The effects of reduced inspired oxygen fraction on the cardiorespiratory response to lower and upper body exercise

Abstract

Exposure to acute hypoxia has been used as a tool to investigate the mechanisms limiting oxygen consumption (VO₂) during predominately lower body (LB) exercise. However, the mechanisms limiting upper body (UB) exercise have been investigated to a lesser extent. Aim: To compare and contrast the cardiorespiratory responses to incremental LB and UB exercise to volitional exhaustion at three inspired oxygen fractions. Participants: Nine healthy, able bodied male participants (age 22 ± 2 years; height 180.6 ± 8.2 cm; body mass 78.7 ± 12.2 kg; estimated body fat 15.1 ± 6.3 %; estimated muscle mass 57.5 ± 6.5 %) gave their informed consent to participate in the study. Methods: In a counter balance designed study participants performed three LB and three UB incremental exercise tests to volitional exhaustion whilst breathing room air (N) or two levels of normobaric hypoxia (H₁ and H₂; F_IO₂ = 0.21, 0.15 and 0.13, respectively). Cycle ergometry (LB) and arm crank ergometry (UB) commenced at 70 and 35 W and were increased by 30 and 15 W every 3 min, respectively. Each workload was separated by 30 s passive recovery for the collection of bloods. Participants maintained a cadence of 70 rev.min^-1. Heart rate (HR), haemoglobin oxygen saturation (S_PO₂) and respiratory gases were collected in the final minute of each workload. Results: Peak power output (PPO) was reduced in both modes of exercise as F_IO₂ declined (P<0.001) and was highest during LB exercise in all conditions (P<0.001). During LB exercise peak oxygen consumption (VO_2 PEAK) declined with F_IO₂ (N 45 ± 7 vs. H₁ 39 ± 6 mL.kg^-1.min^-1; P<0.001 and H₁ vs. H₂ 34 ± 5 mL.kg^-1.min^-1; P<0.05). During UB exercise VO_{2 PEAK} declined between N (32 ± 6 mL.kg^-1.min^-1) and H1 (28 ± 5 mL.kg^-1.min^-1; P<0.001) and tended to be lower between H₁ and H₂ (26 ± 5 mL.kg^-1.min^-1; NS). During LB exercise 13 ± 8 and 24 ± 6 % reductions in VO_{2 PEAK} were evident when FIO2 decreased from N to H₁ and from N to H₂, while during UB exercise 15 ± 7 and 19 ± 9 % reductions were observed from normoxic values for H₁ and H₂, respectively. During LB exercise estimated cardiac output (Q ) was reduced between each F_IO₂ (N, 25.9 ± 2.0 vs. H₁, 23.6 ± 1.8 L.min^-1; P<0.05 and H₁ vs. H₂, 21.1 ± 1.1 L.min^-1, P<0.05). During UB exercise Q declined between N (20.7 ± 3.0 L.min^-1) and H₁ (18.2 ± 3.2 L.min^-1; P<0.01) and tended to be lower between H₁ and H₂ (17.0 ± 2.8 L.min^-1; NS). S_PO₂ declined as F_IO₂ reduced in LB and UB exercise and was lower during LB exercise (P<0.001, main effect). At N, H₁ and H₂ S_PO₂ was (LB vs. UB) 96 ± 2 vs. 97 ± 1 (NS), 83 ± 4 vs. 88 ± 5 (NS) and 74 ± 6 vs. 82 ± 4 (P<0.01) %. Extraction increased as F_IO₂ decreased in both modes of exercise (P<0.001, main effect). At N, H₁ and H₂ extraction (E) was 10 ± 10 (NS), 12 ± 12 (P<0.05) and 13 ± 11 (P<0.01) % lower during UB compared to LB exercise, respectively. Conclusions: Both central and peripheral factors contribute to limiting VO_{2 PEAK}, however their extent differs between LB and UB exercise. As previously shown LB exercise is limited centrally by oxygen delivery. However, the present study shows that during UB exercise although VO_{2 PEAK} declines as F_IO₂ is reduced this mode of exercise is limited by peripheral physiology.

Date of Award	2008
Original language	English
Awarding Institution	Coventry University
Supervisor	Doug Thake (Supervisor)