The neuromodulatory role of dopamine in improved reaction time by acute cardiovascular exercise.

Acute cardiovascular physical exercise improves cognitive performance, as evidenced by a reduction in reaction time (RT). However, the mechanistic understanding of how this occurs is elusive and has not been rigorously investigated in humans. Here, using positron emission tomography (PET) with [11 C]raclopride, in a multi-experiment study we investigated whether acute exercise releases endogenous dopamine (DA) in the brain. We hypothesized that acute exercise augments the brain DA system, and that RT improvement is correlated with this endogenous DA release. The PET study (Experiment 1: n = 16) demonstrated that acute physical exercise released endogenous DA, and that endogenous DA release was correlated with improvements in RT of the Go/No-Go task. Thereafter, using two electrical muscle stimulation (EMS) studies (Experiments 2 and 3: n = 18 and 22 respectively), we investigated what triggers RT improvement. The EMS studies indicated that EMS with moderate arm cranking improved RT, but RT was not improved following EMS alone or EMS combined with no load arm cranking. The novel mechanistic findings from these experiments are: (1) endogenous DA appears to be an important neuromodulator for RT improvement and (2) RT is only altered when exercise is associated with central signals from higher brain centres. Our findings explain how humans rapidly alter their behaviour using neuromodulatory systems and have significant implications for promotion of cognitive health. KEY POINTS: Acute cardiovascular exercise improves cognitive performance, as evidenced by a reduction in reaction time (RT). However, the mechanistic understanding of how this occurs is elusive and has not been rigorously investigated in humans. Using the neurochemical specificity of [11 C]raclopride positron emission tomography, we demonstrated that acute supine cycling released endogenous dopamine (DA), and that this release was correlated with improved RT. Additional electrical muscle stimulation studies demonstrated that peripherally driven muscle contractions (i.e. exercise) were insufficient to improve RT. The current study suggests that endogenous DA is an important neuromodulator for RT improvement, and that RT is only altered when exercise is associated with central signals from higher brain centres.

The effects of manipulating the visual environment on thermal perception: A structured narrative review.

When exposed to ambient temperatures that cause thermal discomfort, a human's behavioral responses are more effective than autonomic ones at compensating for thermal imbalance. These behavioral thermal responses are typically directed by an individual's perception of the thermal environment. Perception of the environment is a holistic amalgamation of human senses, and in some circumstances, humans prioritize visual information. Existing research has considered this in the specific case of thermal perception, and this review investigates the state of the literature examining this effect. We identify the frameworks, research rationales, and potential mechanisms that underpin the evidence base in this area. Our review identified 31 experiments, comprising 1392 participants that met the inclusion criteria. Methodological heterogeneity was observed in the assessment of thermal perception, and a variety of methods were employed to manipulate the visual environment. However, the majority of the included experiments (80%) reported a difference in thermal perception after the visual environment was manipulated. There was limited research exploring any effects on physiological variables (e.g. skin and core temperature). This review has wide-ranging implications for the broad discipline of (thermo)physiology, psychology, psychophysiology, neuroscience, ergonomics, and behavior.

Thalamic Segmentation and Neural Activation Modeling Based on Individual Tissue Microstructure in Deep Brain Stimulation for Essential Tremor.

OBJECTIVE: Thalamic deep brain stimulation (DBS) is the primary surgical therapy for essential tremor (ET). Thalamic DBS traditionally uses an atlas-based targeting approach, which, although nominally accurate, may obscure individual anatomic differences from population norms. The objective of this study was to compare this traditional atlas-based approach with a novel quantitative modeling methodology grounded in individual tissue microstructure (N-of-1 approach). MATERIALS AND METHODS: The N-of-1 approach uses individual patient diffusion tensor imaging (DTI) data to perform thalamic segmentation and volume of tissue activation (VTA) modeling. For each patient, the thalamus was individually segmented into 13 nuclei using DTI-based k-means clustering. DBS-induced VTAs associated with tremor suppression and side effects were then computed for each patient with finite-element electric-field models incorporating DTI microstructural data. Results from N-of-1 and traditional atlas-based modeling were compared for a large cohort of patients with ET treated with thalamic DBS. RESULTS: The size and shape of individual N-of-1 thalamic nuclei and VTAs varied considerably across patients (N = 22). For both methods, tremor-improving therapeutic VTAs showed similar overlap with motor thalamic nuclei and greater motor than sensory nucleus overlap. For VTAs producing undesirable sustained paresthesia, 94% of VTAs overlapped with N-of-1 sensory thalamus estimates, whereas 74% of atlas-based segmentations overlapped. For VTAs producing dysarthria/motor contraction, the N-of-1 approach predicted greater spread beyond the thalamus into the internal capsule and adjacent structures than the atlas-based method. CONCLUSIONS: Thalamic segmentation and VTA modeling based on individual tissue microstructure explain therapeutic stimulation equally well and side effects better than a traditional atlas-based method in DBS for ET. The N-of-1 approach may be useful in DBS targeting and programming, particularly when patient neuroanatomy deviates from population norms.

A Light-Tolerant Wireless Neural Recording IC for Motor Prediction With Near-Infrared-Based Power and Data Telemetry.

