The principle of progressive overload in resistance training states that exercise intensity must exceed normal levels of bodily stress to produce a training effect (2). Overload is most often achieved through dynamic resistance exercise with high resistance (≥70% of maximum strength) and results in improved muscular strength and hypertrophy (11). Low-load (LL) resistance exercise at ≤30% of maximum strength exercise coupled with a blood flow restriction (LLBFR) has been shown to create a state of overload and is an effective modality to increase muscle strength and cross-sectional area (18).
Performing resistance exercise to volitional failure (an inability to maintain the rate of contraction or an inability to maintain full range of motion) increases motor unit activation, recruitment, and synchronization (26,33) and results in strength gains (9). Immediately after resistance exercise to volitional failure, reductions in maximal voluntary force production and fatigue are evident (10). This decline in force can be attributed to central factors related to the brain and/or spinal cord and peripheral factors related to the muscle or peripheral nervous system. For example, central contributions to fatigue include altered motor neuron firing rate, decreased neurotransmitter activity, impaired excitability at the cortex, and inhibition of spinal excitability by afferent feedback (10). Peripheral contributors to muscle fatigue include local acidosis, damage to individual muscle fibers, impaired excitation–contraction coupling, and depleted ATP/PCr availability (5,28).
During acute bouts of dynamic high-load (HL) resistance exercise, muscle activation measured via EMG amplitude increases as individuals approach volitional failure, indicating greater motor unit recruitment and firing rate (26). When acute bouts of LLBFR resistance exercise are performed to volitional failure and compared with HL resistance exercise, similar (36) or lower levels (22) of muscle activation are evident after LLBFR exercise. EMG amplitude during LLBFR exercise has consistently been shown to be greater than that achieved during load- and volume-matched nonrestricted resistance exercise (16,36). Another way to quantify the extent of motor unit activation is by the interpolated twitch technique (3). Karabulut et al. (16) demonstrated that the ability to centrally activate the knee extensors after a bout of LLBFR resistance exercise decreases significantly more than after a bout of load- and volume-matched resistance exercise without a blood flow restriction. Altogether, the increasing motor unit activation followed by subsequent central activation failure implicates central factors as contributors to muscle fatigue. It is unclear if LLBFR and HL resistance exercise result in similar levels of muscle activation, and the roles of central and peripheral factors in muscle fatigue resulting from HL and LLBFR exercise are unknown.
Although many studies comparing LLBFR resistance exercise to nonrestricted exercise have used the approach that matched the volume of exercise, one must consider that the degree of effort put forth by the subjects was not controlled. Subjects experience greater muscle fatigue (16,38) and muscle soreness (38) after performing LLBFR resistance exercise compared with load- and volume-matched conditions, yet when the participants go to volitional failure, they report equal levels of pain (41). Prescribing resistance exercise to volitional failure would allow for the direct comparison of LLBFR, LL, and HL resistance exercise at maximum efforts and varying volumes. It seems likely that regardless of the exercise load, when individuals perform acute bouts of resistance exercise to volitional failure, there is sufficient muscular overload to increase the amplitude of muscle activation, reduce central activation, cause contractile dysfunction and result in decrements in maximal voluntary force production. Over time, this could lead to positive neuromuscular and hypertrophic adaptations. If HL, LLBFR, or LL resistance exercise is performed to volitional failure, it is plausible that any of these training regimens could be effective. Therefore, the purpose of this study was to compare endurance, torque decrement, central activation, muscle activation, and evoked contractile function after acute bouts of LL, HL, and LLBFR resistance exercise to volitional failure. It was hypothesized that 1) endurance, measured by repetitions to volitional failure, would be greatest during the LL condition, 2) peak isometric torque would decrease similarly after the three exercise conditions, 3) central and peripheral factors would contribute to the torque decrements, and 4) EMG amplitude would increase from the beginning to the end of the resistance exercises but would always remain higher in the HL condition.
