title: Effect of exercise-induced arterial O2 desaturation on VO2max in women.
abstract: OBJECTIVE
  We have recently reported that many healthy habitually active women experience exercise induced arterial hypoxemia (EIAH). We questioned whether EIAH affected VO2max in this population and whether the effect was similar to that reported in men.
  
  
  METHODS
  Twenty-five healthy young women with widely varying fitness levels (VO2max, 56.7 +/- 1.5 mL x kg(-1) x min(-1); range: 41-70 mL x kg(-1) x min(-1)) and normal resting lung function performed two randomized incremental treadmill tests to VO2max (FIO2: 0.21 or 0.26) during the follicular phase of their menstrual cycle. Arterial blood samples were taken at rest and near the end of each workload during the normoxic test.
  
  
  RESULTS
  During room air breathing at VO2max, SaO2 decreased to 91.8 +/- 0.4% (range 87-95%). With 0.26 FIO2, SaO2, at VO2max remained near resting levels and averaged 96.8 +/- 0.1% (range 96-98%). When arterial O2 desaturation was prevented via increased FIO2, VO2max increased in 22 of the 25 subjects and in proportion to the degree of arterial O2 desaturation experienced in normoxia (r = 0.88). The improvement in VO2max when systemic normoxia was maintained averaged 6.3 +/- 0.3% (range 0 to +15%) and the slope of the relationship was approximately 2% increase in VO2max for every 1% decrement in the arterial oxygen saturation below resting values. About 75% of the increase in VO2max resulted from an increase in VO2 at a fixed maximal work rate and exercise duration, and the remainder resulted from an increase in maximal work rate.
  
  
  CONCLUSIONS
  These data demonstrate that even small amounts of EIAH (i.e., >3% delta SaO2 below rest) have a significant detrimental effect on VO2max in habitually active women with a wide range of VO2max. In combination with our previous findings documenting EIAH in females, we propose that inadequate pulmonary structure/function in many habitually active women serves as a primary limiting factor in maximal O2 transport and utilization during maximal exercise.
authors.affiliation: Department Preventive Medicine, University of Wisconsin, Madison 53705, USA. caharms@ksu.edu
authors.forename: C A
authors.initials: CA
authors.lastname: Harms
authors.forename: S R
authors.initials: SR
authors.lastname: McClaran
authors.forename: G A
authors.initials: GA
authors.lastname: Nickele
authors.forename: D F
authors.initials: DF
authors.lastname: Pegelow
authors.forename: W B
authors.initials: WB
authors.lastname: Nelson
authors.forename: J A
authors.initials: JA
authors.lastname: Dempsey
mesh_terms: D000293:Adolescent; D000328:Adult; D015444:Exercise / Q000502:physiology*; D005260:Female; D006801:Humans; D018496:Hyperoxia; D000860:Hypoxia / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption / Q000502:physiology; D010809:Physical Fitness / Q000502:physiology
chemical_list: D010100:Oxygen