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Acute physiological responses to low-intensity blood flow restriction cycling
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Original research
Acute physiological responses to low-intensity blood flow restriction cycling H.J. Thomas ∗ , B.R. Scott, J.J. Peiffer School of Psychology and Exercise Science, Murdoch University, Australia
a r t i c l e
i n f o
Article history: Received 13 September 2017 Received in revised form 23 January 2018 Accepted 26 January 2018 Available online xxx Keywords: Blood pressure Aerobic capacity Anaerobic capacity Intermittent exercise Cardiac output Aerobic exercise
a b s t r a c t Objectives: Blood flow restriction (BFR) during interval cycling may stimulate aerobic and anaerobic adaptations. However, acute physiological responses to BFR interval cycling have not been extensively investigated. Design: Eighteen males completed low-intensity (LI), low-intensity with BFR (LIBFR ) and high-intensity (HI) interval cycling sessions in randomised and counterbalanced order. These included a standardised warm-up and three two-min intervals interspersed with two-min recovery. Interval intensity during HI, LI and LIBFR were 85%, 40% and 40% of peak power output obtained during graded exercise tests. Methods: During LIBFR , 80% arterial occlusion was applied to both legs during the interval efforts and removed during recovery. Continuous measures of heart rate (HR), cardiac output (CO) and oxygen con˙ 2 ) were recorded. Blood pressure (BP) and rating of perceived exertion (RPE) were measured sumption (VO following intervals. Blood lactate concentration was measured pre- and post-exercise. ˙ 2 , lactate and RPE were greatest during HI. During the active intervals, BP, HR and Results: BP, HR, CO, VO ˙ 2 during recovery periods were greater in LIBFR than LI. PostCO were greater during LIBFR than LI. VO session lactate was greater during LIBFR than LI. Importantly, mean arterial pressure during interval three was significantly greater in LIBFR (124 ± 2 mmHg) than HI (114 ± 3 mmHg). Conclusions: LIBFR increases cardiovascular and metabolic stress compared with LI and could provide an alternative aerobic training method for individuals unable to perform high-intensity exercise. However, increases in mean arterial pressure during LIBFR indicates high myocardial workload, and practitioners should therefore use caution if prescribing LIBFR for vascular compromised individuals. © 2018 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
1. Introduction Using blood flow restriction (BFR) during very-low-intensity aerobic training has been shown to promote significant increases ˙ 2max ) and anaerobic (2.5%) capacity.1 These in aerobic (11.6%; VO findings are likely the result of peripheral and central stressors which are enhanced through the use of BFR.1,2 Restriction of blood flow during exercise and the resultant tissue hypoxia can improve skeletal muscle oxidative capacity and angiogenesis through increases in vascular endothelial growth factor (VEGF1),2,3 while increasing anaerobic capacity by proposedly enhancing muscle buffering.3 Simultaneously, BFR can increase cardiovascular stress through greater systemic vascular resistance and acute heart rate increase during exercise,4 likely resulting in beneficial cardiac adaptations.5 Importantly, these findings have been
∗ Corresponding author. E-mail address: [email protected] (H.J. Thomas).
observed during very-low-intensity walking with continuous BFR (∼12.5–15 mL kg−1 min−1 )4 and cycling (30% peak aerobic power output) using both continuous and intermittent BFR.6 Cardiovascular responses (i.e. heart rate, blood pressure and cardiac output) to unrestricted submaximal exercise demonstrate a linear relationship with intensity7 ; however, this is not consistent during BFR.6 It is therefore possible that even small changes in intensity could have a disproportionately large impact on cardiovascular stress. For BFR to be widely adopted, it is essential to understand the influence of this modality under increased submaximal workloads. Continuous BFR applied during very-low-intensity aerobic exercise could be beneficial for populations unable to perform exercise that places a large degree of mechanical strain on joints and muscles, such as the elderly, individuals undergoing rehabilitation, and athletes wanting to decrease external training loads.6,8 The use of continuous BFR, however, is associated with greater perceived exertion compared to a similar intensity of exercise without BFR.6 When compared with continuous BFR, the use of intermit-
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tent BFR during low-intensity cycling (30% peak power output achieved during graded exercise test) can provide similar cardiovascular responses; yet, at lower perceived exertion.6 These findings indicate that intermittent BFR may be a more tolerable strategy during exercise, which could improve compliance with training programs and enhance the practicality of this novel training method. It is important to acknowledge that some authors have cited safety concerns as a limitation of using BFR during exercise.4,9 The increased cardiovascular stress associated with adding BFR to lowintensity aerobic exercise could be inappropriate for individuals with a compromised cardiovascular system.4 Therefore, research examining the influence of BFR during exercise, of a higher intensity than previously reported,4,6 is needed to establish the impact of this modality on cardiovascular stress across a range of commonly prescribed intensities.10 Furthermore, the addition of hemodynamic (i.e. blood pressure, cardiac output) responses are needed to provide a wider representation of the cardiovascular stress imposed by this modality. Therefore, the purpose of this study was to investigate acute cardiovascular, metabolic, and perceptual responses to intermittent BFR during interval cycling at a power output above those previously reported. Considering the health benefits of highintensity interval training in healthy and clinical populations,11,12 responses were also compared to a high-intensity interval session as a benchmark for cardiovascular, metabolic and perceptual stress.
2. Methods Eighteen healthy men (age: 23 ± 3 year, height: 176.9 ± 6.8 cm, ˙ 2peak : 49.3 ± 6.7 mL kg−1 min−1 ) volbody mass: 79.4 ± 10.4 kg, VO unteered to participate in this study. Participants were excluded if they were identified as high risk during screening (Exercise and Sports Science Australia pre-exercise screening questionnaire) or if they suffered from musculoskeletal injuries that could be made worse by aerobic exercise or if taking supplements or medications that could influence the study outcomes. Risks and benefits of the study were provided to participants and signed consent was obtained. This study was approved by the institutional Human Research Ethics Committee. Participants were required to complete four exercise sessions consisting of a graded exercise test and three experimental testing sessions. The order of the experimental sessions were counterbalanced for 18 participants and then randomised. Participants were then sequentially allocated to starting condition. The experimental sessions were separated by 5 ± 2 days and consistent within participants. Twelve hours prior to each experimental session, participants were asked to refrain from consuming alcohol, nicotine, or caffeine. Additionally, participants were instructed to consume a similar diet and refrain from heavy exercise for 24 h prior to each session. All testing was conducted at the same time of day to account for diurnal variations in circadian rhythm. During session one, participants completed a maximal graded exercise test using a Velotron cycle ergometer (Racer Mate, Seattle, Washington), starting at 70 W and increasing by 35 W min−1 until volitional exhaustion. Expired gases were measured using a calibrated Parvo TrueOne metabolic cart (Parvo Medics, East Sandy, ˙ 2) Utah) from which the 15 s mean rate of oxygen consumption (VO ˙ and volume of carbon dioxide production (VCO ) were calculated. 2 ˙ 2peak ) was defined as the highest VO ˙ 2 Peak oxygen consumption (VO recorded over three consecutive 15 s values during the final 60 s of the test. During the remaining three visits, participants completed a low-intensity cycling based interval session (LI), low-intensity
