The intermittent activity profile of soccer match play increases the complexity of the physical demands. Laboratory models of soccer match play have value in controlled intervention studies, developed around manipulations of the activity profile to elicit a desired physiological or biomechanical response. Contemporary notational analyses suggest a profile comprising clusters of repeat sprint efforts, with implications for both biomechanical and physiological load. Eighteen male soccer players completed a 90-minute treadmill protocol based on clusters of repeat sprint efforts. Each 15-minute bout of exercise was quantified for uniaxial (medial-lateral [PLML], anterior-posterior [PLAP], and vertical [PLV]) and triaxial PlayerLoad (PLTotal). The relative contributions of the uniaxial PlayerLoad vectors (PLML%, PLAP%, and PLV%) were also examined. In addition to rating of perceived exertion, the physiological response comprised heart rate, blood lactate concentration, and both peak and average oxygen consumption. Triaxial PlayerLoad increased (p = 0.02) with exercise duration (T0-15 = 206.26 ± 14.37 a.u. and T45-60 = 214.51 ± 14.97 a.u.) and remained elevated throughout the second half. This fatigue effect was evident in both the PLML and PLAP movement planes. The mean relative contributions of PLV%:PLAP%:PLML% were consistent at ∼48:28:23. The physiological response was comparable with match play, and a similar magnitude of increase at ∼5% was observed in physiological parameters. Changes in PlayerLoad might reflect a change in movement quality with fatigue, with implications for both performance and injury risk, reflecting observations of match play. The high frequency of speed change elicits a 23% contribution from mediolateral load, negating the criticism of treadmill protocols as "linear."

Chronobiological investigations into core temperature during and after exercise can involve ambulatory measurements of intestinal temperature during actual competitions, esophageal temperature measurements in laboratory simulations, or rectal temperature, which can be measured in both the field and laboratory. These sites have yet to be compared during both morning and afternoon exercise and subsequent recovery. At 08:00 and 17:00 h, seven recreationally active males exercised at 70% peak oxygen uptake for 30 min and then recovered passively for 30 min. During the experiment, esophageal, rectal, intestinal, and skin temperatures, plus sweat loss, heart rate, and ratings of perceived exertion (RPE), were monitored. We found that the diurnal variation in intestinal temperature responses (0.45+/-0.32 degrees C; mean+/-SD) was significantly larger compared with rectal (0.33+/-0.24 degrees C) and, particularly, esophageal temperature responses (0.21+/-0.20 degrees C; p= 0.019). This reflected a greater difference of 0.25-0.40 degrees C between the esophagus and the other two sites in the afternoon, compared to inter-site differences of only 0.13-0.16 degrees C in the morning. Diurnal variation was small for skin temperature, heart rate, sweat loss, and RPE responses during exercise (p>0.05). Our data suggest that the relative differences between intestinal, rectal, and esophageal temperature during exercise and subsequent recovery depend on time of day to the extent that inferences from studies on experimental and applied chronobiology will be affected.

The aim of this study was to assess the physiological, perceptual, and mechanical measures associated with the completion of a simulated period of short-term soccer-specific fixture congestion. Ten male semi-professional soccer players completed three trials of a treadmill-based match simulation, with 48 hours intervening each trial. A repeated measures general linear model identified significantly (P= 0.02) lower knee flexor peak torque (PT) recorded at 300 degs[BULLET OPERATOR]s in the second (141.27 ± 28.51 Nm) and third trials (139.12 ± 26.23 Nm) when compared to the first (154.17 ± 35.25 Nm). Similarly, muscle soreness (MS) and PT data recorded at 60 degs[BULLET OPERATOR]s were significantly (P< 0.05) different in the third trial (MS= 42 ± 25 a.u; PT60= 131.10 ± 35.38 Nm) when compared to the first (MS= 29 ± 29 a.u; PT60= 145.61 ± 42.86 Nm). Significant (P= 0.003) differences were also observed for mean Bicep Femoris electromyography (EMGmean) between the third trial (T0-15= 126.36 ± 15.57 µV; T75-90= 52.18 ± 17.19 µV) and corresponding time points in the first trial (T0-15= 98.20 ± 23.49 µV; T75-90= 99.97 ± 39.81 µV). Cumulative increases in perceived exertion, heart rate, oxygen consumption, blood lactate concentrations, EMGmean, and PlayerLoad were recorded across each trial. MS and PT were also significantly different post-trial. There were however no significant main effects or interactions for the salivary Immunoglobulin A, and the medial-lateral PlayerLoad metrics. These data suggest a biomechanical and muscular emphasis with residual fatigue, with implications for injury risk and the development of recovery strategies.

Although vascular function is lower in the morning than afternoon, previous studies have not assessed the influence of prior sleep on this diurnal variation. The authors employed a semiconstant routine protocol to study the contribution of prior nocturnal sleep to the previously observed impairment in vascular function in the morning. Brachial artery vascular function was assessed using the flow-mediated dilation technique (FMD) in 9 healthy, physically active males (mean ± SD: 27 ± 9 yrs of age), at 08:00 and 16:00 h following, respectively, 3.29 ± .37 and 3.24 ± .57 h prior sleep estimated using actimetry. Heart rate and systolic and diastolic blood pressures were also measured. The data of the experimental sleep condition were compared with the data of the "normal" diurnal sleep condition, in which FMD measurements were obtained from 21 healthy individuals who slept only during the night, as usual, before the morning test session. The morning-afternoon difference in FMD was 1 ± 4% in the experimental sleep condition compared with 3 ± 4% in the normal sleep condition (p = .04). This difference was explained by FMD being 3 ± 3% lower in afternoon following the prior experimental sleep (p = .01). These data suggest that FMD is more dependent on the influence of supine sleep than the endogenous circadian timekeeper, in agreement with our previous finding that diurnal variation in FMD is influenced by exercise. These findings also raise the possibility of a lower homeostatic "set point" for vascular function following a period of sleep and in the absence of perturbing hemodynamic fluctuation.