Joachim Mester

A model analysis of the effects of wobbling mass on whole-body vibration

The effects of wobbling mass on the whole-body vibration are studied in terms of the comparison between two models A and B regarding their detailed behavior during the ‘whole-body vibration,’ where Model A is a system of four degrees of freedom with rigid and wobbling masses in both lower body and upper body, while Model B is a system of three degrees of freedom with a rigid upper body and is otherwise identical to Model A. Various quantities are calculated for both models. It is found that for the frequency range where the foot-to-upper-body transmission is important, the wobbling mass is able to reduce the transmissibility, to reduce the amplitude of the oscillation of the center of mass of the body, and therefore to reduce the amplitude of the fluctuation of the external force from the source of vibration. The model analysis reveals the mechanism for these reductions as follows: The oscillation of the wobbling mass in the upper body is carried by the oscillation of the rigid mass of the upper body and therefore the phase of the wobbling mass lags behind the phase of the rigid mass. For this reason, the average power which the wobbling mass in the upper body gives to the rigid mass of the upper body is negative.

Are electrically induced muscle cramps able to increase the cramp threshold frequency, when induced once a week?

The cramp threshold frequency (CTF) is known to be positively correlated with the individual cramp susceptibility. Here we assessed CTF changes after two bouts of electrically induced muscle cramps (EIMCs). The EIMCs (6×5 sec) were unilaterally induced twice (separated by one week) in the gastrocnemius of an intervention group (n=8), while 5 participants served as control. The CTF increased from 25.1±4.6 Hz at baseline to 31.4±9.0 Hz and 31.7±8.5 Hz 24 h after bout 1 and 2 (P<0.05). Thereafter, the CTF declined following both bouts to reach values of 28.0±6.7 Hz and 29.1±7.7 Hz after 72 h after bout 1 and 2. Creatine kinase (CK) activity and perceived discomfort during cramps was lower after bout 2 (P<0.05). CTF, CK, and discomfort did not change in CG. That is, a single bout of EIMCs induces a 24 h CTF increment and a second bout sustains this effect, while perceived discomfort and muscle damage decreases. This short term effect may help athletes to reduce the cramp susceptibility for an important match.

Plasma prolactin concentration increases during hyperoxia: A new hypothesis for its causes

The acute responses of plasma prolactin (PRL) concentration to inspiration of 80 Vol% oxygen over 45 min at rest were analyzed in 8 male subjects. After 15, 30, and 45 min of oxygen inhalation, a significant increase (p < .01) of arterial partial pressure of carbon dioxide (p CO2) in cerebrospinal fluid (CSF) due to well-established Haldane effect induced by hyperoxia lead to decreased (p 2 at these time points. Plasma PRL concentration was significantly increased (p

Serum cartilage oligomeric matrix protein: is there a repeated bout effect?

The primary aim of the present study was to investigate if there is a repeated bout effect for cartilage tissue, evident in the marker serum cartilage oligomeric matrix protein (sCOMP). Ten healthy male subjects (26.4±3.14 years) performed two high impact interventions (100 drop jumps with a 30 second interval) carried out at a 3 week interval. After each intervention, sCOMP and muscle soreness were assessed on 8 and 6 occasions respectively. Muscle soreness was determined via a visual analog scale with a maximum pain score of 10. sComp levels did not show a blunted response after the second bout (Bout 1: 12.2±3.3 U/L−1; Bout 2: 13.1±4.0 U/L−1; P>0.05). Remarkably, sCOMP increased from baseline levels by 16% after bout 1 and 15% after bout 2. Muscle soreness was blunted following the second intervention (Bout 1: 5.0±1.8; Bout 2: 1.6±0.8). Unlike the known repeated bout effect for muscle damage markers, sCOMP levels do not show a blunted response after two similar loading interventions. This information on biomarker behavior is essential to clinicians attempting to use this marker as an indicator of cartilage damage associated with the development or progression of osteoarthritis.