Resistance Training Augments Cerebral Blood Flow Pulsatility: Cross-Sectional Study

Resistance Training Augments Cerebral Blood Flow Pulsatility: Cross-Sectional Study Abstract BACKGROUND Increased central arterial stiffness and/or decreased compliance reduces buffer function and increases cerebral blood flow (CBF) pulsatility, which leads to increased cerebral microvascular damage, resulting in the augmentation of the risk of cerebrovascular diseases. Resistance-trained men showed higher central arterial stiffness and lower arterial compliance than age-matched, sedentary men. This study examined the effect of increased central arterial stiffness and/or decreased arterial compliance on CBF pulsatility. METHODS The study participants included 31 young healthy men (15 resistance-trained men, aged 21 ± 1 years; and 16 controls, aged 23 ± 1 years). β-Stiffness index and arterial compliance were measured in the right carotid artery as index of central arterial stiffness and compliance, respectively. The pulsatility index (PI) was measured in the middle cerebral artery as index of CBF pulsatility. RESULTS β-Stiffness index and PI were significantly higher in the resistance-trained group than in the control group (β-stiffness index: 5.3 ± 0.3 vs. 3.5 ± 0.3 a.u., P < 0.05, PI: 0.80 ± 0.02 vs. 0.70 ± 0.02, P < 0.05). The resistance-trained group showed significantly lower arterial compliance than the control group (0.16 ± 0.01 vs. 0.23 ± 0.01 mm2/mm Hg, P < 0.05). Positive and negative correlations were observed between β-stiffness index and PI (r = 0.39, P < 0.05), and between arterial compliance and PI (r = −0.59, P < 0.05), respectively. CONCLUSIONS The resistance-trained group showed higher central arterial stiffness and PI and lower arterial compliance. Central arterial stiffness and arterial compliance were associated with PI. Increased arterial stiffness and decreased arterial compliance with resistance training impair buffer function, resulting in increased CBF pulsatility. CLINICAL TRIAL REGISTRATION Trial Number UMIN000023816 URL: http://www.umin.ac.jp/icdr/index.html Official scientific title of the study: effect of increase arterial stiffness by resistance training on cerebral hemodynamic arterial compliance, blood pressure, central arterial stiffness, cerebral blood flow pulsatility, hypertension, resistance training The central arteries such as the aorta and carotid artery are characterized by an abundance of elastic fibers and buffer pulsatile blood flow to continuous flow.1 In addition, buffer function plays a major role in the protection of the cerebral artery, which has low resistance to mechanical damage such as that by high pulsatile blood flow in the central artery.2,3 Previous studies showed that increased central arterial stiffness and decreased arterial compliance with aging and diseases were associated with augmentation of cerebral blood flow (CBF) pulsatility.4,5 In cases of higher pulsatile blood flow over a long period, the arterial wall thickness and wall-to-lumen ratio is increased.6 In addition, increased CBF pulsatility leads to increased cerebral microvascular damage, resulting in elevated risk of cerebrovascular diseases.7,8 Thus, maintaining a lower central arterial stiffness and higher compliance to protect the cerebral artery is of great importance. Moderate- to high-intensity resistance training (RT) has been recently recommended for muscular hypertrophy and maximizing strength.9 However, several studies have reported that moderate- to high-intensity RT increases central arterial stiffness and/or decreases arterial compliance in healthy men.10,11 Resistance-trained men who habitually performed vigorous RT showed higher central arterial stiffness and lower arterial compliance than age-matched, sedentary men.12,13 That is, moderate- to high-intensity RT may increase CBF pulsatility. Although this phenomenon has been considered not a problem because the effect of central artery adaptation with RT on cardiovascular diseases has not been clarified yet, Kamada et al. recently suggested that central arterial adaptation with RT increases cardiovascular disease mortality, including cerebrovascular disease.14 Thus, whether moderate- to high-intensity RT augments CBF pulsatility should be investigated. Nevertheless, to our knowledge, no evidence shows that increased central arterial stiffness and/or decreased arterial compliance with moderate- to high-intensity RT on CBF pulsatility. Therefore, the purpose of this study was to examine the effect of increased central arterial stiffness and decreased arterial compliance by RT on CBF pulsatility. To investigate this purpose, we designed a cross-sectional study in which central arterial stiffness and compliance, and CBF pulsatility in resistance-trained men were compared with those in age-matched non–resistance-trained subjects. MATERIALS AND METHODS Subjects Thirty-one healthy men (15 resistance-trained: mean age, 21 ± 2 years; and 16 sedentary: mean age, 23 ± 2 years) were recruited to participate in this study. The resistance-trained men had been performing vigorous RT for >2 years, >5 days/week. The sedentary subjects recruited were healthy men. None of the subjects in the sedentary group regularly engaged in RT. All the subjects were normotensive (<140/90 mm Hg), and none of them ever used medications such as anabolic steroids. All the subjects provided written informed consent to participate prior to the start of the study. All the procedures and risk of this study were reviewed and approved by the Human Research Committee of Waseda University (approval No. 2016–170). Experimental procedure The studies were performed following a 3-hour fast and required to avoid caffeine intake for at least 12 hours and alcohol intake for at least 24 hours. The subjects were evaluated 24 hours after their last exercise session to avoid the acute effects of exercise. The cardiorespiratory and cerebrohemodynamic variables of the subjects were measured in a temperature-controlled environment (23.0 °C ± 0.1 °C, 50.0% ± 0.1%) after 15 minutes in resting supine position. Body composition Body composition was measured using bioelectrical impedance analysis (InBody 720, InBody Japan, Japan) in the upright position. Muscular strength Hand grip strength was measured using a handheld dynamometer (dynamometer hand grip; Takei Scientific Instruments, Japan) as an index of muscular strength. The subjects were instructed to stand and extend the arms by their sides during a hand grip execution and to grip the handheld dynamometer with full effort for 3 seconds. The values (kg) were recorded as the average of 2 trials. Heart rate and brachial arterial blood pressure Heart rate was measured using 2-lead electrocardiography (Form PWV/ABI; Omron Colin, Japan). Brachial systolic blood pressure, diastolic blood pressure, and mean arterial pressure were measured using a semiautomated device over the brachial artery (Form PWV/ABI; Omron Colin). Central arterial stiffness and compliance The β-stiffness index and arterial compliance of the common carotid artery were measured as an index of central arterial stiffness and compliance, respectively. Both the β-stiffness index and arterial compliance were measured in the right common carotid artery by using a combination of brightness-mode ultrasonography system for carotid artery diameter and applanation tonometry for carotid BP. The carotid diameter was obtained 1.0–2.0 cm proximal to the carotid bifurcation by using an ultrasonography system equipped with a 10-MHz linear transducer (LOGIQ-e; GE Medical Systems, Japan). The diameter was recorded over 10 cardiac cycles by using the brightness mode in the longitudinal section. The images obtained were analyzed using an image analysis software (ImageJ 1.42, NIH), and the systolic diameter (sD) and diastolic diameter (dD) were analyzed in these images. The carotid pressure waveform was obtained in the right common carotid artery with a pencil-type probe incorporating a high-fidelity strain-gauge transducer (SPT-301; Millar Instruments, TX). The obtained pressure waveforms were recorded in the computer. The carotid arterial pressure was calibrated by equating the carotid diastolic blood pressure and mean arterial pressure to the brachial artery value. The β-stiffness index and arterial compliance were calculated as follows10: β−stiffness index=ln(carotid SBP/DBP)/([sD−dD])/dD) Arterial compliance=([dD−sD]/sD)/(2×[carotid SBP–DBP])×π×sD Carotid arterial intima-media thickness The carotid arterial intima-media thickness was measured using the brightness mode of an ultrasonographic system equipped with a 10-MHz linear transducer (LOGIQ-e, GE Medical Systems). The obtained images were analyzed using an image analysis software (ImageJ, NIH). At least 10 carotid intima-media thickness measurements were taken, and the mean value was used for analysis. Internal carotid artery, vertebral artery blood flow, and global CBF The internal carotid artery (ICA) and vertebral artery diameter and velocity were obtained using an ultrasonographic system equipped with a 10-MHz linear transducer (LOGIQ-e; GE Medical Systems). The ICA blood flow was measured 1.0–1.5 cm distal to the carotid bifurcation on the right ICA. Vertebral artery measurements were performed between the transverse processes of C3 and the subclavian artery. The diameter was obtained using the brightness mode in longitudinal section and was analyzed using an image analysis software (ImageJ 1.42, NIH). The mean blood flow velocity was measured in pulse wave mode. The mean blood flow was measured in 10 cardiac cycles to eliminate the effects caused by the breathing cycle. Stability of the probe position was ensured, and the insonation angle did not vary (<60°). The mean diameter, ICA, and vertebral artery blood flow, global CBF (gCBF), and ICA and vertebral artery conductance were calculated as follows15: Mean diameter=(sD×1/3)+(dD×2/3)Blood flow=mean blood flow velocity×(π×[mean diameter/2]2)×60ICA conductance=ICA blood flow/MAPVA conductance=VA blood flow/MAPgCBF=(ICA blood flow+VA blood flow)×2 Middle cerebral artery blood flow velocity and CBF pulsatility The middle cerebral artery blood flow velocity (MCA V) was assessed using an ultrasonographic system equipped with a 2.5-MHz sector transducer (LOGIQ-e, GE Medical Systems) at the right temporal window. The right MCA was confirmed using the color mode, and the blood flow velocity waveform was obtained using the pulse wave mode. The pulsatility index (PI) of the MCA, which indicates CBF pulsatility, and the MCA Vmean were calculated using an automatic-calculation mode. Stroke volume The stroke volume was measured using an ultrasonographic system equipped with a 2.5-MHz sector transducer (LOGIQ-e, GE Medical Systems). The left ventricular image was obtained using a motion mode. The left ventricular end-diastolic and end-systolic dimensions were measured according to the established guidelines.16 The left ventricular volume was calculated using the Teichholz method.17 The left ventricular volume and stroke volume were calculated as follows: Left ventricular volume=(7×end dimension3)/(2.4+end dimension)Stroke volume=left ventricular end−diastolic volume−left ventricular end−systolic volume Partial pressure of arterial carbon dioxide The partial pressure of arterial carbon dioxide (PaCO2) was estimated from the tidal volume (VT) and end-tidal partial pressure of CO2 (PETCO2).18VT and PETCO2 were measured breath by breath from expired gas by using an expired gas analyzer (Aero Monitor AE310s, Minato Medical Science, Japan). The data obtained during the 10-minute collection period were averaged. Statistical analysis All data were presented as mean ± SEM. Statistical analyses were performed using the Statistical Package for the Social Sciences version 22.0 for Windows (IBM, Japan). The mean differences in the 2 groups were examined using the Student unpaired t test. Pearson correlations were used to assess the relationship between β-stiffness index and PI, and between arterial compliance and PI. In all the analyses, the level of significance for all the comparisons was set at P <0.05. RESULTS In the present study, 2 resistance-trained men and 3 control subjects were excluded in the MCA V analysis because obtaining MCA blood flow velocity waveform from them was impossible. As a result, analyzable MCA V recordings in 13 resistance-trained men and 13 control subjects were obtained. Therefore, MCA Vmean and PI, and the association between β-stiffness index and PI, and arterial compliance and PI were analyzed in 26 subjects (13 resistance-trained men and 13 control subjects). Subject characteristics Table 1 shows the characteristics of the subjects. Body weight, body mass index, lean body mass, and hand grip strength were significantly higher in the resistance-trained men than in the control subjects (P < 0.05). However, no significant differences were observed in the other subject characteristics between the 2 groups. Table 1. Characteristics of the control and resistance-trained men Control Resistance-trained Number of subjects 16 15 Age (years) 23 ± 1 21 ± 1 Height (cm) 172.2 ± 1.4 171.0 ± 2.0 Body weight (kg) 69.1 ± 2.6 82.8 ± 3.6* Body fat (%) 18.9 ± 1.3 18.8 ± 1.6 Body mass index (kg/m2) 23.2 ± 0.7 28.6 ± 0.8* Lean body mass (kg) 55.8 ± 1.8 68.5 ± 2.6* Hand grip (kg) 40 ± 2 51 ± 2* Control Resistance-trained Number of subjects 16 15 Age (years) 23 ± 1 21 ± 1 Height (cm) 172.2 ± 1.4 171.0 ± 2.0 Body weight (kg) 69.1 ± 2.6 82.8 ± 3.6* Body fat (%) 18.9 ± 1.3 18.8 ± 1.6 Body mass index (kg/m2) 23.2 ± 0.7 28.6 ± 0.8* Lean body mass (kg) 55.8 ± 1.8 68.5 ± 2.6* Hand grip (kg) 40 ± 2 51 ± 2* The data are presented as mean ± SEM. *P < 0.05 vs. the control subjects. View Large Table 1. Characteristics of the control and resistance-trained men Control Resistance-trained Number of subjects 16 15 Age (years) 23 ± 1 21 ± 1 Height (cm) 172.2 ± 1.4 171.0 ± 2.0 Body weight (kg) 69.1 ± 2.6 82.8 ± 3.6* Body fat (%) 18.9 ± 1.3 18.8 ± 1.6 Body mass index (kg/m2) 23.2 ± 0.7 28.6 ± 0.8* Lean body mass (kg) 55.8 ± 1.8 68.5 ± 2.6* Hand grip (kg) 40 ± 2 51 ± 2* Control Resistance-trained Number of subjects 16 15 Age (years) 23 ± 1 21 ± 1 Height (cm) 172.2 ± 1.4 171.0 ± 2.0 Body weight (kg) 69.1 ± 2.6 82.8 ± 3.6* Body fat (%) 18.9 ± 1.3 18.8 ± 1.6 Body mass index (kg/m2) 23.2 ± 0.7 28.6 ± 0.8* Lean body mass (kg) 55.8 ± 1.8 68.5 ± 2.6* Hand grip (kg) 40 ± 2 51 ± 2* The data are presented as mean ± SEM. *P < 0.05 vs. the control subjects. View Large Cardiorespiratory and cerebrohemodynamic variables Table 2 shows the cardiorespiratory and cerebrovascular variables. The brachial PP, carotid systolic blood pressure, and PP were significantly higher in the resistance-trained men than in the control subjects (P < 0.05). Brachial diastolic blood pressure was significantly lower in the resistance-trained men than in the control subjects (P < 0.05). However, no significant differences were observed in other cardiorespiratory and cerebrovascular variables between the 2 groups. Table 2. Cardiorespiratory and cerebrovascular