Peripheral muscle fatigue during intense exercise

• Main Author: Williams, Craig
• Published: University of Chichester 2005
• Subjects: 612.044; QP Physiology : RC1200 Sports Medicine
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418629

The role of adenine nucleotide metabolism is central to the electro-mechanical processes in muscular contraction. Interventions which alter the cellular micro-environment can impact on the fatigue response during exercise possibly mediated by the balance between ATP and ADP. This thesis examined the response of biochemical and physiological markers of muscle fatigue in dietary interventions aimed to alter the cellular environment. Contractile measures included force and relaxation times from contractions of the knee extensors, whilst biochemical markers included anunonia and lactate after voluntary isometric and incremental cycle exercise. Evoked contractile measurements afforded experimental objectivity independent of voluntary intervention whilst the voluntary measures afforded greater transferability. In Chapter 3 the relaxation time response to a train of evoked fatiguing contractions varied depending on the choice of relaxation method (upper exponential, lower exponential, 60-40 exponential, 100-75,95-45,75-37.5,75-25%). Methods describing the earlier portions of the relaxation curve slowed less during fatigue than those comprising the latter portions. Intra-session variability ranged from 1.3 to 5.02% and inter-session variation ranged from 2.85 to 6.97% dependent upon the adopted relaxation method. Such variability was comparable with other laboratories demonstrating significant intervention-induced changes. This has implications for future studies in the choice of relaxation method and magnitude of change necessary for identification of intervention-induced changes. In chapter 4 the magnitudes of change in MVC and time to fatigue in a voluntary isometric contraction between creatine and placebo supplementation were -3% and 2% respectively. The fatigue-induced slowing of evoked relaxation times was greater by -4% and these changes were not significant. The differences in markers of adenine nucleotide degradation after creatine and placebo supplementation were also insignificant. In chapter 5 the creatine supplementation-induced change in the decline in evoked force during a fatiguing train was -1 % but was insignificant. For the voluntary and evoked relaxation times, in chapter 5, the magnitude of changes between placebo and creatine supplementation were <1 %, and insignificant. The ingestion of NaHCO, accelerated the loss of evoked force during a fatiguing train, with a trend towards shorter relaxation times that was only evident in the 100-75% method. Bicarbonate ingestion resulted in higher plasma lactate but had minimal effect on markers of adenine nucleotide degradation. The rate of evoked force loss was greater when muscle glycogen stores were reduced by exercise and low CHO diet and this trend was reversed by additionally supplementing with creatine, but this was not associated with similar trends in markers of nucleotide degradation during incremental cycling. A novel finding of this study was that reducing muscle glycogen resulted in a more severe slowing of relaxation times that was reversed when combined with creatine supplementation. In this thesis the changes in the biochemical markers of ADP homeostasis (NH,) by dietary interventions were insignificant. However, the force and relaxation time responses may highlight the functional importance of maintaining ADP homeostasis. The fatigue-induced slowing of evoked relaxation times was different depending on the chosen method. Despite a smaller relative slowing during fatigue the 100-75% method appeared to be most sensitive to dietary interventions.