Background: Competitive swimming is a sport that require high muscle strength to overcome the forces in the water. A phenomenon called post activation potentiation (PAP) is known to acutely increase power output. PAP can be defined as an increase in muscle performance after muscle contraction. Previous research on PAP has shown positive effects on different sports, including swimming. However, a limited amount of studies exists on PAP associated with swimming and distances longer than 100 meters. Aim: The aim of the study was to investigate if PAP for triceps brachii and latissimus dorsi with elastic bands can improve the aerobic performance, V4-speed, of elite freestyle swimmers. Methods: 13 elite swimmers participated in this study (mean ±SD: age 18 ±1.15). The participants performed three test sessions on two different days. The first occasion evaluated aerobic performance, V4-speed, where the participants performed a 400-m freestyle swim race and lactate and time were collected. At the second occasion, a 10-repetition maximum (RM) elastic resistance band test was done to get the right resistance band for each individual participant for the PAP exercise. At the third occasion, a PAP exercise, that mimics freestyle swim, with elastic resistance band was performed with 10 repetitions in two sets. After, a rest of six minutes was performed and then the same 400-m freestyle swim test as the first occasion. A paired samples t-test was used to evaluate significant differences between the swim test performed with and without a PAP exercise. Results: The study showed no statistical difference between the V4-speed with or without PAP exercise (p=0.93). An increase in lactate was seen after the PAP exercise (p=0.02). Conclusion: This study could not ensure an improvement of the aerobic performance, V4-speed, of elite swimmers when a PAP exercise, similar to a freestyle stroke, was performed before a 400-m submaximal freestyle swim race with elastic resistance band. Further research must be done in this area before coaches and athletes can apply this in training programs.

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Whole-body vibration (WBV) may positively influence performance acutely through the potentiation of the muscle’s series elastic components and neuromuscular mechanisms. The purpose of this investigation was to examine the acute effects of WBV on sprint performance in NCAA Division I collegiate male sprinters and jumpers. Twenty-one athletes (n=21) completed a control or WBV protocol (30 seconds, 50 Hz, low amplitude ~3mm) one minute before a 30 m flying sprint. Each athlete participated in three separate trials using randomized treatment sessions (1 treatment per session) over 12 weeks of preparation training prior to the indoor season. The control condition consisted of no vibration, while treatment 1 (T1) and treatment 1 repeated (T1-R) incorporated vibration. The vibration-sprint protocol was repeated after a five minute rest period following the first sprint (test-re-test ICC≥0.81). The sprint consisted of a 15 m run-in from a standing start and a 30 m flying sprint with a total distance of 45 m. A two-way factorial ANOVA with repeated measures (p ≤ 0.05) was used to compare treatments. Statistics showed no differences between the treatments at all distances (average sprint time of control vs. T1, control vs. T1-R, and T1 vs. T1-R). The results of this study indicate that WBV at 50 Hz and low amplitude has no potentiation effect on sprint times (15, 30, 45, or 30 m fly). Further research is needed to determine if different WBV protocols may elicit enhanced results in 30 m flying sprint performance. The present WBV protocol does not appear to have practical acute value for sprinting.