variables in the control and resistance-trained men (control subjects: n = 16, resistance-trained men: n = 15) Control Resistance-trained Brachial SBP (mm Hg) 113 ± 2 116 ± 2 Brachial DBP (mm Hg) 65 ± 2 59 ± 1* Brachial MAP (mm Hg) 84 ± 1 83 ± 1 Brachial PP (mm Hg) 48 ± 1 57 ± 1* Carotid SBP (mm Hg) 103 ± 1 112 ± 2* Carotid PP (mm Hg) 38 ± 2 53 ± 1* Carotid diameter (cm) 0.58 ± 0.01 0.60 ± 0.01 Carotid IMT (mm) 0.49 ± 0.01 0.48 ± 0.01 PaCO2 (mm Hg) 41.4 ± 0.4 42.3 ± 0.4 HR (bpm) 62 ± 1 61 ± 3 SV (ml/min) 65 ± 2 66 ± 1 CO (l/min) 4.0 ± 0.9 4.1 ± 2.1 ICA  Blood flow (ml/min) 300 ± 16 325 ± 22  Diameter (cm) 0.48 ± 0.01 0.50 ± 0.02  Velocity (cm/s) 28 ± 1 27 ± 1  Conductance (ml/min/mm Hg) 3.60 ± 0.22 3.95 ± 0.28 VA  Blood flow (ml/min) 94 ± 8 89 ± 11  Diameter (cm) 0.33 ± 0.01 0.34 ± 0.01  Velocity (cm/s) 17 ± 1 15 ± 1  Conductance (ml/min/mm Hg) 1.12 ± 0.10 1.08 ± 0.13 gCBF (ml/min) 789 ± 42 828 ± 46 Control Resistance-trained Brachial SBP (mm Hg) 113 ± 2 116 ± 2 Brachial DBP (mm Hg) 65 ± 2 59 ± 1* Brachial MAP (mm Hg) 84 ± 1 83 ± 1 Brachial PP (mm Hg) 48 ± 1 57 ± 1* Carotid SBP (mm Hg) 103 ± 1 112 ± 2* Carotid PP (mm Hg) 38 ± 2 53 ± 1* Carotid diameter (cm) 0.58 ± 0.01 0.60 ± 0.01 Carotid IMT (mm) 0.49 ± 0.01 0.48 ± 0.01 PaCO2 (mm Hg) 41.4 ± 0.4 42.3 ± 0.4 HR (bpm) 62 ± 1 61 ± 3 SV (ml/min) 65 ± 2 66 ± 1 CO (l/min) 4.0 ± 0.9 4.1 ± 2.1 ICA  Blood flow (ml/min) 300 ± 16 325 ± 22  Diameter (cm) 0.48 ± 0.01 0.50 ± 0.02  Velocity (cm/s) 28 ± 1 27 ± 1  Conductance (ml/min/mm Hg) 3.60 ± 0.22 3.95 ± 0.28 VA  Blood flow (ml/min) 94 ± 8 89 ± 11  Diameter (cm) 0.33 ± 0.01 0.34 ± 0.01  Velocity (cm/s) 17 ± 1 15 ± 1  Conductance (ml/min/mm Hg) 1.12 ± 0.10 1.08 ± 0.13 gCBF (ml/min) 789 ± 42 828 ± 46 The data are presented as mean ± SEM. *P < 0.05, vs. the control subjects. Abbreviations: CO, cardiac output; DBP, diastolic blood pressure; gCBF, global cerebral blood flow; HR, heart rate; ICA, internal carotid artery; IMT, intima-media thickness; MAP, mean arterial pressure; PaCO2, arterial partial pressure of carbon dioxide; PP, pulse pressure; SBP, systolic blood pressure; SV, stroke volume; VA, vertebral artery. View Large Table 2. Cardiorespiratory and cerebrovascular variables in the control and resistance-trained men (control subjects: n = 16, resistance-trained men: n = 15) Control Resistance-trained Brachial SBP (mm Hg) 113 ± 2 116 ± 2 Brachial DBP (mm Hg) 65 ± 2 59 ± 1* Brachial MAP (mm Hg) 84 ± 1 83 ± 1 Brachial PP (mm Hg) 48 ± 1 57 ± 1* Carotid SBP (mm Hg) 103 ± 1 112 ± 2* Carotid PP (mm Hg) 38 ± 2 53 ± 1* Carotid diameter (cm) 0.58 ± 0.01 0.60 ± 0.01 Carotid IMT (mm) 0.49 ± 0.01 0.48 ± 0.01 PaCO2 (mm Hg) 41.4 ± 0.4 42.3 ± 0.4 HR (bpm) 62 ± 1 61 ± 3 SV (ml/min) 65 ± 2 66 ± 1 CO (l/min) 4.0 ± 0.9 4.1 ± 2.1 ICA  Blood flow (ml/min) 300 ± 16 325 ± 22  Diameter (cm) 0.48 ± 0.01 0.50 ± 0.02  Velocity (cm/s) 28 ± 1 27 ± 1  Conductance (ml/min/mm Hg) 3.60 ± 0.22 3.95 ± 0.28 VA  Blood flow (ml/min) 94 ± 8 89 ± 11  Diameter (cm) 0.33 ± 0.01 0.34 ± 0.01  Velocity (cm/s) 17 ± 1 15 ± 1  Conductance (ml/min/mm Hg) 1.12 ± 0.10 1.08 ± 0.13 gCBF (ml/min) 789 ± 42 828 ± 46 Control Resistance-trained Brachial SBP (mm Hg) 113 ± 2 116 ± 2 Brachial DBP (mm Hg) 65 ± 2 59 ± 1* Brachial MAP (mm Hg) 84 ± 1 83 ± 1 Brachial PP (mm Hg) 48 ± 1 57 ± 1* Carotid SBP (mm Hg) 103 ± 1 112 ± 2* Carotid PP (mm Hg) 38 ± 2 53 ± 1* Carotid diameter (cm) 0.58 ± 0.01 0.60 ± 0.01 Carotid IMT (mm) 0.49 ± 0.01 0.48 ± 0.01 PaCO2 (mm Hg) 41.4 ± 0.4 42.3 ± 0.4 HR (bpm) 62 ± 1 61 ± 3 SV (ml/min) 65 ± 2 66 ± 1 CO (l/min) 4.0 ± 0.9 4.1 ± 2.1 ICA  Blood flow (ml/min) 300 ± 16 325 ± 22  Diameter (cm) 0.48 ± 0.01 0.50 ± 0.02  Velocity (cm/s) 28 ± 1 27 ± 1  Conductance (ml/min/mm Hg) 3.60 ± 0.22 3.95 ± 0.28 VA  Blood flow (ml/min) 94 ± 8 89 ± 11  Diameter (cm) 0.33 ± 0.01 0.34 ± 0.01  Velocity (cm/s) 17 ± 1 15 ± 1  Conductance (ml/min/mm Hg) 1.12 ± 0.10 1.08 ± 0.13 gCBF (ml/min) 789 ± 42 828 ± 46 The data are presented as mean ± SEM. *P < 0.05, vs. the control subjects. Abbreviations: CO, cardiac output; DBP, diastolic blood pressure; gCBF, global cerebral blood flow; HR, heart rate; ICA, internal carotid artery; IMT, intima-media thickness; MAP, mean arterial pressure; PaCO2, arterial partial pressure of carbon dioxide; PP, pulse pressure; SBP, systolic blood pressure; SV, stroke volume; VA, vertebral artery. View Large Central arterial stiffness and compliance β-Stiffness index and arterial compliance are presented in Figure 1a and b, respectively. β-Stiffness index was significantly higher in the resistance-trained men than in the control subjects (5.3 ± 0.3 vs. 3.5 ± 0.3 a.u., P < 0.05). By contrast, arterial compliance was significantly lower in the resistance-trained men than in the control subjects (0.16 ± 0.01 vs. 0.23 ± 0.01 mm2/mm Hg, P < 0.05). Figure 1. View largeDownload slide β-Stiffness index (a) and arterial compliance (b) in the control subjects and resistance-trained men (control subjects: n = 16 and resistance-trained men: n = 15). The data are presented as SEM. *P < 0.05, vs. control subjects. Figure 1. View largeDownload slide β-Stiffness index (a) and arterial compliance (b) in the control subjects and resistance-trained men (control subjects: n = 16 and resistance-trained men: n = 15). The data are presented as SEM. *P < 0.05, vs. control subjects. MCA V and CBF pulsatility Figure 2 presents the MCA Vmean (a) and PI (b). No significant differences were observed in the MCA Vmean in the 2 groups (50 ± 4 vs. 51 ± 3 cm/s, P = 0.85). On the other hand, PI was significantly higher in the resistance-trained men than in the control subjects (PI: 0.80 ± 0.02 vs. 0.70 ± 0.02, P < 0.05). Figure 2. View largeDownload slide MCA Vmean (a) and pulsatility index (b) in the control and resistance-trained men (control subjects: n = 13 and resistance-trained men: n = 13). The data are presented as SEM. *P < 0.05, vs. the control subjects. Abbreviations: MCA Vmean, middle cerebral artery mean blood flow velocity; PI, pulsatility index. Figure 2. View largeDownload slide MCA Vmean (a) and pulsatility index (b) in the control and resistance-trained men (control subjects: n = 13 and resistance-trained men: n = 13). The data are presented as SEM. *P < 0.05, vs. the control subjects. Abbreviations: MCA Vmean, middle cerebral artery mean blood flow velocity; PI, pulsatility index. Association between central arterial stiffness, arterial compliance, and CBF pulsatility The associations between β-stiffness index and PI, and between arterial compliance and PI are shown in Figure 3a and b, respectively. A positive correlation was found between β-stiffness index and PI (r = 0.39, P < 0.05), and a negative correlation was found between arterial compliance and PI (r = −0.63, P < 0.05). Figure 3. View largeDownload slide Association between β-stiffness index and PI (a), between arterial compliance and PI (b) (control subjects: n = 13, resistance-trained men: n = 13). Close rhombus (◆): control subjects. Open rhombus (◇): resistance-trained men. Abbreviation: PI, pulsatility index. Figure 3. View largeDownload slide Association between β-stiffness index and PI (a), between arterial compliance and PI (b) (control subjects: n = 13, resistance-trained men: n = 13). Close rhombus (◆): control subjects. Open rhombus (◇): resistance-trained men. Abbreviation: PI, pulsatility index. DISCUSSION The present study showed that resistance-trained men had higher central arterial stiffness and PI, and lower arterial compliance than the control subjects. In addition, a positive correlation was observed between the β-stiffness index and