Post-activation potentiation (PAP) has been shown to increase force generation due to prior muscu... more Post-activation potentiation (PAP) has been shown to increase force generation due to prior muscular activity which can acutely improve strength and power performance. Typically, heavy-loaded bench press has been used as a conditioning contraction for a PAP stimulus. However, a heavy loaded weight exercise is frequently not available prior to performance, due to varying factors such as regulations or practicality for athletes. The aim of this study was to examine whether lower load exercises can cause an induction of PAP.
Fourteen male, competitive university level athletes (mean ± SD: age, 21.9 ± 2.2 years; height 1.8 ± 0.05 m; body mass 76.3 ± 8.2 kg) performed an explosive bench press (with 50% 1RM load) immediately prior to one of four conditioning contractions; 2 x 45 seconds of suspended chest press, 3 x 8 repetitions of resistance band lying bench press, 3 x 10 repetitions of push-ups, or no conditioning contractions. Rest between all sets was 30 seconds and the conditioning contraction order was randomised. The explosive bench press was performed again at 2, 4, 6 and 8 minutes after the conditioning contraction. Peak power (Ppeak), peak force (Fpeak), peak velocity (Vpeak), rate of force development (RFD) and a percentage of EMG from the Pectoralis Major, Anterior Deltoid and Triceps Brachii were recorded for all trials and a maximum voluntary contraction (MVC). Normality of data was checked using the Shapiro-Wilks test and confirmed for Ppeak, Fpeak, Vpeak, and EMG triceps but not for RFD, EMG chest and EMG shoulder. Repeated measures ANOVA with Bonferroni correction was used to check for differences between normally distributed data, while a Friedman’s test was used to check for differences in RFD, EMG chest and EMG shoulder. A Wilcoxon Signed Ranks test was used to analyse the difference found in the data for EMG shoulder.
The results showed no significant difference between the variables for any of the conditioning contractions between baseline, 2, 4, 6 and 8 minutes. Similarly, there was no significant difference in any variables was shown between conditioning contractions at baseline, 2, 4, 6 and 8 minutes. Whereas, EMG shoulder showed a difference in the RB intervention between trials 1 and 2 (Z = -2.480, p = 0.013), 1 and 4 (Z = -2.480, p = 0.013), 1 and 5 (Z = -2.103, p= 0.035) and trials 2 and 3 (Z = -2.103, p = 0.035), with a difference also found in the PU intervention, between trials 2 and 3 (Z = -2.229, p = 0.026) and trials 2 and 4 (Z = -2.103, p = 0.035).
The findings suggest that PAP was not induced by any of the conditioning contractions used in this study. As the design employed in the current study has been used previously showing higher weighted exercises inducing PAP, we conclude that a) the loading used in the current study was insufficient to induce PAP, b) there is a ‘load threshold’ below which PAP cannot be induced, c) the stimulus from the EMG was not high enough to induce PAP, and d) muscle excitation is not a contributing mechanism to an induction of PAP.
Post-activation potentiation (PAP) has been shown to increase force generation due to prior muscu... more Post-activation potentiation (PAP) has been shown to increase force generation due to prior muscular activity which can acutely improve strength and power performance. Typically, heavy-loaded bench press has been used as a conditioning contraction for a PAP stimulus. However, a heavy loaded weight exercise is frequently not available prior to performance, due to varying factors such as regulations or practicality for athletes. The aim of this study was to examine whether lower load exercises can cause an induction of PAP.
Fourteen male, competitive university level athletes (mean ± SD: age, 21.9 ± 2.2 years; height 1.8 ± 0.05 m; body mass 76.3 ± 8.2 kg) performed an explosive bench press (with 50% 1RM load) immediately prior to one of four conditioning contractions; 2 x 45 seconds of suspended chest press, 3 x 8 repetitions of resistance band lying bench press, 3 x 10 repetitions of push-ups, or no conditioning contractions. Rest between all sets was 30 seconds and the conditioning contraction order was randomised. The explosive bench press was performed again at 2, 4, 6 and 8 minutes after the conditioning contraction. Peak power (Ppeak), peak force (Fpeak), peak velocity (Vpeak), rate of force development (RFD) and a percentage of EMG from the Pectoralis Major, Anterior Deltoid and Triceps Brachii were recorded for all trials and a maximum voluntary contraction (MVC). Normality of data was checked using the Shapiro-Wilks test and confirmed for Ppeak, Fpeak, Vpeak, and EMG triceps but not for RFD, EMG chest and EMG shoulder. Repeated measures ANOVA with Bonferroni correction was used to check for differences between normally distributed data, while a Friedman’s test was used to check for differences in RFD, EMG chest and EMG shoulder. A Wilcoxon Signed Ranks test was used to analyse the difference found in the data for EMG shoulder.
The results showed no significant difference between the variables for any of the conditioning contractions between baseline, 2, 4, 6 and 8 minutes. Similarly, there was no significant difference in any variables was shown between conditioning contractions at baseline, 2, 4, 6 and 8 minutes. Whereas, EMG shoulder showed a difference in the RB intervention between trials 1 and 2 (Z = -2.480, p = 0.013), 1 and 4 (Z = -2.480, p = 0.013), 1 and 5 (Z = -2.103, p= 0.035) and trials 2 and 3 (Z = -2.103, p = 0.035), with a difference also found in the PU intervention, between trials 2 and 3 (Z = -2.229, p = 0.026) and trials 2 and 4 (Z = -2.103, p = 0.035).
