Geoffrey L. Hartley

The effect of a covert manipulation of ambient temperature on heat storage and voluntary exercise intensity.

The modulation of sub-maximal voluntary exercise intensity during heat stress has been suggested as a behavioral response to maintain homeostasis; however, the relationship between thermophysiological cues and the associated response remains unclear. Awareness of an environmental manipulation may influence anticipatory planning before the start of exercise, making it difficult to isolate the dynamic integration of thermophysiological afferents during exercise itself. The purpose of the present study was to examine the direct real-time relationship between thermophysiological afferents and the behavioral response of voluntary exercise intensity. Participants were tasked with cycling at a constant rating of perceived exertion while ambient temperature (T(a)) was covertly changed from 20 °C to 35 °C and then back to 20 °C at 20-minute intervals. Overall, power output (PO) and heat storage, quantified using repeated measures ANOVA, changed significantly over 20-minute intervals (135 ± 39 W, 133 ± 46 W, 120 ± 45 W; 52.35 ± 36.15 W·m(-2), 66.34 ± 22.02 W·m(-2), -66.53 ± 56.01 W·m(-2)). The synchronicity of PO fluctuations with changes in thermophysiological status was quantified using Auto-Regressive Integrated Moving Average (ARIMA) time series analysis. Fluctuations in PO were not synchronized in real time with changes in T(a); heat storage; rectal, skin, or mean body temperature; or sweat rate (stationary-r(2) ≤ 0.10 and Ljung-Box statistic > 0.05 for all variables). We conclude that, while the thermal environment affects physiological responses and voluntary power output while cycling at a constant perceived effort, the behavioral response of voluntary exercise intensity did not depend on a direct response to real-time integration of thermal afferent inputs.

Oxidative fuel selection and shivering thermogenesis during a 12- and 24-h cold-survival simulation

Because the majority of cold exposure studies are constrained to short-term durations of several hours, the long-term metabolic demands of cold exposure, such as during survival situations, remain largely unknown. The present study provides the first estimates of thermogenic rate, oxidative fuel selection, and muscle recruitment during a 24-h cold-survival simulation. Using combined indirect calorimetry and electrophysiological and isotopic methods, changes in muscle glycogen, total carbohydrate, lipid, protein oxidation, muscle recruitment, and whole body thermogenic rate were determined in underfed and noncold-acclimatized men during a simulated accidental exposure to 7.5 °C for 12 to 24 h. In noncold-acclimatized healthy men, cold exposure induced a decrease of ∼0.8 °C in core temperature and a decrease of ∼6.1 °C in mean skin temperature (range, 5.4-6.9 °C). Results showed that total heat production increased by approximately 1.3- to 1.5-fold in the cold and remained constant throughout cold exposure. Interestingly, this constant rise in Ḣprod and shivering intensity was accompanied by a large modification in fuel selection that occurred between 6 and 12 h; total carbohydrate oxidation decreased by 2.4-fold, and lipid oxidation doubled progressively from baseline to 24 h. Clearly, such changes in fuel selection dramatically reduces the utilization of limited muscle glycogen reserves, thus extending the predicted time to muscle glycogen depletion to as much as 15 days rather than the previous estimates of approximately 30-40 h. Further research is needed to determine whether this would also be the case under different nutritional and/or colder conditions.

Corticospinal excitability is associated with hypocapnia but not changes in cerebral blood flow

Reductions in cerebral blood flow (CBF) may be implicated in the development of neuromuscular fatigue; however, the contribution from hypocapnic‐induced reductions (i.e. P ETC O2 ) in CBF versus reductions in CBF per se has yet to be isolated. We assessed neuromuscular function while using indomethacin to selectively reduce CBF without changes in P ETC O2 and controlled hyperventilation‐induced hypocapnia to reduce both CBF and P ETC O2 . Increased corticospinal excitability appears to be exclusive to reductions in P ETC O2 but not reductions in CBF, whereas sub‐optimal voluntary output from the motor cortex is moderately associated with decreased CBF independent of changes in P ETC O2 . These findings suggest that changes in CBF and P ETC O2 have distinct roles in modulating neuromuscular function.

Effect of Segmental, Localized Lower Limb Cooling on Dynamic Balance.