cycling based interval session with BFR (LIBFR ) and a high-intensity cycling based interval session (HI) on a Velotron cycle ergometer. Each session commenced with a seven-min standardised warm-up at 30% of peak aerobic power measured during the graded exercise test (96 ± 3 W). The interval protocol consisted of three rounds of two-min efforts interspersed with two-min of very-low-intensity active recovery (10 W). Finally, participants completed a five-min cool-down (30% peak aerobic power). To allow comparison of the acute influence of low-intensity exercise with BFR to a theoretical maximum, the interval program was designed to match the duration and number of efforts achievable in the high-intensity condition. Two-min efforts at 85% of peak aerobic power (272 ± 9 W) were selected as this type of training is consistent with increases in aerobic performance13 and through pilot testing, it was determined that some participants may not have been able to complete four efforts. Further pilot testing was conducted to determine the appropriate percentage of peak aerobic power output for the BFR condition (40%; 128 ± 4 W) that would allow participants to complete three, two-min efforts under the BFR protocol. The LI intervals were completed at the same intensity as the LIBFR session. During the LIBFR , restriction was applied to the proximal portion of both thighs using a pressurised cuff (10 cm wide) only during the active interval and was released during recovery. Occlusion pressure was maintained via an E20 rapid cuff inflator and AG101 air source (Hokanson, Bellevue, Washington) and set to 80% (143.4 ± 19.2 mmHg) of participants’ pre-determined arterial occlusion pressure14 (179.2 ± 24.1 mmHg). Arterial occlusion pressure was determined with participants lying supine using a handheld bi-directional ultrasound Doppler probe (MD6 Doppler, Hokanson, Bellevue, Washington) in accordance with previous methods in current BFR research.14 ˙ 2 and VCO ˙ Within all sessions, VO 2 were measured continuously at a frequency of 1 Hz using a metabolic cart, while heart rate (HR), cardiac output (CO) and stroke volume (SV), were measured at a beat-by-beat frequency and reported as 10 s mean values using automated impedance cardiography (ICG; Q-Link PhysioFlow PF-07, Manatec Biomedical; France). This method has been shown to be valid and reliable at rest and during submaximal exercise in patients with normal cardiorespiratory function.15 Systolic (SBP) and diastolic blood pressure (DBP) were measured manually by the same researcher at the end of warm-up and cool-down, as well as approximately 90 s (measured started at one min and completed in 30 s) into the two-min working and recovery intervals. The use of manual recording of SBP and DBP has demonstrated smallest detectable differences of 7.6 and 7.0 mmHg, respectively, during rest conditions.16 These data were entered into the ICG software following each BP reading, to calculate mean arterial pressure (MAP). Using HR and blood pressure measures, the rate pressure product (RPP) and pulse pressure (PP) were calculated. Blood lactate concentrations were measured via a finger stick blood sample and hand-held analyser (Lactate plus, Nova biomedical, Waltham, Massachusetts) immediately before the warm-up and at completion of the last recovery interval. Finally, a 0–10 Borg scale17 was used to obtain a rating of perceived exertion (RPE) at the end of each active interval, as well as a sessional-RPE (sRPE) 30-min after completion of exercise. Differences in cardiovascular, metabolic, and perceptual responses between conditions and time points were analysed using a two-way ANOVA with repeated measures. Significant main effects or interactions were assessed using Fisher’s least significant difference post hoc test. Differences in sRPE between conditions were analysed using a one-way ANOVA with repeated measures. Where necessary, Cohen’s d effect sizes were calculated. Statistical analy-
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Fig. 1. Systolic (a), diastolic (b), and mean (c) arterial blood pressure measured throughout the low-intensity, low-intensity with blood flow restriction and highintensity conditions. SBP = systolic arterial blood pressure, DBP = diastolic arterial blood pressure, MAP = mean arterial pressure, LI = low-intensity, LIBFR = low-intensity with blood flow restriction, HI = high-intensity. *LIBFR significantly different to HI, ‡ LIBFR significantly different to LI, # HI significantly different to LI. B = baseline, WU = warm-up, Int1–3 = interval 1–3, Rec1–3 = recovery 1–3, CD = cooldown.
sis was conducted using SPSS (v.22, IBM) with a level of significance of p < 0.05. All data are presented as mean ± SEM. 3. Results A condition × time interaction was observed for differences in SBP, DBP and MAP (p < 0.01) (Fig. 1). SBP was greater during LIBFR than LI at all time points from warm-up to cool-down (range: p < 0.01–0.05; ES = 0.34–2.04). Additionally, SBP was greater during HI compared with LI for the entire exercise session (range: p < 0.01–0.04; ES = 0.14–2.90). Compared with LIBFR , SBP measured during HI was greater at recovery one (p < 0.01; ES = 1.09) and intervals two (p = 0.04; ES = 0.65) and three (p = 0.02; ES = 0.44). Compared with LI, DBP was greater in LIBFR measured at baseline (p = 0.05; ES = 0.51) and intervals one (p = 0.02; ES = 0.71), two
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(p < 0.01; ES = 0.98) and three (p < 0.01; ES = 1.39). Greater DBP were observed in LI compared to HI during warm-up (p < 0.01; ES = 0.56), recovery periods one (p < 0.01; ES = 0.89), two (p < 0.01; ES = 0.83) and three (p = 0.02; ES = 0.74) and the cool-down (p < 0.01; ES = 0.60). DBP during LIBFR was greater than HI from interval one until cool-down (range: p < 0.01–0.04; ES = 0.45–1.60). Greater MAP were observed in LIBFR compared to LI during intervals one (p < 0.01; ES = 1.28), two (p < 0.01; ES = 1.41) and three (p = 0.01; ES = 2.1) and recovery periods two (p < 0.01; ES = 0.69) and three (p < 0.01; ES = 0.83). During the HI condition, MAP was greater than LI during intervals one (p < 0.01; ES = 0.80), two (p < 0.01; ES = 0.91), and three (p < 0.01; ES = 1.13). Of note, MAP was greater in LIBFR when compared with HI during interval three (124.2 ± 2.3 mmHg vs. 113.9 ± 2.5 mmHg; ES = 1.00) and cool-down (98.6 ± 2 mmHg vs. 94.7 ± 2.1 mmHg; ES = 0.44). Within the LIBFR condition, MAP was greater during interval three (124.2 ± 2.3 mmHg) compared with intervals one (115.2 ± 2.6 mmHg) and two (118.0 ± 2.7 mmHg). A condition × time interaction (p < 0.01) was observed for differences in CO and HR (Fig. 2b and a; respectively). Measures of CO were greater in LIBFR than LI during intervals two (p = 0.04; ES = 0.50) and three (p < 0.01; ES = 0.64) and recovery periods one (p < 0.01; ES = 0.78), two (p < 0.01; ES = 0.84) and three (p < 0.01; ES = 0.84). Greater CO was observed during HI compared with LIBFR from interval one to the cool-down (range: p < 0.01; ES = 0.99–1.29) and in LI from interval one to the cool-down (range: p < 0.01; ES = 0.98–1.84). HR was greater in HI compared with LI at all time points (range: p < 0.01; ES = 0.60–4.37) except baseline. Similarly, HR was greater in LIBFR compared with LI measured at all points (range: p < 0.03; ES = 0.32–1.93) except baseline. Compared with LIBFR , HR was greater during HI from interval one through the cool-down (range: p < 0.01; ES = 1.26–2.12). No main effects or interactions were observed for SV between conditions (Fig. 2c). A condition × time interaction was observed for PP and RPP (p < 0.01; Fig. 4). Compared with HI, PP was lower in LI from interval one to recovery three (range: p < 0.01; ES = 1.58–3.07) and in LIBFR from interval one to recovery three (range: p = 0.01–0.03; ES = 0.64–1.53). Measured at warmup, PP was less in LI (64 ± 3 mmHg) compared with HI (71 ± 2 mmHg) and LIBFR (72 ± 3 mmHg). Additionally LI was less at cooldown (77 ± 4 mmHg) compared with HI (91 ± 4 mmHg) and LIBFR (88 ± 4 mmHg). Compared with HI, the RPP was lower in LI from interval one onward (range: p < 0.01; ES = 2.70–4.83) with similar differences observed between HI and LIBFR (range: p < 0.01; ES = 1.21–2.21). Additionally, RPP measured during LIBFR was greater than during LI from interval one through the cool-down (range: p < 0.01; ES = 1.32–2.42). Measured at the warmup, RPP was less during LI (127 ± 530 bpm mmHg) compared with both HI (136 ± 415 bpm mmHg) and LIBFR (133 ± 360 bpm mmHg). ˙ 2 and VCO ˙ A condition × time interaction was observed for VO 2 ˙ 2 was observed in LIBFR compared with (p < 0.01) (Fig. 3). Greater VO LI from baseline (p < 0.01; ES = 1.24), recovery periods one (p < 0.01; ES = 1.17), two (p < 0.01; ES = 1.37) and three (p < 0.01; ES = 1.35) ˙ 2 was greater and the cool-down (p = 0.02; ES = 0.40). During HI, VO than LI at all time points (range: p < 0.01–0.04; ES = 0.27–4.53) and greater than LIBFR from interval one through cool-down (range: ˙ p < 0.01; ES = 0.92–4.33). Measures of VCO 2 were greater in LIBFR compared with LI from baseline until recovery three (p < 0.01; ˙ ES = 0.49–2.13). Additionally, greater levels of VCO 2 were observed in HI than LI at all time points (range: p < 0.01; ES = 0.52–5.87) and LIBFR (range: p < 0.01; ES = 1.92–4.78) from interval one through cool-down. There were no differences in blood lactate pre-exercise in HI (1.2 ± 0.09), LIBFR (1.3 ± 0.08) and LI (1.2 ± 0.08). A condition × time interaction (p < 0.01) was observed with greater post-exercise values in HI (13.2 ± 0.61) than LIBFR (6.3 ± 0.49) (+125%; p < 0.01) and
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Fig. 2. Heart rate (a), cardiac output (b) and stroke volume (c) measured throughout the low-intensity, low-intensity with blood flow restriction and high-intensity conditions. HR = heart rate, CO = cardiac output, SV = stroke volume, LI = low-intensity, LIBFR = low-intensity with blood flow restriction, HI = high-intensity. *LIBFR significantly different to HI, ‡ LIBFR significantly different to LI, # HI significantly different to LI. B = baseline, WU = warm-up, Int1–3 = interval 1–3, Rec1–3 = recovery 1–3, CD = cool-down.
