Specifically how the brain operates to regulate exercise and acts to terminate or extend an exercise bout is not fully known or understood. Several models exist and go some way to provide insight in to what processes might be occurring but we have much to learn about the neural correlates of exercise tolerance, regulation and termination. All models of exercise; the time trial, constant load tests to exhaustion and maximal oxygen uptake tests; involve a degree of tolerance to physiological signals but we have yet to elucidate how these signals are integrated in such a way that exercise continues or is terminated. Evidence of both neurotransmitter and psychological manipulations allowing for improved performance during exercise suggests the brain plays a key role in our capacity to prolong exercise to a greater extent than without these interventions. Thus, the aim of this thesis is to examine the cerebral responses to different exercise models and further to this, evaluate the role of changes within the internal and external environment on exercise performance. This is achieved by examining the neurophysiological responses to the three aforementioned exercise models in studies 1 and 3 and by evaluating the effects of the provision of exogenous cortisol in study 2 and via the provision of a motivational factor in study 3 on exercise performance. Study 1 examined the EEG response in the prefrontal cortex (PFC) and motor cortex (MC) during incremental exercise in relation to ventilatory parameters. Electroencephalography (EEG) activity at the motor (MC) and frontal cortices was measured during an incremental exercise test (IET) in 11 cyclists (peak oxygen uptake (푉̇푂2 푝푒푎푘 ) 4.1 0.74 (SD) l.min-1). EEG power spectral densities were calculated for alpha slow (S) (8-10Hz), alpha fast, (F) (10- 13Hz), Beta () (13-30Hz), and Gamma ( ) (30-40Hz) bandwidths. EEG data were calculated as % change from eyes open (EO) at baseline and a repeated measures analysis of variance (ANOVA) was performed on regions of interest (ROI), time and bandwidth. All EEG activity increased from 50% 푉̇푂2 푝푒푎푘 to ventilatory threshold (VT) (P= 0.045) and the respiratory compensation point (RCP; P = 0.019) and decreased from the RCP to end of exercise (END) (P=0.04). Significant differences between regions were found at the ventrolateral prefrontal cortex (VLPFC) and MC for both S and F. Both S and F increased from 50% 푉̇푂2 푝푒푎푘 to RCP (14.9 10.2 to 23.8 15.5 and 18.9 10.6 to 26.12 12.7 respectively) and then decreased to END (23.8 15.5 to 14.4 10.3 and 26.1 12.7, to 17.7 8.8 respectively) (P<0.01) and concomitantly only decreased significantly in MC in F from VT to END (P<0.05). These data show a decline in the EEG response to exercise in the PFC following the RCP, whilst alpha activity in the MC is preferentially maintained. Therefore, in this exercise model, changes within the PFC appear to play a role in exercise termination. Study 2 measured the cerebral responses to rest and the cerebral and neuromuscular responses to exercise in 10 male cyclists, when exogenous cortisol was provided prior to exercise. Using a double blind counterbalanced design, cyclists completed a placebo (PLA) and a cortisol (COR) trial (50mg cortisol; EXCOR). Each trial consisted of a rest period of 60 min followed by a 30 min time trial (TT) with 5 x 30s sprints at the following time intervals; 5, 11, 17, 23 and 29 min. Salivary cortisol (SaCOR), EEG and cerebral near infrared spectroscopy (NIRS) were measured at 15 30 45 and 60 min post ingestion. During exercise EEG, cerebral NIRS and electromyography (EMG) of the Vastus Lateralis (VL) and Rectus Femoris (RF) were measured during steady state periods and NIRS and EMG were measured during the 5 x 30s sprints. SaCOR was measured 10 min post exercise. At rest, SaCOR levels were higher (P<0.01) in COR compared to PLA (29.7 +/- 22.7 and 3.27 +/- 0.7 nmol/l, respectively). At 60 min S EEG response was higher in COR than PLA in the PFC (5.5 +/- 6.4% vs -0.02 +/- 8.7% change) (P<0.01). During the TT there was no difference in total km, average power or average sprint power. Peak power (PP) achieved was lower in COR than PLA (465.3 +/- 83.4 and 499.8 +/- 104.3) (P<0.05) and cerebral oxygenation