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The effects of flexibility conditioning on neuromuscular and sensorimotor performance were assessed near to full knee extension (25°). Eighteen males who were randomly assigned into two groups underwent eight weeks (three-times per week) of flexibility conditioning (hip region/knee flexor musculature; dominant limb) involving either proprioceptive neuromuscular facilitation (PNF) (n=9) or passive stretching (PASS) (n=9). Both modes of flexibility conditioning are popular within contemporary exercise and clinical settings and have demonstrated efficacy in improving range of motion. The contralateral limb and a prior ‘no exercise’ condition were used as controls. The PNF and PASS modes of conditioning improved passive hip flexibility to a similar extent (mean 19.3% vs. baseline, intervention limb,p<0.01) but did not alter knee flexor strength (overall mean 309.6±81 N) or sensorimotor performance (force and positional errors: 2.3±8.2% and 0.48±7.1%). Voluntary and magnetically evoked electromechanical delays (EMDVand EMDE, respectively) were increased but to a greater extent following PASS compared to PNF (PASS: 10.8% and 16.9% lengthening of EMDVand EMDE, respectively vs. PNF: 3.2% and 6.2%,p<0.01).The attenuated change to electromechanical delay (EMD) performance during PNF conditioning suggests a preserved capability for rapid muscle activation, which is important in the maintenance of dynamic joint stability. That PNF was also equally efficacious in flexibility conditioning would suggest that this mode of flexibility training should be used over passive to help preserve dynamic joint stability capabilities at this extended and vulnerable joint position. [ABSTRACT FROM PUBLISHER]

This study examined the concurrent effects of exercise-induced muscle damage and superimposed acute fatigue on the neuromuscular activation performance of the knee flexors of nine males (age: 26.7±6.1 years; height 1.81±0.05 m; body mass 81.2±11.7 kg [mean±s]). Measures were obtained during three experimental conditions: (i) ‘fatigue-muscle damage’, involving acute fatiguing exercise performed on each assessment occasion plus a single episode of eccentric exercise performed on the first occasion and after the fatigue trial; (ii) ‘fatigue’, involving the fatiguing exercise only; and (iii) ‘control’ consisting of no exercise. Assessments were performed prior to (pre) and at 1 h, 24 h, 48 h, 72 h, and 168 h relative to the muscle damaging eccentric exercise. Repeated-measures analyses of variance (ANOVAs) showed that muscle damage elicited reductions of up to 38%, 24% and 65% in volitional peak force, electromechanical delay and rate of force development compared to baseline and controls, respectively (F [10, 80] = 2.3 to 4.6; P < 0.05) with further impairments (6.2% to 30.7%) following acute fatigue (F [2, 16] = 4.3 to 9.1; P < 0.05). By contrast, magnetically-evoked electromechanical delay was not influenced by muscle damage and was improved during the superimposed acute fatigue (∼14%; F [2, 16] = 3.9; P < 0.05). The safeguarding of evoked muscle activation capability despite compromised volitional performance might reveal aspects of capabilities for emergency and protective responses during episodes of fatigue and antecedent muscle damaging exercise. [ABSTRACT FROM PUBLISHER]

The effects of serial episodes of fatigue and recovery on volitional and magnetically evoked neuromuscular performance of the knee flexors were assessed in 20 female soccer players during: (i) an intervention comprising 4 × 35 s maximal static exercise, and (ii) a control condition. Volitional peak force was impaired progressively (∼16% vs. baseline: 235.3 ± 54.7 to 198.1 ± 38.5 N) by the fatiguing exercise and recovered to within ∼97 % of baseline values following 6 min of rest. Evoked peak twitch force was diminished subsequent to the fourth episode of exercise (23.3%: 21.4 ± 13.8 vs. 16.4 ± 14.6 N) and remained impaired at this level throughout the recovery. Impairment of volitional electromechanical delay performance following the first episode of exercise (25.5%: 55.3 ± 11.9 vs. 69.5 ± 24.5 ms) contrasted with concurrent improvement (10.0%: 24.5 ± 4.7 vs. 22.1 ± 5.0 ms) in evoked electromechanical delay (P < 0.05), and this increased disparity between evoked and volitional electromechanical delay remained during subsequent periods of intervention and recovery. The fatiguing exercise provoked substantial impairments to volitional strength and volitional electromechanical delay that showed differential patterns of recovery. However, improved evoked electromechanical delay performance might identify a dormant capability for optimal muscle responses during acute stressful exercise and an improved capacity to maintain dynamic joint stabilty during critical episodes of loading. [ABSTRACT FROM PUBLISHER]