USING CRITICAL VELOCITIES TO SET TRAINING INTENSITIES

Determining training intensities is a real challenge for a swimming coach because of the few physiological variables measurable on pool-side. The use of blood markers such as lactate can help in the assessment of a swimmer’s aerobic endurance through the identification of a lactate threshold although a) blood sampling is not necessary an option and b) lactate threshold is such a low intensity (maintainable for hours) that it is not necessary very pertinent for setting training intensities. Similarly, performances over long distances (2-km or 3-km time trials) have been suggested to help defining training intensities but have their own limitations (pacing issues; physiological meaning). This talk will focus on the critical velocity concept, which in swimming research, and since the early nineties, has been suggested to be a valuable tool to assess aerobic endurance. A stop watch is the only equipment required to determine a swimmer’s critical velocity. The method relies solely on the measure of two or more performances (from 3 to 15-20 min) from which a distance vs time relationship is plotted and modelled using a 2-parameter model (y=ax+b). The slope of this relationship (a) is recognised as critical velocity, an intensity a swimmer would maintain, in theory, indefinitely. In reality, critical velocity can be sustained for around 30 minutes. This presentation will focus on the latest findings on critical velocity and the reasons why it can be seen as an attractive tool to set training intensities. Critical velocity will be compared with more classical “thresholds” and the findings will lead the audience to consider their own ways of setting their aerobic training zones. Some concepts such as aerobic power and capacity will be challenged in an attempt to gain an appreciation of the physiological mechanisms behind swimming endurance

Interactions between perceptions of fatigue, effort and affect decrease knee extensor endurance performance following upper body motor activity, independent of alterations to neuromuscular function

Prior exercise has previously been shown to impair subsequent endurance performance in non‐activated muscles. Declines in the neuromuscular function and altered perceptual/affective responses offer possible mechanisms through which endurance performance may be limited in these remote muscle groups. We thus conducted two experiments to better understand these performance‐limiting mechanisms. In the first experiment, we examined the effect of prior handgrip exercise on the behavioral, perceptual, and affective responses to a sustained, sub‐maximal contraction of the knee extensors. In the second experiment, transcranial magnetic stimulation was used to assess the neuromuscular function of the knee extensors before and after the handgrip exercise. The results of the first experiment demonstrated prior handgrip exercise increased the perceptions of effort and reduced affective valence during the subsequent knee extensor endurance exercise. Both effort and affect were associated with endurance performance. Subjective ratings of fatigue were also increased by the preceding handgrip exercise but were not directly related to knee extensor endurance performance. However, perceptions of fatigue were correlated with heightened effort perception and reduced affect during the knee extensor contraction. In the second experiment, prior handgrip exercise did not significantly alter the neuromuscular function of the knee extensors. The findings of the present study indicate that motor performance in the lower limbs following demanding exercise in the upper body appears to be regulated by complex, cognitive‐emotional interactions, which may emerge independent of altered neuromuscular function. Subjective fatigue states are implicated in the control of perceptual and affective processes responsible for the regulation of endurance performance

Toward the unity of pathological and exertional fatigue: a predictive processing model

Fatigue is a common experience in both health and disease. Yet, pathological (i.e., prolonged or chronic) and transient (i.e., exertional) fatigue symptoms are traditionally considered distinct, compounding a separation between interested research fields within the study of fatigue. Within the clinical neurosciences, nascent frameworks position pathological fatigue as a product of inference derived through hierarchical predictive processing. The metacognitive theory of dyshomeostasis (Stephan et al., 2016) states that pathological fatigue emerges from the metacognitive mechanism in which the detection of persistent mismatches between prior interoceptive predictions and ascending sensory evidence (i.e., prediction error) signals low evidence for internal generative models, which undermine an agent’s feeling of mastery over the body and is thus experienced phenomenologically as fatigue. Although acute, transient subjective symptoms of exertional fatigue have also been associated with increasing interoceptive prediction error, the dynamic computations that underlie its development have not been clearly defined. Here, drawing on the metacognitive theory of dyshomeostasis, we extend this account to offer an explicit description of the development of fatigue during extended periods of (physical) exertion. Accordingly, it is proposed that a loss of certainty or confidence in control predictions in response to persistent detection of prediction error features as a common foundation for the conscious experience of both pathological and nonpathological fatigue

The effects of a 6-week strength training on critical velocity, anaerobic running distance, 30-m sprint and yo-yo intermittent running test performances in male soccer players

The objectives of this study were to examine the effects of a moderate intensity strength training on changes in critical velocity (CV), anaerobic running distance (D'), sprint performance and Yo-Yo intermittent running test (Yo-Yo IR1) performances. Methods: two recreational soccer teams were divided in a soccer training only group (SO; n = 13) and a strength and soccer training group (ST; n = 13). Both groups were tested for values of CV, D', Yo-Yo IR1 distance and 30-m sprint time on two separate occasions (pre and post intervention). The ST group performed a concurrent 6-week upper and lower body strength and soccer training, whilst the SO group performed a soccer only training. Results: after the re-test of all variables, the ST demonstrated significant improvements for both, YoYo IR1 distance (p = 0.002) and CV values (p<0.001) with no significant changes in the SO group. 30-m sprint performance were slightly improved in the ST group with significantly decreased performance times identified in the SO group (p<0.001). Values for D' were slightly reduced in both groups (ST -44.5 m, 95% CI = -90.6 to 1.6; SO -42.6 m, 95% CI = -88.7 to 3.5). Conclusions: combining a 6-week moderate strength training with soccer training significantly improves CV, Yo-Yo IR1 whilst moderately improving 30-m sprint performances in non-previously resistance trained male soccer players. Critical Velocity can be recommended to coaches as an additional valid testing tool in soccer

High-intensity interval training improves VO2peak, maximal lactate accumulation, time trial and competition performance in 9–11-year-old swimmers

Training volume in swimming is usually very high when compared to the relatively short competition time. High-intensity interval training (HIIT) has been demonstrated to improve performance in a relatively short training period. The main purpose of the present study was to examine the effects of a 5-week HIIT versus high-volume training (HVT) in 9–11-year-old swimmers on competition performance, 100 and 2,000 m time (T100 m and T2,000 m), VO2peak and rate of maximal lactate accumulation (Lacmax). In a 5-week crossover study, 26 competitive swimmers with a mean (SD) age of 11.5 ± 1.4 years performed a training period of HIIT and HVT. Competition (P < 0.01; effect size = 0.48) and T2,000 m (P = 0.04; effect size = 0.21) performance increased following HIIT. No changes were found in T100 m (P = 0.20). Lacmax increased following HIIT (P < 0.01; effect size = 0.43) and decreased after HVT (P < 0.01; effect size = 0.51). VO2peak increased following both interventions (P < 0.05; effect sizes = 0.46–0.57). The increases in competition performance, T2,000 m, Lacmax and VO2peak following HIIT were achieved in significantly less training time (~2 h/week)