Countermovement vertical jump (CMVJ) performance may be acutely facilitated via potentiation (PAP) due to central and peripheral factors. PURPOSE: To investigate the effects of two methods of PAP in trained weightlifters (n=16); group 1: stronger (n=7) and group 2: weaker (n=9) upon unweighted countermovement jumps (CMVJs) over a 15 minute time period. METHODS: A series of maximal unweighted CMVJs were performed prior to, then at, 30, 60, 120, 180, 300, 480, 660, 780, and 900 seconds following two conditions: isometric mid-thigh clean pulls (C1) and dynamic mid-thigh clean pulls (C2). Dependent variables included, jump height (JH, cm), peak power (PP, W), peak velocity (PV, m·s-1), and peak force (PF, N). RESULTS: A series of repeated measures ANOVA: conditions (2); time points (10); groups (2) were performed on JH, PP, PV, and PF (p>.05). Significant main effects for JH existed by condition (C1>C2) (p=.001, ES=.571, 1-β=.979, mean diff=.053cm), group (G1>G2) (p=.018, ES=.339, 1-β=.702, mean diff=.053), and time (60s>900s, 120s>900s, 180s>900s) (p=.014, ES=.148, 1-β=.910).Within subjects main effects for JH were seen for the stronger group for JH by condition (C1>C2) (p=.055, ES=.757, 1-β=.947, mean diff=.053cm), and weaker group by condition (C1>C2) (p=.025, ES=.487, 1-β=.676, mean diff=.054cm). Significant main effects existed for PP by condition (C1>C2) (p=.000, ES=.631, 1-β=.995, mean diff=427.9W), group (G1>G2) (p=.008, ES=.405, 1-β=.819, mean diff=1660.1W), and time (60s>480s, 60s>660s, 60s>780s, 60s>900s>120s>900s, 180s>480s, 180s>660s, 180s>780s) (p=.000, ES=.355, 1-β=1.00, mean diff=240.1W ).Within subjects main effects for PP were seen for the stronger group for condition (C1>C2) (p=.055, ES=.761, 1-β=.951, mean diff=516.8W), and time (120s>900s) (p=.000, ES=.471,1-β=.999, mean diff=319.5W). In the weaker group; significant main effects by condition (C1>C2) (p=.025, ES=.485, 1-β=.672, mean diff=339.1W) and time (120s>900s, 180s>480s, 180s>900s, 300s>900s) (p=.003, ES=.281, 1-β=.963, mean diff=319.5W). Significant main effects were seen for jump PV by condition (C1>C2) (p=.001, ES=.536,1-β=.962, mean diff=.177 m·s-1), group (G1>G2) (p=.022, ES=.320, 1-β=.665, mean diff=.298m/s) and by time (60s>900s, 120s>900s, 180s>900s) (p=.016, ES=.145, 1-β=.904). Within subjects main effects for jump PV in the stronger group by condition (C1>C2) (p=.007, ES=.727, 1-β=.911, mean diff=.165m/s), and time (120s>900s) (p=.036, ES=.269, 1-β=.840, mean diff=.073 m·s-1). In the weaker group there were significant main effects for jump PV by condition (C1>C2) (p=.028, ES=.474, 1-β=.654, mean diff=.188 m·s-1). A significant main effect for jump PF by group (G1>G2) (p=.014, ES=.363, 1-β=.747, mean diff=647.0N) and time (60s>baseline) (p=.05, ES=.122, 1-β=.824, mean diff=71.0N) was seen. Within subjects, a significant main effect for jump PF in the weaker group by time (60s>780s) (p=.012, ES=.247, 1-β=.919). There were no significant interactions for any of the dependent variables (p >.05). CONCLUSION: Isometric mid-thigh clean pulls appear to have a greater potentiating effect than dynamic mid-thigh pulls on PP and PV during subsequent CMVJ0’s, and stronger weightlifters tend to have a more favorable response to both conditions. PRACTICAL APPLICATION: Whole-body isometric movements may be a more effective at eliciting a potentiation response than dynamic movements in strength and power athletes.

Limited research exists examining the effect of moderately loaded conditioning activities that are employed as part of a strength-power potentiating complex (SPPC). Additionally, no studies to date have explored the effects of using a concentric-only quarter back squat protocol as part of an SPPC. Therefore, the purpose of this study was to examine the effects of a moderately loaded (50–65% of 1RM) concentric-only quarter back squat protocol on the occurrence of potentiation effects at various time points. Twenty men who could quarter back squat a minimum of 2.4 times their body mass (3.7 ± 0.7 kg·per body mass) participated in this investigation. All subjects participated in 3 conditions: control (CT), a 50% of 1RM trial (50POT), and a 65% of 1RM trial (65POT). One minute before each condition, a maximal countermovement vertical jump (CMJ) was performed. One minute later, the subject performed 1 of 3 conditions: CT condition, 50POT, or 65POT, followed by vertical jumps at 0.5, 3, 5, 10, and 15 minutes after conditioning activity. A force plate was used to quantify displacement, peak power output, peak force, and the rate of force development for each CMJ. There were no significant differences (p > 0.05) in any of the performance measures quantified during the CMJ trials when comparing the CT, 50POT, and 65POT treatment conditions. However, 48% of the subjects demonstrated some degree of potentiation at the 30 seconds after completing the 65POT trial, but this percent increase was not statistically significant. From a practical perspective, if the goal of the SPPC is to create a maximization of the potentiation effect, moderately loaded activities may not be the best alternative.

