Combined effects of low-intensity blood flow restriction training and high-intensity resistance training on muscle strength and size

We investigated the combined effect of low-intensity blood flow restriction and high-intensity resistance training on muscle adaptation. Forty young men (aged 22–32 years) were randomly divided into four groups of ten subjects each: high-intensity resistance training (HI-RT, 75% of one repetition maximum [1-RM]), low-intensity resistance training with blood flow restriction (LI-BFR, 30% 1-RM), combined HI-RT and LI-BFR (CB-RT, twice-weekly LI-BFR and once-weekly HI-RT), and nontraining control (CON). Three training groups performed bench press exercises 3 days/week for 6 weeks. During LI-BFR training sessions, subjects wore pressure cuffs on both arms that were inflated to 100–160 mmHg. Increases in 1-RM were similar in the HI-RT (19.9%) and CB-RT (15.3%) groups and lower in the LI-BFR group (8.7%, p < 0.05). Maximal isometric elbow extension (MVC) increased in the HI-RT (11.3%) and CB-RT (6.6%) groups; there was no change in the LI-BFR group (−0.2%). The cross-sectional area (CSA) of the triceps brachii (TB) increased (p < 0.05) in the HI-RT (8.6%), CB-RT (7.2%), and LI-BFR (4.4%) groups. The change in relative isometric strength (MVC divided by TB CSA) was greater (p < 0.05) in the HI-RT group (3.3%) than in the LI-BFR (−3.5%) and CON (−0.1%) groups. Following training, relative dynamic strength (1-RM divided by TB CSA) was increased (p < 0.05) by 10.5% in the HI-RT group and 6.7% in the CB-RT group. None of the variables in the CON group changed. Our results show that low-intensity resistance training with BFR-induced functional muscle adaptations is improved by combining it with HI-RT.     

Effects of high-intensity resistance training and low-intensity resistance training with vascular restriction on bone markers in older men

The aim of this study was to examine and compare the effects of different resistance training protocols on bone marker concentrations in older men. Thirty-seven healthy older male subjects were assigned to one of three groups: high-intensity resistance training (HI-RT, age?=?57.5?±?0.8); low-intensity resistance training with vascular restriction (LI-VRT, age?=?59.9?±?1.0); and control (CON, age?=?57.0?±?1.1). Blood samples were collected before and after 6?weeks of resistance training to measure the changes in bone formation [bone alkaline phosphatase, (Bone ALP)] and resorption (C-terminal cross-linking telopeptide of Type-I collagen, CTX) marker concentrations. A significant main effect for time was detected in Bone ALP to CTX ratio for the exercise groups (p??LI-VRT, p?相似文献   

Effect of low-intensity resistance training on arterial function

Although high-intensity resistance training increases central arterial stiffness, moderate-intensity resistance training does not. However, the effects of low-intensity resistance training on arterial stiffness are unknown. The aim of this study was to investigate the effect of low-intensity resistance training with short inter-set rest period (LSR) on arterial stiffness. Twenty-six young healthy subjects were randomly assigned to training (10 males, 3 females) and control groups (9 males, 4 females). The subjects performed LSR twice a week at 50% of one repetition maximum for 10 weeks. Training consisted of five sets of ten repetitions with an inter-set rest period of 30 s. Changes in brachial-ankle pulse wave velocity (baPWV) and brachial flow-mediated dilation (FMD) were assessed before and after the intervention period. After the intervention period, one repetition maximum strength increased (by 9–38%, P < 0.05 to <0.001; increases varied among the exercise types), baPWV decreased (from 1,093 ± 148 to 1,020 ± 128 cm/s, P < 0.05), and brachial FMD increased (from 9.7 ± 1.3 to 11.8 ± 1.9%, P < 0.05). These values did not change in the control group. These results suggest that LSR reduced arterial stiffness and improved vascular endothelial function.     