A within-subjects experimental design was used to investigate the neuromuscular effects of acute bouts of HL, LL, and LLBFR dynamic knee extension exercise. Participants first underwent a familiarization session in which isometric and dynamic peak torque were assessed. During this session, they became familiar with the exercise protocol and the blood flow restriction cuff that was used in the LLBFR condition. All subjects then completed the exercise conditions in a randomized order on visits separated by approximately 1 wk. During the sessions, the subjects performed three sets of unilateral dynamic knee extensions on the right leg to volitional task failure with 30 s of rest between sets. Exercise volume, decrement in peak isometric torque, Borg ratings of perceived exertion, heart rate, central activation, contractile function (rate of torque development and rate of half relaxation), and surface root mean square (RMS) EMG of the superficial quadriceps were measured during each condition.
Eight recreationally active males who have not been engaged in resistance training of the legs in the past 6 months (aged 22 ± 2 yr; height, 177.6 ± 3.9 cm; mass, 71.8 ± 17.4 kg) were recruited from the University of New Hampshire and the surrounding community. Sample size for the present study was powered (>0.80) to detect significant decreases in isometric force immediately after HL and LLBFR fatigue protocols at a P < 0.05 level based on a previous study (7). Subjects provided their written informed consent, and the study was approved by the University of New Hampshire Institutional Review Board. Participants also completed a health history questionnaire. Individuals with cardiovascular disease, neurological or neuromuscular disorders, and musculoskeletal abnormalities or injuries of the legs were excluded from the study.
Peak dynamic and isometric knee extensor torque of the right leg was assessed during the familiarization session and was used to set the exercise load for subsequent visits. To determine peak torque, participants were seated at an 85° hip angle on a constant resistance HUMAC Norm dynamometer (CSMI, Stoughton, MA) linked to a BIOPAC MP150 data acquisition system (BIOPAC Systems Inc., Goleta, CA). A seat belt was secured over the torso to prevent hip joint movement. Participants completed a warm-up of 10 dynamic knee extensions at a very light load. To assess peak dynamic torque, single attempts at progressively higher torques were performed, and participants rested approximately 1–2 min between loads. The highest torque achieved for only one repetition through a full range of motion (70°–180°) was recorded as the dynamic peak torque. Peak torque was typically obtained within four to six attempts, and this method has a reliability intraclass correlation 0.98, as previously determined in our laboratory.
Isometric torque testing was assessed at the familiarization session and before each exercise condition. The knee joint angle was set at 60° from extension, and the ankle and thigh were strapped to minimize movement. Subjects pushed as hard as possible against an immovable pad attached to a force transducer for 4–5 s. Three to five maximum contractions were performed until two consecutive trials were less than 5% different, and the highest isometric torque achieved was recorded. Participants rested approximately 1–2 min between attempts. Verbal encouragement was provided to the subjects during all voluntary contractions. The measurement of peak isometric torque has a reliability intraclass correlation of 0.95, as previously determined in our laboratory.
Evoked torque was elicited by transcutaneous stimulation of the femoral nerve using a cathode in the inguinal triangle (Ag–AgCl, 36-mm diameter, Kendall MediTrace 200 [Kendall-LTP, Chicopee, MA]) and an anode placed on the skin over the greater trochanter (Ag–AgCl, 48-mm diameter, Kendall MediTrace 530). The optimum site for stimulation was located by delivering a series of single, submaximal stimuli via a hand-held stimulation probe while the subject was supine. Each stimulus consisted of a 1-ms rectangular pulse with 400-V maximal voltage (Digitimer constant current stimulator model DS7AH coupled with the train/delay generator, Hertfordshire, UK). Once the optimal site for stimulation was determined, the area was shaved, abraded with sandpaper, and cleaned with isopropyl alcohol to reduce impedance. The subject was seated in the dynamometer with a knee angle fixed at 60° from extension. Stimuli were then progressively intensified until peak isometric twitch torque was obtained. Supramaximal stimulation was achieved by increasing the stimulus intensity 10% beyond that required to elicit peak twitch torque. Doublet (interpulse duration was 6 ms) frequencies were obtained, and postactivation potentiated doublet torque was measured approximately 2 s after the cessation of a maximal isometric contraction.
