75% of maximal heart rate in different age groups of men [3]. The exercise-induced hemoconcentration is multifactorial [2] and the reductions in plasma volume after exercise found in the present study could be attributed to the significant increase in mean arterial blood pressure [24] that was observed immediately after both HIIE protocols. Mean arterial pressure rises during heavy exercise in proportion to exercise intensity [23], a rise that leads to filtration of blood fluid into the interstitial space [11]. Furthermore, although the exercise intensity in the HIIE_1/8 (110% of VO_2max) was higher than HIIE_1/1 (85% of VO_2max), the duration of active rest was 8 times more in proportion to activity in HIIE_1/8 trial compared to HIIE_1/1 trial that duration of active rest (2 min) was equal to the activity (2 min). It could be speculated that the longer duration of active rest in HIIE_1/8 has resulted in reducing the physiological strain and consequently lowering mean arterial pressure as was found in the present study. Despite the energy expenditure being equal in both protocols and lower exercise intensity in our HIIE_1/1 protocol, this protocol has led to higher physiological strain and consequently higher hemoconcentration because, 1) the duration of exercise worked at 85% is longer, 2) the work to recovery ratio is higher (the recovery after each exercise is shorter), and 3) the 85% of VO_2max is still considered high intensity exercise.

Another main finding of the present study was that increases in blood viscosity following HIIE_1/1 (14.6%) were significantly higher than that for HIIE_1/8 (4.2%). Exercise-induced increases in blood viscosity are mediated by elevated plasma viscosity and hematocrit [31]. Our findings confirm this, because we found higher increases in plasma viscosity and hematocrit following HIIE_1/1 compared to HIIE_1/8. On the other hand, higher hemoconcentration (11.8%) observed following HIIE_1/1 is in agreement to findings of previous studies that showed 10 to 15% plasma volume losses following short term exercise [25, 29]. Therefore, the increases in blood viscosity might be attributed to HIIE_1/1–induced hemoconcentration, as well as increases in hematocrit and plasma viscosity. Our findings for higher plasma viscosity following HIIE_1/1 confirm those of Alis et al. [5] who employed the same protocol as ours (HIIE protocols including 2 min activity interspersed by 2 min recovery) and showed that the HIIE protocol increased plasma viscosity compared to moderate intensity continuous exercise. The increases in plasma viscosity in our study and that of Alis et al. [5] could not be attributed to changes in fibrinogen concentration, because we both could not find significant changes in fibrinogen following the HIIE protocol. For two reasons this finding is interesting. Firstly, it indicates that recovery periods used after each exercise during HIIE might has resulted in the reducing the stress and inflammation which consequently leads to suppression of exercise-induced increases in fibrinogen. Secondly, the reductions in plasma volume found after the HIIE was not accompanied by increases in fibrinogen that questioning the previous mechanisms that related the exercise-induced increases in fibrinogen to hemoconcentration, which of course it needs to be investigated further. Based on the data of the present study we are not able to justify the mechanisms related to lack of changes in fibrinogen and this warrants further studies. However, the increases in plasma viscosity following HIIE_1/1 could be associated with rises in mean arterial pressure during heavy exercise, a rise that leads to filtration of blood fluid into the interstitial space and hemoconcentration.

Moreover, compared to HIIE_1/8, HIIE_1/1 was followed by increases in RBC count that might be partly explained by increased flow and shear forces that might lead to recruitment of RBCs from various circulatory beds [16].

Rises in markers of blood fluidity and hemoconcentration observed following HIIE_1/1 in the present study could be considered as a potential risk for cardiovascular events during this exercise protocol. Therefore, prescribing HIIE for patients with cardiovascular diseases and endothelial dysfunction should be done with care and cautions.

In general, based on the findings of the present study it could be concluded that 1) the intensity of HIIE might not be used as the only key factor in designing HIIT, and the other factors such as the duration of exercise and work/rest ratio are important as much, and 2) HIIE with work/rest ratio of 1/1 induces a physiological strain more than the other HIIEs with lower work/rest ratios, therefore, the risk of this type of HIIE is high and employing this exercise protocols for sedentary individuals and in particular patients might put them at risk. Although, the aim of present study was to clarify the risk of performing the acute HIIT by looking at the hemorheological variables, further studies are needed to determine the effects of regular high training interval exercise or HIIT with different protocols on hemorheological variables in different populations.

Footnotes

Acknowledgments

The authors wish to thank volunteers for their enthusiastic participation in this study. No research fund has been received for this study and the authors have no conflict of interest to declare.

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