Fig. 3. Rate of oxygen consumption (a) and volume of carbon dioxide production (b) measured throughout the low-intensity, low-intensity with blood flow restriction and high-intensity conditions. ˙ ˙ 2 = rate of oxygen consumption, VCO VO 2 = volume of carbon dioxide production, LI = low-intensity, LIBFR = low-intensity with blood flow restriction, HI = highintensity. *LIBFR significantly different to HI, ‡ LIBFR significantly different to LI, # HI significantly different to LI. B = baseline, WU = warm-up, Int1–3 = interval 1–3, Rec1–3 = recovery 1–3, CD = cooldown.
Fig. 4. Pulse pressure (A) and the rate pressure product (B) calculated throughout the low-intensity, low-intensity with blood flow restriction and high-intensity conditions. LI = low-intensity, LIBFR = low-intensity with blood flow restriction, HI = highintensity. *LIBFR significantly different to HI, ‡ LIBFR significantly different to LI, # HI significantly different to LI. B = baseline, WU = warm-up, Int1–3 = interval 1–3, Rec1–3 = recovery 1–3, CD = cooldown.
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LI (2.8 ± 0.29) (+371%; p < 0.01). In addition, post-exercise lactate was 110% greater in LIBFR than LI (p < 0.01). A condition × time interaction was observed for RPE (p < 0.01) measured during each interval. Greater RPE were observed during HI in all intervals (5.5 ± 0.3, 6.9 ± 0.3 and 8.1 ± 0.3, respectively) than both LIBFR (4.6 ± 0.3, 5.1 ± 0.2 and 5.6 ± 0.3, respectively) and LI (2.1 ± 0.2, 2.6 ± 0.1 and 2.8 ± 0.2, respectively). Furthermore, RPE was greater in all intervals during LIBFR than LI. sRPE was greater in HI (8.1 ± 0.7) compared with LIBFR (5.7 ± 1.6; p < 0.01) and LI (2.4 ± 0.8; p < 0.01) and between LIBFR compare with LI (p < 0.01).
4. Discussion Throughout the interval sessions HR was greater during LIBFR than LI alone (Fig. 2a). The difference in HR (∼15 bpm during active and ∼18 bpm during recovery intervals) is consistent with, albeit larger than, previous aerobic based BFR research which observed ∼10 bpm increases in HR during very-low-intensity (∼12.5–15 mL kg−1 min−1 ) walking with BFR.4 The elevated HR response during BFR is likely due to the activation of the muscle chemoreflex18 in response to an increase in hypoxic stress.19 Indeed, the use of BFR during exercise decreases available oxygen at the working muscle20,21 resulting in increased levels of lactate22 and carbon dioxide.23,24 Efferent signalling in response to these changes is known to stimulate an increase in HR through sympathetic output.17,19 Increases in CO observed in the current study (Fig. 2b) is not consistent with previous BFR research4 and is likely due to the BFR methodology employed. For instance, utilising a continuous restriction protocol, Renzi et al.4 observed no change in CO, which was explained by reductions in venous return and a resultant decrease in SV.4,22 In the present study, deflation of the BFR cuffs and the addition of the muscle pump effect during the active recovery, may have allowed pooled blood in the limbs to return to the heart, maintaining SV (Fig. 2) and increasing CO.20 Additionally, we set BFR to 80% of the participant’s arterial occlusion pressure to allow some arterial inflow whereas Renzi et al.4 utilised a standard pressure of 160 mmHg. It is also plausible that the use of an arbitrary standard pressure by Renzi et al.4 may have resulted in higher levels of occlusion in some or their participants leading to the differences in our findings. However, with the current available information this hypothesis cannot be confirmed. In agreement with Renzi et al.,4 the addition of BFR to low-intensity aerobic exercise resulted in increased myocardial work as measured through changes in PP and RPP (Fig. 4). However, these responses were not elevated to the same magnitude as during the HI condition, indicating that the increased cardiac stress associated with LIBFR is not consistent with traditional high-intensity exercise. Consistent with a hypoxic environment within the working ˙ muscle,21,23,24 we observed increased lactate and VCO 2 during the LIBFR compared with LI. Indeed, hypoxia is associated with an increase in anaerobic metabolism22 from which lactate and carbon dioxide are main bi-products.25,26 The current findings support previous BFR research4 and represent an increase in anaerobic ˙ 2 during metabolism under these conditions.1,25 The higher VO ˙ 2 recovery in LIBFR compared with LI, combined with similar VO during the exercise intervals resulted in a higher accumulated O2 uptake throughout the duration of the session. These findings indicate that overall aerobic metabolism was greater during LIBFR ; however, the peak rate of aerobic energy release during exercise was not. In comparison, HI demonstrated the greatest peak rate of aerobic energy release, as well as highest accumulated O2 uptake, across the exercise session. It is common, following exercise of high ˙ 2 post exercise in anaerobic demand, to observe an increased VO response to an initial oxygen deficit,27 a response that was likely
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exacerbated by the BFR. When considered together with previously discussed differences in lactate, a greater accumulated O2 uptake during BFR exercise compared to the intensity matched exercise without BFR indicate this technique may provide enhanced stimulus for both aerobic and anaerobic adaptations.1,2 When compared with HI exercise, the addition of BFR to low-intensity cycling did not result in similar metabolic or cardiovascular stress (Figs. 1–4). This is even evident during the cool-down periods following each trial, where higher HR, CO, VO2 and VCO2 were observed for HI trials compared with both LI and LIBFR conditions. This indicates a greater overall physiological demand being posed by the HI session, and suggests that lowintensity aerobic exercise with BFR should not be used as a sole replacement of high-intensity training if an individual can safely tolerate high-intensity exercise. However, for individuals that cannot tolerate high-intensity exercise, the additional cardiovascular and metabolic stress associated with LIBFR when compared with LI alone indicate that method of exercise delivery could provide benefit. Furthermore, lower interval RPE and sRPE scores were reported following the low-intensity BFR session compared with the highintensity session. These findings are in agreement with Corvino et al.,6 and indicate that this low-intensity BFR exercise may be better tolerated by a wider population compared with high-intensity exercise.26 Notably, MAP during interval three was greater (10.3 ± 0.3 mmHg) for LIBFR compared with HI. A greater CO measured during HI compared with LIBFR would indicate that the observed difference in MAP between the two conditions was a consequence of the higher DBP during LIBFR (Figs. 1b and 2d). During the recovery periods, cuff deflation was associated with a decrease in DBP in LIBFR to levels consistent with the LI condition. Together these findings indicate that bi-lateral BFR of the low limbs overrides normal vasodilation responses associated with exercise.28 When analysing the LIBFR condition separately, greater MAP was noted during interval three compared with intervals one and two (Fig. 1c). It is possible that the inclusion of additional intervals, longer intervals, increased work:rest ratio or continuous BFR could have resulted in even higher MAP. Indeed, many of the hemodynamic variables associated with MAP demonstrated a systemic increase following each working interval, further supporting our hypothesis. This finding is important, as majority of BFR research has utilised continuous BFR at intensities equal to or less than 30% peak power,1,4,5 and it is therefore likely that continuous BFR would be used within current practice. The increased myocardial workload,4 in terms of MAP, HR and CO seen during the LIBFR trial, is likely not problematic for many clinical populations.20 While resting MAP measures >99 mmHg are associated with an increased risk of cardiac events,29,30 we are not aware of exercise-specific guidelines to indicate potentially dangerous levels of MAP. Nevertheless, considering that MAP reached values of 124.2 ± 2.3 mmHg in the final interval of the LIBFR condition, we suggest that practitioners use caution when implementing BFR in populations with compromised vascular function. While this study provides new information regarding the acute responses to interval cycling with BFR, it would be remiss not to acknowledge some limitations. Firstly, the current findings are specific to the interval protocol completed (i.e. number of intervals, duration of efforts and work:rest ratio). Considering that MAP appeared to increase with each interval in the LIBFR condition, it is possible that longer intervals, additional intervals or an increased work:rest ratio could lead to even greater increases in the physiological stress associated with BFR exercise. We observed similar VO2 and HR responses to Corvino et al.,6 despite implementing a higher intensity during intervals; this may be due to the greater work:rest ratio prescribed by Corvino et al.6 (2:1), compared with the 1:1 ratio used in the current study. This finding highlights
