Emma Kate Zadow

Validity of Power Settings of the Wahoo KICKR Power Trainer.

PURPOSE To assess the validity of power output settings of the Wahoo KICKR Power Trainer (KICKR) using a dynamic calibration rig (CALRIG) over a range of power outputs and cadences. METHODS Using the KICKR to set power outputs, powers of 100-999 W were assessed at cadences (controlled by the CALRIG) of 80, 90, 100, 110, and 120 rpm. RESULTS The KICKR displayed accurate measurements of power of 250-700 W at cadences of 80-120 rpm with a bias of -1.1% (95% limits of agreement [LoA] -3.6% to 1.4%). A larger mean bias in power was observed across the full range of power tested, 100-999 W (4.2%, 95% LoA -20.1% to 28.6%), due to larger biases of 100-200 and 750-999 W (4.5%, 95% LoA -2.3% to 11.3%, and 13.0%, 95% LoA -24.4% to 50.3%), respectively. CONCLUSIONS Compared with a CALRIG, the KICKR has acceptable accuracy reporting a small mean bias and narrow LoA in the measurement of power output of 250-700 W at cadences of 80-120 rpm. Caution should be applied by coaches and sports scientists when using the KICKR at power outputs of <200 W and >750 W due to the greater variability in recorded power.

Time of day and short-duration high-intensity exercise influences on coagulation and fibrinolysis

Abstract Exercise has been demonstrated to have considerable effects upon haemostasis, with activation dependent upon the duration and intensity of the exercise bout. In addition, markers of coagulation and fibrinolysis have been shown to possess circadian rhythms, peaking within the morning (0600–1200 h). Therefore, the time of day in which exercise is performed may influence the activation of the coagulation and fibrinolytic systems. This study aimed to examine coagulation and fibrinolytic responses to short-duration high-intensity exercise when completed at different times of the day. Fifteen male cyclists (VO2max: 60.3 ± 8.1 ml kg−1 min−1) completed a 4-km cycling time trial (TT) on five separate occasions at 0830, 1130, 1430, 1730 and 2030. Venous blood samples were obtained pre- and immediately post-exercise, and analysed for tissue factor (TF), tissue factor pathway inhibitor (TFPI), thrombin–anti-thrombin complexes (TAT) and D-Dimer. Exercise significantly increased plasma concentrations of TF (p < .0005), TFPI (p < .0006), TAT complexes (p < .0012) and D-Dimer (p < .0003). There was a time-of-day effect in pre-exercise TF (p = .004) and TFPI (p = .031), with 0830 greater than 1730 (p  .001), while 1730 was less than 2030 h (p = .008), respectively. There was no significant effect of time of day for TAT (p = .364) and D-Dimer (p = .228). Power output, TT time and heart rate were not significantly different between TTs (p > .05); however, percentage VO2max was greater at 1730 when compared to 2030 (p = .04). Due to a time-of-day effect present within TF, peaking at 0830, caution should be applied when prescribing short-duration high-intensity exercise bout within the morning in populations predisposed to hypercoagulability.

Acquired and Genetic Thrombotic Risk Factors in the Athlete

Abstract While athletes are often considered the epitome of health due to their physique and lowered potential for metabolic and cardiovascular diseases, they may also be at risk for the onset and development of venous thromboembolism (VTE). In an attempt to achieve and remain competitive, athletes are frequently exposed to numerous athlete‐specific risk factors, which may predispose them to VTE through the disruption of factors associated with Virchows triad (i.e., hypercoagulability, venous stasis, and vessel wall injury). Indeed, hypercoagulability within an athletic population has been well documented to occur due to a combination of multiple factors including exercise, dehydration, and polycythemia. Furthermore, venous stasis within an athletic population may occur as a direct result of prolonged periods of immobilization experienced when undertaking long‐distance travels for training and competition, recovery from injury, and overdevelopment of musculature. While all components of Virchows triad are disrupted, injury to the vessel wall has emerged as the most important factor contributing to thrombosis formation within an athletic population, due to its ability to influence multiple hemostatic mechanisms. Vessel wall injury within an athletic population is often related to repetitive microtrauma to the venous and arterial walls as a direct result of sport‐dependent trauma, in addition to high metabolic rates and repetitive blood monitoring. Although disturbances to Virchows triad may not be detrimental to most individuals, approximately 1 in 1,000 athletes will experience a potentially fatal post‐exercise thrombotic incidence. When acquired factors are considered in conjunction with genetic predispositions to hypercoagulability present in some athletes, an overall increased risk for VTE is present.

