Degree Type


Date of Award


Degree Name

Master of Science




Exercise & Sport Science (Biological Basis of Physical Activity)


Muscle H+ accumulation may be the primary causal factor in limiting high-intensity exercise (HIE) performance. It is proposed that eccentric-induced muscle damage caused by unaccustomed eccentric muscle contractions may lead to higher muscle lactate and H+ concentrations during HIE and an impaired ability to remove these metabolites after completion of the exercise bout. Impaired clearance of muscle lactate and H+ may be a direct effect of damage to the primary inter-cellular (and intra-cellular) transporters of lactate and H+, the monocarboxylate transporters (MCT). Eight male college-aged subjects performed either a muscle-damaging eccentric resistance exercise bout (ECC) or a maximal concentric (CON) bout of 100 maximal isokinetic repetitions. Two days following the resistance bout, subjects performed a graded HIE cycling bout to exhaustion. Muscle samples were taken from the right vastus lateralis prior to the HIE bout, immediately post-HIE, and 10 minutes following the HIE bout. Muscle lactate concentration, muscle pH, and muscle buffer capacity (β[subscript m]) were calculated. The ECC bout led to considerable muscle soreness (8 ± 2 arbitrary units vs 0 ± 0 for CON) and raised concentrations of plasma creatine kinase (ECC: 847 ± 330 U/L; CON: 226 ± 40 U/L). There was no significant interaction between ECC and CON across time in muscle lactate concentration, muscle pH, in-vivo β[subscript m] or in-vitro β[subscript m]. However, a moderate-to-large effect size for muscle lactate and H+ concentrations both immediately post-HIE and 10 minutes post-HIE indicate lower concentrations for ECC than in CON. Both groups showed similar rate of recovery of muscle lactate concentration over the 10 minutes post-HIE. There were no significant differences between groups in exercise performance. The slightly lower accumulation of lactate and H+ during the HIE bout following ECC, without a subsequent change in either the rate of recovery post-HIE or in the β[subscript m], suggests that eccentric-induced muscle damage may lead to lower production of lactate and H+ during HIE. The impaired ability of eccentrically damaged muscle to produce lactate and H+ during subsequent HIE may represent reduced glycolytic potential.


Copyright Owner

Andrew Keech



OCLC Number


File Format


File Size

107 pages