Search

Saddle position affects mechanical variables during submaximal cycling, but little is known about its effect on mechanical performance during maximal cycling. Therefore, this study relates saddle position to experimentally obtained maximal power output and theoretically calculated moment generating capacity of hip, knee and ankle muscles during isokinetic cycling. Ten subjects performed maximal cycling efforts (5 s at 100 rpm) at different saddle positions varying ± 2 cm around the in literature suggested optimal saddle position (109% of inner leg length), during which crank torque and maximal power output were determined. In a subgroup of 5 subjects, lower limb kinematics were additionally recorded during submaximal cycling at the different saddle positions. A decrease in maximal power output was found for lower saddle positions. Recorded changes in knee kinematics resulted in a decrease in moment generating capacity of biceps femoris, rectus femoris and vastus intermedius at the knee. No differences in muscle moment generating capacity were found at hip and ankle. Based on these results we conclude that lower saddle positions are less optimal to generate maximal power output, as it mainly affects knee joint kinematics, compromising mechanical performance of major muscle groups acting at the knee. [ABSTRACT FROM AUTHOR]

Isometric muscle force after active shortening is reduced [force depression (FD)]. The mechanism is incompletely understood but work delivered during shortening has been suggested to be the main determinant of FD. However, whether muscle length affects the sensitivity of FD to work is unknown, although this information might add to the understanding of the phenomenon. The aim of this study is to investigate the length dependence of the FD/work ratio (Q). Therefore, isometric force production (ISO) of 10 incubated mouse soleus muscles was compared to isometric force after 0.6, 1.2, and 2.4 mm shortening (IAS) at different end lengths ranging from L(0) - 3 to L(0) + 1.8 mm in steps of 0.6 mm. FD was calculated as the force difference between an ISO and IAS contraction at the same activation time (6 s) and end length. We confirm the strong relation between FD and work at L(0) (R² = 0.92) and found that FD is length dependent with a maximum of 8.8 ± 0.3% at L(0) + 1.2 mm for 0.6 mm shortening amplitude. Q was only constant for short muscle lengths (<85% L(0)) but increased exponentially with increasing muscle length. The observed length dependence of Q indicates that FD is not only determined by work produced during shortening but also by a length-dependent factor, possibly actin compliance, which should be incorporated in any mechanism explaining FD. [ABSTRACT FROM AUTHOR]

The ACTN3 gene encodes for the alpha-actinin-3 protein, which has an important structural function in the Z line of the sarcomere in fast muscle fibers. A premature stop codon (R577X) polymorphism in the ACTN3 gene causes a complete loss of the protein in XX homozygotes. This study investigates a possible role for the alpha-actinin-3 protein in protecting the fast fiber from eccentric damage and studies repair mechanisms after a single eccentric exercise bout. Nineteen healthy young men (10 XX, 9 RR) performed 4 series of 20 maximal eccentric knee extensions with both legs. Blood (creatine kinase; CK) and muscle biopsy samples were taken to study differential expression of several anabolic (MyoD1, myogenin, MRF4, Myf5, IGF-1), catabolic (myostatin, MAFbx, and MURF-1), and contraction-induced muscle damage marker genes [cysteine- and glycine-rich protein 3 (CSRP3), CARP, HSP70, and IL-6] as well as a calcineurin signaling pathway marker (RCAN1). Baseline mRNA content of CSRP3 and MyoD1 was 49 + or - 12 and 67 + or - 25% higher in the XX compared with the RR group (P = 0.01-0.045). However, satellite cell number was not different between XX and RR individuals. After eccentric exercise, XX individuals tended to have higher serum CK activity (P = 0.10) and had higher pain scores than RR individuals. However, CSRP3 (P = 0.058) and MyoD1 (P = 0.08) mRNA expression tended to be higher after training in RR individuals compared with XX alpha-actinin-3-deficient subjects. This study suggests a protective role of alpha-actinin-3 protein in muscle damage after eccentric training and an improved stress-sensor signaling, although effects are small.