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that further research is necessary to understand the combined impacts of different training variables during BFR modalities on cardiovascular demands, particularly to enhance the safety of such training. In addition, this study involved only healthy participants, and the results may not translate to clinical populations. It is important, however, to take these first steps towards understanding the potential cardiovascular risk of BFR exercise using populations who are less likely to suffer adverse events. Lastly, while the method used to determine arterial occlusion pressure is widely accepted in BFR research, arterial occlusion pressure was assessed in a resting supine position, which may be different when participants are in a seated position, and during exercise. 5. Conclusion The findings of this study suggest that addition of intermittent BFR to low-intensity interval cycling represents a useful training modality which can increase metabolic and cardiovascular demands compared to low-intensity cycling alone. This subsequent stress could result in beneficial aerobic and anaerobic adaptations, and should be considered by individuals who are not able to tolerate high-intensity exercise. However, the increase in MAP observed toward the conclusion of LIBFR trials indicates a high myocardial workload, which was greater than that observed during the highintensity session. Therefore, practitioners should use caution if prescribing this modality within a vascular compromised population. Practical implications • Low-intensity BFR cycling may be useful for individuals unable to perform exercise at a high-intensity, such as those undergoing rehabilitation, elderly or clinical populations. • Low-intensity cycling with BFR provides greater aerobic and anaerobic stress then low-intensity cycling alone. • Caution should be used by practitioners when prescribing BFR exercise to individuals with compromised vascular function. Acknowledgments The results of this study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. Results of the present study do not constitute endorsement by SMA. We would like to thank the participants in this study for dedicating their time to this project, and Mr Cameron Lilly for his extensive assistance in data collection. References 1. Park S, Kim JK, Choi HM et al. Increase in maximal oxygen uptake following 2-week walk training with blood flow occlusion in athletes. Eur J Appl Physiol 2010; 109(4):591–600. 2. de Oliveira MF, Caputo F, Corvino RB et al. Short-term low-intensity blood flow restricted interval training improves both aerobic fitness and muscle strength. Scand J Med Sci Sports 2016; 26(9):1017–1025. 3. Pope ZK, Willardson JM, Schoenfeld BJ. Exercise and blood flow restriction. J Strength Cond Res 2013; 27(10):2914–2926. 4. Renzi CP, Tanaka H, Sugawara J. Effects of leg blood flow restriction during walking on cardiovascular function. Med Sci Sport Exerc 2010; 42(4):726–732.
5. Abe T, Fujita S, Nakajima T et al. Effects of low-intensity cycle training with restricted leg blood flow on thigh muscle volume and VO2max in young men. J Sports Sci Med 2010; 9(3):452–458. 6. Corvino RB, Rossiter HB, Loch T et al. Physiological responses to interval endurance exercise at different levels of blood flow restriction. Eur J Appl Physiol 2017; 117(1):39–52. 7. Arts FJ, Kuipers H. The relation between power output, oxygen uptake and heart rate in male athletes. Int J Sports Med 1994; 15(5):228–231. 8. Scott BR, Loenneke JP, Slattery KM et al. Exercise with blood flow restriction: an updated evidence-based approach for enhanced muscular development. Sport Med 2015; 45(3):313–325. 9. Tabata S, Suzuki Y, Azuma K et al. Rhabdomyolysis after performing blood flow restriction training: a case report. J Strength Cond Res 2016; 30(7):2064–2068. 10. American College of Sports Medicine, ACSMs guidelines for exercise testing and prescription, 9th ed., Philadelphia, Lippincott Williams and Wilkins, 2014. 11. Weston KS, Wisløff U, Coombes JS. High-intensity interval training in patients with lifestyle-induced cardiometabolic disease: a systematic review and metaanalysis. Br J Sport Med 2014; 48(16):1227–1234. 12. Helgerud J, Hoydal K, Wang E et al. Aerobic high-intensity intervals improve VO2max more than moderate training. Med Sci Sports Exerc 2007; 39(4):665–671. 13. Buchheit M, Laursen PB. High-intensity interval training, solutions to the programming puzzle: part I: cardiopulmonary emphasis. Sports Med 2013; 43(5):313–338. 14. Loenneke JP, Fahs CA, Rossow LM et al. Effects of cuff width on arterial occlusion: implications for blood flow restricted exercise. Eur J Appl Physiol 2012; 112(8):2903–2912. 15. Charloux A, Lonsdorfer-Wolf E, Richard R et al. A new impedance cardiograph device for the non-invasive evaluation of cardiac output at rest and during exercise: comparison with the direct Fick method. Eur J Appl Physiol 2000; 82(4):313–320. 16. Keavney B, Bird R, Caiazza A et al. Measurement of blood pressure using the auscultatory and oscillometric methods in the same cuff deflation: validation and field trial of the A&D TM2421 monitor. J Hum Hypertens 2000; 14(9):573–579. 17. Borg GA. Psychophysical bases of perceived exertion. Med Sci Sports Exerc 1982; 14(5):377–381. 18. Victor RG, Seals DR. Reflex stimulation of sympathetic outflow during rhythmic exercise in humans. Am J Physiol 1989; 257(6):H2017–H2024. 19. Vieira PJ, Chiappa GR, Umpierre D et al. Hemodynamic responses to resistance exercise with restricted blood flow in young and older men. J Strength Cond Res 2013; 27(8):2288–2294. 20. Neto GR, Novaes JS, Dias I et al. Effects of resistance training with blood flow restriction on haemodynamics: a systematic review. Clin Physiol Funct Imaging 2017; 37(6):567–574. 21. Takarada Y, Nakamura Y, Aruga S et al. Rapid increase in plasma growth hormone after low-intensity resistance exercise with vascular occlusion. J Appl Physiol 2000; 88(1):61–65. 22. Takano H, Morita T, Iida H et al. Hemodynamic and hormonal responses to a short-term low-intensity resistance exercise with the reduction of muscle blood flow. Eur J Appl Physiol 2005; 95(1):65–73. 23. Vallet B, Teboul J-L, Cain S et al. Venoarterial CO2 difference during regional ischemic or hypoxic hypoxia. J Appl Physiol 2000; 89(4):1317–1321. 24. Wasserman K, Whipp BJ, Koyl S et al. Anaerobic threshold and respiratory gas exchange during exercise. J Appl Physiol 1973; 35(2):236–243. 25. Green H. Mechanisms of muscle fatigue in intense exercise. J Sport Sci 1997; 15(3):247–256. 26. Wasserman K. The anaerobic threshold measurement to evaluate exercise performance. Am Rev Respir Dis 1984; 129(2):S35–S40. 27. Bangsbo J, Gollnick P, Graham T et al. Anaerobic energy production and O2 deficit-debt relationship during exhaustive exercise in humans. J Physiol 1990; 422:539–559. 28. Boutcher YN, Hopp JP, Boutcher SH. Acute effect of a single bout of aerobic exercise on vascular and baroreflex function of young males with a family history of hypertension. J Hum Hypertens 2011; 25(5):311–319. 29. Benetos A, Safar M, Rudnichi A et al. Pulse pressure: a predictor of longterm cardiovascular mortality in a French male population. Hypertension 1997; 30(6):1410–1415. 30. Sesso HD, Stampfer MJ, Rosner B et al. Systolic and diastolic blood pressure, pulse pressure, and mean arterial pressure as predictors of cardiovascular disease risk in men. Hypertension 2000; 36(5):801–807.
