With increased professionalism in sport there has been a greater interest in the scientific approach to training and recovery of athletes. Applying appropriate training loads along with adequate recovery, is essential in gaining maximal adaptation in athletes, while minimizing harm such as overreaching, overtraining, injury and illness. Although appropriate physical stress is essential, stress for many athletes may come from areas other than training. Stress from may arise from social or environmental pressure, and for many athletes who combine elite athletic training with university study, academic workloads create significant stress which adds to the constant pressure to perform athletically. This research aimed to determine if subjective stressors were associated with counterproductive training adaptations in university athletes. Moreover, it aimed to elucidate if, and when, such stressors are most harmful (i.e., certain times of the academic year or sports training season). We monitored subjective (mood state, energy levels, academic stress, sleep quality/quantity, muscle soreness, training load) and objective (injury and illness) markers in 182 young (18–22 years) elite athletes over a 4-year period using a commercially available software package. Athletes combined full-time university study with elite sport and training obligations. Results suggest athletes were relatively un-stressed with high levels of energy at the beginning of each university semester, however, energy levels deteriorated along with sleep parameters toward the examination periods of the year. A logistical regression indicated decreased levels of perceived mood (0.89, 0.85–0.94, Odds Ratio and 95% confidence limits), sleep duration (0.94, 0.91–0.97) and increased academic stress (0.91, 0.88–0.94) and energy levels (1.07, 1.01–1.14) were able to predict injury in these athletes. Examination periods coincided with the highest stress levels and increased likelihood of illness. Additionally, a sudden and high increase in training workload during the preseason was associated with an elevated incidence of injury and illness (r = 0.63). In conclusion, young elite athletes undertaking full-time university study alongside their training and competition loads were vulnerable to increased levels of stress at certain periods of the year (pre-season and examination time). Monitoring and understanding these stressors may assist coaches and support staff in managing overall stress in these athletes.

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While the effects of instantaneous, single-bout exposure to hypoxia have been well researched, little is known about the autonomic response during, or as an adaptation to, repeated intermittent hypoxic exposure (IHE) in a sedentary population. Resting heart rate variability (HRV) and exercise capacity was assessed in 16 participants (8 receiving IHE, [Hyp] and 8 receiving a placebo treatment [C]) before and after a 4-week IHE intervention. Heart rate variability was also measured during an IHE session in the last week of the intervention. Post-intervention, the root mean squared successive difference (rMSSD) increased substantially in Hyp (71.6 ± 52.5%, mean change ± 90% confidence limits) compared to C suggesting an increase in vagal outflow. However, aside from a likely decrease in submaximal exercise heart rate in the Hyp group (-5.0 ± 6.4%) there was little evidence of improved exercise capacity. During the week 4 IHE measurement, HRV decreased during the hypoxic exposure (reduced R-R interval: -7.5 ± 3.2%; and rMSSD: -24.7 ± 17.3%) suggesting a decrease in the relative contribution of vagal activity. In summary, while 4 weeks of IHE is unlikely to improve maximal exercise capacity, it may be a useful means of increasing HRV in people unable to exercise.Keywords: autonomic nervous system, sedentary lifestyle, interval hypoxia, simulated altitude, physical fitness, health Heart rate variability (HRV) is the analysis of the variation in the beat to beat intervals in the heart rhythm, which reflects the autonomic nervous system (ANS) innervation on the sinus node (25). Heart rate variability is also responsive to the changes in the ANS associated with external stimuli such as real or simulated altitude (21). For example, an initially sharp increase in sympathetic activity is observed upon arrival at altitude (7, 28), which gradually declines through the acclimatization process (14, 23). The reduction in HRV is largely due to a reduction in the parasympathetic drive at the sinus node during hypoxia, the mechanism behind which has been well described by Roche et al. (20). The recovery of HRV to baseline levels upon return to normoxic ambient air depends on the length and severity of the initial exposure. That is, after 12 hours of continuous hypoxic exposure, a pronounced (dampened) effect on HRV is still evident an hour after returning to normoxic ambient air (7), but after a brief hypoxic exposure of 15 min, recovery is almost immediate (20).