Effects of acute carbohydrate supplementation during sessions of high-intensity intermittent exercise

Abs tract The present study evaluated the acute effects of carbohydrate supplementation on heart rate (HR), rate of perceived exertion (RPE), metabolic and hormonal responses during and after sessions of high-intensity intermittent running exercise. Fifteen endurance runners (26 ± 5 years, 64.5 ± 4.9 kg) performed two sessions of intermittent exercise under carbohydrate (CHO) and placebo (PLA) ingestion. The sessions consisted of 12 × 800 m separated by intervals of 1 min 30 s at a mean velocity corresponding to the previously performed 3-km time trial. Both the CHO and PLA sessions were concluded within ∼28 min. Blood glucose was significantly elevated in both sessions (123.9 ± 13.2 mg dl⁻¹ on CHO and 147.2 ± 16.3 mg dl⁻¹ on PLA) and mean blood lactate was significantly higher in the CHO (11.4 ± 4.9 mmol l⁻¹) than in the PLA condition (8.4 ± 5.1 mmol l⁻¹) (P < 0.05). The metabolic stress induced by the exercise model used was confirmed by the elevated HR (∼182 bpm) and RPE (∼18 on the 15-point Borg scale) for both conditions. No significant differences in plasma insulin, cortisol or free fatty acids were observed during exercise between the two trials. During the recovery period, free fatty acid and insulin concentrations were significantly lower in the CHO trial. Supplementation with CHO resulted in higher lactate associated with lipolytic suppression, but did not attenuate the cortisol, RPE or HR responses.     

Effect of whole body resistance training on arterial compliance in young men

The effect of resistance training on arterial stiffening is controversial. We tested the hypothesis that resistance training would not alter central arterial compliance. Young healthy men (age, 23 +/- 3.9 (mean +/- s.e.m.) years; n = 28,) were whole-body resistance trained five times a week for 12 weeks, using a rotating 3-day split-body routine. Resting brachial blood pressure (BP), carotid pulse pressure, carotid cross-sectional compliance (CSC), carotid initima-media thickness (IMT) and left ventricular dimensions were evaluated before beginning exercise (PRE), after 6 weeks of exercise (MID) and at the end of 12 weeks of exercise (POST). CSC was measured using the pressure-sonography method. Results indicate reductions in brachial (61.1 +/- 1.4 versus 57.6 +/- 1.2 mmHg; P < 0.01) and carotid pulse pressure (52.2 +/- 1.9 versus 46.8 +/- 2.0 mmHg; P < 0.01) PRE to POST. In contrast, carotid CSC, beta-stiffness index, IMT and cardiac dimensions were unchanged. In young men, central arterial compliance is unaltered with 12 weeks of resistance training and the mechanisms responsible for cardiac hypertrophy and reduced arterial compliance are either not inherent to all resistance-training programmes or may require a prolonged stimulus.     

Dynamics of the short-term regulation of arterial pressure: Frequency dependence and role of arterial compliance

The purpose of this study was to investigate the role of the interaction between peripheral resistance regulation and arterial compliance in the overall short-term regulation of mean arterial pressure. A nonlinear model previously proposed was linearised about control values of mean arterial pressure and cardiac output so that it could be reformulated in terms of transfer functions. The resulting pressure to pressure open-loop transfer function H(s) consists of a complex conjugate pair of poles (pertaining to the resistance regulating system) and a real pole (pertaining to the arterial system, 1/(R₀ C), R₀=control resistance). Such a structure suggests an interaction between the resistance regulation and the arterial compliance (C). Quantitative evaluation of this interaction was obtained by estimating the model parameters during partial vena cava occlusions in four cats. Using these parameters the time response of the open-loop control system to a pressure step was found to be underdamped and oscillatory in all four cats (damping factor ξ ranged from 0·20 to 0·66), the amplitude of oscillations depending on the value of ξ and on the relative amplitude of the arterial time constant (compliance and peripheral resistance) with respect to the time constant 1/(ξω_n). Bode diagrams of H(jω) showed that the resonance peak due to the resistance regulating system may not be detectable, either because of the relatively high value of ξ or because it is masked by the pole of the arterial system.     

