Cardiovascular Responses to Blood Flow-Restricted Exercise
Cardiovascular Responses to Blood Flow-Restricted Exercise
The main goal of this study was to characterize local artery blood flow and StO2, and the acute cardiovascular response to unilateral BFR, HL, and LL resistance exercise. The main findings are as follows: (a) the exercise-induced increase in blood flow was reduced by the cuff pressure, most notably in the BFRSBP condition; (b) Q· did not increase during exercise in the BFRSBP condition; and (c) SBP and DBP were elevated above baseline during the rest intervals in BFR exercise conditions. The reduced blood flow and heightened BP responses to the BFR conditions agree with our original hypothesis, demonstrating that HL and BFR exercise affect the cardiovascular system differently. The cuff pressure clearly affected blood flow and the ability to perform work in subsequent exercise sets. In our study, subjects experienced ischemia at the exercising muscle for ~6 min and ~9 min in the BFRSBP and BFRDBP conditions, respectively. No ischemia-related effects were observed other than localized tingling or numbness, which subsided immediately upon cuff release. Previous investigations have shown that significant and irreversible limb skeletal muscle injury did not occur until approximately 3 h of ischemia in rats.
During leg press, the rate of fatigue (decrease in repetitions performed) from the first to second set of exercise was greater in the BFR conditions (BFRDBP = 65% and BFRSBP = 82%) compared with the LL and HL conditions (LL = 46% and HL = 36%). During heel raise, cuff pressure in the BFRSBP condition also resulted in a high rate of fatigue (82%). The rate of fatigue was approximately 10%–15% lower for BFRDBP, HL, and LL conditions for heel raise compared with leg press exercise. Although we did not design the study to compare differences between the leg press and heel raise exercises, it is possible that the metabolic profile or fiber type distribution in the active calf muscles resulted in an increased capacity to work under ischemic conditions. These results suggest that the required minimal cuff pressure may be different between muscle groups and may also depend on the muscle fiber type.
Our "exercise" measurements were obtained within 15 s of exercise cessation. Acquiring ultrasound images immediately after exercise allowed for better image quality and more precise and repeatable location of the measurements; however, we do recognize that blood flow obtained during the dynamic resistance exercise would likely be different, particularly in the HL and LL conditions. Specifically, the 15-s postexercise measurements may have been higher than blood flow during exercise in the HL and LL conditions because of the presence of postexercise reactive hyperemia. Alternatively, the weight lifted in the LL condition was fairly light relative to the subjects' 1RM, and it may not have been sufficient to cause significant arterial or venous constriction. Blood flow measurements obtained within 15 s of exercise completion in the BFR conditions were likely similar during exercise because very little mechanical work was performed and the cuff pressure was maintained during the rest period. The BP measurements reported in this study were obtained during the rest intervals and are likely lower than the BP during exercise because the muscle pump stops and sympathetic activity changes upon exercise cessation. In the BFR conditions, BP may be similar during the rest intervals and during exercise because of the maintained cuff pressure and activation of the mechanosensors.
Recent studies have shown that artery blood flow is highly correlated with perfusion, indicating that changes in blood flow can be used to estimate relative change in muscle oxygen availability. Our NIRS data support the notion that measurements of blood flow under the different exercise conditions likely reflect changes in muscle perfusion and oxygen availability, suggesting that oxygen availability is one of the limiting factors in the ability to perform multiple sets of BFR exercise. The NIRS data collected throughout the leg press exercise suggest that the muscle was depleted of oxygen during the first set of exercise and rest in the BFR conditions, so that the start of each exercise set occurred in a condition of low oxygen availability. In contrast, in the HL and LL conditions, StO2 was low during exercise and returned to or near baseline before the start of the next exercise set. Because of drop outs in the BP data collected during exercise, we were not able to calculate changes in vascular conductance (calculated as blood flow/MAP) from rest to exercise to further support the NIRS data. However, on the basis of baseline and immediate postexercise blood flow and BP (collected during the 90-s postexercise rest period), conductance during exercise in the BFRDBP and BFRSBP conditions would be similar or less than baseline, respectively, whereas in the LL and HL conditions, conductance during exercise would be nearly double baseline values. Although the NIRS data have been shown to correlate well with muscle perfusion under normal conditions, it is possible that the cuff affects perfusion kinetics via externally applied pressure on the microvasculature, which could ultimately affect the ability to perform work. This particular NIRS system is reliable and well validated, but it is possible that changes in blood volume due to the cuff pressure and muscle contraction during exercise could have affected the accuracy of the StO2 measurements. However, they should still be reliable because such movement should be consistent within a subject.