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Original research
Acute physiological responses to low-intensity blood flow restriction cycling H.J. Thomas ∗ , B.R. Scott, J.J. Peiffer School of Psychology and Exercise Science, Murdoch University, Australia
a r t i c l e
i n f o
Article history: Received 13 September 2017 Received in revised form 23 January 2018 Accepted 26 January 2018 Available online xxx Keywords: Blood pressure Aerobic capacity Anaerobic capacity Intermittent exercise Cardiac output Aerobic exercise
a b s t r a c t Objectives: Blood flow restriction (BFR) during interval cycling may stimulate aerobic and anaerobic adaptations. However, acute physiological responses to BFR interval cycling have not been extensively investigated. Design: Eighteen males completed low-intensity (LI), low-intensity with BFR (LIBFR ) and high-intensity (HI) interval cycling sessions in randomised and counterbalanced order. These included a standardised warm-up and three two-min intervals interspersed with two-min recovery. Interval intensity during HI, LI and LIBFR were 85%, 40% and 40% of peak power output obtained during graded exercise tests. Methods: During LIBFR , 80% arterial occlusion was applied to both legs during the interval efforts and removed during recovery. Continuous measures of heart rate (HR), cardiac output (CO) and oxygen con˙ 2 ) were recorded. Blood pressure (BP) and rating of perceived exertion (RPE) were measured sumption (VO following intervals. Blood lactate concentration was measured pre- and post-exercise. ˙ 2 , lactate and RPE were greatest during HI. During the active intervals, BP, HR and Results: BP, HR, CO, VO ˙ 2 during recovery periods were greater in LIBFR than LI. PostCO were greater during LIBFR than LI. VO session lactate was greater during LIBFR than LI. Importantly, mean arterial pressure during interval three was significantly greater in LIBFR (124 ± 2 mmHg) than HI (114 ± 3 mmHg). Conclusions: LIBFR increases cardiovascular and metabolic stress compared with LI and could provide an alternative aerobic training method for individuals unable to perform high-intensity exercise. However, increases in mean arterial pressure during LIBFR indicates high myocardial workload, and practitioners should therefore use caution if prescribing LIBFR for vascular compromised individuals. © 2018 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
1. Introduction Using blood flow restriction (BFR) during very-low-intensity aerobic training has been shown to promote significant increases ˙ 2max ) and anaerobic (2.5%) capacity.1 These in aerobic (11.6%; VO findings are likely the result of peripheral and central stressors which are enhanced through the use of BFR.1,2 Restriction of blood flow during exercise and the resultant tissue hypoxia can improve skeletal muscle oxidative capacity and angiogenesis through increases in vascular endothelial growth factor (VEGF1),2,3 while increasing anaerobic capacity by proposedly enhancing muscle buffering.3 Simultaneously, BFR can increase cardiovascular stress through greater systemic vascular resistance and acute heart rate increase during exercise,4 likely resulting in beneficial cardiac adaptations.5 Importantly, these findings have been
∗ Corresponding author. E-mail address: [email protected] (H.J. Thomas).
observed during very-low-intensity walking with continuous BFR (∼12.5–15 mL kg−1 min−1 )4 and cycling (30% peak aerobic power output) using both continuous and intermittent BFR.6 Cardiovascular responses (i.e. heart rate, blood pressure and cardiac output) to unrestricted submaximal exercise demonstrate a linear relationship with intensity7 ; however, this is not consistent during BFR.6 It is therefore possible that even small changes in intensity could have a disproportionately large impact on cardiovascular stress. For BFR to be widely adopted, it is essential to understand the influence of this modality under increased submaximal workloads. Continuous BFR applied during very-low-intensity aerobic exercise could be beneficial for populations unable to perform exercise that places a large degree of mechanical strain on joints and muscles, such as the elderly, individuals undergoing rehabilitation, and athletes wanting to decrease external training loads.6,8 The use of continuous BFR, however, is associated with greater perceived exertion compared to a similar intensity of exercise without BFR.6 When compared with continuous BFR, the use of intermit-
https://doi.org/10.1016/j.jsams.2018.01.013 1440-2440/© 2018 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
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tent BFR during low-intensity cycling (30% peak power output achieved during graded exercise test) can provide similar cardiovascular responses; yet, at lower perceived exertion.6 These findings indicate that intermittent BFR may be a more tolerable strategy during exercise, which could improve compliance with training programs and enhance the practicality of this novel training method. It is important to acknowledge that some authors have cited safety concerns as a limitation of using BFR during exercise.4,9 The increased cardiovascular stress associated with adding BFR to lowintensity aerobic exercise could be inappropriate for individuals with a compromised cardiovascular system.4 Therefore, research examining the influence of BFR during exercise, of a higher intensity than previously reported,4,6 is needed to establish the impact of this modality on cardiovascular stress across a range of commonly prescribed intensities.10 Furthermore, the addition of hemodynamic (i.e. blood pressure, cardiac output) responses are needed to provide a wider representation of the cardiovascular stress imposed by this modality. Therefore, the purpose of this study was to investigate acute cardiovascular, metabolic, and perceptual responses to intermittent BFR during interval cycling at a power output above those previously reported. Considering the health benefits of highintensity interval training in healthy and clinical populations,11,12 responses were also compared to a high-intensity interval session as a benchmark for cardiovascular, metabolic and perceptual stress.