PI, and a negative correlation was observed between arterial compliance and PI. These results suggest that increased central arterial stiffness and decreased arterial compliance with RT impair buffer function, resulting in increased CBF pulsatility. Central arterial stiffness and compliance The β-stiffness index was significantly higher in the resistance-trained men than in the control subjects. By contrast, the arterial compliance in the resistance-trained men was significantly lower than that in the control subjects. A previous study showed that adiposity and inflammation impaired central arterial stiffness and arterial compliance.19,20 Physical exercise commonly improves these indices, resulting in improvements in central arterial stiffness and compliance. Also, RT induces similar benefits for adiposity and inflammation.21 However, several studies have shown that resistance-trained men have higher arterial stiffness and lower compliance than age-matched sedentary men.12,13 Moderate- to high-intensity RT was also demonstrated to increase arterial stiffness and/or to decrease arterial compliance in sedentary young men.10,11 Thus, this arterial adaptation has been thought to be caused by RT. Increased central arterial stiffness and decreased arterial compliance with aging and diseases may be impaired by the vascular endothelial function and arterial structure.22–24 In case of impaired vascular endothelial function, production and/or bioavailability of nitric oxide are decreased,25 resulting in increased central arterial stiffness and/or reduced compliance.26 However, no differences were observed in the vascular endothelial function between the resistance-trained men and the age-matched sedentary.12,13 Other studies have shown that moderate- and high-intensity RT does not alter or improve vascular endothelial function in sedentary young men.27,28 Previous studies reported that arterial structure was not altered in both intervention and cross-sectional studies.10,12 These results indicate that RT increases central arterial stiffness and decreases arterial compliance without impairment in vascular endothelial function and unchanged arterial structure. Elevation of muscle sympathetic nerve activity causes vasoconstriction,29 resulting in increasing arterial stiffness.30 Recent studies have suggested that increased central arterial stiffness and decreased arterial compliance with moderate- to high-intensity RT are associated with elevation of sympathetic nerve activity.13,31 Smith et al. showed that muscle sympathetic nerve activity and central arterial stiffness are higher in resistance-trained men than in endurance-trained subjects, and a positive correlation was observed between muscle sympathetic nerve activity and central arterial stiffness.13 In addition, Okamoto et al. reported that upper limb RT increased norepinephrine concentration in the blood and central arterial stiffness, but no such changes were observed in lower limb RT.31 The study showed a positive correlation between the changes in norepinephrine concentration in the blood and central arterial stiffness. These results demonstrate that altered sympathetic nerve activity is associated with central arterial stiffness following RT because norepinephrine concentration in the blood indicates sympathetic nerve activity.32 Pressor response during moderate- to high-intensity resistance exercise may also be associated with increased central arterial stiffness and decreased arterial compliance. Previous study reported that RT alters the arterial load-bearing properties, thereby causing arterial stiffening,10 because moderate- and high-intensity resistance exercise elevates blood pressure to as high as 320/250 mm Hg.33 However, evidence on the mechanism of increased central arterial stiffness and/or decreased arterial compliance with moderate- to high-intensity RT is limited. Thus, further studies are needed to investigate the correct mechanism of increased central arterial stiffness and/or decreased arterial compliance with RT. CBF pulsatility Previous studies demonstrated that CBF pulsatility is increased with aging and diseases,34 and elevation of central arterial stiffness and/or reduction in arterial compliance are thought to be factors in this phenomenon.34,35 The central arteries such as the aorta and carotid artery have abundant elasticity-buffer pulsatile blood flow to protect end-organ function, such as cerebral circulation.1 A previous study showed that arterial enlargement may blunt pulsatile blood flow,36 and hypotensive episodes may induce higher CBF pulsatility.37 However, no significant differences were observed in carotid diameter and carotid blood pressure in resistance-trained men is higher compared with control subjects in present study. Therefore, arterial diameter and hypotensive episodes may not have changed CBF pulsatility in the present study. Central arteries repeatedly expand and recoil against the intermittent flow generated by cardiac pulsation to buffer the pulsatility of blood flow. However, increased central arterial stiffness and decreased arterial compliance impair this function. Impairment of this function occurs to increase systolic blood flow and decrease diastolic blood flow,38 resulting in elevated pulsatility of blood flow.34 Previous studies showed that increased central arterial stiffness and decreased arterial compliance with aging and diseases were associated with enhancement of CBF pulsatility4,5 and decline cognitive function.39 In addition, this phenomenon leads to increased risk of cerebrovascular diseases.7,8 Moderate- to high-intensity RT may increase the risk of cerebrovascular diseases. Therefore, this study may support a previous study that suggested that central artery adaptation with RT increases cardiovascular disease mortality, including cerebrovascular disease.14 However, a limitation of this study is that the study population consisted of young subjects. Hence, further research is needed to investigate the effect of RT on CBF pulsatility. In conclusion, β-stiffness index and PI were significantly higher in the resistance-trained men than in the control subjects. By contrast, the arterial compliance in the resistance-trained men was significantly lower than that in the control subjects. Moreover, PI was correlated with β-stiffness index and arterial compliance. These results suggest that increased central arterial stiffness and decreased central arterial compliance by RT elevate CBF pulsatility. As this cerebrohemodynamic changes may place an excessive mechanical stress to the cerebrovascular system, moderate- to high-intensity RT should be performed carefully. DISCLOSURE The authors declared no conflict of interest. ACKNOWLEDGMENT We appreciate all the participants of this study. REFERENCES 1. O’Rourke MF , Hashimoto J . Mechanical factors in arterial aging: a clinical perspective . J Am Coll Cardiol 2007 ; 50 : 1 – 13 . Google Scholar CrossRef Search ADS PubMed 2. O’Rourke MF , Safar ME . Relationship between aortic stiffening and microvascular disease in brain and kidney: cause and logic of therapy . Hypertension 2005 ; 46 : 200 – 204 . Google Scholar CrossRef Search ADS PubMed 3. Mitchell GF . Effects of central arterial aging on the structure and function of the peripheral vasculature: implications for end-organ damage . J Appl Physiol (1985) 2008 ; 105 : 1652 – 1660 . Google Scholar CrossRef Search ADS PubMed 4. Hirata K , Yaginuma T , O’Rourke MF , Kawakami M . Age-related changes in carotid artery flow and pressure pulses: possible implications for cerebral microvascular disease . Stroke 2006 ; 37 : 2552 – 2556 . 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For Permissions, please email: journals.permissions@oup.com This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Hypertension Oxford University Press