In this study, immediate postexercise blood flow and total work (sum of the entire exercise session) were higher after the HL and LL conditions than after the BFR conditions, and the reduction in work from the first to third set of exercise for each condition (leg press: BFRDBP ~80%, BFRSBP ~96%, LL ~60%, HL ~55%) was inversely related to postexercise blood flow. Because perfusion was also likely lower in the BFR conditions than that in the HL and LL conditions, our results suggest that the cuff pressure reduces oxygen supply to an extent that limits the ability to perform work and increases the rate of fatigue in the BFR conditions, and to a greater extent in the BFRSBP than that in the BFRDBP condition. Importantly, because LL exercise alone and ischemia alone do not provide a potent hypertrophic stimulus, the balance between the amount of work performed and the level of ischemia necessary to induce muscle hypertrophy needs to be more clearly defined.
The resting DBP in this study was notably low in all subjects. These results may be due to the supine exercise position and the healthy cohort of subjects. SBP and DBP were higher during the BFR sessions than the LL and HL sessions. HR was highest in the LL and HL conditions and was elevated from rest in all conditions. Exercise (with or without ischemia) excites group III and group IV mechano- and metabolic-sensitive afferent nerves, which provide feedback to cardiovascular areas and lead to an increase in sympathetic activity. Activation of the sympathetic nervous system causes a reflex increase in arterial pressure (i.e., muscle metaboreflex). During postexercise ischemia, the exercise-induced BP response is maintained due the sustained sympathetic activity, whereas HR returns to near resting levels because of parasympathetic reactivation. The maintained sympathetic activation observed in our study during postexercise ischemia is likely due to a combination of reduced blood flow and oxygen availability, as well as pressure on the muscle from the cuff. Although the BFR condition elicited a heightened pressor response, the reported SBP and DBP for all conditions were well within the values prescribed for cardiac rehabilitation.
The isometric and slow dynamic components of high-load resistance exercise cause vasoconstriction and rapid spikes in SBP and DBP, which places a pressure load on the myocardium. In contrast, mounting evidence suggests that dynamic resistance training does not cause myocardial ischemia or threatening arrhythmias in patients with normal left ventricular function, possibly because elevated DBP and decreased venous return are associated with a pattern of blood flow distribution that favors coronary circulation. With these varying outcomes, there is a need to evaluate the cardiovascular responses that are specific to BFR exercise in clinical populations because the cardiovascular responses to the resistance exercise conditions may be different in a less healthy population. For example, hypertensive individuals are known to have an exaggerated BP response to resistance exercise and ischemia, likely because of enhanced activation of the metaboreceptors. Muller et al. demonstrated that the augmented BP response to muscle contraction in peripheral artery disease patients was mitigated by 50% when an ascorbic acid supplement was provided before exercise. Pairing antioxidant supplements with BFR exercise may provide a unique approach means to control the BP response to BFR exercise in hypertensives and those with vascular dysfunction.
We showed that SV, HR, and Q· increased more during the HL and LL conditions than that in the BFR conditions. The blunted exercise-induced rise in SV observed in the BFR conditions may be caused by increased vascular resistance (i.e., increased cardiac afterload) and/or reduced venous return (i.e., decreased cardiac preload) associated with the cuff pressure. Renzi et al. measured HR and estimated Q· and SV from finger BP waveforms during walking with and without blood flow restriction. HR was higher and SV was lower during walking with blood flow restriction than normal walking, and Q· was not different between conditions. Although the cardiovascular requirements of resistance and aerobic exercise are inherently different, the occlusion cuff does seem to mitigate the rise in SV during exercise. The measurements of vein CSA showed that the cuff pressure caused significant venodilation distal to the cuff, indicating that cardiac return from the femoral and popliteal arteries was reduced by the cuff pressure, which could affect cardiac preload and, consequently, SV. However, it is likely that muscle metaboreflex activation caused an increase in ventricular contractility as well as central blood volume mobilization, which allowed for SV and Q· to be maintained at or above baseline levels in the BFR conditions. We were not able to acquire measures of left ventricular end-diastolic volume because of the complexity of the data collection protocol; however, future studies should include measurements of ventricular function.
