Abstract
Eccentric exercise-induced muscle damage (EEIMD) is experienced following unaccustomed
eccentric-biased exercise. Gaps in knowledge on aspects of the metabolic response to
EEIMD exist, particularly on in vivo metabolism. The aim of this thesis is to provide empirical
evidence to advance the scientific knowledge and understanding of EEIMD by investigating the
metabolic responses following acute and adaptive bouts of eccentric exercise. Eccentric exercise
causes changes to the ultrastructure of skeletal muscle and may alter the ability of the muscle to
store and utilise intracellular substrates such as glycogen and intramyocellular lipid
(IMCL). Using expired respiratory gases collected during one legged cycling to estimate whole body
substrate utilisation, the first study showed that acute bouts of eccentric exercise alter the
pattern of substrate selection. The effect of EEIMD on substrate utilisation during one legged
cycling revealed significantly higher rates of CHO oxidation in EEIMD and that the CHO oxidation
further increased during one legged cycling at 48 hours. This is suggestive of greater reliance
upon muscle glycogen during subsequent bouts of exercise. The utilisation of nuclear magnetic
resonance (NMR) spectroscopy to measure phosphate compounds and IMCL content of the vastus
lateralis allowed for examination of changes in substrate storage following exposure to an acute
bout of eccentric exercise. The second study showed that, following EEIMD, using proton
spectroscopy (1H-MRS), alterations occur in the IMCL pool within skeletal muscle with
a higher concentration evident in the eccentric leg at 24 hours but the trend had been reversed at
48 hours with higher concentrations of IMCL in the concentric leg at 48 hours. Using phosphorous
spectroscopy (31P-MRS) there was also a significant alteration for resting phosphate stores
with increases in inorganic phosphate concentration ([Pi]) in EEIMD. Eccentric exercise also
alters the physiological response to normal levels of insulin and can be defined as "transient
insulin resistance". Repeated eccentric exercise training initiates a protective adaptation so
that recovery results in reduced symptoms of damage in the repeat bout compared to the initial
bout. The third study investigated; via a standard 75g oral glucose tolerance test (OGTT), whether
disruptions to glucose and insulin responses following eccentric exercise could be attenuated after
a repeated bout of eccentric exercise. There was no change in the
insulin response, in comparison to a control trial, 48 hours after a bout of 100 squats of
30% body mass; this formed the eccentric exercise for the study. A subsequent bout of the same eccentric exercise did not attenuate the insulin response. It is not known if repeated exposure to eccentric exercise can attenuate increases in indirect measures of intracellular metabolism (Pi / PCr) following EEIMD, as seen in study two. Study four utilised 31P-MRS to examine the effect of EEIMD on intramyocellular phosphate stores in skeletal muscle, which had been concentrically or eccentrically trained. The data revealed that increases in skeletal muscle phosphate metabolism were not attenuated following exposure to repeated bouts of eccentric exercise and decrements in force generating capacity of muscle following EEIMD must be mediated by central factors. The four studies have provided novel insights into the influence of eccentric, muscle-damaging exercise on the metabolic response of skeletal muscle.
Date
2011
Rights
The Author
Publisher
Massey University
Description
The contents of chapter 4 form the basis of the following publication: Hughes, J. D., Johnson, N. A., Brown, S. J., Sachinwalla, T., Walton, D. W., & Stannard, S. R. (2010). Effects of eccentric exercise-induced muscle damage on intramyocellular lipid concentration and high energy phosphates. European Journal of Applied Physiology, 110(6), 1135-1141. doi: 10.1007/s00421-010-1605-5 (The original publication is available at www.springerlink.com)