Effect of different types of resistance exercise on arterial compliance and calf blood flow

Low-intensity blood flow restricted (LI-BFR) resistance training has been shown to produce comparable increases in muscle hypertrophy to traditional high-intensity (HI) resistance training. However, a comparison of the acute vascular responses between the two types of exercise has not been made. The purpose of this study is to compare the acute vascular responses of HI, low-intensity (LI), and LI-BFR resistance exercise. Using a randomized, cross-over design, 11 young (28 ± 5 years) males completed three acute resistance exercise bouts (HI, LI and LI-BFR). Before (Pre), and starting at 15- and 45-min after each exercise bout, large (LAEI) and small (SAEI) artery compliance and calf blood flow were assessed. Calf blood flow was normalized per unit pressure as calf vascular conductance (CVC). Repeated measures (condition × time) ANOVA revealed a main time effect for LAEI and a main condition effect for SAEI. LAEI increased following exercise but returned to baseline at 45-min post. SAEI was greater during the HI condition compared to the LI or LI-BFR conditions. There was a significant condition × time interaction for CVC. CVC was elevated at 15- and 45-min post during the HI condition and at 15-min following the LI condition. CVC was not altered following the LI-BFR condition. These results suggest that HI, LI, and LI-BFR resistance exercise cause similar acute increases in large artery compliance but HI causes greater increases in small artery compliance and calf vascular conductance than LI or LI-BFR resistance exercise.     

Characteristics of the carotid baroreflex in man during normal and flow-restricted exercise

EIKEN, O., CONVERTINO, V. A., DOERR, D. F., DUDLEY, G. A., MORARIU, G. & Mekjavic; I. B. 1992. Characteristics of the carotid baroreflex in man during normal and flow-restricted exercise. Acta Physiol Scand 144 , 325–331. Received 27 May 1 991 , accepted 29 October 1991. ISSN 0001–6772. School of Kinesiology, Simon Fraser University, Burnaby, B.C., Canada. Eight subjects were studied in the supine position at rest, during normal dynamic leg exercise (control exercise) and with blood-flow restriction in the working legs (flow-restricted exercise). Graded muscle blood-flow restriction was accomplished by applying a supra-atmospheric pressure of 50 mmHg to the working legs. During incremental-load exercise, flow restriction reduced exercise performance and peak heart rate by 36% and 13%, respectively. The function of the cardiac branch of the carotid baroreflex was studied over its full operational range, at rest and during constant-load control and flow-restricted exercise, by measuring R-R intervals during application of pulse-synchronous graded pressures (40 to -65 mmHg) in a neck-chamber device. Heart rate and arterial pressure were higher during flow-restricted than control exercise, indicating that the flow restriction activated the muscle chemoreflex. Raising the carotid transmural pressure (systolic arterial pressure minus neck-chamber pressure) was accompanied by increasing R-R intervals in all conditions. The set point (point of baseline carotid transmural pressure and R-R interval) coincided with the midportion of the pressure-response curve at rest and with the threshold point of the curve during exercise. The maximal rate of change in relative R-R intervals and the corresponding carotid transmural pressure range were higher during control exercise than at rest and highest during flow-restricted exercise, indicating that exercise and especially flow-restricted exercise increased carotid baroflex sensitivity, and shifted the carotid baroreflex optimal buffering range to higher pressures. The results suggest that the carotid baroflex attenuates exercise heart rate increases mediated by the muscle chemoreflex and/or by central command.     

Characteristics of the carotid baroreflex in man during normal and flow-restricted exercise.

Eight subjects were studied in the supine position at rest, during normal dynamic leg exercise (control exercise) and with blood-flow restriction in the working legs (flow-restricted exercise). Graded muscle blood-flow restriction was accomplished by applying a supra-atmospheric pressure of 50 mmHg to the working legs. During incremental-load exercise, flow restriction reduced exercise performance and peak heart rate by 36% and 13%, respectively. The function of the cardiac branch of the carotid baroreflex was studied over its full operational range, at rest and during constant-load control and flow-restricted exercise, by measuring R-R intervals during application of pulse-synchronous graded pressures (40 to -65 mmHg) in a neck-chamber device. Heart rate and arterial pressure were higher during flow-restricted than control exercise, indicating that the flow restriction activated the muscle chemoreflex. Raising the carotid transmural pressure (systolic arterial pressure minus neck-chamber pressure) was accompanied by increasing R-R intervals in all conditions. The set point (point of baseline carotid transmural pressure and R-R interval) coincided with the midportion of the pressure-response curve at rest and with the threshold point of the curve during exercise. The maximal rate of change in relative R-R intervals and the corresponding carotid transmural pressure range were higher during control exercise than at rest and highest during flow-restricted exercise, indicating that exercise and especially flow-restricted exercise increased carotid baroflex sensitivity, and shifted the carotid baroreflex optimal buffering range to higher pressures. The results suggest that the carotid baroflex attenuates exercise heart rate increases mediated by the muscle chemoreflex and/or by central command.     