BP and HR responses to HL, LL, and BFR resistance exercise have been measured in one other study; however, it should be noted that the measurements were taken 15 and 45 min after exercise. In that study, HR was elevated after exercise in all conditions and to a greater extent in the HL condition at both 15 and 45 min postexercise. At 15 min postexercise, SBP and DBP were not different from baseline. It is likely that arterial resistance imparted by the BP cuff recovered before the 15-min measurement in the data presented by Fahs et al., whereas the increases in BP reported in our study reflect the acute effect of exercise and the cuff pressure. Assessment of BP and HR variability via frequency analysis during the postexercise time (i.e., during 45 min of recovery) may provide important information about autonomic nervous system activity during resistance training that we were not able to detect in the immediate postexercise data.
Our results provide information about the relations between blood flow, total work, and StO2 during and immediately post-HL, LL, and BFR resistance exercise; however, further work is necessary to improve the comfort of and most effectively prescribe BFR exercise. We demonstrated that cuff pressure does blunt the exercise-induced increase in blood flow to muscle, and the maintained cuff pressure limits recovery and the ability to perform further work. Because little to no work was performed in the BFRSBP condition after the first set of exercise, it is possible that the training adaptations to BFR exercise could be achieved in one set of exercise rather than three. Alternatively, it may be possible to increase the effectiveness and mitigate the discomfort of BFR exercise by using a lower cuff pressure, such as that used in the BFRDBP condition. This configuration would favor more work under a less severe ischemic environment. A future study should measure blood flow using a variety of cuff pressures that are evenly spaced between the low and high pressures in order to accomplish this goal and to establish a method to individualize cuff pressure. We also provided a comprehensive examination of the acute cardiovascular responses to each exercise condition and showed that BFR and HL resistance exercises stress the cardiovascular system differently. Our results suggest that BFR is safe for healthy individuals; however, further evaluations are warranted before prescribing LBFR exercise to individuals with compromised cardiac function.
Discussion
The main goal of this study was to characterize local artery blood flow and StO2, and the acute cardiovascular response to unilateral BFR, HL, and LL resistance exercise. The main findings are as follows: (a) the exercise-induced increase in blood flow was reduced by the cuff pressure, most notably in the BFRSBP condition; (b) Q· did not increase during exercise in the BFRSBP condition; and (c) SBP and DBP were elevated above baseline during the rest intervals in BFR exercise conditions. The reduced blood flow and heightened BP responses to the BFR conditions agree with our original hypothesis, demonstrating that HL and BFR exercise affect the cardiovascular system differently. The cuff pressure clearly affected blood flow and the ability to perform work in subsequent exercise sets. In our study, subjects experienced ischemia at the exercising muscle for ~6 min and ~9 min in the BFRSBP and BFRDBP conditions, respectively. No ischemia-related effects were observed other than localized tingling or numbness, which subsided immediately upon cuff release. Previous investigations have shown that significant and irreversible limb skeletal muscle injury did not occur until approximately 3 h of ischemia in rats.
During leg press, the rate of fatigue (decrease in repetitions performed) from the first to second set of exercise was greater in the BFR conditions (BFRDBP = 65% and BFRSBP = 82%) compared with the LL and HL conditions (LL = 46% and HL = 36%). During heel raise, cuff pressure in the BFRSBP condition also resulted in a high rate of fatigue (82%). The rate of fatigue was approximately 10%–15% lower for BFRDBP, HL, and LL conditions for heel raise compared with leg press exercise. Although we did not design the study to compare differences between the leg press and heel raise exercises, it is possible that the metabolic profile or fiber type distribution in the active calf muscles resulted in an increased capacity to work under ischemic conditions. These results suggest that the required minimal cuff pressure may be different between muscle groups and may also depend on the muscle fiber type.