Voluntary activation of the knee extensors was assessed using the interpolated twitch technique. Subjects performed a 4- to 5-s maximum voluntary isometric contraction. During that time, a supramaximal doublet was delivered to the femoral nerve. The increase in torque after the doublet was expressed relative to a postactivation potentiated doublet obtained 1–2 s after the voluntary isometric contraction and expressed as follows:
To identify changes in the functional properties of the knee extensors, the torque–time curve obtained from the postactivation potentiated doublet was evaluated. Peak-evoked torque was assessed, and the absolute time-to-peak torque (TPT) from 10% to 90% of peak torque was measured. Relative rate of torque development (+dF/dt) from 10% to 90% of peak torque was calculated by normalizing the absolute TPT to the post-activation potentiation torque. The absolute time to 1/2 relaxation (1/2 RT) and the relative rate of torque relaxation (−dF/dt) from 90% to 50% of peak torque were also calculated.
Surface EMG signals were collected from the vastus lateralis, vastus medialis, and rectus femoris muscles using preamplified electrodes with a gain of 300 times and band-pass filtered between 12 and 3200 Hz (B&L Engineering, Santa Ana, CA). A reference electrode was placed at the patella. Before electrode placement, the skin was shaved, abraded, and cleaned with isopropyl alcohol to minimize skin impedance. Anatomical locations were recorded by measuring from the superficial aspect of the patella to the center of the electrode. All electrodes were taped down, and the upper leg was wrapped with an elastic bandage to prevent movement of the electrodes. Using the BIOPAC MP150 data acquisition system, the signal was amplified 1000 times, band-pass filtered between 10 and 500 Hz, and sampled at a frequency of 1000 Hz. The interference EMG signals recorded during the peak isometric torque trials were analyzed in 1024-sample epochs (approximately 1.02 s) centered about the peak torque. The amplitude of the surface EMG signals was quantified by calculating the RMS EMG of the vastus lateralis, vastus medialis, and rectus femoris. During the dynamic exercise conditions, RMS EMG was analyzed on the concentric portion of each repetition at peak torque for a 1024-sample epoch preceding and including full knee extension. The first five repetitions in the first set and the last five repetitions of the third set were considered during analysis, and the average RMS EMG from the first five and last five repetitions during the entire exercise session was expressed as a percentage of RMS EMG at peak isometric torque as assessed before the exercise condition.
Before each protocol, subjects performed a brief warm-up of 10–15 repetitions at a light load. Isometric peak torque was measured and central activation was assessed. The loads used in each condition were as follows: HL = 70% of peak dynamic torque; LL = 20% of peak dynamic torque, and LLBFR = 20% of peak dynamic torque. Exercise during the LLBFR condition was coupled with a 5-cm-wide blood flow restriction cuff (Kaatsu Master Mini, Sato Sports Plaza, Tokyo, Japan) placed around the proximal portion of the thigh at an initial pressure of 30–40 mm Hg and inflated to approximately 180 mm Hg immediately before exercise. The cuff remained inflated for the duration of the exercise, including the rest periods. A restriction pressure of about 1.3–1.5 times systolic pressure is commonly used in blood flow–restricted resistance exercise studies (7,22,23,35,38).
