Abstract
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.
Original language | English |
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Qualification | Doctor of Philosophy |
Awarding Institution |
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Supervisors/Advisors |
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Award date | 20 Mar 2016 |
Place of Publication | Australia |
Publisher | |
Publication status | Published - 2016 |