Resistance Training Augments Cerebral Blood Flow Pulsatility: Cross-Sectional Study

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Oxford University Press
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© American Journal of Hypertension, Ltd 2018. All rights reserved. For Permissions, please email: journals.permissions@oup.com
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0895-7061
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1941-7225
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10.1093/ajh/hpy034
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Abstract

Abstract BACKGROUND Increased central arterial stiffness and/or decreased compliance reduces buffer function and increases cerebral blood flow (CBF) pulsatility, which leads to increased cerebral microvascular damage, resulting in the augmentation of the risk of cerebrovascular diseases. Resistance-trained men showed higher central arterial stiffness and lower arterial compliance than age-matched, sedentary men. This study examined the effect of increased central arterial stiffness and/or decreased arterial compliance on CBF pulsatility. METHODS The study participants included 31 young healthy men (15 resistance-trained men, aged 21 ± 1 years; and 16 controls, aged 23 ± 1 years). β-Stiffness index and arterial compliance were measured in the right carotid artery as index of central arterial stiffness and compliance, respectively. The pulsatility index (PI) was measured in the middle cerebral artery as index of CBF pulsatility. RESULTS β-Stiffness index and PI were significantly higher in the resistance-trained group than in the control group (β-stiffness index: 5.3 ± 0.3 vs. 3.5 ± 0.3 a.u., P < 0.05, PI: 0.80 ± 0.02 vs. 0.70 ± 0.02, P < 0.05). The resistance-trained group showed significantly lower arterial compliance than the control group (0.16 ± 0.01 vs. 0.23 ± 0.01 mm2/mm Hg, P < 0.05). Positive and negative correlations were observed between β-stiffness index and PI (r = 0.39, P < 0.05), and between arterial compliance and PI (r = −0.59, P < 0.05), respectively. CONCLUSIONS The resistance-trained group showed higher central arterial stiffness and PI and lower arterial compliance. Central arterial stiffness and arterial compliance were associated with PI. Increased arterial stiffness and decreased arterial compliance with resistance training impair buffer function, resulting in increased CBF pulsatility. CLINICAL TRIAL REGISTRATION Trial Number UMIN000023816 URL: http://www.umin.ac.jp/icdr/index.html Official scientific title of the study: effect of increase arterial stiffness by resistance training on cerebral hemodynamic arterial compliance, blood pressure, central arterial stiffness, cerebral blood flow pulsatility, hypertension, resistance training The central arteries such as the aorta and carotid artery are characterized by an abundance of elastic fibers and buffer pulsatile blood flow to continuous flow.1 In addition, buffer function plays a major role in the protection of the cerebral artery, which has low resistance to mechanical damage such as that by high pulsatile blood flow in the central artery.2,3 Previous studies showed that increased central arterial stiffness and decreased arterial compliance with aging and diseases were associated with augmentation of cerebral blood flow (CBF) pulsatility.4,5 In cases of higher pulsatile blood flow over a long period, the arterial wall thickness and wall-to-lumen ratio is increased.6 In addition, increased CBF pulsatility leads to increased cerebral microvascular damage, resulting in elevated risk of cerebrovascular diseases.7,8 Thus, maintaining a lower central arterial stiffness and higher compliance to protect the cerebral artery is of great importance. Moderate- to high-intensity resistance training (RT) has been recently recommended for muscular hypertrophy and maximizing strength.9 However, several studies have reported that moderate- to high-intensity RT increases central arterial stiffness and/or decreases arterial compliance in healthy men.10,11 Resistance-trained men who habitually performed vigorous RT showed higher central arterial stiffness and lower arterial compliance than age-matched, sedentary men.12,13 That is, moderate- to high-intensity RT may increase CBF pulsatility. Although this phenomenon has been considered not a problem because the effect of central artery adaptation with RT on cardiovascular diseases has not been clarified yet, Kamada et al. recently suggested that central arterial adaptation with RT increases cardiovascular disease mortality, including cerebrovascular disease.14 Thus, whether moderate- to high-intensity RT augments CBF pulsatility should be investigated. Nevertheless, to our knowledge, no evidence shows that increased central arterial stiffness and/or decreased arterial compliance with moderate- to high-intensity RT on CBF pulsatility. Therefore, the purpose of this study was to examine the effect of increased central arterial stiffness and decreased arterial compliance by RT on CBF pulsatility. To investigate this purpose, we designed a cross-sectional study in which central arterial stiffness and compliance, and CBF pulsatility in resistance-trained men were compared with those in age-matched non–resistance-trained subjects. MATERIALS AND METHODS Subjects Thirty-one healthy men (15 resistance-trained: mean age, 21 ± 2 years; and 16 sedentary: mean age, 23 ± 2 years) were recruited to participate in this study. The resistance-trained men had been performing vigorous RT for >2 years, >5 days/week. The sedentary subjects recruited were healthy men. None of the subjects in the sedentary group regularly engaged in RT. All the subjects were normotensive (<140/90 mm Hg), and none of them ever used medications such as anabolic steroids. All the subjects provided written informed consent to participate prior to the start of the study. All the procedures and risk of this study were reviewed and approved by the Human Research Committee of Waseda University (approval No. 2016–170). Experimental procedure The studies were performed following a 3-hour fast and required to avoid caffeine intake for at least 12 hours and alcohol intake for at least 24 hours. The subjects were evaluated 24 hours after their last exercise session to avoid the acute effects of exercise. The cardiorespiratory and cerebrohemodynamic variables of the subjects were measured in a temperature-controlled environment (23.0 °C ± 0.1 °C, 50.0% ± 0.1%) after 15 minutes in resting supine position. Body composition Body composition was measured using bioelectrical impedance analysis (InBody 720, InBody Japan, Japan) in the upright position. Muscular strength Hand grip strength was measured using a handheld dynamometer (dynamometer hand grip; Takei Scientific Instruments, Japan) as an index of muscular strength. The subjects were instructed to stand and extend the arms by their sides during a hand grip execution and to grip the handheld dynamometer with full effort for 3 seconds. The values (kg) were recorded as the average of 2 trials. Heart rate and brachial arterial blood pressure Heart rate was measured using 2-lead electrocardiography (Form PWV/ABI; Omron Colin, Japan). Brachial systolic blood pressure, diastolic blood pressure, and