In each exercise condition, the subjects completed three sets of unilateral, dynamic knee extensions on a constant load dynamometer to volitional failure with 30 s of rest between sets. Subjects performed the contractions to a metronome set at a cadence of 2 s for the concentric portion of the movement and 2 s for the eccentric portion (15 repetitions per min). Subjects were verbally encouraged throughout each protocol and were instructed to continue exercise until they could not maintain the pace of the contractions or obvious decrements in range of motion were observed for more than two consecutive contractions. During the LLBFR condition, the cuff was inflated before the start of exercise and remained inflated for the duration of the exercise protocol, including rest periods. It was released at the completion of the exercise before any follow-up measurements. Within 30 s of completing each exercise condition, maximum isometric torque was assessed during a 5-s contraction with a doublet superimposed on the contraction followed by another doublet stimulus approximately 2 s after relaxation (postactivation potentiated doublet). Heart rate was measured using a Polar FS1 heart rate monitor (Polar Electro Inc., Kempele, Finland) and was recorded at the beginning and the end of each set of knee extensions. Before the start of exercise, participants were told to rate their overall perceived level of exertion with respect to muscular fatigue at the working limb from 6 to 20 according to the Borg ratings of perceived exertion scale where 6 corresponds to very, very light and 20 corresponds to maximum effort (4). Participants rated their perceived exertion immediately upon completion of the exercise. To track the postexercise recovery in strength, one isometric contraction was performed at 2, 3, 4, and 5 min postexercise and peak torque was recorded. Exercise volume was calculated as the product of the exercise load and the total number of repetitions completed over all three sets. Time-to-task failure was calculated based on repetitions performed and lifting cadence. Angular impulse, which is the area under the torque–time curve, was assessed as a total amount of muscular work performed. This measurement accounts for the amount of torque produced and the time the muscle was under tension.
A within-subjects repeated-measures ANOVA was used to determine significant differences (P < 0.05) in all dependent variables between conditions (HL, LL, and LLBFR) with respect to time (pre- and postexercise). If the assumptions of ANOVA were violated, the Greenhouse–Geisser correction factor was applied. Significant interactions and main effects were followed with appropriate post hoc analyses with Bonferroni adjustments, and partial eta squared (ηp2) values were reported. A Friedman two-way ANOVA by rank test was performed on the ratings of perceived exertion between the conditions followed by the Wilcoxon signed rank test with Bonferroni adjustments. Statistics were computed using PASW Statistics Version 18.0 (SPSS, Chicago, IL). Data are presented as means ± SD unless otherwise noted.
The average peak dynamic torque of the sample was 179 ± 31 N·m. The exercise load in the HL condition was 125 ± N·m, and the LL and LLBFR conditions used a load of 36 ± 6 N·m. Subjects performed significantly more repetitions in the LL and LLBFR conditions than the HL condition (P = 0.01, ηp2 = 0.48), and as a result, it took longer to reach task failure (P < 0.01). There was not a significant difference in exercise volume (P = 0.07, ηp2 = 0.27) or angular impulse between conditions (P = 0.13, ηp2 = 0.26, Table 1). Peak isometric torque was similar before the performance of exercise among all conditions (HL, 289.9 ± 36.1 N·m; LL, 286.7 ± 58.8 N·m; LLBFR, 267.3 ± 41.6 N·m; P = 0.61, ηp2 = 0.26). Immediately after the exercise protocols, there was a significant time main effect because isometric peak torque declined an average of 37% in the three conditions (P < 0.01, ηp2 = 0.94) (Fig. 1). There was not a significant condition main effect that indicated the reductions in peak torque were similar among the conditions (P = 0.35, ηp2 = 0.14). Peak isometric torque remained depressed at 5 min after exercise in all conditions.
Central activation values were similar before each exercise condition because subjects had an overall mean of 92.7% ± 5.1% (P = 0.1, ηp2 = 0.02). Central activation showed nonsignificant changes of +3.8%, −6.1%, and −3.6% in the HL, LL, and LLBFR conditions, respectively (P = 0.1, ηp2 = 0.34).
