Research Article: Rate dependent influence of arterial desaturation on self-selected exercise intensity during cycling

Date Published: March 3, 2017

Publisher: Public Library of Science

Author(s): Saro D. Farra, Stephen S. Cheung, Scott G. Thomas, Ira Jacobs, Alejandro Lucía.


The purpose of this study was to clarify if Ratings of Perceived Exertion (RPE) and self-selected exercise intensity are sensitive not only to alterations in the absolute level of arterial saturation (SPO2) but also the rate of change in SPO2. Twelve healthy participants (31.6 ± 3.9 y, 175.5 ± 7.7 cm, 73.3 ± 10.3 kg, 51 ± 7 mL·kg-1·min-1V˙O2peak) exercised four times on a cycle ergometer, freely adjusting power output (PO) to maintain RPE at 5 on Borg’s 10-point scale with no external feedback to indicate their exercise intensity. The fraction of inspired oxygen (FIO2) was reduced during three of those trials such that SPO2 decreased during exercise from starting values (>98%) to 70%. These trials were differentiated by the time over which the desaturation occurred: 3.9 ± 1.4 min, -8.7 ± 4.2%•min-1 (FAST), 11.0 ± 3.7 min, -2.8 ± 1.3%•min-1 (MED), and 19.5 ± 5.8 min, -1.5 ± 0.8%•min-1 (SLOW) (P < 0.001). Compared to stable PO throughout the control condition (no SPO2 manipulation), PO significantly decreased across the experimental conditions (FAST = 2.8 ± 2.1 W•% SPO2-1; MED = 2.5 ± 1.8 W•% SPO2-1; SLOW = 1.8 ± 1.6 W•% SPO2-1; P < 0.001). The rates of decline in PO during FAST and MED were similar, with both greater than SLOW. Our results confirm that decreases in absolute SPO2 impair exercise performance and that a faster rate of oxygen desaturation magnifies that impairment.

Partial Text

There are a myriad of mediators that have been associated with the development of fatigue during voluntary exercise such as increasing core body temperature (TC) [1, 2], accumulating concentrations of muscle and blood metabolites [3, 4], energy availability [5–7], and insufficient oxygen (O2) availability and/or transport [8, 9]. The research conducted to date in the area of exercise-induced fatigue demonstrates how the magnitude of changes in various ambient stressors, or the absolute magnitude of physiological strain associated with those stressors, augment the development of exercise-induced fatigue. Much less is known about how the rate of change of these same stressors and strains influence the homeostatic control systems that are thought to regulate the neuromuscular system during exercise. Should the rate of change in physiological strain be shown to influence exercise performance, it would support the proposition that the neuromuscular system is sensitive to feed-forward homeostatic control during exercise [10, 11], because feed-forward systems can be characterized as being able to differentiate between the instantaneous physiological state and the instantaneous rate of change within the system [12, 13].

This study is the first report of the influence of different rates of change in SPO2 on self-selected exercise intensity during constant RPE exercise. Despite exercising for less time, reaching a similar absolute change in SPO2 and achieving a comparable estimated oxygenation status in cerebral and muscle tissues, the relationship between self-selected exercise intensity and muscle activation with SPO2 was altered, such that a faster arterial deoxygenation rate was associated with a greater decline in submaximal self-selected work rate. These results suggest that the rate of arterial deoxygenation has a central depressant effect on submaximal self-selected exercise intensity, which is independent from the absolute level of SPO2. In contrast, the decline in PPO, and the associated sEMG, during the 5 s sprint was not affected by the rate of change of SPO2, suggesting that the magnitude of impairment to the overall capacity of the neuromuscular system was similar.




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