mean arterial pressure were measured using a semiautomated device over the brachial artery (Form PWV/ABI; Omron Colin). Central arterial stiffness and compliance The β-stiffness index and arterial compliance of the common carotid artery were measured as an index of central arterial stiffness and compliance, respectively. Both the β-stiffness index and arterial compliance were measured in the right common carotid artery by using a combination of brightness-mode ultrasonography system for carotid artery diameter and applanation tonometry for carotid BP. The carotid diameter was obtained 1.0–2.0 cm proximal to the carotid bifurcation by using an ultrasonography system equipped with a 10-MHz linear transducer (LOGIQ-e; GE Medical Systems, Japan). The diameter was recorded over 10 cardiac cycles by using the brightness mode in the longitudinal section. The images obtained were analyzed using an image analysis software (ImageJ 1.42, NIH), and the systolic diameter (sD) and diastolic diameter (dD) were analyzed in these images. The carotid pressure waveform was obtained in the right common carotid artery with a pencil-type probe incorporating a high-fidelity strain-gauge transducer (SPT-301; Millar Instruments, TX). The obtained pressure waveforms were recorded in the computer. The carotid arterial pressure was calibrated by equating the carotid diastolic blood pressure and mean arterial pressure to the brachial artery value. The β-stiffness index and arterial compliance were calculated as follows10: β−stiffness index=ln(carotid SBP/DBP)/([sD−dD])/dD) Arterial compliance=([dD−sD]/sD)/(2×[carotid SBP–DBP])×π×sD Carotid arterial intima-media thickness The carotid arterial intima-media thickness was measured using the brightness mode of an ultrasonographic system equipped with a 10-MHz linear transducer (LOGIQ-e, GE Medical Systems). The obtained images were analyzed using an image analysis software (ImageJ, NIH). At least 10 carotid intima-media thickness measurements were taken, and the mean value was used for analysis. Internal carotid artery, vertebral artery blood flow, and global CBF The internal carotid artery (ICA) and vertebral artery diameter and velocity were obtained using an ultrasonographic system equipped with a 10-MHz linear transducer (LOGIQ-e; GE Medical Systems). The ICA blood flow was measured 1.0–1.5 cm distal to the carotid bifurcation on the right ICA. Vertebral artery measurements were performed between the transverse processes of C3 and the subclavian artery. The diameter was obtained using the brightness mode in longitudinal section and was analyzed using an image analysis software (ImageJ 1.42, NIH). The mean blood flow velocity was measured in pulse wave mode. The mean blood flow was measured in 10 cardiac cycles to eliminate the effects caused by the breathing cycle. Stability of the probe position was ensured, and the insonation angle did not vary (<60°). The mean diameter, ICA, and vertebral artery blood flow, global CBF (gCBF), and ICA and vertebral artery conductance were calculated as follows15: Mean diameter=(sD×1/3)+(dD×2/3)Blood flow=mean blood flow velocity×(π×[mean diameter/2]2)×60ICA conductance=ICA blood flow/MAPVA conductance=VA blood flow/MAPgCBF=(ICA blood flow+VA blood flow)×2 Middle cerebral artery blood flow velocity and CBF pulsatility The middle cerebral artery blood flow velocity (MCA V) was assessed using an ultrasonographic system equipped with a 2.5-MHz sector transducer (LOGIQ-e, GE Medical Systems) at the right temporal window. The right MCA was confirmed using the color mode, and the blood flow velocity waveform was obtained using the pulse wave mode. The pulsatility index (PI) of the MCA, which indicates CBF pulsatility, and the MCA Vmean were calculated using an automatic-calculation mode. Stroke volume The stroke volume was measured using an ultrasonographic system equipped with a 2.5-MHz sector transducer (LOGIQ-e, GE Medical Systems). The left ventricular image was obtained using a motion mode. The left ventricular end-diastolic and end-systolic dimensions were measured according to the established guidelines.16 The left ventricular volume was calculated using the Teichholz method.17 The left ventricular volume and stroke volume were calculated as follows: Left ventricular volume=(7×end dimension3)/(2.4+end dimension)Stroke volume=left ventricular end−diastolic volume−left ventricular end−systolic volume Partial pressure of arterial carbon dioxide The partial pressure of arterial carbon dioxide (PaCO2) was estimated from the tidal volume (VT) and end-tidal partial pressure of CO2 (PETCO2).18VT and PETCO2 were measured breath by breath from expired gas by using an expired gas analyzer (Aero Monitor AE310s, Minato Medical Science, Japan). The data obtained during the 10-minute collection period were averaged. Statistical analysis All data were presented as mean ± SEM. Statistical analyses were performed using the Statistical Package for the Social Sciences version 22.0 for Windows (IBM, Japan). The mean differences in the 2 groups were examined using the Student unpaired t test. Pearson correlations were used to assess the relationship between β-stiffness index and PI, and between arterial compliance and PI. In all the analyses, the level of significance for all the comparisons was set at P <0.05. RESULTS In the present study, 2 resistance-trained men and 3 control subjects were excluded in the MCA V analysis because obtaining MCA blood flow velocity waveform from them was impossible. As a result, analyzable MCA V recordings in 13 resistance-trained men and 13 control subjects were obtained. Therefore, MCA Vmean and PI, and the association between β-stiffness index and PI, and arterial compliance and PI were analyzed in 26 subjects (13 resistance-trained men and 13 control subjects). Subject characteristics Table 1 shows the characteristics of the subjects. Body weight, body mass index, lean body mass, and hand grip strength were significantly higher in the resistance-trained men than in the control subjects (P < 0.05). However, no significant differences were observed in the other subject characteristics between the 2 groups. Table 1. Characteristics of the control and resistance-trained men Control Resistance-trained Number of subjects 16 15 Age (years) 23 ± 1 21 ± 1 Height (cm) 172.2 ± 1.4 171.0 ± 2.0 Body weight (kg) 69.1 ± 2.6 82.8 ± 3.6* Body fat (%) 18.9 ± 1.3 18.8 ± 1.6 Body mass index (kg/m2) 23.2 ± 0.7 28.6 ± 0.8* Lean body mass (kg) 55.8 ± 1.8 68.5 ± 2.6* Hand grip (kg) 40 ± 2 51 ± 2* Control Resistance-trained Number of subjects 16 15 Age (years) 23 ± 1 21 ± 1 Height (cm) 172.2 ± 1.4 171.0 ± 2.0 Body weight (kg) 69.1 ± 2.6 82.8 ± 3.6* Body fat (%) 18.9 ± 1.3 18.8 ± 1.6 Body mass index (kg/m2) 23.2 ± 0.7 28.6 ± 0.8* Lean body mass (kg) 55.8 ± 1.8 68.5 ± 2.6* Hand grip (kg) 40 ± 2 51 ± 2* The data are presented as mean ± SEM. *P < 0.05 vs. the control subjects. View Large Table 1. Characteristics of the control and resistance-trained men Control Resistance-trained Number of subjects 16 15 Age (years) 23 ± 1 21 ± 1 Height (cm) 172.2 ± 1.4 171.0 ± 2.0 Body weight (kg) 69.1 ± 2.6 82.8 ± 3.6* Body fat (%) 18.9 ± 1.3 18.8 ± 1.6 Body mass index (kg/m2) 23.2 ± 0.7 28.6 ± 0.8* Lean body mass (kg) 55.8 ± 1.8 68.5 ± 2.6* Hand grip (kg) 40 ± 2 51 ± 2* Control Resistance-trained Number of subjects 16 15 Age (years) 23 ± 1 21 ± 1 Height (cm) 172.2 ± 1.4 171.0 ± 2.0 Body weight (kg) 69.1 ± 2.6 82.8 ± 3.6* Body fat (%) 18.9 ± 1.3 18.8 ± 1.6 Body mass index (kg/m2) 23.2 ± 0.7 28.6 ± 0.8* Lean body mass (kg) 