Power-generating capacity should be a primary training outcome for football athletes. The ability to be explosive and use high levels of strength seems to differentiate between athletes and teams. Developing training interventions that can improve both strength- and power-generating capacity would therefore be considered a paramount endeavor when attempting to optimize the physiological and performance adaptations necessary for competitive success. Too often, strength and conditioning coaches forget that the foundation of powergenerating capacity is in fact high levels of muscular strength. When the development of strength is minimized or excluded from the training plan, the ability to express high-power outputs is compromised. In addition, a failure to use sequenced and integrated training programs decreases the possibility of successfully increasing strength- and power-generating capacity, thus decreasing the potential for competitive success. Therefore, this brief review attempts to explain how strength- and powergenerating capacity can be enhanced to increase the potential for developing the physiological and performance foundation necessary for competitive success with the football athlete.

The short-term enhancement of physical performance known as post-activation potentiation could be exploited in the design of sport-specific training sessions. The purpose of this study was to compare the potentiation of softball throwing velocity following two kinds of resistance-training session: a control session consisting of traditional heavy-load sets, and an experimental "Pmax" session consisting of sets of loads selected to maximise the mean power output during explosive bench presses. Both sessions included plyometric medicine ball chest passes. Eight male softball players of premier grade, with at least 2 yr experience of resistance training, performed the two sessions in a crossover fashion, with 30 min recovery between sessions. Softball throwing velocity was measured with a radar gun immediately before and at 2-min intervals 4-10 min after each session. Percent effects on throwing speed were analyzed via log transformation, and t statistics were used to make magnitude-based inferences with respect to the smallest important change of 2%. The average throwing velocity increased between pre and post tests for both treatments; the average increase was a substantial 2.3% (0.5 to 4.1%). Throwing velocity after Pmax training was a trivial 0.4% slower relative to that after heavy-load training (90% confidence limits -1.2 to 1.9%). There was a greater change in throwing velocity by 10 min post treatment than by 4 min post treatment; the change by 10 min was 5.0% (3.2 to 6.7%) for the Pmax training session and 5.3% (2.1 to 8.6%) for the heavy-load session. These effects were almost certainly beneficial for throwing speed, but the difference between them was unclear (-0.3%; -3.7 to 3.1%). The mean change between 4 and 10 min for both treatments combined was 5.1% (90% confidence limits 3.6 to 6.7%). The short-term enhancement of throwing performance following heavy-load and Pmax training sets has implications for the design of softball warm-up routines. There is also the potential for softball players to use such training to improve their throwing velocity during games.

We have recently established that aberrant alkylacylglycerophosphocholine metabolism results in the increased tissue concentration of platelet activating factors (PAFs) in the temporal cortex of Alzheimer Disease (AD) patients and in TgCRND8 mice over-expressing mutant human amyloid precursor protein. PAF lipids activate a G-protein coupled receptor (PAFR) reported to be expressed by microglia and subsets of neurons in rat. It is not known whether this same expression pattern is recapitulated in mice however, as the expression has only been inferred by use of pharmacological PAFR antagonists, many of which impact on both PAFR-dependent and PAFR-independent signalling pathways. PAFR plays a role in long term potentiation (LTP) induction in rats. PAFR has also been implicated in behavioural indices of spatial learning and memory in rats. Contradictory reports using mice provide ambiguity regarding the role of PAFR in LTP induction in mice. To assess whether PAFR is expressed in murine neurons, I localized PAFR mRNA in wild-type C57BL/6 mice using PAFR KO mice as a negative control. I further showed that the loss of PAFR did not impair learning and memory although this assessment must be considered preliminary as the behavioural test employed was not optimized to detect changes in learning and memory of C57BL/6 mice over time adequately.Finally, I showed that the loss of PAFR in TgCRND8 mouse model of AD had no impact upon Aβ plaque number. My observations suggest that PAFR is restricted to microglial-like cells in mouse hippocampus and as such, it may not play a role in learning and memory.