Effects of hemorrhage on vasopressin secretion and arterial blood pressure during experimental diabetes insipidus in goats

The effect of hypotensive hemorrhage on plasma vasopressin (AVP) concentration and carotid blood pressure before and after induction of experimental diabetes insipidus (DI) was studied in the conscious goat. Bleeding to the point of blood pressure fall (blood loss 15–25% of the estimated blood volume) caused an immediate, approximately hundred fold, increase in the plasma AVP concentration in the normal animal. Hemorrhage to the same extent during DI did not affect the plasma AVP levels. A rather transient hypotensive response to bleeding was seen before disruption of the pituitary stalk, but during DI the recovery of the hemorrhage-induced hypotension was less effective. However, the normalization of the blood pressure after bleeding was slightly more efficient during the permanent than during the temporary phase of DI. It is concluded that an intact hypothalamoneurohypophysial connection is necessary for the massive release of AVP normally seen in response to hypotensive hemorrhage. It is also confirmed that the lack of this hormonal response to bleeding is accompanied by an increased susceptibility to the hypotensive effect of hemorrhage.     

Cardiac and vasomotor components of the carotid baroreflex control of arterial blood pressure during isometric exercise in humans

We sought to examine the importance of the cardiac component of the carotid baroreflex (CBR) in control of blood pressure during isometric exercise. Nine subjects performed 4 min of ischaemic isometric calf exercise at 20% of maximum voluntary contraction. Trials were repeated with β₁-adrenergic blockade (metoprolol, 0.15 ± 0.003 mg kg⁻¹) or parasympathetic blockade (glycopyrrolate, 13.6 ± 1.5 μg kg⁻¹). CBR function was determined using rapid pulses of neck pressure and neck suction from +40 to −80 mmHg, while heart rate (HR), mean arterial pressure (MAP) and changes in stroke volume (SV, Modelflow method) were measured. Metoprolol decreased and glycopyrrolate increased HR and cardiac output both at rest and during exercise ( P < 0.05), while resting and exercising blood pressure were unchanged. Glycopyrrolate reduced the maximal gain ( G _max) of the CBR-HR function curve (−0.58 ± 0.10 to −0.06 ± 0.01 beats min⁻¹ mmHg⁻¹, P < 0.05), but had no effect on the G _max of the CBR-MAP function curve. During isometric exercise the CBR-HR curve was shifted upward and rightward in the metoprolol and no drug conditions, while the control of HR was significantly attenuated with glycopyrrolate ( P < 0.05). Regardless of drug administration isometric exercise produced an upward and rightward resetting of the CBR control of MAP with no change in G _max. Thus, despite marked reductions in CBR control of HR following parasympathetic blockade, CBR control of blood pressure was well maintained. These data suggest that alterations in vasomotor tone are the primary mechanism by which the CBR modulates blood pressure during low intensity isometric exercise.     