2. Methods Eighteen healthy men (age: 23 ± 3 year, height: 176.9 ± 6.8 cm, ˙ 2peak : 49.3 ± 6.7 mL kg−1 min−1 ) volbody mass: 79.4 ± 10.4 kg, VO unteered to participate in this study. Participants were excluded if they were identified as high risk during screening (Exercise and Sports Science Australia pre-exercise screening questionnaire) or if they suffered from musculoskeletal injuries that could be made worse by aerobic exercise or if taking supplements or medications that could influence the study outcomes. Risks and benefits of the study were provided to participants and signed consent was obtained. This study was approved by the institutional Human Research Ethics Committee. Participants were required to complete four exercise sessions consisting of a graded exercise test and three experimental testing sessions. The order of the experimental sessions were counterbalanced for 18 participants and then randomised. Participants were then sequentially allocated to starting condition. The experimental sessions were separated by 5 ± 2 days and consistent within participants. Twelve hours prior to each experimental session, participants were asked to refrain from consuming alcohol, nicotine, or caffeine. Additionally, participants were instructed to consume a similar diet and refrain from heavy exercise for 24 h prior to each session. All testing was conducted at the same time of day to account for diurnal variations in circadian rhythm. During session one, participants completed a maximal graded exercise test using a Velotron cycle ergometer (Racer Mate, Seattle, Washington), starting at 70 W and increasing by 35 W min−1 until volitional exhaustion. Expired gases were measured using a calibrated Parvo TrueOne metabolic cart (Parvo Medics, East Sandy, ˙ 2) Utah) from which the 15 s mean rate of oxygen consumption (VO ˙ and volume of carbon dioxide production (VCO ) were calculated. 2 ˙ 2peak ) was defined as the highest VO ˙ 2 Peak oxygen consumption (VO recorded over three consecutive 15 s values during the final 60 s of the test. During the remaining three visits, participants completed a low-intensity cycling based interval session (LI), low-intensity
cycling based interval session with BFR (LIBFR ) and a high-intensity cycling based interval session (HI) on a Velotron cycle ergometer. Each session commenced with a seven-min standardised warm-up at 30% of peak aerobic power measured during the graded exercise test (96 ± 3 W). The interval protocol consisted of three rounds of two-min efforts interspersed with two-min of very-low-intensity active recovery (10 W). Finally, participants completed a five-min cool-down (30% peak aerobic power). To allow comparison of the acute influence of low-intensity exercise with BFR to a theoretical maximum, the interval program was designed to match the duration and number of efforts achievable in the high-intensity condition. Two-min efforts at 85% of peak aerobic power (272 ± 9 W) were selected as this type of training is consistent with increases in aerobic performance13 and through pilot testing, it was determined that some participants may not have been able to complete four efforts. Further pilot testing was conducted to determine the appropriate percentage of peak aerobic power output for the BFR condition (40%; 128 ± 4 W) that would allow participants to complete three, two-min efforts under the BFR protocol. The LI intervals were completed at the same intensity as the LIBFR session. During the LIBFR , restriction was applied to the proximal portion of both thighs using a pressurised cuff (10 cm wide) only during the active interval and was released during recovery. Occlusion pressure was maintained via an E20 rapid cuff inflator and AG101 air source (Hokanson, Bellevue, Washington) and set to 80% (143.4 ± 19.2 mmHg) of participants’ pre-determined arterial occlusion pressure14 (179.2 ± 24.1 mmHg). Arterial occlusion pressure was determined with participants lying supine using a handheld bi-directional ultrasound Doppler probe (MD6 Doppler, Hokanson, Bellevue, Washington) in accordance with previous methods in current BFR research.14 ˙ 2 and VCO ˙ Within all sessions, VO 2 were measured continuously at a frequency of 1 Hz using a metabolic cart, while heart rate (HR), cardiac output (CO) and stroke volume (SV), were measured at a beat-by-beat frequency and reported as 10 s mean values using automated impedance cardiography (ICG; Q-Link PhysioFlow PF-07, Manatec Biomedical; France). This method has been shown to be valid and reliable at rest and during submaximal exercise in patients with normal cardiorespiratory function.15 Systolic (SBP) and diastolic blood pressure (DBP) were measured manually by the same researcher at the end of warm-up and cool-down, as well as approximately 90 s (measured started at one min and completed in 30 s) into the two-min working and recovery intervals. The use of manual recording of SBP and DBP has demonstrated smallest detectable differences of 7.6 and 7.0 mmHg, respectively, during rest conditions.16 These data were entered into the ICG software following each BP reading, to calculate mean arterial pressure (MAP). Using HR and blood pressure measures, the rate pressure product (RPP) and pulse pressure (PP) were calculated. Blood lactate concentrations were measured via a finger stick blood sample and hand-held analyser (Lactate plus, Nova biomedical, Waltham, Massachusetts) immediately before the warm-up and at completion of the last recovery interval. Finally, a 0–10 Borg scale17 was used to obtain a rating of perceived exertion (RPE) at the end of each active interval, as well as a sessional-RPE (sRPE) 30-min after completion of exercise. Differences in cardiovascular, metabolic, and perceptual responses between conditions and time points were analysed using a two-way ANOVA with repeated measures. Significant main effects or interactions were assessed using Fisher’s least significant difference post hoc test. Differences in sRPE between conditions were analysed using a one-way ANOVA with repeated measures. Where necessary, Cohen’s d effect sizes were calculated. Statistical analy-
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Fig. 1. Systolic (a), diastolic (b), and mean (c) arterial blood pressure measured throughout the low-intensity, low-intensity with blood flow restriction and highintensity conditions. SBP = systolic arterial blood pressure, DBP = diastolic arterial blood pressure, MAP = mean arterial pressure, LI = low-intensity, LIBFR = low-intensity with blood flow restriction, HI = high-intensity. *LIBFR significantly different to HI, ‡ LIBFR significantly different to LI, # HI significantly different to LI. B = baseline, WU = warm-up, Int1–3 = interval 1–3, Rec1–3 = recovery 1–3, CD = cooldown.
