Simultaneous 31p nmr spectroscopy and emg in exercising and
recovering human skeletal muscle - a correlation study.
Vestergaard-Poulsen, P., C. Thomsen, T. Sinkjer, and O. Henriksen.
Danish Research Center of Magnetic Resonance, Hvidovre Hospital,
University of Copenhagen, Hvidovre, Denmark and Center for Sensory
-Motor Interaction, Aalborg University, Aalborg, Denmark
APStracts 2:0282A, 1995.
A large number of studies have shown amplitude and spectral changes of
the electromyogram during exercise, leading to several theories of
how these changes might be related to the underlying metabolic
changes. The amplitude and spectral changes are generally interpreted
as changes in motor unit recruitment and a reduction of the muscle
fiber conduction velocity due to proton or lactate accumulation. This
study focuses on the causality of spectral changes of the surface
electromyogram and proton/lactate accumulation, and how the changes
in motor unit recruitment are related to the metabolic status of the
muscle. Simultaneous 31P nuclear magnetic resonance spectroscopy and
surface electromyography were performed during sustained static
exercise and recovery in healthy volunteers and a patient with
McArdles syndrome. A clear dissociation between the median power
frequency of the surface electromyogram and pH was seen in the
healthy volunteers during recovery and during exercise in the McArdle
patient. The results indicate that proton or lactate accumulation is
not primarily responsible for the spectral changes of the surface
electromyogram as previously suggested. The motor unit recruitment
(as judged by the root-mean-square of the surface electromyogram)
increased hyperbolically during the submaximal static exercise, with
decreasing phosphocreatine/inorganic phosphate ratio (PCr/Pi)
reaching maximum at PCr/Pi=0.6 (exhaustion), and seems to constitute
a consistent metabolic limit to the exercise. The increased
myoelectrical activity seen after exercise is not caused by an
incomplete recovery of phosphorous metabolism, pH or lactate, but
could probably be an impairment of the excitation-contraction
coupling.
Received 28 September 1994; accepted in final form 12 June 1995.
APS Manuscript Number A1005-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 11 July 1995.