european college of sport science

OP-PH16 Physiology 16
tween the contractile filaments often in the I-band (10-20% of total glycogen). And (3) also a minor population is located in the subsarcolemmal
space just beneath the sarcolemma together with e.g. nuclei, mitochondria, golgi complex and lysosomes (5-20% of total
glycogen). Their individual roles in muscle function remain today elusive.
Method
In this study 11 young (24 ± 0.5 years) and 9 old (67 ± 1 years) men had their quadriceps muscle immobilised for 14 days by casting from
hip to ankle of one of their legs chosen by random. Muscle biopsies were obtained from vastus lateralis before and after the immobilisation
period and muscle specimens were prepared for TEM contrasting in favour of glycogen as described by Marchand et al. (2002).
From each of the young and old men 5 were randomly selected for the TEM analysis, which was carried out on images of x40 000 magnifications
photographed on systematically randomised locations. All fibres were fibre typed based on mitochondria volume and z-line
width. Values are presented as means ± SEM.
Results: There was a strong interaction of immobilisation and subcellular glycogen population (p < 0.0001), post hoc analysis showed that
immobilisation induced a decrement of intramyofibrillar glycogen by 44 ± 5 % (p < 0.001), which was independent of fibre type and age
group. In contrast, immobilisation did not change the glycogen content localised in the intermyofibrillar or subsarcolemmal spaces. Thus,
immobilisation lowered the intra- to intermyofibrillar glycogen ratio from 0.15 ± 0.01 to 0.07 ± 0.005.
Discussion: This study showed a novel regulation of subcellular glycogen content in human skeletal muscle: a halving in one population
and no change in two other populations due to 14 days of immobilisation. This can be interpreted as follows. Firstly, a translocation
mechanism of glycogen from the relatively minor store in the intramyofibrillar space to the major intermyofibrillar store exists and is active
during immobilisation. Secondly, during the 14 days of immobilisation a degradation of intramyofibrillar glycogen is incompletely replenished
suggesting suboptimal glucose uptake signalling.
References
Marchand I, Chorneyko K, Tarnopolsky M, Hamilton S, Shearer J, Potvin J and Graham T. E. (2002). J Appl Physiol, 93, 1598-1607
ELECTROMYOGRAPHIC ACTIVITY DURING WHOLE BODY VIBRATION: MOTION ARTIFACTS OR STRETCH REFLEX RE-
SPONSES?
KRAMER, A., RITZMANN, R., GRUBER, M., GOLLHOFER, A., TAUBE, W.
ALBERT-LUDWIGS-UNIVERSITÄT FREIBURG, UNIVERSITÄT POTSDAM
Introduction: The validity of electromyographic (EMG) data recorded during whole body vibration (WBV) is discussed controversially. Some
authors have suggested filtering because of vibration-induced motion artifacts (Abercromby et al., 2007; Fratini et al., 2008) while others
have interpreted the EMG signals as muscular activity caused at least partly by stretch reflexes (Mesters et al., 2002; Rittweger et al.,
2003; Kvorning et al., 2006). The aim of this study was to investigate the origin of the EMG signal during WBV using several independent
approaches.
Methods: The EMG activity of four leg muscles was determined in ten healthy subjects during WBV. Additionally, to test whether the
movement of the cables and electrodes during WBV caused motion artifacts in the EMG signal, special dummy electrodes were developed,
thus providing a signal only influenced by motion artifacts, without interference from muscle signals. The three following protocols
had the same goal, but used a physiological approach and in addition they were designed to verify whether the characteristics of the
EMG signal were consistent with the characteristics of a stretch reflex response. For that purpose, frequency spectra and latencies of
mechanically evoked stretch reflexes and of the EMG signal during WBV were evaluated and compared. Moreover, pressure application
via a blood pressure cuff served to reduce the amplitude of the short latency component of the stretch reflex, thus allowing an estimation
of the stretch reflex contribution to the EMG signal.
Results: The dummy electrodes, designed to monitor motion artifacts, showed almost no activity during WBV. The frequency analyses
showed no evidence of motion artifacts. The latencies of the stretch reflex responses evoked by the dorsiflexions in an ankle ergometer
were almost identical to the supposed stretch reflex responses during vibration (differences of less than one millisecond). Pressure application
significantly reduced the amplitude of both the supposed stretch reflexes during vibration (by 61±17 %, p