PURPOSE This study aimed to determine the effect of cooling progressively greater portions of the lower extremities on dynamic balance and neuromuscular activation. METHODS Ten healthy males (22.8 ± 3.4 yr, 76.5 ± 9.1 kg) performed one room air temperature control (22.4°C ± 0.8°C) and three trials of cold water immersion at 12°C (lateral malleolus, ankle; lateral femoral epicondyle, knee; anterior superior iliac spine, hip) for 10 min before performing a unipedal balance test (Star Excursion Balance Test (SEBT)) with their dominant limb. Muscle activation of the vastus lateralis, biceps femoris, tibialis anterior, and lateral gastrocnemius was measured with surface EMG during the SEBT. RESULTS Core temperature remained euthermic throughout all trials. Gastrocnemius temperature decreased from control (30.4°C ± 0.5°C) with knee (23.7°C ± 1.7°C) and hip immersion (22.4°C ± 1.0°C), whereas vastus lateralis temperature decreased from control (33.7°C ± 1.7°C) with hip immersion (27.3°C ± 2.0°C) (P < 0.01 for all comparisons). Cold water immersion influenced mean anterior and posterior reach distance on the SEBT in a dose-dependent fashion. Compared with those in control, mean anterior and posterior SEBT reach distances were not decreased with ankle (-1.38% and -0.74%, respectively) and knee immersion (-2.48% and -2.74%), whereas hip immersion significantly reduced SEBT by 4.73% and 4.05% (P < 0.05, d = 0.52-0.58). Muscle activation was largely unaffected as the lower extremities were cooled, with only the lateral gastrocnemius during the anterior SEBT approaching a decrease (P = 0.059). CONCLUSIONS Cooling larger portions of the lower extremities progressively affect dynamic balance, and thermal protection strategies should focus on maintaining temperature in the large muscle mass of the thigh.

Neither Short-term Sprint nor Endurance Training Enhances Thermal Response to Exercise in a Hot Environment

Improvements in fitness from a brief period of physical training may elicit sufficient physiological adaptations to decrease thermal strain during exercise in the heat. This study tested heat adaptation from short-term endurance (ET) and sprint-interval (SIT) training in moderately fit individuals. The ET group (n = 8) cycled at 65% for 8 sessions (4 sessions each at 60 and 90 min, respectively) over two weeks, while the SIT group (n = 8) performed repeated 30-s Wingate sprints (resistance 7.5% body mass; 4 sessions each of 4 and 5 sprints, respectively). and heat stress testing (HST; 60 min cycling at 65% at 35ºC, 40% relative humidity) were performed pre- and post-training. increased by 11% (p = 0.025) and 14% (p = 0.020) for the ET and SIT groups post-training, respectively. Thermal stress was similar pre- and post-training, with no significant difference in the rate of whole-body metabolic heat production (p = 0.106) for either group post-training. Cardiovascular improvement was evident with both ET and SIT, with a significant mean decrease (p = 0.014) in HR for both groups (ET: 146 ± 15 beats·min−1pre vs. 142 ± 12 beats·min−1post; SIT: 149 ± 15 beats·min−1pre vs. 146 ± 12 beats·min−1post) during the HST post-training. However, mean sweat loss (p = 0.248) and the rise in core temperature (p = 0. 260) did not change significantly comparing pre- and post-training HST. While short-term ET and SIT both induced significant improvements in aerobic fitness and decreased cardiovascular strain, neither elicited improved thermal responses during exercise in the heat and do not replace heat acclimatization.

Cognitive Performance during a 24-Hour Cold Exposure Survival Simulation

Survivor of a ship ground in polar regions may have to wait more than five days before being rescued. Therefore, the purpose of this study was to explore cognitive performance during prolonged cold exposure. Core temperature (T c) and cognitive test battery (CTB) performance data were collected from eight participants during 24 hours of cold exposure (7.5°C ambient air temperature). Participants (recruited from those who have regular occupational exposure to cold) were instructed that they could freely engage in minimal exercise that was perceived to maintaining a tolerable level of thermal comfort. Despite the active engagement, test conditions were sufficient to significantly decrease T c after exposure and to eliminate the typical 0.5–1.0°C circadian rise and drop in core temperature throughout a 24 h cycle. Results showed minimal changes in CTB performance regardless of exposure time. Based on the results, it is recommended that survivors who are waiting for rescue should be encouraged to engage in mild physical activity, which could have the benefit of maintaining metabolic heat production, improve motivation, and act as a distractor from cold discomfort. This recommendation should be taken into consideration during future research and when considering guidelines for mandatory survival equipment regarding cognitive performance.

Neuromuscular fatigue during hypoxia is mediated by the hypoxic ventilatory response

Neurons of the corticospinal tract are inherently sensitive to oxygen availability and, in response to hypoxia, reduce their metabolic requirements and activity [1]. Consequently, hypoxia is associated with neuromuscular fatigue, attributed in part to central (i.e., CNS) mechanisms [2]. Although changes in cerebral blood flow (CBF), mediated by the ratio of hypoxia induced vasodilation to hypoxic ventilatory response (HVR) induced hypocapnia (i.e., PETCO2) [3], may be implicated in the development of central fatigue, the contribution from the chemoreflex control of HVR and CBF vs. reductions in CBF per se has yet to be isolated.