EFFECTS OF DIFFERENT RELATIVE LOADS ON POWER PERFORMANCE DURING THE BALLISTIC PUSH-UP

The purpose of this investigation was to examine the effect of load on force and power performance during a ballistic push-up. Sixty (24.5 +/- 4.3 years, 1.75 +/- 0.07 m, and 80.8 +/- 13.5 kg) recreationally active men who participated in this investigation completed all testing and were included in the data analysis. All participants were required to perform a 1 repetition maximum bench press, and ballistic push-ups without external load (T1), with 10% (T2) and 20% (T3) of their body mass. Ballistic push-ups during T2 and T3 were performed using a weight loaded vest. Peak and mean force, power, as well as net impulse and flight time were determined for each ballistic push-up. Peak and mean force were both significantly greater (p > 0.01) during T3 (1,062 +/- 202 and 901 +/- 154 N, respectively), than both T2 (1,017 +/- 202 and 842 +/- 151 N, respectively) and T1 (960 +/- 188 and 792 +/- 140 N, respectively). Peak and mean power were significantly greater (p < 0.01) during T1 (950 +/- 257 and 521 +/- 148 W, respectively), than both T2 (872 +/- 246 and 485 +/- 143 W, respectively) and T3 (814 +/- 275 and 485 +/- 162 W, respectively). Peak and mean power were greatest during T1, regardless of participants' strength levels. Significant (p > 0.01) greater net impulse and smaller peak velocity and flight time were also noted from T1 to T3. Results of this investigation indicated that maximal power outputs were achieved without the use of an external load when performing the ballistic push-up, regardless of the participants' level of strength

Comparison of a new pmp22 transgenic mouse line with other mouse models and human patients with CMT1A*

Charcot-Marie-Tooth disease type 1A is a dominantly inherited demyelinating disorder of the peripheral nervous system. It is most frequently caused by overexpression of peripheral myelin protein 22 (PMP22), but is also caused by point mutations in the PMP22 gene. We describe a new transgenic mouse model (My41) carrying the mouse, rather than the human, pmp22 gene. The My41 strain has a severe phenotype consisting of unstable gait and weakness of the hind limbs that becomes obvious during the first 3 weeks of life. My41 mice have a shortened life span and breed poorly. Pathologically, My41 mice have a demyelinating peripheral neuropathy in which 75% of axons do not have a measurable amount of myelin. We compare the peripheral nerve pathology seen in My41 mice, which carry the mouse pmp22 gene, with previously described transgenic mice over-expressing the human PMP22 protein and Trembler-(J) (Tr(J)) mice which have a P16L substitution. We also look at the differences between CMT1A duplication patients, patients with the P16L mutation and their appropriate mouse models