The effect of resistance training on blood pressure in normotensive women

The purpose of the present study was to determine whether conventional resistance training alters 24-h ambulatory and manually determined casual blood pressure of normotensive women. Seven individuals (23 +/- 2 years old) trained 2 days week-1 for 20 weeks emphasizing the hip and knee extensor muscle groups. Three sets to exhaustion of the knee extension, squat, knee flexion and leg press exercises were performed. The load for each exercise represented approximately 80-85% of the one-repetition maximum. Average values for 24-h ambulatory blood pressure were not different (P greater than 0.05) pre- and post-training (systolic, 107 +/- 4 vs. 109 +/- 1 mmHg; diastolic, 73 +/- 2 vs. 71 +/- 2 mmHg). Ambulatory values over 8-h segments of the 24 h (day, evening, night) and casual resting determinations of blood pressure were also not affected. The lack of change in blood pressure cannot be explained by an insufficient training response. Knee extensor strength during dynamic or isokinetic actions increased (approximately 43%, P less than 0.05). In addition, biopsies from the vastus lateralis muscle showed an increase (P less than 0.05) in average muscle fibre cross-sectional area of 32%. This hypertrophic response was further substantiated by an increase (P less than 0.05) in lean body mass (41.2 +/- 1.3 kg to 43.4 +/- 1.5 kg). These results indicate that resistance training, which increases muscular strength, muscle fibre area and lean body mass, does not alter ambulatory or casual blood pressure. Thus, the concern that conventional resistance training may chronically elevate blood pressure does not appear warranted, at least in normotensive women.     

Effects of high-intensity interval training on pulmonary function

To determine whether high-intensity interval training (HIT) would increase respiratory muscle strength and expiratory flow rates more than endurance training (ET), 15 physically active, healthy subjects (untrained) were randomly assigned to an ET group (n = 7) or a HIT group (n = 8). All subjects performed an incremental test to exhaustion (VO2max) on a cycle ergometer before and after training. Standard pulmonary function tests, maximum inspiratory pressure (PImax), maximum expiratory pressure (PEmax), and maximal flow volume loops were performed pre training and after each week of training. HIT subjects performed a 4-week training program, 3 days a week, on a cycle ergometer at 90% of their VO2max final workload, while the ET subjects performed exercise at 60-70% VO2max. The HIT group performed five 1-min bouts with 3-min recovery periods and the ET group cycled for 45 min continuously. A five-mile time trial (TT) was performed prior to, after 2 weeks, and after completion of training. Both groups showed improvements (P < 0.05) in VO2max (~8-10%) and TT (HIT 6.5 ± 1.3%, ET 4.4 ± 1.8%) following training with no difference (P > 0.05) between groups. Both groups increased (P < 0.05) PImax post training (ET ~ 25%, HIT ~ 43%) with values significantly higher for HIT than ET. There was no change (P > 0.05) in expiratory flow rates with training in either group. These data suggest that both whole-body exercise training and HIT are effective in increasing inspiratory muscle strength with HIT offering a time-efficient alternative to ET in improving aerobic capacity and performance.     

Endurance training regimen based upon arterial blood lactate: Effects on anaerobic threshold

Summary The purpose of this investigation was to assess the effect of endurance training based upon the intensity as determined by the arterial blood lactate concentration (LA). Seven healthy male college students performed endurance training on a Monark bicycle ergometer for 15 min on 3 days/week for 8 weeks, at an intensity corresponding to 4 mmol·l⁻¹ arterial blood LA determined during an incremental exercise test (25 watts increment every minute on a bicycle at 50 rpm). Another six male students served as the control group. To assess the training effect, both an incremental exercise test and a submaximal exercise test were performed before and after the endurance training. In the incremental exercise test, at , anaerobic threshold (AT), and the onset of respiratory compensation for metabolic acidosis (RCMA) were measured. AT was determined as the point at which arterial LA rose above the resting value, and RCMA was determined as the point at which Paco₂ decreased during the incremental exercise test. After training, AT increased significantly (37% increment expressed in ,p<0.05). There was a significant increase (p<0.05) in RCMA (17%) and (14%). This training decreased (4%), (15%), heart rate (10%), respiratory exchange ratio (5%), and LA (23%) significantly (p<0.05) during the submaximal exercise test after training. On the other hand, there were no significant changes in the control group through the period when the training group performed their training. These results showed that the endurance training intensity corresponding to 4 mmol·l₋₁ arterial blood LA was effective for the improvement in AT as well as . It is suggested that the present training regimen could delay the onset of anaerobic glycolysis, thus shifting AT to the higher workload and decreasing LA at a given submaximal exercise after training.     