55.8 ± 1.8 68.5 ± 2.6* Hand grip (kg) 40 ± 2 51 ± 2* The data are presented as mean ± SEM. *P < 0.05 vs. the control subjects. View Large Cardiorespiratory and cerebrohemodynamic variables Table 2 shows the cardiorespiratory and cerebrovascular variables. The brachial PP, carotid systolic blood pressure, and PP were significantly higher in the resistance-trained men than in the control subjects (P < 0.05). Brachial diastolic blood pressure was significantly lower in the resistance-trained men than in the control subjects (P < 0.05). However, no significant differences were observed in other cardiorespiratory and cerebrovascular variables between the 2 groups. Table 2. Cardiorespiratory and cerebrovascular variables in the control and resistance-trained men (control subjects: n = 16, resistance-trained men: n = 15) Control Resistance-trained Brachial SBP (mm Hg) 113 ± 2 116 ± 2 Brachial DBP (mm Hg) 65 ± 2 59 ± 1* Brachial MAP (mm Hg) 84 ± 1 83 ± 1 Brachial PP (mm Hg) 48 ± 1 57 ± 1* Carotid SBP (mm Hg) 103 ± 1 112 ± 2* Carotid PP (mm Hg) 38 ± 2 53 ± 1* Carotid diameter (cm) 0.58 ± 0.01 0.60 ± 0.01 Carotid IMT (mm) 0.49 ± 0.01 0.48 ± 0.01 PaCO2 (mm Hg) 41.4 ± 0.4 42.3 ± 0.4 HR (bpm) 62 ± 1 61 ± 3 SV (ml/min) 65 ± 2 66 ± 1 CO (l/min) 4.0 ± 0.9 4.1 ± 2.1 ICA  Blood flow (ml/min) 300 ± 16 325 ± 22  Diameter (cm) 0.48 ± 0.01 0.50 ± 0.02  Velocity (cm/s) 28 ± 1 27 ± 1  Conductance (ml/min/mm Hg) 3.60 ± 0.22 3.95 ± 0.28 VA  Blood flow (ml/min) 94 ± 8 89 ± 11  Diameter (cm) 0.33 ± 0.01 0.34 ± 0.01  Velocity (cm/s) 17 ± 1 15 ± 1  Conductance (ml/min/mm Hg) 1.12 ± 0.10 1.08 ± 0.13 gCBF (ml/min) 789 ± 42 828 ± 46 Control Resistance-trained Brachial SBP (mm Hg) 113 ± 2 116 ± 2 Brachial DBP (mm Hg) 65 ± 2 59 ± 1* Brachial MAP (mm Hg) 84 ± 1 83 ± 1 Brachial PP (mm Hg) 48 ± 1 57 ± 1* Carotid SBP (mm Hg) 103 ± 1 112 ± 2* Carotid PP (mm Hg) 38 ± 2 53 ± 1* Carotid diameter (cm) 0.58 ± 0.01 0.60 ± 0.01 Carotid IMT (mm) 0.49 ± 0.01 0.48 ± 0.01 PaCO2 (mm Hg) 41.4 ± 0.4 42.3 ± 0.4 HR (bpm) 62 ± 1 61 ± 3 SV (ml/min) 65 ± 2 66 ± 1 CO (l/min) 4.0 ± 0.9 4.1 ± 2.1 ICA  Blood flow (ml/min) 300 ± 16 325 ± 22  Diameter (cm) 0.48 ± 0.01 0.50 ± 0.02  Velocity (cm/s) 28 ± 1 27 ± 1  Conductance (ml/min/mm Hg) 3.60 ± 0.22 3.95 ± 0.28 VA  Blood flow (ml/min) 94 ± 8 89 ± 11  Diameter (cm) 0.33 ± 0.01 0.34 ± 0.01  Velocity (cm/s) 17 ± 1 15 ± 1  Conductance (ml/min/mm Hg) 1.12 ± 0.10 1.08 ± 0.13 gCBF (ml/min) 789 ± 42 828 ± 46 The data are presented as mean ± SEM. *P < 0.05, vs. the control subjects. Abbreviations: CO, cardiac output; DBP, diastolic blood pressure; gCBF, global cerebral blood flow; HR, heart rate; ICA, internal carotid artery; IMT, intima-media thickness; MAP, mean arterial pressure; PaCO2, arterial partial pressure of carbon dioxide; PP, pulse pressure; SBP, systolic blood pressure; SV, stroke volume; VA, vertebral artery. View Large Table 2. Cardiorespiratory and cerebrovascular variables in the control and resistance-trained men (control subjects: n = 16, resistance-trained men: n = 15) Control Resistance-trained Brachial SBP (mm Hg) 113 ± 2 116 ± 2 Brachial DBP (mm Hg) 65 ± 2 59 ± 1* Brachial MAP (mm Hg) 84 ± 1 83 ± 1 Brachial PP (mm Hg) 48 ± 1 57 ± 1* Carotid SBP (mm Hg) 103 ± 1 112 ± 2* Carotid PP (mm Hg) 38 ± 2 53 ± 1* Carotid diameter (cm) 0.58 ± 0.01 0.60 ± 0.01 Carotid IMT (mm) 0.49 ± 0.01 0.48 ± 0.01 PaCO2 (mm Hg) 41.4 ± 0.4 42.3 ± 0.4 HR (bpm) 62 ± 1 61 ± 3 SV (ml/min) 65 ± 2 66 ± 1 CO (l/min) 4.0 ± 0.9 4.1 ± 2.1 ICA  Blood flow (ml/min) 300 ± 16 325 ± 22  Diameter (cm) 0.48 ± 0.01 0.50 ± 0.02  Velocity (cm/s) 28 ± 1 27 ± 1  Conductance (ml/min/mm Hg) 3.60 ± 0.22 3.95 ± 0.28 VA  Blood flow (ml/min) 94 ± 8 89 ± 11  Diameter (cm) 0.33 ± 0.01 0.34 ± 0.01  Velocity (cm/s) 17 ± 1 15 ± 1  Conductance (ml/min/mm Hg) 1.12 ± 0.10 1.08 ± 0.13 gCBF (ml/min) 789 ± 42 828 ± 46 Control Resistance-trained Brachial SBP (mm Hg) 113 ± 2 116 ± 2 Brachial DBP (mm Hg) 65 ± 2 59 ± 1* Brachial MAP (mm Hg) 84 ± 1 83 ± 1 Brachial PP (mm Hg) 48 ± 1 57 ± 1* Carotid SBP (mm Hg) 103 ± 1 112 ± 2* Carotid PP (mm Hg) 38 ± 2 53 ± 1* Carotid diameter (cm) 0.58 ± 0.01 0.60 ± 0.01 Carotid IMT (mm) 0.49 ± 0.01 0.48 ± 0.01 PaCO2 (mm Hg) 41.4 ± 0.4 42.3 ± 0.4 HR (bpm) 62 ± 1 61 ± 3 SV (ml/min) 65 ± 2 66 ± 1 CO (l/min) 4.0 ± 0.9 4.1 ± 2.1 ICA  Blood flow (ml/min) 300 ± 16 325 ± 22  Diameter (cm) 0.48 ± 0.01 0.50 ± 0.02  Velocity (cm/s) 28 ± 1 27 ± 1  Conductance (ml/min/mm Hg) 3.60 ± 0.22 3.95 ± 0.28 VA  Blood flow (ml/min) 94 ± 8 89 ± 11  Diameter (cm) 0.33 ± 0.01 0.34 ± 0.01  Velocity (cm/s) 17 ± 1 15 ± 1  Conductance (ml/min/mm Hg) 1.12 ± 0.10 1.08 ± 0.13 gCBF (ml/min) 789 ± 42 828 ± 46 The data are presented as mean ± SEM. *P < 0.05, vs. the control subjects. Abbreviations: CO, cardiac output; DBP, diastolic blood pressure; gCBF, global cerebral blood flow; HR, heart rate; ICA, internal carotid artery; IMT, intima-media thickness; MAP, mean arterial pressure; PaCO2, arterial partial pressure of carbon dioxide; PP, pulse pressure; SBP, systolic blood pressure; SV, stroke volume; VA, vertebral artery. View Large Central arterial stiffness and compliance β-Stiffness index and arterial compliance are presented in Figure 1a and b, respectively. β-Stiffness index was significantly higher in the resistance-trained men than in the control subjects (5.3 ± 0.3 vs. 3.5 ± 0.3 a.u., P < 0.05). By contrast, arterial compliance was significantly lower in the resistance-trained men than in the control subjects (0.16 ± 0.01 vs. 0.23 ± 0.01 mm2/mm Hg, P < 0.05). Figure 1. View largeDownload slide β-Stiffness index (a) and arterial compliance (b) in the control subjects and resistance-trained men (control subjects: n = 16 and resistance-trained men: n = 15). The data are presented as SEM. *P < 0.05, vs. control subjects. Figure 1. View largeDownload slide β-Stiffness index (a) and arterial compliance (b) in the control subjects and resistance-trained men (control subjects: n = 16 and resistance-trained men: n = 15). The data are presented as SEM. *P < 0.05, vs. control subjects. MCA V and CBF pulsatility Figure 2 presents the MCA Vmean (a) and PI (b). No significant differences were observed in the MCA Vmean in the 2 groups (50 ± 4 vs. 51 ± 3 cm/s, P = 0.85). On the other hand, PI was significantly higher in the resistance-trained men than in the control subjects (PI: 0.80 ± 0.02 vs. 0.70 ± 0.02, P < 0.05). Figure 2. View largeDownload slide MCA Vmean (a) and pulsatility index (b) in the control and resistance-trained men (control subjects: n = 13 and resistance-trained men: n = 13). The data are presented as SEM. *P < 0.05, vs. the control subjects. Abbreviations: MCA Vmean, middle cerebral artery mean blood flow velocity; PI, pulsatility index. Figure 2. View largeDownload slide MCA Vmean (a) and pulsatility index (b) in the control and resistance-trained men (control subjects: n = 13 and resistance-trained men: n = 13). The data are presented as SEM. *P < 0.05, vs. the control subjects. Abbreviations: MCA Vmean, middle cerebral artery mean blood flow velocity; PI, pulsatility index. Association between central arterial stiffness, arterial compliance, and CBF pulsatility The associations between β-stiffness index and PI, and between arterial compliance and PI are shown in Figure 3a and b, respectively. A positive correlation was found between β-stiffness index and PI (r = 0.39, P < 0.05), and a negative correlation was found between arterial compliance and PI (r = −0.63, P < 0.05). Figure 3. View largeDownload slide Association between β-stiffness index and PI (a), between arterial compliance and PI (b) (control