This study investigated the effects of frequent low-load ischemic resistance exercise performed to failure on quadriceps size and performance, muscle activation, oxygen kinetics and cardiovascular responses. Ten healthy males performed knee-extension exercise for 4 weeks (4 sessions/week) at 15% maximal voluntary muscle contraction (MVC). One leg was trained with free blood flow (C-leg) while in the other leg (I-leg) ischemia was induced by an inflatable cuff (≥230 mmHg). Quadriceps cross-sectional area (CSA) of the I-leg increased by 3.4% (P<0.05). A tendency for smaller increase in muscle CSAs at the cuff level was observed. MVC force did not change in either leg, whereas the number of repetitions during exercise test to failure increased (P<0.01) by 63% in I-leg and 36% in C-leg. The decrease in muscle oxygenated hemoglobin concentration acquired by NIRS was attenuated (P<0.01) by 56% in I-leg and 21% in C-leg. Electromyographic amplitude of rectus femoris in I-leg was ∼45% lower (P<0.025) during the ischemic test. Also, ∼9% increase (P<0.05) in pre-exercise diastolic pressure was observed. In conclusion, substantial gains in muscle endurance capacity were induced, which were associated with enhanced muscle oxygen delivery. The potential negative effects of ischemic exercise with high cuff pressure on muscle and nerve and on arterial pressure regulation need further investigation.
Surgical ACL reconstruction performed with a tourniquet induces compression and ischemic stress of the quadriceps femoris (QF) muscle which can accelerate postoperative weakness. Given that low-load blood flow restricted (BFR) exercise is potent in enhancing muscle oxygenation and vascular function, we hypothesized that short-term preconditioning with low-load BFR exercise can attenuate QF muscle endurance deterioration in the postoperative period. Twenty subjects undergoing arthroscopic ACL reconstruction performed 5 exercise sessions in the last 8 days prior to surgery. They were assigned into either BFR group, performing low-load BFR knee-extension exercise, or SHAM-BFR group, replicating equal training volume with sham occlusion. Blood flow (near-infrared spectroscopy) and surface EMG of QF muscle during sustained isometric contraction at 30% of maximal voluntary isometric contraction (MVIC) torque performed to volitional failure were measured prior to the intervention and again 4 and 12 weeks after surgery. There was an overall decrease (p = 0.033) in MVIC torque over time, however, no significant time-group interaction was found. The time of sustained QF contraction shortened (p = 0.002) in SHAM-BFR group by 97 ± 85 s at week 4 and returned to preoperative values at week 12. No change in the time of sustained contraction was detected in BFR group at any time point after surgery. RMS EMG amplitude increased (p = 0.009) by 54 ± 58% at week 4 after surgery in BFR group only. BFm increased (p = 0.004) by 52 ± 47% in BFR group, and decreased (p = 0.023) by 32 ± 19% in SHAM-BFR group at week 4 after surgery. Multivariate regression models of postoperative changes in time of sustained QF contraction revealed its high correlation (R2 = 0.838; p < 0.001) with changes in BFm and RMS EMG in the SHAM-BFR group, whereas no such association was found in the BFR group. In conclusion, enhanced endurance of QF muscle was triggered by combination of augmented muscle fiber recruitment and enhanced muscle perfusion. The latter alludes to a preserving effect of preconditioning with BFR exercise on density and function of QF muscle microcirculation within the first 4 weeks after ACL reconstruction.
We compared the quality of debridement of chondral lesions performed by four arthroscopic (SH, shaver; CU, curette; SHCU, shaver and curette; BP, bipolar electrodes) and one open technique (OPEN, scalpel and curette) which are used prior to autologous chondrocyte implantation (ACI). The ex vivo simulation of all five techniques was carried out on six juvenile equine stifle joints. The OPEN, SH and SHCU techniques were tested on knees harvested from six adult human cadavers. The most vertical walls with the least adjacent damage to cartilage were obtained with the OPEN technique. The CU and SHCU methods gave inferior, but still acceptable results whereas the SH technique alone resulted in a crater-like defect and the BP method undermined the cartilage wall. The subchondral bone was severely violated in all the equine samples which might have been peculiar to this model. The predominant depth of the debridement in the adult human samples was at the level of the calcified cartilage. Some minor penetrations of the subchondral end-plate were induced regardless of the instrumentation used. Our study suggests that not all routine arthroscopic instruments are suitable for the preparation of a defect for ACI. We have shown that the preferred debridement technique is either open or arthroscopically-assisted manual curettage. The use of juvenile equine stifles was not appropriate for the study of the cartilage-subchondral bone interface.
The aim of our study was to evaluate adaptive changes in the dominant shoulders of female professional overhead athletes, their mutual association, and relation between adaptive changes and shoulder injury. Thirty-six female professional volleyball and handball players were divided into two groups: 14 athletes were included in the symptomatic group (positive shoulder injury history and specific shoulder tests) and 22 athletes were included in the asymptomatic group (negative shoulder injury history and specific shoulder tests). Clinical examinations with specific shoulder tests, evaluation of rotational mobility, and symptoms of malposition and dyskinesis of the dominant scapula (SICK scapula syndrome) were performed. Glenohumeral rotators were isokinetically tested at 60 and 150°/s, with evaluation of stability ratios and rotator fatigability. On average, the participants had decreased internal rotation (P<0.001) and increased external rotation (P<0.001), lower spiking (P<0.01 at 60 and 150°/s) and conventional ratios (P≤0.01 at 60 and 150°/s), lower eccentric external rotator peak torques (eER) (P≤0.05 at 60 and 150°/s), and marginally lower eccentric internal rotator peak torques at 60°/s (P=0.061) on the dominant side compared with the nondominant side. The symptomatic group showed decreased ER (P=0.021), higher deficit of dominant eER at 60°/s (P=0.049), and higher fatigability of internal (P=0.013) and external rotators (P=0.028). The athletes with increased ER had more scapular lateralization (ρ=0.340, P=0.042), higher spiking ratios at 60°/s (ρ=0.349, P=0.037) and 150°/s (ρ=0.330, P=0.049), and lower cocking ratios at 60°/s (ρ=-0.477, P=0.003). Decreased dominant ER, higher deficit of dominant eccentric ER peak torques, and higher dominant rotator fatigability correlate with previous shoulder pain/injury. Different adaptive changes (rotational mobility, SICK scapula signs, and glenohumeral muscular imbalance) are inter-related. As a form of both prevention and rehabilitation for the athletes at risk, we recommend individually adjusted shoulder training on the basis of clinical and isokinetic testing.
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