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Running economy is a key component of distance running performance and is associated with gait parameters. However, there is no consensus of the link between the running economy (RE), ground contact time, and footstrike patterns. Thus, this study aimed to clarify the relationship between RE, ground contact time, and thigh muscle cross-sectional area (CSA) in highly trained distance runners and to compare these parameters between 2 habitual footstrike patterns (midfoot vs. rearfoot). Seventeen male distance runners ran on a treadmill to measure RE and gait parameters. We collected the CSAs of the right thigh muscle using a magnetic resonance imaging scanner. The RE had a significant negative relationship with distance running performance (r = -0.50) and ground contact time (r = -0.51). The ground contact time had a significant negative relationship with the normalized CSAs of the vastus lateralis muscle (r = -0.60) and hamstrings (r = -0.54). No significant differences were found in RE, ground contact time, or normalized CSAs of muscles between midfoot (n = 10) and rearfoot (n = 7) strikers. These results suggest that large CSAs of knee extensor muscles results in short ground contact time and worse RE. The effects of the footstrike pattern on the RE appear insignificant, and the preferred footstrike pattern can be recommended for running in highly trained runners. [ABSTRACT FROM AUTHOR]

Purpose: Increases in maximal oxygen uptake (VO2max) and running economy improve performance in long-distance runners. Nevertheless, long-distance runners require sprinting ability to win, especially in the final phase of competitions. The authors determined the relationships between performance and sprinting ability, as well as other abilities in elite long-distance runners. Methods: The subjects were 12 elite long-distance runners. Mean official seasonal best times in 5000-m (5000 m-SB) and 10,000-m (10,000 m-SB) races within 1 year before or after the examination were 13:58.5 (0:18.7) and 28:37.9 (0:25.2) (mean [SD]), respectively. The authors measured 100-m and 400-m sprint times as the index of sprinting ability. They also measured VO2max and running economy (VO2 at 300 m·min-1 of running velocity). They used a single correlation analysis to assess relationships between 5000 m-SB or 10,000 m-SB and other elements. Results: There were significant correlations between 5000 m-SB was significantly correlated with 100-m sprint time (13.3 [0.7] s; r = .68, P = .014), 400-m sprint time (56.6 [2.7] s; r = .69, P = .013), and running economy (55.5 [3.9] mL·kg-1· min-1; r = .59, P = .045). There were significant correlations between 10,000 m-SB and 100-m sprint time (r = .72, P = .009) and 400-m sprint time (r = .85, P < .001). However, there was no significant correlation between 5000 m-SB or 10,000 m-SB and VO2max (72.0 [3.8] mL·kg-1·min-1). Conclusions: The authors' data suggest that sprinting ability is an important indicator of performance in elite long-distance runners. [ABSTRACT FROM AUTHOR]

Background: The DMD gene encoding dystrophin is mutated in Duchenne muscular dystrophy, a fatal progressive muscle wasting disease. DMD has also been shown to act as a tumor suppressor gene. Rhabdomyosarcoma (RMS) is a mesodermal sarcoma that shares characteristics of skeletal muscle precursors. Products of the DMD gene in RMS have not yet been fully clarified. Here, DMD products were analyzed in CRL-2061 cells established from alveolar RMS. Methods: The 14-kb long DMD cDNA was PCR amplified as 20 separated fragments, as were nine short intron regions. Dystrophin was analyzed by Western blotting using an antibody against the C-terminal region of dystrophin. Results: Sixteen of the 20 DMD cDNA fragments could be amplified from CRL-2061 cells as muscle cDNA. Three fragments included aberrant gene products, including one in which exon 71 was omitted and one each with retention of introns 40 and 58. In one fragment, extending from exon 70 to 79, no normally spliced product was obtained. Rather, six alternatively spliced products were identified, including a new product deleting exon 73, with the most abundant product showing deletion of exon 78. Although dystrophin expression was expected in CRL-2061 cells, western blotting of cell lysates showed no evidence of dystrophin, suggesting that translation of full-length DMD mRNA was inhibited by intron retention that generated a premature stop codon. Intron specific PCR amplification of nine short introns, showed retention of introns 40, 58, and 70, which constituted about 60, 25 and 9%, respectively, of the total PCR amplified products. The most abundant DMD transcript contained two abnormalities, intron 40 retention and exon 78 skipping. Conclusions: Intron-specific PCR amplification showed that DMD transcripts contained high levels of introns 40, 58 and 70. Retention of these introns may have been responsible for the lack of dystrophin expression by CRL-2061 cells, thereby abolishing the tumor suppressor activity of dystrophin. [ABSTRACT FROM AUTHOR]