Our "exercise" measurements were obtained within 15 s of exercise cessation. Acquiring ultrasound images immediately after exercise allowed for better image quality and more precise and repeatable location of the measurements; however, we do recognize that blood flow obtained during the dynamic resistance exercise would likely be different, particularly in the HL and LL conditions. Specifically, the 15-s postexercise measurements may have been higher than blood flow during exercise in the HL and LL conditions because of the presence of postexercise reactive hyperemia. Alternatively, the weight lifted in the LL condition was fairly light relative to the subjects' 1RM, and it may not have been sufficient to cause significant arterial or venous constriction. Blood flow measurements obtained within 15 s of exercise completion in the BFR conditions were likely similar during exercise because very little mechanical work was performed and the cuff pressure was maintained during the rest period. The BP measurements reported in this study were obtained during the rest intervals and are likely lower than the BP during exercise because the muscle pump stops and sympathetic activity changes upon exercise cessation. In the BFR conditions, BP may be similar during the rest intervals and during exercise because of the maintained cuff pressure and activation of the mechanosensors.
Recent studies have shown that artery blood flow is highly correlated with perfusion, indicating that changes in blood flow can be used to estimate relative change in muscle oxygen availability. Our NIRS data support the notion that measurements of blood flow under the different exercise conditions likely reflect changes in muscle perfusion and oxygen availability, suggesting that oxygen availability is one of the limiting factors in the ability to perform multiple sets of BFR exercise. The NIRS data collected throughout the leg press exercise suggest that the muscle was depleted of oxygen during the first set of exercise and rest in the BFR conditions, so that the start of each exercise set occurred in a condition of low oxygen availability. In contrast, in the HL and LL conditions, StO2 was low during exercise and returned to or near baseline before the start of the next exercise set. Because of drop outs in the BP data collected during exercise, we were not able to calculate changes in vascular conductance (calculated as blood flow/MAP) from rest to exercise to further support the NIRS data. However, on the basis of baseline and immediate postexercise blood flow and BP (collected during the 90-s postexercise rest period), conductance during exercise in the BFRDBP and BFRSBP conditions would be similar or less than baseline, respectively, whereas in the LL and HL conditions, conductance during exercise would be nearly double baseline values. Although the NIRS data have been shown to correlate well with muscle perfusion under normal conditions, it is possible that the cuff affects perfusion kinetics via externally applied pressure on the microvasculature, which could ultimately affect the ability to perform work. This particular NIRS system is reliable and well validated, but it is possible that changes in blood volume due to the cuff pressure and muscle contraction during exercise could have affected the accuracy of the StO2 measurements. However, they should still be reliable because such movement should be consistent within a subject.
In this study, immediate postexercise blood flow and total work (sum of the entire exercise session) were higher after the HL and LL conditions than after the BFR conditions, and the reduction in work from the first to third set of exercise for each condition (leg press: BFRDBP ~80%, BFRSBP ~96%, LL ~60%, HL ~55%) was inversely related to postexercise blood flow. Because perfusion was also likely lower in the BFR conditions than that in the HL and LL conditions, our results suggest that the cuff pressure reduces oxygen supply to an extent that limits the ability to perform work and increases the rate of fatigue in the BFR conditions, and to a greater extent in the BFRSBP than that in the BFRDBP condition. Importantly, because LL exercise alone and ischemia alone do not provide a potent hypertrophic stimulus, the balance between the amount of work performed and the level of ischemia necessary to induce muscle hypertrophy needs to be more clearly defined.
The resting DBP in this study was notably low in all subjects. These results may be due to the supine exercise position and the healthy cohort of subjects. SBP and DBP were higher during the BFR sessions than the LL and HL sessions. HR was highest in the LL and HL conditions and was elevated from rest in all conditions. Exercise (with or without ischemia) excites group III and group IV mechano- and metabolic-sensitive afferent nerves, which provide feedback to cardiovascular areas and lead to an increase in sympathetic activity. Activation of the sympathetic nervous system causes a reflex increase in arterial pressure (i.e., muscle metaboreflex). During postexercise ischemia, the exercise-induced BP response is maintained due the sustained sympathetic activity, whereas HR returns to near resting levels because of parasympathetic reactivation. The maintained sympathetic activation observed in our study during postexercise ischemia is likely due to a combination of reduced blood flow and oxygen availability, as well as pressure on the muscle from the cuff. Although the BFR condition elicited a heightened pressor response, the reported SBP and DBP for all conditions were well within the values prescribed for cardiac rehabilitation.
