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Canterbury Christ Church University Introduction The training stimulus responsible for blood pressure reductions after isometric training remains equivocal. It has previously been suggested that increased exposure to shear stress during isometric exercise may mediate endothelial adaptations, similar to that seen in dynamic exercise training. This may lead to a reduced peripheral resistance and thus a lower resting blood pressure (McGowan et al, 2007). However the role of shear stress in isometric training induced blood pressure reductions remains uninvestigated. The purpose of this study was to train participants at two intensities that either elicited a high or low shear stress stimulus to determine the role of conduit femoral artery shear stress in blood pressure reductions after an isometric leg training intervention. Methods 35 male normotensive participants (age = 23.79 ± 6.30 yrs, height = 180 ± 5.71 cm, mass = 75.70 ± 11.11 kg ) were allocated to one of three groups: high shear stress (HI), low shear stress (LO) or control (CON). The HI and LO groups undertook an 8 week training programme of 4 x 2minute bilateral-leg isometric contractions, 3 times per week. Mean shear rate (MSR), peak shear rate(PSR) and change in shear rate ( SR) were used as an estimation of shear stress, and was measured using doppler ultrasound during training intervention in the common femoral artery.
GREATER VISCOSITY AND SMALLER ELASTICITY OF CENTRAL ARTERY IN RESISTANCE-TRAINED YOUNG MENKawano, H., Gando, Y., Asaka, M., Ise, R., Higuchi, M.
Waseda University Introduction: Arterial mechanical characteristics include both elastic and viscous properties. Arterial elastic property, such as dynamic arterial compliance, beta-stiffness, and pulse wave velocity, are often used for assessment of vascular health, and arterial elasticity is attenuated by resistance training, leading to increases in risk of cardiovascular diseases. On the other hand, arterial wall viscosity is a source of energy dissipation, considering viscosity as an energy-dissipating phenomenon during mechanical transduction (conversion of cardiac pulsatile energy into arterial elastic energy). It remains unclear, however, whether arterial wall viscosity is affected by habitual resistance training. Accordingly, the purpose of the present study is to compare elasticity and viscosity of central artery between resistance-trained and sedentary men. We hypothesized that if resistance-trained men have less elasticity of artery, there is greater viscosity in them. Methods: Twelve resistance-trained (age, 21.0 ± 2.7 yrs; height, 167.6 ± 5.9 cm; body weight, 75.2 ± 12.2 kg) and 12 sedentary control peers (age, 22.3 ± 1.8 yrs; height, 174.3 ± 5.6 cm; body weight, 65.7 ± 8.9 kg) were participated in this study. All resistance-trained men had been performing moderate to high-intensity ‘full-body’ resistance training involving large muscle groups. All subjects were normotensive ( 140/90 mmHg), non-obese and smoker, and free of overt chronic diseases as assessed by medical history, physical examination and complete blood chemistry and haematological evaluation. All participants were measured as follows; static and dynamic compliance, beta-stiffness index, and wall viscosity in carotid artery. Results and Discussion: Resistance-trained men had smaller static arterial compliance and carotid beta-stiffness index compared with sedentary control men (P0.05 for both), but not statistical difference in dynamic arterial compliance (P=0.0655), which suggests habitual resistance training may induce dysfunction of elastic artery. On the other hand, carotid arterial wall viscosity in resistance-trained men is greater than control peers (1700 ± 548 vs 1296 ± 355 mmHg·s/mmHg, P0.05).This result indicates that chronic resistance training augments to dissipate pulsatile energy from heart, leading to less elasticity of central artery. Conclusion: The present study first examined the impact of resistance training-induced arterial stiffening on wall viscosity carotid artery, and found that there were greater wall viscosity and smaller elasticity of artery in resistancetrained men compared with sedentary young men.