The findings suggest that PAP was not induced by any of the conditioning contractions used in this study. As the design employed in the current study has been used previously showing higher weighted exercises inducing PAP, we conclude that a) the loading used in the current study was insufficient to induce PAP, b) there is a ‘load threshold’ below which PAP cannot be induced, c) the stimulus from the EMG was not high enough to induce PAP, and d) muscle excitation is not a contributing mechanism to an induction of PAP.
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Fourteen male, competitive university level athletes (mean ± SD: age, 21.9 ± 2.2 years; height 1.8 ± 0.05 m; body mass 76.3 ± 8.2 kg) performed an explosive bench press (with 50% 1RM load) immediately prior to one of four conditioning contractions; 2 x 45 seconds of suspended chest press, 3 x 8 repetitions of resistance band lying bench press, 3 x 10 repetitions of push-ups, or no conditioning contractions. Rest between all sets was 30 seconds and the conditioning contraction order was randomised. The explosive bench press was performed again at 2, 4, 6 and 8 minutes after the conditioning contraction. Peak power (Ppeak), peak force (Fpeak), peak velocity (Vpeak), rate of force development (RFD) and a percentage of EMG from the Pectoralis Major, Anterior Deltoid and Triceps Brachii were recorded for all trials and a maximum voluntary contraction (MVC). Normality of data was checked using the Shapiro-Wilks test and confirmed for Ppeak, Fpeak, Vpeak, and EMG triceps but not for RFD, EMG chest and EMG shoulder. Repeated measures ANOVA with Bonferroni correction was used to check for differences between normally distributed data, while a Friedman’s test was used to check for differences in RFD, EMG chest and EMG shoulder. A Wilcoxon Signed Ranks test was used to analyse the difference found in the data for EMG shoulder.
The results showed no significant difference between the variables for any of the conditioning contractions between baseline, 2, 4, 6 and 8 minutes. Similarly, there was no significant difference in any variables was shown between conditioning contractions at baseline, 2, 4, 6 and 8 minutes. Whereas, EMG shoulder showed a difference in the RB intervention between trials 1 and 2 (Z = -2.480, p = 0.013), 1 and 4 (Z = -2.480, p = 0.013), 1 and 5 (Z = -2.103, p= 0.035) and trials 2 and 3 (Z = -2.103, p = 0.035), with a difference also found in the PU intervention, between trials 2 and 3 (Z = -2.229, p = 0.026) and trials 2 and 4 (Z = -2.103, p = 0.035).
The findings suggest that PAP was not induced by any of the conditioning contractions used in this study. As the design employed in the current study has been used previously showing higher weighted exercises inducing PAP, we conclude that a) the loading used in the current study was insufficient to induce PAP, b) there is a ‘load threshold’ below which PAP cannot be induced, c) the stimulus from the EMG was not high enough to induce PAP, and d) muscle excitation is not a contributing mechanism to an induction of PAP.
Fourteen male, competitive university level athletes (mean ± SD: age, 21.9 ± 2.2 years; height 1.8 ± 0.05 m; body mass 76.3 ± 8.2 kg) performed an explosive bench press (with 50% 1RM load) immediately prior to one of four conditioning contractions; 2 x 45 seconds of suspended chest press, 3 x 8 repetitions of resistance band lying bench press, 3 x 10 repetitions of push-ups, or no conditioning contractions. Rest between all sets was 30 seconds and the conditioning contraction order was randomised. The explosive bench press was performed again at 2, 4, 6 and 8 minutes after the conditioning contraction. Peak power (Ppeak), peak force (Fpeak), peak velocity (Vpeak), rate of force development (RFD) and a percentage of EMG from the Pectoralis Major, Anterior Deltoid and Triceps Brachii were recorded for all trials and a maximum voluntary contraction (MVC). Normality of data was checked using the Shapiro-Wilks test and confirmed for Ppeak, Fpeak, Vpeak, and EMG triceps but not for RFD, EMG chest and EMG shoulder. Repeated measures ANOVA with Bonferroni correction was used to check for differences between normally distributed data, while a Friedman’s test was used to check for differences in RFD, EMG chest and EMG shoulder. A Wilcoxon Signed Ranks test was used to analyse the difference found in the data for EMG shoulder.
The results showed no significant difference between the variables for any of the conditioning contractions between baseline, 2, 4, 6 and 8 minutes. Similarly, there was no significant difference in any variables was shown between conditioning contractions at baseline, 2, 4, 6 and 8 minutes. Whereas, EMG shoulder showed a difference in the RB intervention between trials 1 and 2 (Z = -2.480, p = 0.013), 1 and 4 (Z = -2.480, p = 0.013), 1 and 5 (Z = -2.103, p= 0.035) and trials 2 and 3 (Z = -2.103, p = 0.035), with a difference also found in the PU intervention, between trials 2 and 3 (Z = -2.229, p = 0.026) and trials 2 and 4 (Z = -2.103, p = 0.035).
The findings suggest that PAP was not induced by any of the conditioning contractions used in this study. As the design employed in the current study has been used previously showing higher weighted exercises inducing PAP, we conclude that a) the loading used in the current study was insufficient to induce PAP, b) there is a ‘load threshold’ below which PAP cannot be induced, c) the stimulus from the EMG was not high enough to induce PAP, and d) muscle excitation is not a contributing mechanism to an induction of PAP.