was lower in COR (P<0.05). PP was negatively correlated with peak SaCOR levels (r=-0.79 P<0.01). These data show EXCOR significantly altered cerebral responses at rest and exercise. Overall exercise performance was not affected. However, PP achieved in the TT was reduced with EXCOR. These results have implications for our understanding of how stress and neuroendocrine function might affect exercise regulation. Study 3 was divided into two parts. Part 1 examined the cerebral responses to three different exercise models; time trial (TT), maximal oxygen uptake (푉̇푂2max), and a Time to Exhaustion test (TTE). Part 2 of the study was to examine the effect of the presence of time on performance, emotional and cerebral responses to exercise to a further TTE trial. 14 cyclists (11 male and 3 female) completed the study. Each participant completed the study in the following order; 푉̇푂2max test, TT, first time to exhaustion test (TTE1) and second time to exhaustion test (TTE2). To allow comparisons across exercise models where the intensity would vary (i.e. 푉̇푂2max vs TT) the exercise bouts were controlled for work done (kJ). The average power (W) achieved in the TT was then used as the intensity for both the TTE trials. During exercise EEG, NIRS and EMG of the VL and RF were measured throughout. In part 1, rate of perceived exertion (RPE) and the Feeling scale (FS) were recorded immediately post exercise. In part 2, emotional regulation (ER) was also scored. In part 1, there were no differences in total work done between all three tests 150.8 54.6 Kj for 푉̇푂2푚푎푥 and TT and 194.1 135.1 Kj for TTE. In the EMG response TT showed a trend (P = 0.051-0.08) to be higher than 푉̇푂2푚푎푥 at 50, 60, 80 and 90% of test complete and was significantly higher at 10, 20 and 30% (P <0.01) and at 40 and 70% (P <0.05). All tests changed significantly over time in each NIRs response; tissue oxygenation index (TOI), oxyhaemoglobin (OHb) and deoxyhaemoglobin (HHb). TOI was significantly lower over time (P<0.05) in TTE and TT compared to 푉̇푂2max. TTE elicited greater increases in HHb compared to 푉̇푂2max (P<0.05) and (OHb) was higher in TTE (P<0.05). At exercise termination in both prefrontal (PFC) and motor (MC) cortices EEG responses of alpha slow (s) and alpha fast (f) were higher than Beta () and Ga ( ) in 푉̇푂2푚푎푥 (P < 0.001 and P < 0.01 respectively). showed a trend to be higher in TTE1 compared to VO2 (P = 0.08). Normalised FS data showed that participants rated how they felt at the end of the 푉̇푂2푚푎푥 test as more pleasant (6.7 2.9) than either the TT (5.9 3.0) or the TTE (4.9 2.3) (P < 0.05). During the ES there was a significant increase in W, EMG, OHb and HHb (P<0.05). In part 2, TTE2 was significantly longer than TTE1 by 157.7 136.4 s (P < 0.01). TTE2 resulted in significantly higher TOI compared to TTE1 (-10.5 3.0 vs -3.8 3.1) (P < 0.001). OHb and HHb were higher at TTE2 compared to isotime (P <0.05). Overall change in EEG activity was greater in the PFC than the MC (P < 0.001) by 7.0 2.9 %. AS was elevated to a greater degree by the end of exercise in isotime and at TTE2 (P <0.05) compared to TTE1 in the MC and PFC by 7.57 5.7 and 9.9 11.2 % and by 18.2 18.2 and 19.4 16.7 % respectively. There were no differences in emotional scores. The novel findings were that each exercise model displayed different cerebral characteristics and that the ES preceded an increase in power output, EMG activity and was related to greater deoxygenation at the PFC. Further, the availability of time as a stimulus in a TTE test allowed participants to prolong their time to exhaustion. This was also associated with specific changes in cerebral responses. Chapter 5 examined the role of the PFC in exercise tolerance and termination and presents a model of potential cerebral pathways involved in the interpretation of physiological signals, combined with internal and external factors present in exercise environments, to determine exercise tolerance. These studies provide novel data on the cerebral responses to exercise and the neural correlates of exercise tolerance, termination and regulation.
|Qualification||Doctor of Philosophy|
|Award date||20 Mar 2016|
|Place of Publication||Australia|
|Publication status||Published - 2016|