Table 2 displays the results of the contractile activity after the evoked postactivation potentiated doublet torque. There was not a time × condition interaction for postactivation potentiated doublet torque (P = 0.32, ηp2 = 0.18), but there was a significant main effect of time (P = 0.004, ηp2 = 0.78) as torque declined an average of 40% after exercise. The decrement was similar between conditions (P = 0.26, ηp2 = 0.18). Only a time main effect was observed for +dPt/dt because it declined an average of 26% after the exercise conditions (P = 0.003, ηp2 = 0.63). This decrement was similar between conditions (P = 0.27, ηp2 = 0.21). There was a significant time × condition interaction for −dPt/dt (P = 0.002, ηp2 = 0.59), and further analysis revealed a significant 48% decline in the HL condition only (P = 0.006). A time × condition interaction was also evident in absolute 1/2 RT (P = 0.004, ηp2 = 0.55), and post hoc analysis indicated a 40% decrease in 1/2 RT after the LLBFR condition only.
There was not a significant time × condition × muscle interaction for RMS EMG amplitude (P = 0.24, ηp2 = 0.12), but there was a significant main effect of condition (P < 0.01, ηp2 = 0.90) and time (P = 0.02, ηp2 = 0.67). All exercise conditions yielded an overall increase of 19% in RMS EMG activity of the vastus lateralis, vastus medialis, and rectus femoris during exercise (Fig. 2). The condition main effect indicated that HL exercise consistently had higher muscle activity than LL (P = 0.02) and LLBFR (P = 0.04) before and after the exercise in all three muscles (Fig. 2).
There was a significant time main effect of heart rate (P < 0.01, ηp2 = 0.65). The average heart rate of all conditions at preexercise was 78 ± 10 beats·min−1 and was 116 ± 22 beats·min−1 at the cessation of exercise. At the completion of exercise, the ratings of perceived exertion (presented as median (range)) was 18.5 (16–20), 19.5 (16–20), and 19.5 (17–20) (P = 0.046). Post hoc analyses did not reveal significant differences between the conditions (P > 0.05).
Acute bouts of HL, LLBFR, and LL exercise to volitional failure resulted in similar amounts of muscle fatigue as demonstrated by significant torque decrements after each bout of exercise. The volume of exercise and angular impulse tended to be highest in the LL exercise but was not statistically different between conditions. In accordance with our hypothesis, muscle activation increased throughout all three exercise conditions, and the highest levels of activation were evident in HL exercise. Contrary to our hypothesis, peripheral, but not central factors, contributed to the decrements in torque after the various exercise conditions.
The loss of approximately 30% isometric muscle strength immediately after HL and LLBFR resistance exercise to volitional failure is similar to a previous study (7). Despite analogous torque decrements among the three exercise conditions, neuromuscular differences were evident. Throughout the bout of HL exercise, subjects exhibited higher RMS EMG amplitudes in the quadriceps femoris than during LL and LLBFR exercise. Moreover, at the end of the LL and LLBFR exercise protocols, the average RMS EMG levels were still less than the amplitudes achieved during the HL condition at the beginning of the exercise. Our data support the reports of Manini and Clark (22) that higher muscle activation levels are apparent during HL exercise compared with LLBFR exercise. Higher RMS EMG amplitudes during HL exercise indicate greater motor unit recruitment, firing rate, and/or synchronization throughout the exercise (34). Assuming the size principle is upheld (2,14), this would suggest a greater absolute amount of Type II muscle fiber activation compared with the LLBFR and LL conditions. The number of active muscle fibers and the propensity of Type II fibers to undergo hypertrophy (17) could be a major factor in the magnitude of potential muscle strength and hypertrophic gains during HL exercise. However, short-term LLBFR resistance training (18,36) and LL resistance training (24) have yielded similar muscular hypertrophy and strength gains as HL training, suggesting that transcription factors, local growth factors, and satellite cells may be additional mechanisms of hypertrophy (21) that need to be further investigated.
