August 2018 - Volume 50 - Issue 8

  • L. Bruce Gladden, PhD, FACSM
  • 0195-9131
  • 1530-0315
  • 12 issues / year
  • 7/81 in Sports Sciences
  • 4.291

​​​​​​​​​​​​​​​​​​​​​​​​​Allow me to direct your attention to three particularly intriguing articles in this month's issue of MSSE® (August 2018). In the first of these, Guest et al. recruited 101 male athletes to determine whether their genes affected their response to supplemental caffeine, and subsequent performance during a 10-km cycling time trial. Overall, caffeine appears to be beneficial to endurance exercise; however, there is considerable interindividual variability with studies showing improved, neutral, or impaired performance with caffeine use. Variation in the CYP1A2 gene, which affects the rate of caffeine metabolism, may explain some of these differences. Findings from this paper showed that low and moderate doses of caffeine improved cycling time, but only in those with the AA genotype who are "fast" metabolizers. Caffeine had no effect or diminished performance in those with the AC and CC genotypes, respectively. This study demonstrates that not all athletes benefit from caffeine and that CYP1A2 genotype is a factor in the effects of caffeine supplementation.

Klass and colleagues explored the effect of noradrenergic neuromodulation on the maximal force and fine control of muscle force in association with changes in corticospinal and spinal excitability. To that end, they compared motor performance after ingestion of Reboxetine, a norepinephrine reuptake inhibitor, to that in a placebo condition. Their results showed an increase in both maximal force and force steadiness under Reboxetine. These motor performance improvements were accompanied by greater voluntary activation and corticospinal excitability which was mainly related to an increase in spinal excitability. These results suggest that, through its impact at both cortical and spinal levels, norepinephrine enhances motor performance.

Practitioners prescribing aerobic activities often utilize a percentage of HRpeak to identify the desired exercise intensity, assuming a linear relationship between HR and VO2. In young physically active subjects, during constant work rate exercise, Zuccarelli et al. observed a slow component of the HR kinetics in the moderate-intensity domain and, above the gas exchange threshold, a greater relative amplitude of the HR slow component compared to the VO2 slow component. Thus, the ''translation'' of work rates, or of percentages of VO2peak associated with variables such as the gas exchange threshold or critical power, into HR values, may not be straightforward. Exercise prescriptions at specific HR values, when carried out for periods longer than a few minutes, should consider this phenomenon, particularly in patients in whom this dissociation of the heart rate and VO2 slow components may be more pronounced.​


L. Bruce Gladden

School of Kinesiology
Auburn University

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