subjects: n = 13, resistance-trained men: n = 13). Close rhombus (◆): control subjects. Open rhombus (◇): resistance-trained men. Abbreviation: PI, pulsatility index. Figure 3. View largeDownload slide Association between β-stiffness index and PI (a), between arterial compliance and PI (b) (control subjects: n = 13, resistance-trained men: n = 13). Close rhombus (◆): control subjects. Open rhombus (◇): resistance-trained men. Abbreviation: PI, pulsatility index. DISCUSSION The present study showed that resistance-trained men had higher central arterial stiffness and PI, and lower arterial compliance than the control subjects. In addition, a positive correlation was observed between the β-stiffness index and PI, and a negative correlation was observed between arterial compliance and PI. These results suggest that increased central arterial stiffness and decreased arterial compliance with RT impair buffer function, resulting in increased CBF pulsatility. Central arterial stiffness and compliance The β-stiffness index was significantly higher in the resistance-trained men than in the control subjects. By contrast, the arterial compliance in the resistance-trained men was significantly lower than that in the control subjects. A previous study showed that adiposity and inflammation impaired central arterial stiffness and arterial compliance.19,20 Physical exercise commonly improves these indices, resulting in improvements in central arterial stiffness and compliance. Also, RT induces similar benefits for adiposity and inflammation.21 However, several studies have shown that resistance-trained men have higher arterial stiffness and lower compliance than age-matched sedentary men.12,13 Moderate- to high-intensity RT was also demonstrated to increase arterial stiffness and/or to decrease arterial compliance in sedentary young men.10,11 Thus, this arterial adaptation has been thought to be caused by RT. Increased central arterial stiffness and decreased arterial compliance with aging and diseases may be impaired by the vascular endothelial function and arterial structure.22–24 In case of impaired vascular endothelial function, production and/or bioavailability of nitric oxide are decreased,25 resulting in increased central arterial stiffness and/or reduced compliance.26 However, no differences were observed in the vascular endothelial function between the resistance-trained men and the age-matched sedentary.12,13 Other studies have shown that moderate- and high-intensity RT does not alter or improve vascular endothelial function in sedentary young men.27,28 Previous studies reported that arterial structure was not altered in both intervention and cross-sectional studies.10,12 These results indicate that RT increases central arterial stiffness and decreases arterial compliance without impairment in vascular endothelial function and unchanged arterial structure. Elevation of muscle sympathetic nerve activity causes vasoconstriction,29 resulting in increasing arterial stiffness.30 Recent studies have suggested that increased central arterial stiffness and decreased arterial compliance with moderate- to high-intensity RT are associated with elevation of sympathetic nerve activity.13,31 Smith et al. showed that muscle sympathetic nerve activity and central arterial stiffness are higher in resistance-trained men than in endurance-trained subjects, and a positive correlation was observed between muscle sympathetic nerve activity and central arterial stiffness.13 In addition, Okamoto et al. reported that upper limb RT increased norepinephrine concentration in the blood and central arterial stiffness, but no such changes were observed in lower limb RT.31 The study showed a positive correlation between the changes in norepinephrine concentration in the blood and central arterial stiffness. These results demonstrate that altered sympathetic nerve activity is associated with central arterial stiffness following RT because norepinephrine concentration in the blood indicates sympathetic nerve activity.32 Pressor response during moderate- to high-intensity resistance exercise may also be associated with increased central arterial stiffness and decreased arterial compliance. Previous study reported that RT alters the arterial load-bearing properties, thereby causing arterial stiffening,10 because moderate- and high-intensity resistance exercise elevates blood pressure to as high as 320/250 mm Hg.33 However, evidence on the mechanism of increased central arterial stiffness and/or decreased arterial compliance with moderate- to high-intensity RT is limited. Thus, further studies are needed to investigate the correct mechanism of increased central arterial stiffness and/or decreased arterial compliance with RT. CBF pulsatility Previous studies demonstrated that CBF pulsatility is increased with aging and diseases,34 and elevation of central arterial stiffness and/or reduction in arterial compliance are thought to be factors in this phenomenon.34,35 The central arteries such as the aorta and carotid artery have abundant elasticity-buffer pulsatile blood flow to protect end-organ function, such as cerebral circulation.1 A previous study showed that arterial enlargement may blunt pulsatile blood flow,36 and hypotensive episodes may induce higher CBF pulsatility.37 However, no significant differences were observed in carotid diameter and carotid blood pressure in resistance-trained men is higher compared with control subjects in present study. Therefore, arterial diameter and hypotensive episodes may not have changed CBF pulsatility in the present study. Central arteries repeatedly expand and recoil against the intermittent flow generated by cardiac pulsation to buffer the pulsatility of blood flow. However, increased central arterial stiffness and decreased arterial compliance impair this function. Impairment of this function occurs to increase systolic blood flow and decrease diastolic blood flow,38 resulting in elevated pulsatility of blood flow.34 Previous studies showed that increased central arterial stiffness and decreased arterial compliance with aging and diseases were associated with enhancement of CBF pulsatility4,5 and decline cognitive function.39 In addition, this phenomenon leads to increased risk of cerebrovascular diseases.7,8 Moderate- to high-intensity RT may increase the risk of cerebrovascular diseases. Therefore, this study may support a previous study that suggested that central artery adaptation with RT increases cardiovascular disease mortality, including cerebrovascular disease.14 However, a limitation of this study is that the study population consisted of young subjects. Hence, further research is needed to investigate the effect of RT on CBF pulsatility. In conclusion, β-stiffness index and PI were significantly higher in the resistance-trained men than in the control subjects. By contrast, the arterial compliance in the resistance-trained men was significantly lower than that in the control subjects. Moreover, PI was correlated with β-stiffness index and arterial compliance. These results suggest that increased central arterial stiffness and decreased central arterial compliance by RT elevate CBF pulsatility. As this cerebrohemodynamic changes may place an excessive mechanical stress to the cerebrovascular system, moderate- to high-intensity RT should be performed carefully. 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American Journal of HypertensionOxford University Press

Published: Feb 28, 2018

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