Intestinal Damage Following Short Duration Exercise at the Same Relative Intensity is Similar in Temperate and Hot Environments

Increasing temperature and exercise disrupt tight junctions of the gastrointestinal tract although the contribution of environmental temperature to intestinal damage when exercising is unknown. This study investigated the effect of 2 different environmental temperatures on intestinal damage when exercising at the same relative intensity. Twelve men (mean ± SD; body mass, 81.98 ± 7.95 kg; height, 182.6 ± 7.4 cm) completed randomised cycling trials (45 min, 70% maximal oxygen uptake) in 30 °C/40% relative humidity (RH) and 20 °C/40%RH. A subset of participants (n = 5) also completed a seated passive trial (30 °C/40%RH). Rectal temperature and thermal sensation (TSS) were recorded during each trial and venous blood samples collected at pre- and post-trial for the analysis of intestinal fatty acid-binding protein (I-FABP) level as a marker of intestinal damage. Oxygen uptake was similar between 30 °C and 20 °C exercise trials, as intended (p = 0.94). I-FABP increased after exercise at 30 °C (pre-exercise: 585 ± 188 pg·mL-1; postexercise: 954 ± 411 pg·mL-1) and 20 °C (pre-exercise: 571 ± 175 pg·mL-1; postexercise: 852 ± 317 pg·mL-1) (p < 0.0001) but the magnitude of damage was similar between temperatures (p = 0.58). There was no significant increase in I-FABP concentration following passive heat exposure (p = 0.59). Rectal temperature increased during exercise trials (p < 0.001), but not the passive trial (p = 0.084). TSS increased more when exercising in 30 °C compared with 20 °C (p < 0.001). There was an increase in TSS during the passive heat trial (p = 0.03). Intestinal damage, as measured by I-FABP, following exercise in the heat was similar to when exercising in a cooler environment at the same relative intensity. Passive heat exposure did not increase I-FABP. It is suggested that when exercising in conditions of compensable heat stress, the increase in intestinal damage is predominantly attributable to the exercise component, rather than environmental conditions.

Validity of the Wahoo KICKR Power Trainer and Reliability of a 4 km Cycle Time Trial

Purpose : To assess the validity of power and the reliability of a 4 km cycle time trial (TT) using the Wahoo KICKR Power Trainer. Methods : The Wahoo KICKR power output was assessed using a dynamic calibration rig (DCR) over power outputs of 100-600 W at cadences of 80, 90 and 100 rpm. Twelve trained male cyclists (mean ± SD; age: 34.0 ± 6.5 years, height: 178.4 ± 6.2 cm, body mass: 76.8 ± 9.6 kg) completed three 4 km TTs on the Wahoo KICKR, each separated by a minimum of two and a maximum of three days. Mean power (W), cadence (rpm), speed (km.h-1), heart rate (bpm) and total time (s) were recorded for each TT while ratings of effort (0-10) and sessional ratings of perceived exertion (6-20) were collected immediately and 10 mins post each TT. Results: Bias for differences in power (%) recorded by the Wahoo KICKR to the DCR was 0.8% (95%LOA -4.0- 5.6%) (Figure 1). Average ICC between trials (2-1, 3-2, 3-1) for power was 0.95 (95%CI 0.89-0.98), cadence 0.80 (95 %CI 0.60- 0.92), speed 0.70 (95%CI 0.46- 0.88), heart rate 0.93 (95%CI 0.85- 0.98) and total time 0.75 (95%CI 0.53-0.90). Coefficient of variation was 2.9%, 4.5%, 3.7%, 1.5%, 3.6% for power, cadence, speed, heart rate and total time, respectively (Table 2). Results: sIgA concentrations ( I¼ g.m l I„ U° ) before and after the treadmill were [mean 595 , s = 64.6 and mean 841 , s = 76.3 ] and before and after the bike were [mean 593.9 , s = 51.1 and 778.8 s = 99.3 ]. sIgA secretion rates ( I¼ g.min I„ U° ) before and after the treadmill were [mean 396.2, s = 73.7 and 223 s = 99.6 ] and before and after the bike were [mean 284.1 , s = 74.3 and 216.6 , s = 29.5 ]. Saliva flow rates ( I¼ l.min I„ U° ) before and after the treadmill were [mean 657.8, s = 92.2 and 289.3, s = 56.6] and before and after the bike were [mean 487.2, s = 123.3 and 319.5, s = 66.5]. The results indicated that sIgA secretion rate (P < 0.028) and saliva flow rate (P < 0.01) were significantly decreased following the 2 hour treadmill protocol but not the 2 hour bike protocol. sIgA concentration was also significantly elevated following the treadmill (P < 0.01), with no significant increase following the bike protocol. Conclusion: These results suggest that when compared to a DCR, the Wahoo KICKR Power Trainer displays a small mean bias across all measures of power, with caution to be applied at the lower ranges of power output (<200 W). When completed on the Wahoo KICKR Power Trainer, a 4 km TT in trained cyclists is highly reproducible.