sis was conducted using SPSS (v.22, IBM) with a level of significance of p < 0.05. All data are presented as mean ± SEM. 3. Results A condition × time interaction was observed for differences in SBP, DBP and MAP (p < 0.01) (Fig. 1). SBP was greater during LIBFR than LI at all time points from warm-up to cool-down (range: p < 0.01–0.05; ES = 0.34–2.04). Additionally, SBP was greater during HI compared with LI for the entire exercise session (range: p < 0.01–0.04; ES = 0.14–2.90). Compared with LIBFR , SBP measured during HI was greater at recovery one (p < 0.01; ES = 1.09) and intervals two (p = 0.04; ES = 0.65) and three (p = 0.02; ES = 0.44). Compared with LI, DBP was greater in LIBFR measured at baseline (p = 0.05; ES = 0.51) and intervals one (p = 0.02; ES = 0.71), two
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(p < 0.01; ES = 0.98) and three (p < 0.01; ES = 1.39). Greater DBP were observed in LI compared to HI during warm-up (p < 0.01; ES = 0.56), recovery periods one (p < 0.01; ES = 0.89), two (p < 0.01; ES = 0.83) and three (p = 0.02; ES = 0.74) and the cool-down (p < 0.01; ES = 0.60). DBP during LIBFR was greater than HI from interval one until cool-down (range: p < 0.01–0.04; ES = 0.45–1.60). Greater MAP were observed in LIBFR compared to LI during intervals one (p < 0.01; ES = 1.28), two (p < 0.01; ES = 1.41) and three (p = 0.01; ES = 2.1) and recovery periods two (p < 0.01; ES = 0.69) and three (p < 0.01; ES = 0.83). During the HI condition, MAP was greater than LI during intervals one (p < 0.01; ES = 0.80), two (p < 0.01; ES = 0.91), and three (p < 0.01; ES = 1.13). Of note, MAP was greater in LIBFR when compared with HI during interval three (124.2 ± 2.3 mmHg vs. 113.9 ± 2.5 mmHg; ES = 1.00) and cool-down (98.6 ± 2 mmHg vs. 94.7 ± 2.1 mmHg; ES = 0.44). Within the LIBFR condition, MAP was greater during interval three (124.2 ± 2.3 mmHg) compared with intervals one (115.2 ± 2.6 mmHg) and two (118.0 ± 2.7 mmHg). A condition × time interaction (p < 0.01) was observed for differences in CO and HR (Fig. 2b and a; respectively). Measures of CO were greater in LIBFR than LI during intervals two (p = 0.04; ES = 0.50) and three (p < 0.01; ES = 0.64) and recovery periods one (p < 0.01; ES = 0.78), two (p < 0.01; ES = 0.84) and three (p < 0.01; ES = 0.84). Greater CO was observed during HI compared with LIBFR from interval one to the cool-down (range: p < 0.01; ES = 0.99–1.29) and in LI from interval one to the cool-down (range: p < 0.01; ES = 0.98–1.84). HR was greater in HI compared with LI at all time points (range: p < 0.01; ES = 0.60–4.37) except baseline. Similarly, HR was greater in LIBFR compared with LI measured at all points (range: p < 0.03; ES = 0.32–1.93) except baseline. Compared with LIBFR , HR was greater during HI from interval one through the cool-down (range: p < 0.01; ES = 1.26–2.12). No main effects or interactions were observed for SV between conditions (Fig. 2c). A condition × time interaction was observed for PP and RPP (p < 0.01; Fig. 4). Compared with HI, PP was lower in LI from interval one to recovery three (range: p < 0.01; ES = 1.58–3.07) and in LIBFR from interval one to recovery three (range: p = 0.01–0.03; ES = 0.64–1.53). Measured at warmup, PP was less in LI (64 ± 3 mmHg) compared with HI (71 ± 2 mmHg) and LIBFR (72 ± 3 mmHg). Additionally LI was less at cooldown (77 ± 4 mmHg) compared with HI (91 ± 4 mmHg) and LIBFR (88 ± 4 mmHg). Compared with HI, the RPP was lower in LI from interval one onward (range: p < 0.01; ES = 2.70–4.83) with similar differences observed between HI and LIBFR (range: p < 0.01; ES = 1.21–2.21). Additionally, RPP measured during LIBFR was greater than during LI from interval one through the cool-down (range: p < 0.01; ES = 1.32–2.42). Measured at the warmup, RPP was less during LI (127 ± 530 bpm mmHg) compared with both HI (136 ± 415 bpm mmHg) and LIBFR (133 ± 360 bpm mmHg). ˙ 2 and VCO ˙ A condition × time interaction was observed for VO 2 ˙ 2 was observed in LIBFR compared with (p < 0.01) (Fig. 3). Greater VO LI from baseline (p < 0.01; ES = 1.24), recovery periods one (p < 0.01; ES = 1.17), two (p < 0.01; ES = 1.37) and three (p < 0.01; ES = 1.35) ˙ 2 was greater and the cool-down (p = 0.02; ES = 0.40). During HI, VO than LI at all time points (range: p < 0.01–0.04; ES = 0.27–4.53) and greater than LIBFR from interval one through cool-down (range: ˙ p < 0.01; ES = 0.92–4.33). Measures of VCO 2 were greater in LIBFR compared with LI from baseline until recovery three (p < 0.01; ˙ ES = 0.49–2.13). Additionally, greater levels of VCO 2 were observed in HI than LI at all time points (range: p < 0.01; ES = 0.52–5.87) and LIBFR (range: p < 0.01; ES = 1.92–4.78) from interval one through cool-down. There were no differences in blood lactate pre-exercise in HI (1.2 ± 0.09), LIBFR (1.3 ± 0.08) and LI (1.2 ± 0.08). A condition × time interaction (p < 0.01) was observed with greater post-exercise values in HI (13.2 ± 0.61) than LIBFR (6.3 ± 0.49) (+125%; p < 0.01) and
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Fig. 2. Heart rate (a), cardiac output (b) and stroke volume (c) measured throughout the low-intensity, low-intensity with blood flow restriction and high-intensity conditions. HR = heart rate, CO = cardiac output, SV = stroke volume, LI = low-intensity, LIBFR = low-intensity with blood flow restriction, HI = high-intensity. *LIBFR significantly different to HI, ‡ LIBFR significantly different to LI, # HI significantly different to LI. B = baseline, WU = warm-up, Int1–3 = interval 1–3, Rec1–3 = recovery 1–3, CD = cool-down.
Fig. 3. Rate of oxygen consumption (a) and volume of carbon dioxide production (b) measured throughout the low-intensity, low-intensity with blood flow restriction and high-intensity conditions. ˙ ˙ 2 = rate of oxygen consumption, VCO VO 2 = volume of carbon dioxide production, LI = low-intensity, LIBFR = low-intensity with blood flow restriction, HI = highintensity. *LIBFR significantly different to HI, ‡ LIBFR significantly different to LI, # HI significantly different to LI. B = baseline, WU = warm-up, Int1–3 = interval 1–3, Rec1–3 = recovery 1–3, CD = cooldown.
Fig. 4. Pulse pressure (A) and the rate pressure product (B) calculated throughout the low-intensity, low-intensity with blood flow restriction and high-intensity conditions. LI = low-intensity, LIBFR = low-intensity with blood flow restriction, HI = highintensity. *LIBFR significantly different to HI, ‡ LIBFR significantly different to LI, # HI significantly different to LI. B = baseline, WU = warm-up, Int1–3 = interval 1–3, Rec1–3 = recovery 1–3, CD = cooldown.
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LI (2.8 ± 0.29) (+371%; p < 0.01). In addition, post-exercise lactate was 110% greater in LIBFR than LI (p < 0.01). A condition × time interaction was observed for RPE (p < 0.01) measured during each interval. Greater RPE were observed during HI in all intervals (5.5 ± 0.3, 6.9 ± 0.3 and 8.1 ± 0.3, respectively) than both LIBFR (4.6 ± 0.3, 5.1 ± 0.2 and 5.6 ± 0.3, respectively) and LI (2.1 ± 0.2, 2.6 ± 0.1 and 2.8 ± 0.2, respectively). Furthermore, RPE was greater in all intervals during LIBFR than LI. sRPE was greater in HI (8.1 ± 0.7) compared with LIBFR (5.7 ± 1.6; p < 0.01) and LI (2.4 ± 0.8; p < 0.01) and between LIBFR compare with LI (p < 0.01).
