Abstract
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-1 ) 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.
Highlights
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 [5,6,7], and insufficient oxygen (O2) availability and/or transport [8, 9]
SPO2 decreased from starting values to approximately 70%, in 3.9 ± 1.4 min, 11.0 ± 3.7 min, 19.5 ± 5.8 min for the FAST, MED, and SLOW conditions respectively, with the rate of arterial desaturation significantly different between the conditions (Table 2)(P < 0.001)
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
Summary
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 [5,6,7], and insufficient oxygen (O2) availability and/or transport [8, 9]. Isolating the feed-forward contribution to voluntary exercise performance can be challenging, Tucker [11] proposed a conceptual model, known as ‘constant RPE exercise’, that may be useful to further this line of research In this model, the investigator dictates a target RPE (known as the RPE template), and the subject maintains that RPE by freely adjusting exercise intensity. Other forms of self-paced exercise, such as a time trial does not allow for this consistency, as exercise intensity and the associated physiological responses are constantly changing Such a consistent and reproducible steady state over the duration of an exercise trial lends itself to experimental manipulation seeking to separate the impact of the absolute magnitude of physiological strain from the rate of physiological strain development on exercise performance as the manipulation can be applied irrespective of time
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