The finding that muscle activity increases similarly during LL and LLBFR exercise to volitional failure agrees with Wernbom et al. (41), but the magnitude of this increase is discrepant because our data indicate lower levels of muscle activation occur during all exercise conditions. This could be related to methodological differences between the studies. In the present study, RMS EMG was measured at peak torque during the first five and last five contractions on a constant resistance dynamometer. It has been shown that on constant resistance dynamometers, more muscle activation may be required at more acute knee angles and not necessarily where torque is the greatest (12). Therefore, it is possible that higher levels of muscle activation occurred in our study but were not evident through our analyses. Furthermore, the study performed by Wernbom et al. (41) implemented a wider (13.5 cm) cuff and lower blood flow restriction pressure (100 mm Hg) than the present study (5 cm and 180 mm Hg, respectively). The application of a wider cuff transmits the pressure to soft tissue differently than a narrow cuff (20) and could affect muscle activation if the cuff covers a portion of the exercising muscles. Nevertheless, the present study and the study by Wernbom et al. (41) indicate that when LL or LLBFR resistance exercise is performed to volitional failure, there is an increase in muscle activation. Although there are studies that have reported higher levels of muscle activity during LLBFR exercise when compared with LL exercise (16,36), it must be considered that the exercise was volume matched. In one such study (16), the researchers reported increases in EMG amplitude during LL and LLBFR exercise conditions and then observed decrements in muscle activation upon completion of the LLBFR exercise only and attributed this to an inhibition of central drive to motor units.
In the present study, the lack of change in central activation and the increase in RMS EMG amplitude throughout the HL, LL, and LLBFR resistance exercise suggest that central factors do not have a predominant role in the neuromuscular fatigue. The activation of the knee extensors in our sample was high but incomplete (>92%) during maximum contractions before the fatigue protocol. The high percentage of Type II muscle fibers within the quadriceps femoris has high recruitment thresholds, which could make it difficult to fully activate those muscles (3), especially in individuals who do not regularly engage in resistance exercise (1,40). Our data showed nonsignificant changes in central activation after each exercise protocol. This disagrees with the study by Karabulut et al. (16) that demonstrated a 13% reduction in central activation and decreased EMG amplitude at the end of a bout of LLBFR resistance exercise on the knee extensors. The subjects in that study were classified as untrained, yet they had lower central activation values than the participants in the present study. Greater decrements in central activation after a fatiguing bout of resistance exercise have been observed in untrained individuals when compared with trained individuals (13). Although the subjects in our study were not resistance trained, they were not sedentary and did engage in other forms of physical activity such as cycling and jogging. Although impossible to determine, differences in physical activity levels could contribute to the discrepant findings.
The depressed evoked torque and the slowed relative rates of torque development imply that peripheral factors were apparent in the neuromuscular fatigue observed after HL, LL, and LLBFR resistance exercise. The evoked torque from the postactivation potentiated doublet torque declined approximately 40% after the three conditions and suggests that there may be a failure in excitation contraction coupling and/or impairments in the contractile process leading to a reduced number of active cross-bridges (31). Although not able to be determined from our measurements, the depressed torque could be the result of dysfunction in the phosphorylation of myosin regulatory chains, making them less sensitive to the calcium released from the sarcoplasmic reticulum (29). In addition, there were alterations in the rates of torque development and relaxation after the exercise conditions. The rate of torque development and relaxation can be influenced by the amplitude of evoked torque (37), and therefore, the data were also analyzed when normalized to the postactivation potentiated doublet torque. A slowing in the relative rate of torque development, +dPt/dt, was evident after the three conditions, possibly suggesting there was a disruption in calcium kinetics related to the amount and rate of release of calcium from the sarcoplasmic reticulum (19). A slowing in the relative rate of relaxation, −dPt/dt, was evident only in the HL condition, possibly indicating that at higher loads, the additional recruitment of Type II fibers magnify the alterations in excitation–contraction coupling and contractile speed (39).
