Possible mechanisms underlying the decrease in performance associated with overtraining syndrome (ots)

Introduction

While high-intensity interval training can improve performance [1] it is also well known that performing large amounts of high-intensity training may result in the athlete developing overtraining syndrome (OTS) [2]. To date, most research has been directed towards determining indicators of OTS in an effort to predict and therefore prevent overtraining in athletes. However, less attention has been given to determining why overtraining limits performance.  Possible mechanisms that can limit performance include an increase in metabolic end products such as lactate and hydrogen ions, muscle glycogen depletion,  earlier attainment of VO_2peak and increased "sensation" of fatigue, among others. The purpose of this study was to examine possible mechanisms underlying the performance limiting effects associated with OTS.

Methods

Twelve moderately-trained males performed a graded exercise test (GXT) to determine VO_2peak and lactate threshold (LT). Time-to-fatigue (TTF) at 20% of the difference between VO_2peak and LT was also assessed. Following these tests, subjects were randomly assigned to either a control (N=6) or training group (N=6). Those assigned to the training group were required to complete two high-intensity interval-training sessions per day, seven days per week for up to 3 weeks. Training consisted of up to 14, two-minute intervals performed at 150% of LT with one-minute rest. A TTF test replaced one of the training sessions every second day. Training continued until TTF decreased to 75% of the initial TTF test. Those assigned to the control group performed a TTF test every second day. Within 48 h of this final TTF test, a GXT was performed by the subject and their matched pair in the control group. Capillary blood was sampled and RPE determined at 75% of initial TTF and at TTF for all tests. VO₂ was also determined during all TTF tests.

Results

TTF was significantly different between the training and control groups on the final TTF test (P< 0.05). VO_2peak (L.min^-1) was not significantly different for either the training or control group pre or post training (P >0.05). For the training group, there was no significant difference between blood lactate concentration measured at 75% of TTF on day one and blood lactate concentration measured at fatigue on the final TTF test (P > 0.05). There were also no significant differences in VO₂ (L.min^-1) on day one at 75% fatigue, day one at fatigue or at fatigue on the final TTF test for either group. Final ratings of perceived exertion for the training group did not differ significantly from those measured on day one at TTF (P > 0.05).

Discussion / Conclusions

The high-intensity interval-training protocol resulted in significant performance decrements as assessed by the TTF test. These results are comparable to those of Fry et al. [3] who showed decreased time to exhaustion in five well-trained men after a period of intense training performed twice per day for ten days. Earlier accumulation of maximal levels of blood lactate, earlier attainment of VO_2peak and earlier sensation of fatigue did not seem to be the mechanisms underlying the performance decrement associated with this training protocol. There is little data reporting the effects of OTS on physiological and psychological responses at fatigue after training. However, the present results are similar to a previous study that also reported that maximal blood lactate concentrations did not change significantly during a time trial (approximately 60 minutes) after intensified training designed to induce OTS [4]. Future research should therefore examine additional mechanisms that may be associated with the earlier attainment of fatigue following overtraining.

 

References

[1]. Edge, J. et al. (2002). 7^th Annual Congress of the ECSS, Athens, Greece: 622.

[2]. Fry, R. et al. (1991). Sports Medicine, 12 (1), 32-65.

[3]. Fry, R. et al. (1994). British Journal of Sports Medicine, 28(4), 241-246.

[4[. Halsom, S. et al. (2002). Journal of Applied Physiology, 93, 947-956.