Alleviating the negative effects of heat stress upon intermittent sprint exercise
The aim of this thesis was to quantify the physiological strain during intennittent sprint
exercise while under heat stress and to investigate interventions that may alleviate this strain.
In study one agreement between measures of body temperature from the rectum (criterion),
aural (ear) canal and intestines was assessed during a 40 min Cycling Intennittent Sprint
Protocol (CISP). Peak rectal temperatures in the temperate and hot conditions were 38.4 ± 0.3°C and 38.8 ± 0.6 °C, respectively. Both aural and intestinal temperature displayed
statistically acceptable agreement with rectal temperature within a range of 1.2°C. However,
this range of agreement was not deemed clinically acceptable, so rectal thermometry remained
the criterion measure.
In study two, heat strain was quantified using a physiological strain index (PSI) that classified
strain on a scale of 0 (no strain) to 10 (very high strain). The PSI was higher (8.2 ± 0.5 Units;
P < 0.05) whilst perfonning the CISP in hot compared to temperate conditions (7.0 ± 0.5
Units). The PSI was negatively correlated to peak power output (PPo; r = -0.80, P < 0.01) in
the heat and PPO declined after 10 sprints (P < 0.05). In the temperate condition, PSI showed
no correlation with PPO and no decline in PPO occurred.
Heat strain (PSI) in study three was lower during the CISP using a recovery intensity of 35%
peak oxygen consumption (VOzpeak) compared to 50% VOzpeak as had been used in studies
one and two. Concomitantly, the reduction in PPO of individual sprints was delayed by 5
sprints and average PPO was ~ 4% higher during 35% V02peak in the heat (1165 ± 154 W)
than during 50% VOzpeak in the heat (1120 ± 190 W; Main effect; P < 0.05).
To determine if pre-cooling could alleviate heat strain further, study four examined 20 minutes
of water immersion, or wearing an ice vest, or ice packs placed on the legs, compared to a
control condition. All pre-cooling techniques reduced the PSI and rectal temperature, and
water immersion and ice packs also reduced muscle temperature (0.7 ± 2.3 °C and 1.0 ± 6.6
°C; P < 0.05, respectively). Peak power output in the control condition (1132 ± 112 W) was
reduced by ~ 1% after water immersion (1126 ± 118 W), increased by ~1% after wearing the
ice vest (1149 ± 127 W) and ice packs improved PPO by ~4% (1181 ± 149 W; P < 0.05).
The combination of ice pack pre-cooling and heat acclimation was investigated for the final
study. Muscle damage and the cellular response to exercise induced heat strain were also
investigated. These were assessed through the changes in blood plasma creatine kinase (CK)
and heat stress protein 70 (HSP70) concentrations, respectively. Ten days of heat acclimation
improved PPO (~3%; Main effect, P < 0.05) during the CISP in the heat, but the further precooling
was not additionally ergogenic. During the CISP in the heat, prior to heat acclimation,
significant changes of plasma CK (208 ± 233 U/L; P < 0.05) and HSP70 (0.027 ± 0.016 ng'ml
1; P < 0.05) concentrations were observed. However these changes were not observed after
heat acclimation. This indicated increased cellular thermo-tolerance against temperature and
exercise induced muscle damage and may be linked to the ergogenic response observed.
This thesis confirms a direct relationship between heat strain and intermittent sprint exercise
performance whilst under heat stress. Manipulation of heat strain can be achieved by using
different interventions that can improve intermittent sprint exercise performance. These
results are most relevant to unacclimated games players competing in hot, humid conditions.