Effects of rhythmic muscle compression on arterial blood pressure at rest and during dynamic exercise in humans

This study was designed to examine the hypothesis that a rhythmic mechanical compression of muscles would affect systemic blood pressure regulation at rest and during dynamic exercise in humans. We measured the changes in mean arterial pressure (MAP) occurring (a) at rest with pulsed (350 ms pulses at 50 pulses min^–1) or static compression (50 and 100 mmHg) of leg muscles with or without upper thigh occlusion, and (b) during 12‐min supine bicycle exercise (75 W, 50 r.p.m.) with or without pulsed compression (50, 100, 150 mmHg) of the legs in synchrony with the thigh extensor muscle contraction. At rest with thigh occlusion, MAP increased by 4–8 mmHg during static leg compression, and by 5–9 mmHg during pulsed leg compression. This suggests that at rest pulsed leg compression elicits a reflex pressor response of similar magnitude to that evoked by static compression. During dynamic exercise without leg compression, MAP (having risen initially) gradually declined, but imposition of graded pulsed leg compression prevented this decline, the MAP values being significantly higher than those recorded without pulsed leg compression by 7–10 mmHg. These results suggest that the rhythmic increase in intramuscular pressure that occurs during dynamic exercise evokes a pressor response in humans.     

Effect of multiple set on intramuscular metabolic stress during low-intensity resistance exercise with blood flow restriction

Our previous study reported that intramuscular metabolic stress during low-intensity resistance exercise was significantly enhanced by combining blood flow restriction (BFR); however, they did not reach the levels achieved during high-intensity resistance exercise. That study was performed using a single set of exercise; however, usual resistance exercise consists of multiple sets with rest intervals. Therefore, we investigated the intramuscular metabolic stress during multiple-set BFR exercises, and compared the results with those during multiple-set high-intensity resistance exercise. Twelve healthy young subjects performed 3 sets of 1-min unilateral plantar flexion (30 repetitions) with 1-min intervals under 4 different conditions: low intensity (L, 20 % 1 RM) and high intensity (H, 65 % 1 RM) without BFR, and L with intermittent BFR (IBFR, only during exercise) and with continuous BFR (CBFR, during rest intervals as well as exercise). Intramuscular metabolic stress, defined as intramuscular metabolites and pH, and muscle fiber recruitment were evaluated by ³¹P-magnetic resonance spectroscopy. The changes of intramuscular metabolites and pH during IBFR were significantly greater than those in L but significantly lower than those in H. By contrast, those changes in CBFR were similar to those in H. Moreover, the fast-twitch fiber recruitment, evaluating by a splitting Pi peak, showed a similar level to H. In conclusion, the multiple sets of low-intensity resistance exercise with continuous BFR could achieve with the same metabolic stress as multiple sets of high-intensity resistance exercise.     

Contribution of systemic arterial compliance and systemic vascular resistance to effective arterial elastance changes during exercise in humans

Background: Effective arterial elastance (Ea), an index of arterial load, increases with elevations in left ventricular elastance to maximize the efficiency of left ventricular stroke work during exercise. Systemic arterial compliance (C) and vascular resistance (R) are the primary components contributing to Ea, and R plays a greater role in determining Ea at rest. We hypothesized that the contribution of C to Ea increases during exercise to maintain an optimal balance between arterial load and ventricular elastance, and that the increase in Ea is due primarily to a reduction in C. Aim: The aim of this study was to investigate the contributions of C and R to Ea during exercise. Methods: Ea (0.9 × systolic blood pressure/stroke volume), C (stroke volume/pulse pressure), R (mean blood pressure/cardiac output), and cardiac cycle length (T) were measured at rest and during exercise of 40%, 60% and 80% maximal oxygen uptake (O_2max) using Doppler echocardiography in 45 healthy men. Results: Ea did not differ between rest and 40%O_2max, but it was greater at 60% and 80%O_2max. C markedly decreased during exercise in an exercise intensity‐dependent manner. The changes in R/T during exercise were small, whereas it decreased at 40%O_2max and gradually increased at 60% and 80%O_2max. Conclusions: The present results suggest that the contribution of systemic arterial compliance to effective arterial elastance increases during exercise. Therefore, we propose that the increase in arterial load during exercise is mainly driven by a reduction in systemic arterial compliance.