The isometric and slow dynamic components of high-load resistance exercise cause vasoconstriction and rapid spikes in SBP and DBP, which places a pressure load on the myocardium. In contrast, mounting evidence suggests that dynamic resistance training does not cause myocardial ischemia or threatening arrhythmias in patients with normal left ventricular function, possibly because elevated DBP and decreased venous return are associated with a pattern of blood flow distribution that favors coronary circulation. With these varying outcomes, there is a need to evaluate the cardiovascular responses that are specific to BFR exercise in clinical populations because the cardiovascular responses to the resistance exercise conditions may be different in a less healthy population. For example, hypertensive individuals are known to have an exaggerated BP response to resistance exercise and ischemia, likely because of enhanced activation of the metaboreceptors. Muller et al. demonstrated that the augmented BP response to muscle contraction in peripheral artery disease patients was mitigated by 50% when an ascorbic acid supplement was provided before exercise. Pairing antioxidant supplements with BFR exercise may provide a unique approach means to control the BP response to BFR exercise in hypertensives and those with vascular dysfunction.
We showed that SV, HR, and Q· increased more during the HL and LL conditions than that in the BFR conditions. The blunted exercise-induced rise in SV observed in the BFR conditions may be caused by increased vascular resistance (i.e., increased cardiac afterload) and/or reduced venous return (i.e., decreased cardiac preload) associated with the cuff pressure. Renzi et al. measured HR and estimated Q· and SV from finger BP waveforms during walking with and without blood flow restriction. HR was higher and SV was lower during walking with blood flow restriction than normal walking, and Q· was not different between conditions. Although the cardiovascular requirements of resistance and aerobic exercise are inherently different, the occlusion cuff does seem to mitigate the rise in SV during exercise. The measurements of vein CSA showed that the cuff pressure caused significant venodilation distal to the cuff, indicating that cardiac return from the femoral and popliteal arteries was reduced by the cuff pressure, which could affect cardiac preload and, consequently, SV. However, it is likely that muscle metaboreflex activation caused an increase in ventricular contractility as well as central blood volume mobilization, which allowed for SV and Q· to be maintained at or above baseline levels in the BFR conditions. We were not able to acquire measures of left ventricular end-diastolic volume because of the complexity of the data collection protocol; however, future studies should include measurements of ventricular function.
BP and HR responses to HL, LL, and BFR resistance exercise have been measured in one other study; however, it should be noted that the measurements were taken 15 and 45 min after exercise. In that study, HR was elevated after exercise in all conditions and to a greater extent in the HL condition at both 15 and 45 min postexercise. At 15 min postexercise, SBP and DBP were not different from baseline. It is likely that arterial resistance imparted by the BP cuff recovered before the 15-min measurement in the data presented by Fahs et al., whereas the increases in BP reported in our study reflect the acute effect of exercise and the cuff pressure. Assessment of BP and HR variability via frequency analysis during the postexercise time (i.e., during 45 min of recovery) may provide important information about autonomic nervous system activity during resistance training that we were not able to detect in the immediate postexercise data.
Our results provide information about the relations between blood flow, total work, and StO2 during and immediately post-HL, LL, and BFR resistance exercise; however, further work is necessary to improve the comfort of and most effectively prescribe BFR exercise. We demonstrated that cuff pressure does blunt the exercise-induced increase in blood flow to muscle, and the maintained cuff pressure limits recovery and the ability to perform further work. Because little to no work was performed in the BFRSBP condition after the first set of exercise, it is possible that the training adaptations to BFR exercise could be achieved in one set of exercise rather than three. Alternatively, it may be possible to increase the effectiveness and mitigate the discomfort of BFR exercise by using a lower cuff pressure, such as that used in the BFRDBP condition. This configuration would favor more work under a less severe ischemic environment. A future study should measure blood flow using a variety of cuff pressures that are evenly spaced between the low and high pressures in order to accomplish this goal and to establish a method to individualize cuff pressure. We also provided a comprehensive examination of the acute cardiovascular responses to each exercise condition and showed that BFR and HL resistance exercises stress the cardiovascular system differently. Our results suggest that BFR is safe for healthy individuals; however, further evaluations are warranted before prescribing LBFR exercise to individuals with compromised cardiac function.
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