4. Discussion Throughout the interval sessions HR was greater during LIBFR than LI alone (Fig. 2a). The difference in HR (∼15 bpm during active and ∼18 bpm during recovery intervals) is consistent with, albeit larger than, previous aerobic based BFR research which observed ∼10 bpm increases in HR during very-low-intensity (∼12.5–15 mL kg−1 min−1 ) walking with BFR.4 The elevated HR response during BFR is likely due to the activation of the muscle chemoreflex18 in response to an increase in hypoxic stress.19 Indeed, the use of BFR during exercise decreases available oxygen at the working muscle20,21 resulting in increased levels of lactate22 and carbon dioxide.23,24 Efferent signalling in response to these changes is known to stimulate an increase in HR through sympathetic output.17,19 Increases in CO observed in the current study (Fig. 2b) is not consistent with previous BFR research4 and is likely due to the BFR methodology employed. For instance, utilising a continuous restriction protocol, Renzi et al.4 observed no change in CO, which was explained by reductions in venous return and a resultant decrease in SV.4,22 In the present study, deflation of the BFR cuffs and the addition of the muscle pump effect during the active recovery, may have allowed pooled blood in the limbs to return to the heart, maintaining SV (Fig. 2) and increasing CO.20 Additionally, we set BFR to 80% of the participant’s arterial occlusion pressure to allow some arterial inflow whereas Renzi et al.4 utilised a standard pressure of 160 mmHg. It is also plausible that the use of an arbitrary standard pressure by Renzi et al.4 may have resulted in higher levels of occlusion in some or their participants leading to the differences in our findings. However, with the current available information this hypothesis cannot be confirmed. In agreement with Renzi et al.,4 the addition of BFR to low-intensity aerobic exercise resulted in increased myocardial work as measured through changes in PP and RPP (Fig. 4). However, these responses were not elevated to the same magnitude as during the HI condition, indicating that the increased cardiac stress associated with LIBFR is not consistent with traditional high-intensity exercise. Consistent with a hypoxic environment within the working ˙ muscle,21,23,24 we observed increased lactate and VCO 2 during the LIBFR compared with LI. Indeed, hypoxia is associated with an increase in anaerobic metabolism22 from which lactate and carbon dioxide are main bi-products.25,26 The current findings support previous BFR research4 and represent an increase in anaerobic ˙ 2 during metabolism under these conditions.1,25 The higher VO ˙ 2 recovery in LIBFR compared with LI, combined with similar VO during the exercise intervals resulted in a higher accumulated O2 uptake throughout the duration of the session. These findings indicate that overall aerobic metabolism was greater during LIBFR ; however, the peak rate of aerobic energy release during exercise was not. In comparison, HI demonstrated the greatest peak rate of aerobic energy release, as well as highest accumulated O2 uptake, across the exercise session. It is common, following exercise of high ˙ 2 post exercise in anaerobic demand, to observe an increased VO response to an initial oxygen deficit,27 a response that was likely
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exacerbated by the BFR. When considered together with previously discussed differences in lactate, a greater accumulated O2 uptake during BFR exercise compared to the intensity matched exercise without BFR indicate this technique may provide enhanced stimulus for both aerobic and anaerobic adaptations.1,2 When compared with HI exercise, the addition of BFR to low-intensity cycling did not result in similar metabolic or cardiovascular stress (Figs. 1–4). This is even evident during the cool-down periods following each trial, where higher HR, CO, VO2 and VCO2 were observed for HI trials compared with both LI and LIBFR conditions. This indicates a greater overall physiological demand being posed by the HI session, and suggests that lowintensity aerobic exercise with BFR should not be used as a sole replacement of high-intensity training if an individual can safely tolerate high-intensity exercise. However, for individuals that cannot tolerate high-intensity exercise, the additional cardiovascular and metabolic stress associated with LIBFR when compared with LI alone indicate that method of exercise delivery could provide benefit. Furthermore, lower interval RPE and sRPE scores were reported following the low-intensity BFR session compared with the highintensity session. These findings are in agreement with Corvino et al.,6 and indicate that this low-intensity BFR exercise may be better tolerated by a wider population compared with high-intensity exercise.26 Notably, MAP during interval three was greater (10.3 ± 0.3 mmHg) for LIBFR compared with HI. A greater CO measured during HI compared with LIBFR would indicate that the observed difference in MAP between the two conditions was a consequence of the higher DBP during LIBFR (Figs. 1b and 2d). During the recovery periods, cuff deflation was associated with a decrease in DBP in LIBFR to levels consistent with the LI condition. Together these findings indicate that bi-lateral BFR of the low limbs overrides normal vasodilation responses associated with exercise.28 When analysing the LIBFR condition separately, greater MAP was noted during interval three compared with intervals one and two (Fig. 1c). It is possible that the inclusion of additional intervals, longer intervals, increased work:rest ratio or continuous BFR could have resulted in even higher MAP. Indeed, many of the hemodynamic variables associated with MAP demonstrated a systemic increase following each working interval, further supporting our hypothesis. This finding is important, as majority of BFR research has utilised continuous BFR at intensities equal to or less than 30% peak power,1,4,5 and it is therefore likely that continuous BFR would be used within current practice. The increased myocardial workload,4 in terms of MAP, HR and CO seen during the LIBFR trial, is likely not problematic for many clinical populations.20 While resting MAP measures >99 mmHg are associated with an increased risk of cardiac events,29,30 we are not aware of exercise-specific guidelines to indicate potentially dangerous levels of MAP. Nevertheless, considering that MAP reached values of 124.2 ± 2.3 mmHg in the final interval of the LIBFR condition, we suggest that practitioners use caution when implementing BFR in populations with compromised vascular function. While this study provides new information regarding the acute responses to interval cycling with BFR, it would be remiss not to acknowledge some limitations. Firstly, the current findings are specific to the interval protocol completed (i.e. number of intervals, duration of efforts and work:rest ratio). Considering that MAP appeared to increase with each interval in the LIBFR condition, it is possible that longer intervals, additional intervals or an increased work:rest ratio could lead to even greater increases in the physiological stress associated with BFR exercise. We observed similar VO2 and HR responses to Corvino et al.,6 despite implementing a higher intensity during intervals; this may be due to the greater work:rest ratio prescribed by Corvino et al.6 (2:1), compared with the 1:1 ratio used in the current study. This finding highlights
Please cite this article in press as: Thomas HJ, et al. Acute physiological responses to low-intensity blood flow restriction cycling. J Sci Med Sport (2018), https://doi.org/10.1016/j.jsams.2018.01.013
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that further research is necessary to understand the combined impacts of different training variables during BFR modalities on cardiovascular demands, particularly to enhance the safety of such training. In addition, this study involved only healthy participants, and the results may not translate to clinical populations. It is important, however, to take these first steps towards understanding the potential cardiovascular risk of BFR exercise using populations who are less likely to suffer adverse events. Lastly, while the method used to determine arterial occlusion pressure is widely accepted in BFR research, arterial occlusion pressure was assessed in a resting supine position, which may be different when participants are in a seated position, and during exercise. 5. Conclusion The findings of this study suggest that addition of intermittent BFR to low-intensity interval cycling represents a useful training modality which can increase metabolic and cardiovascular demands compared to low-intensity cycling alone. This subsequent stress could result in beneficial aerobic and anaerobic adaptations, and should be considered by individuals who are not able to tolerate high-intensity exercise. However, the increase in MAP observed toward the conclusion of LIBFR trials indicates a high myocardial workload, which was greater than that observed during the highintensity session. Therefore, practitioners should use caution if prescribing this modality within a vascular compromised population. Practical implications • Low-intensity BFR cycling may be useful for individuals unable to perform exercise at a high-intensity, such as those undergoing rehabilitation, elderly or clinical populations. • Low-intensity cycling with BFR provides greater aerobic and anaerobic stress then low-intensity cycling alone. • Caution should be used by practitioners when prescribing BFR exercise to individuals with compromised vascular function. Acknowledgments The results of this study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. Results of the present study do not constitute endorsement by SMA. We would like to thank the participants in this study for dedicating their time to this project, and Mr Cameron Lilly for his extensive assistance in data collection. References 1. Park S, Kim JK, Choi HM et al. Increase in maximal oxygen uptake following 2-week walk training with blood flow occlusion in athletes. Eur J Appl Physiol 2010; 109(4):591–600. 2. de Oliveira MF, Caputo F, Corvino RB et al. Short-term low-intensity blood flow restricted interval training improves both aerobic fitness and muscle strength. Scand J Med Sci Sports 2016; 26(9):1017–1025. 3. Pope ZK, Willardson JM, Schoenfeld BJ. Exercise and blood flow restriction. J Strength Cond Res 2013; 27(10):2914–2926. 4. Renzi CP, Tanaka H, Sugawara J. Effects of leg blood flow restriction during walking on cardiovascular function. Med Sci Sport Exerc 2010; 42(4):726–732.
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Please cite this article in press as: Thomas HJ, et al. Acute physiological responses to low-intensity blood flow restriction cycling. J Sci Med Sport (2018), https://doi.org/10.1016/j.jsams.2018.01.013