The present study tracked strength recovery for 5 min postexercise, and during that time, knee extensor isometric torque after all three conditions returned to approximately 80% of peak isometric torque. Raastad and Hallen (27) noted losses in knee extension strength after bouts of moderate and high-intensity squats and tracked the recovery of muscle strength for 36 h after the exercise. They found that after the moderate intensity exercise, muscle strength recovered within 11 h after exercise, whereas it took more than 1 d to recover after high-intensity exercise (27). Reduced creatine phosphate concentration and increased inorganic phosphate and hydrogen ions are possible metabolic causes of fatigue (42). Suga et al. (32) observed these metabolic changes after 2-min bouts of HL, LL, and LLBFR plantarflexion exercise and found that HL resistance exercise led to greater reductions in creatine phosphate and pH and larger increases in inorganic phosphate when compared with LLBFR and LL resistance exercise, thus insinuating that LLBFR exercise was not as strenuous as HL exercise. Despite that, these metabolic factors have been shown to almost fully recover to preexercise values within 5 min after the completion of exhausting resistance exercise (30). The inability to recover muscle strength after the HL, LL, and LLBFR resistance exercise in our study further implies that peripheral fatigue was evident and impairments in excitation–contraction coupling likely occurred. Prolonged contractile dysfunction and muscle weakness could be related to muscle damage and inflammation (27). Tracking the time course of neuromuscular recovery and muscle damage after LLBFR could provide valuable information regarding adaptation and exercise prescription.
Based on the results of the present study, when HL, LLBFR, and LL resistance exercise are performed to volitional failure, similar torque decrements are evident. However, the duration of exercise to volitional failure in the LL and LLBFR conditions was approximately three to five times longer than that of HL exercise. It has been reported that for loads lighter than 75% of maximum strength, there are large differences in the number of repetitions that subjects can complete and that weaker individuals tend to perform more repetitions (8). This variability in LLBFR conditions was also noted in a previous study (7). From a practical standpoint, if individuals engage in these LL high-volume protocols, the greater time commitment for exercising one muscle group must be considered. It must be recognized that LLBFR resistance training studies have demonstrated muscular improvements without the participants’ resistance training to muscular failure (15,18,25) . If HL exercise is unavailable or contraindicated, in such situations as microgravity, injury, or postsurgery, LLBFR resistance exercise has been shown to maintain or improve muscle strength and cross-sectional area (6,25).
After completing each set of knee extension exercise to volitional failure, subjects rated a slightly lower, nonsignificant perceived exertion (approximately 17–18) after the HL condition. The ratings of perceived exertion in the LL and LLBFR conditions (approximately 18–19) are consistent with those found by Wernbom et al. (41). After the three conditions of exercise, the high ratings of perceived exertion, the similar heart rate values observed at exercise completion, and the equivalent changes in postexercise isometric torque suggest that HL, LL, and LLBFR resistance exercise are of comparable intensity when performed at maximum effort and to volitional failure. The low levels of muscle activation and alterations in neuromuscular function after LL and LLBFR resistance exercise imply that there are differences among HL, LL, and LLBFR resistance exercise that over time could result in diverse neuromuscular adaptations.
A limitation to our study and other LLBFR resistance exercise studies is the regulation of the blood flow restriction. Pressures typically range from 160 to 180 mm Hg (1.3 to 1.5 times systolic blood pressure), and this caused 70% attenuation in femoral artery blood flow in a previous study (35). It has recently been suggested that cuff pressures be based on thigh circumference rather than systolic blood pressure (20). Therefore, blood flow and thigh circumference were not measured in our study, and the degree of blood flow restriction was not controlled. Future studies should be used to develop guidelines for pressures based on thigh circumference.
In conclusion, HL, LL, and LLBFR knee extension exercise performed to volitional failure resulted in similar torque decrements despite the LL and LLBFR conditions requiring a higher volume of exercise and having lower levels of muscle activation. The muscular fatigue that ensued after HL, LL, and LLBFR resistance exercise was primarily attributed to peripheral factors because central activation levels were unchanged and postactivation potentiated double torque and relative rate of torque development were depressed. HL resistance exercise also resulted in a slower relative rate of relaxation. Further evaluation of the neuromuscular responses and recovery after chronic LLBFR resistance training could provide valuable insight into the neuromuscular adaptations and aid in the development of appropriate LLBFR resistance exercise prescriptions.
Funding for the present study was provided by the University of New Hampshire, Durham, NH.
The authors report no conflicts of interest.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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