We have recently established that aberrant alkylacylglycerophosphocholine metabolism results in the increased tissue concentration of platelet activating factors (PAFs) in the temporal cortex of Alzheimer Disease (AD) patients and in TgCRND8 mice over-expressing mutant human amyloid precursor protein. PAF lipids activate a G-protein coupled receptor (PAFR) reported to be expressed by microglia and subsets of neurons in rat. It is not known whether this same expression pattern is recapitulated in mice however, as the expression has only been inferred by use of pharmacological PAFR antagonists, many of which impact on both PAFR-dependent and PAFR-independent signalling pathways. PAFR plays a role in long term potentiation (LTP) induction in rats. PAFR has also been implicated in behavioural indices of spatial learning and memory in rats. Contradictory reports using mice provide ambiguity regarding the role of PAFR in LTP induction in mice. To assess whether PAFR is expressed in murine neurons, I localized PAFR mRNA in wild-type C57BL/6 mice using PAFR KO mice as a negative control. I further showed that the loss of PAFR did not impair learning and memory although this assessment must be considered preliminary as the behavioural test employed was not optimized to detect changes in learning and memory of C57BL/6 mice over time adequately.Finally, I showed that the loss of PAFR in TgCRND8 mouse model of AD had no impact upon Aβ plaque number. My observations suggest that PAFR is restricted to microglial-like cells in mouse hippocampus and as such, it may not play a role in learning and memory.

The mesolimbic dopamine system, including dopaminergic projections from the ventral tegmental area (VTA) to nucleus accumbens (NAc), is critically involved in the development of addiction to many drugs of abuse, including cocaine (CA). Although there is an attractive hypothesis that the modifications of mesolimbic reward circuit following repeated drug exposure are responsible for cocaine-addicted causes behaviors change, however, our understanding in the underlying molecular mechanisms at the neural circuit level is still in its infancy. It has been suggested PKMzeta, a constitutively active atypical isoform of PKC, plays a critical role in spatial memory formation and long-term synaptic potentiation in hippocampus. To define the relationship among PKMzeta, CA-induced synaptic long-term potentiation and CA addiction, we examined the regulation of PKMzeta after CA administration in Sprague-Dawley rat. We found single CA injection elicits an increase in PKMzeta protein expression in the VTA region. The increase was first observed 10 min after CA administration and lasted for 7 days, the longest sampling time point of our experimental design. The PKMzeta protein expression can also be induced in 10 minutes while incubating the acute isolated brain slice with CA, the expression within 1 hr can be eliminated at the present of Chelerythrine (PKC inhibitor) and ZIP (PKMzeta inhibitor) suggests a positive feedback loop. The PKMzeta mRNA expression can be induced within 1 hr, and Actinomycin d (transcription inhibitor) had no effect on the PKMzeta protein expression indicating CA increases PKM£a translation from preexisting PKM£a mRNA. Furthermore,real time PCR-based analysis showed resembling increase profile ofPKM£a mRNA after single CA injection, suggesting a co-upregulation of transcription and translation of PKM£a after CA administration in VTA. Eticlopride (dopamine receptor D2-subtype antagonist) ¡BSCH-23390(dopamine receptor D1-subtype antagonist)¡BH-89 (PKA inhibitor)¡B Wortmannin (PI3K inhibitor)¡BPD98059 (MEK1 inhibitor) decreasedcocaine-induced PKM£a expression within 1 hr in VTA. On the contrary, KN-62 (CaMK II inhibitor) has no obvious effect on PKM£a expression. CA challenge not only induces the PKM£a expression in the VTA region but also in the NAc and hippocampus region. The CA-induced PKM£a expression is more obvious in elder group (>45 days in age) than younger group (18~30 days in age), similar results also showed in the locomotor activity assay. Prenatal CA exposure decreased the postnatal CA-induced PKM£a expression and the locomotor sensitivity in younger group. Overall, results from our current experiments have raised the possibility of PKM£a involvement in CA addiction. How CA regulates PKM£a expression and the context dependence between PKM£a and CA-induced behavior change and synaptic long-term potentiation remains further elucidation.