7 DAYS ISCHEMIC PRECONDITONING IMPROVES LOCAL AND SYSTEMIC ENDOTHELIAL FUNCTION AND MICROCIRCULATION IN HEALTHY HUMANS
Liverpool John Moores University Introduction: Ischemic preconditioning (IPC) is able to protect tissue against ischemia-induced injury within and beyond the ischaemic area. We examined the hypothesis that daily exposure to IPC leads to improvement in endothelial function and skin microcirculation in the arm exposed to IPC, but also in the contra-lateral arm. Given that late phase of protection from IPC has been shown to be evident for up to 4 days, we hypothesised that improvements in vascular function would remain for 7 days following the daily IPC intervention. Methods: Thirteen healthy young males (age 22.5±2.5 yrs; BMI 22.8±1.0 kg/m2) completed a 7-day IPC-intervention, consisting of daily exposure of the arm to an IPC protocol (4x5-min at 220 mmHg with 5 min deflation). Bilateral assessment of brachial artery endothelial function (flow-mediated dilation (FMD)) and forearm microcirculation [cutaneous vascular conductance (CVC) calculated from skin flux (laserDoppler) and blood pressure at rest and during local heating] was performed before (pre) and after 7 days of IPC (post). Bilateral assessment allowed for examination of the local (i.e. intervention-arm) and remote (i.e. contralateral-arm) effect of IPC. Since the late phase of protection from IPC extends up to 4 days, we repeated tests 8 days following cessation of the intervention (post+8). FMD and forearm microcirculation were also examined in a no intervention group (control) of 8 healthy males (age 26.0±4.8 yrs; BMI 26.4±2.0 kg/m2), on two occasions separated by 15 days. Differences over time and between arms were analysed using repeated measures general linear models. Data are presented as mean±SD. Results: Brachial artery FMD increased during the 15 day protocol (P=0.03). FMD was significantly elevated at Post+8 (7.0±1.6%) when compared to pre (5.2±1.5%; P0.01). Forearm resting CVC also increased during the protocol (P=0.006). CVC was elevated at Post+8 (0.16±0.04 mV/mm Hg) when compared to pre (0.13±0.04 mV/mm Hg) (P=0.01). No interaction
between IPC arm and time were evident (P0.05), indicating similar changes in both the IPC and contralateral arm. The IPC-intervention did not effect CVC-responses to local heating in either arm (P0.05). No significant changes were evident in the control group across the 15 day time period in FMD or CVC. Conclusion: These data indicate that daily exposure to 7-days of IPC leads to local (IPC arm) and systemic (contra-lateral arm) improvements in brachial artery endothelial function and resting skin microcirculation that remains after cessation of the intervention and beyond the late phase of protection. These novel findings may have clinical relevance, as our data suggest local and systemic potency for the IPC-stimulus to improve endothelial function in small and large arteries both acutely and chronically.
ACUTE RESPONSES OF HEART RATE VARIABILITY AFTER BLOOD FLOW RESTRICTION EXERCISEChacon-Mikahil, M.P., Souza, L.C., Bonganha, V., Souza, G.V., Ferreira, M.L.V., Andrade, M.P.C., Rocha, J., Cavaglieri, C.R., Ugrinowitsch, C., Libardi, C.A.
State University of Campinas Introduction Resistance exercise with high-intensity (RE-HI) ( 70% 1-RM) has been recommended to increase in skeletal muscle mass. It is suggested that high-intensity resistance training may induce orthopedic and cardiovascular problems (1). On the other hand, resistance exercise low intensity (e.g. 20% 1-RM), with restriction of blood flow (RE-RBF) seems to promote increased muscle mass similar to RE-HI (2).
Although the RE-RBF promotes a lower stress on joints, and its efficacy is well established (3), little is known about its effect on the cardiovascular system, especially in autonomic function after exercise. One way to measure the cardiovascular stress is the measuring behavior of heart rate variability (HRV) after exercise. Indeed, sympathetic hyperactivity or reduced cardiac vagal tone (4) after exercise may represent a greater cardiovascular risk (5) and underlie ischemic heart disease and the pathogenesis of malignant ventricular arrhythmias and sudden cardiac death. Therefore, the purpose of the present study was to determine the effect of the RE-HI and RE-RBF in the sympathetic and parasympathetic balance by the HRV analyses. Methods Fifteen middle-age men (47.6±5.28 y, 76.81±10.95 kg,
1.74±0.08 m), non-physically active performed 3 sets of 10 at 80% 1-RM (RE-HI) and 3 sets of 15 at 20% 1-RM (RE-RBF) in leg press, with the session randomized, counterbalanced order with 72h between session. The rest intervals between sets were 1 min. The cuff pressure used during the RE-RBF was determined as 50% of the necessary pressure for complete blood flow restriction in a resting condition.
Autonomic measures were made before and during 60min after session. Random coefficient growth curve analysis allowed comparison between slopes during the 60 minute recovery for R-R interval, RMSSD, SDNN, LF, HF and LF/HF ratio. Results The random coefficient growth curve analysis identified greater increase post-exercise in LFnu for RE-HI compared to RE-RBF (P = 0.004). The RE-HI also showed greater reduction in HFnu compared to RE-RBF (P = 0.004). In addition, there was a tendency for higher LF/HF ratio for RE-HI (P = 0.059).
No differences between slopes for R-R interval, RMSSD, SDNN. Discussion The results suggest that sympathetic hyperactivity and greater reduction cardiac vagal tone after RE-HI may represent a greater cardiovascular risk compared RE-RBF. These results may be important especially for aging people and patients with various disorders, seen that the RE-RBF may promote increased skeletal muscle mass similar to RE-HI (2), but with less cardiovascular stress as seen by the sympathetic and parasympathetic modulation in the HRV analyses References 1) Williams et al. (2007). Circulation, 116:572–584. 2) Takarada et al. (2000). J Appl Physiol, 88, 2097–2106. 3) Loenneke (2012).
Acta Physiol Hung, 99(3):235-50. 4) Billman (2002). J Appl Physiol, 92: 446–454 5) Albert et al. (2000). The New England J of Med, 343 (19):