Purpose This study aimed to investigate the effects of different work and recovery characteristics on the W′ reconstitution and to test the predictive capabilities of the W′BAL model. Methods Eleven male participants (22 ± 3 yr, 55 ± 4 mL·kg−1⋅min−1) completed three to five constant work rate tests to determine CP and W′. Subsequently, subjects performed 12 experimental trials, each comprising two exhaustive constant work rate bouts (i.e., WB1 and WB2), interspersed by an active recovery interval. In each trial, work bout characteristics (P4 or P8, i.e., the work rate predicted to result in exhaustion in 4 and 8 min, respectively), recovery work rate (33% CP or 66% CP), and recovery duration (2, 4, or 6 min) were varied. Actual (W′ACT) and model-predicted (W′PRED) reconstitution values of W′ were calculated. Results After 2, 4, and 6 min recovery, W′ACT averaged 46% ± 2.7%, 51.2% ± 3.3%, and 59.4% ± 4.1%, respectively (P = 0.003). W′ACT was 9.4% higher after recovery at 33% CP than at 66% CP (56.9% ± 3.9% vs 47.5% ± 3.2%) (P = 0.019). P4 exercise yielded a 11.3% higher W′ACT than P8 exercise (57.8% ± 3.9% vs 46.5% ± 2.7%) (P = 0.001). W′ACT was higher than W′PRED in the conditions P4-2 min (+29.7%), P4-4 min (+18.4%), and P8-2 min (+18%) (P < 0.01). A strong correlation (R = 0.68) between the rate of W′ depletion and W′ recovery was found (P = 0.001). Conclusion This study demonstrated that both the work and recovery characteristics of a prior exhaustive exercise bout can affect the W′ reconstitution. Results revealed a slower W′ reconstitution when the rate of W′ depletion was slower as well. Furthermore, it was shown that the current W′BAL model underestimates actual W′ reconstitution, especially after shorter recovery.
Purpose: The aims of this study were 1) to model the temporal profile of W′ recovery after exhaustion, 2) to estimate the contribution of changing V ˙O2 kinetics to this recovery, and 3) to examine associations with aerobic fitness and muscle fiber type (MFT) distribution. Methods: Twenty-one men (age = 25 ± 2 yr, V ˙O2peak = 54.4 ± 5.3 mL•min −1 •kg −1 ) performed several constant load tests to determine critical power and W′ followed by eight trials to quantify W′ recovery. Each test consisted of two identical exhaustive work bouts (WB1 and WB2), separated by a variable recovery interval of 30, 60, 120, 180, 240, 300, 600, or 900 s. Gas exchange was measured and muscle biopsies were collected to determine MFT distribution. W′ recovery was quantified as observed W′ recovery (W′ OBS ), model-predicted W′ recovery (W′ BAL ), and W′ recovery corrected for changing V ˙O2 kinetics (W′ ADJ ). W′ OBS and W′ ADJ were modeled using mono-and biexponential fitting. Root-mean-square error (RMSE) and Akaike information criterion (ΔAIC C ) were used to evaluate the models' accuracy. Results: The W′ BAL model (τ = 524 ± 41 s) was associated with an RMSE of 18.6% in fitting W′ OBS and underestimated W′ recovery for all durations below 5 min (P < 0.002). Monoexponential modeling of W′ OBS resulted in τ = 104 s with RMSE = 6.4%. Biexponential modeling of W′ OBS resulted in τ 1 = 11 s and τ 2 = 256 s with RMSE = 1.7%. W′ ADJ was 11% ± 1.5% lower than W′ OBS (P < 0.001). ΔAIC C scores favored the biexponential model for W′ OBS , but not for W′ ADJ . V ˙O2peak (P = 0.009) but not MFT distribution (P = 0.303) was associated with W′ OBS . Conclusion: We showed that W′ recovery from exhaustion follows a two-phase exponential time course that is dependent on aerobic fitness. The appearance of a fast initial recovery phase was attributed to an enhanced aerobic energy provision resulting from changes in V ˙O2 kinetics.
Results of the present study strongly question true equivalence of CP, RCP, m[HHb]BP, and c[O2Hb]BP during ramp incremental exercise. Therefore, these exercise thresholds should not be used interchangeably.
The purpose of the present study was to assess the effects of aerobic interval training on muscle and brain oxygenation to incremental ramp exercise. Eleven physically active subjects performed a 6-week interval training period, proceeded and followed by an incremental ramp exercise to exhaustion (25 W min–1). Throughout the tests pulmonary gas exchange and muscle (Vastus Lateralis) and brain (prefrontal cortex) oxygenation [concentration of deoxygenated and oxygenated hemoglobin, HHb and O2Hb, and tissue oxygenation index (TOI)] were continuously recorded. Following the training intervention V.O2peak had increased with 7.8 ± 5.0% (P < 0.001). The slope of the decrease in muscle TOI had decreased (P = 0.017) 16.6 ± 6.4% and the amplitude of muscle HHb and totHb had increased (P < 0.001) 40.4 ± 15.8 and 125.3 ± 43.1%, respectively. The amplitude of brain O2Hb and totHb had increased (P < 0.05) 40.1 ± 18.7 and 26.8 ± 13.6%, respectively. The training intervention shifted breakpoints in muscle HHb, totHb and TOI, and brain O2Hb, HHb, totHb and TOI to a higher absolute work rate and V.O2 (P < 0.05). The relative (in %) change in V.O2peak was significantly correlated to relative (in %) change slope of muscle TOI (r = 0.69, P = 0.011) and amplitude of muscle HHb (r = 0.72, P = 0.003) and totHb (r = 0.52, P = 0.021), but not to changes in brain oxygenation. These results indicate that interval training affects both muscle and brain oxygenation, coinciding with an increase in aerobic fitness (i.e., V.O2peak). The relation between the change in V.O2peak and muscle but not brain oxygenation suggests that brain oxygenation per se is not a primary factor limiting exercise tolerance during incremental exercise.
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