May 2017 - Volume 49 - Issue 5

  • L. Bruce Gladden, PhD, FACSM
  • 0195-9131
  • 1530-0315
  • 12 issues / year
  • 6/81 in Sports Sciences
  • 4.041
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Again this month, I am directing attention to three particular articles. First, exercise-induced arterial hypoxemia (EIAH) is known to occur during heavy exercise in many highly endurance-trained individuals. In a large cohort of male distance runners (VO2max > 68 mL·kg-1·min-1), Constantini et al. demonstrated that EIAH prevalence is substantially higher during maximal treadmill exercise than the historically reported rate of about 50% for cy​cling. In fact, across all 124 subjects tested, 84% experienced at least moderate EIAH (arterial oxyhemoglobin saturation ≤ 93%). It is likely that exercise mode, sex, and age influence the prevalence and degree of arterial oxyhemoglobin desaturation. Therefore, the authors assert that a set prevalence percentage should not be used collectively to characterize EIAH, and each sub-population and mode of exercise should be considered separately.

On a different topic, the fatigue experienced after a soccer match is known to be multifactorial, sometimes taking days to fully resolve. Thomas and coauthors investigated recovery of both central and peripheral fatigue after a simulated soccer match. Simulated soccer elicited significant fatigue, which was both central and peripheral in origin, and persisted for up to 3 days post-match. The recovery of central nervous system function was more rapid, with a full recovery by 48 h post, whereas the decline in peripheral function persisted for up to 72 h. These data suggest that decrements in central nervous system function do contribute to the fatigue experienced after soccer, but the slower recovery of peripheral function indicates that processes at the muscle should remain the primary target of post-match recovery strategies.

Finally, cigarette smoke exposure is a primary risk factor for lung disease, but there are also numerous extrapulmonary risks. Yet there remains a paucity of studies on the effects of smoke exposure on the extrapulmonary organs in the period that precedes lung impairments. Bowen et al. used an integrative approach to reveal that mice exposed to cigarette-smoke experienced deterioration of the heart, the peripheral vascular endothelium, and the diaphragm, which all occurred before the onset of overt emphysema. However, 6 weeks of high-intensity treadmill training reversed or attenuated these extrapulmonary impairments and this was associated with an improved exercise capacity. If these results translate to humans, they suggest that cigarette smokers, even prior to lung impairments, may be predisposed to extrapulmonary damage to the heart, peripheral endothelium, and diaphragm which collectively reduce exercise capacity. However, these may be ameliorated by exercise training, a non-pharmacological intervention. 


​L. Bruce Gladden

School of Kinesiology
Auburn University

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