Miniaturized and wireless near-infrared (NIR) based neural recorders with optical powering and data telemetry have been introduced as a promising approach for safe long-term monitoring with the smallest physical dimension among state-of-the-art standalone recorders. However, a main challenge for the NIR based neural recording ICs is to maintain robust operation in the presence of light-induced parasitic short circuit current from junction diodes. This is especially true when the signal currents are kept small to reduce power consumption. In this work, we present a light-tolerant and low-power neural recording IC for motor prediction that can fully function in up to 300 µW/mm2 of light exposure. It achieves best-in-class power consumption of 0.57 µW at 38° C with a 4.1 NEF pseudo-resistorless amplifier, an on-chip neural feature extractor, and individual mote level gain control. Applying the 20-channel pre-recorded neural signals of a monkey, the IC predicts finger position and velocity with correlation coefficient up to 0.870 and 0.569, respectively, with individual mote level gain control enabled. In addition, wireless measurement is demonstrated through optical power and data telemetry using a custom PV/LED GaAs chip wire bonded to the proposed IC.

Previous recreational cold exposure does not alter endothelial function or sensory thermal thresholds in the hands or feet.

NEW FINDINGS: What is the central question of this study? Does recreational cold exposure result in cold sensitivity and is this associated with endothelial dysfunction and impaired sensory thermal thresholds? What is the main finding and its importance? Previous cold exposure was correlated with cold sensitivity of the foot, which might indicate the development of a subclinical non-freezing cold injury. Endothelial function and thermal detection were not impaired in cold-sensitive individuals; therefore, further research is required to understand the pathophysiology of subclinical and clinical forms of non-freezing cold injury. ABSTRACT: In this study, we investigated whether cold-sensitive (CS) individuals, who rewarm more slowly after a mild cold challenge, have impaired endothelial function and sensory thermal thresholds (STTs) and whether this is related to reported cold exposure. Twenty-seven participants with varying previous cold exposure undertook three tests: an STT test, i.e. determination of warm and cold STTs of the fingers and dorsal foot; an endothelial function test, i.e. measurement of cutaneous vascular conductance (CVC) during iontophoresis of ACh on the forearm, finger and foot; and a CS test, involving immersion of a foot for 2 min in water at 15°C followed by 10 min of rewarming in air at 30°C. Toe skin temperature (Tsk ) measured during the CS test was used to form a CS group (<32°C before and 5 min after immersion) and an otherwise closely matched control group [Tsk >32°C; n = 9 (four women) for both groups]. A moderate relationship was found between cold exposure ranking and Tsk rewarming (r = 0.408, P = 0.035, n = 27) but not STT or endothelial function. The Tsk and blood flow were lower in CS compared with control subjects before and after foot immersion [Tsk , mean (SD): 30.3 (0.9) versus 34.8 (0.8) and 27.9 (0.8) versus 34.3 (0.8)°C, P < 0.001; and CVC: 1.08 (0.79) versus 3.82 (1.21) and 0.79 (0.52) versus 3.45 (1.07) flux mmHg-1 , n = 9, P < 0.001, respectively]. However, no physiologically significant differences were observed between groups for endothelial function or STT. A moderate correlation between previous cold exposure and toe Tsk rewarming after foot immersion was observed; however, CS was not associated with impaired endothelial function or reduced thermal detection.

A network physiology approach to oxygen saturation variability during normobaric hypoxia.

NEW FINDINGS: What is the central question of this study? What is the physiological interpretation of SpO2 fluctuations observed during normobaric hypoxia in healthy individuals? What is the main finding and its importance? There is a significant flow of information between SpO2 and other cardio-respiratory time series during graded hypoxia. Analysis of the pattern of SpO2 variations has potential for non-invasive assessment of the engagement of respiratory control system in health and disease. ABSTRACT: Peripheral capillary oxygen saturation ( SpO2 ) exhibits a complex pattern of fluctuations during hypoxia. The physiological interpretation of SpO2 variability is not well understood. In this study, we tested the hypothesis that SpO2 fluctuation carries information about integrated cardio-respiratory control in healthy individuals using a network physiology approach. We explored the use of transfer entropy in order to compute the flow of information between cardio-respiratory signals during hypoxia. Twelve healthy males (mean (SD) age 22 (4) years) were exposed to four simulated environments (fraction of inspired oxygen ( FIO2 ): 0.12, 0.145, 0.17, and 0.2093) for 45 min, in a single blind randomized controlled design. The flow of information between different physiological parameters ( SpO2 , respiratory frequency, tidal volume, minute ventilation, heart rate, end-tidal pressure of O2 and CO2 ) were analysed using transfer entropy. Normobaric hypoxia was associated with a significant increase in entropy of the SpO2 time series. The transfer entropy analysis showed that, particularly at FIO2 0.145 and 0.12, the flow of information between SpO2 and other physiological variables exhibits a bidirectional relationship. While reciprocal interactions were observed between different cardio-respiratory parameters during hypoxia, SpO2 remained the main hub of this network. SpO2 fluctuations during graded hypoxia exposure carry information about cardio-respiratory control. Therefore, SpO2 entropy analysis has the potential for non-invasive assessment of the functional connectivity of respiratory control system in various healthcare settings.

The interactive effects of acute exercise and hypoxia on cognitive performance: A narrative review.

Acute moderate intensity exercise has been shown to improve cognitive performance. In contrast, hypoxia is believed to impair cognitive performance. The detrimental effects of hypoxia on cognitive performance are primarily dependent on the severity and duration of exposure. In this review, we describe how acute exercise under hypoxia alters cognitive performance, and propose that the combined effects of acute exercise and hypoxia on cognitive performance are mainly determined by interaction among exercise intensity and duration, the severity of hypoxia, and duration of exposure to hypoxia. We discuss the physiological mechanism(s) of the interaction and suggest that alterations in neurotransmitter function, cerebral blood flow, and possibly cerebral metabolism are the primary candidates that determine cognitive performance when acute exercise is combined with hypoxia. Furthermore, acclimatization appears to counteract impaired cognitive performance during prolonged exposure to hypoxia although the precise physiological mechanism(s) responsible for this amelioration remain to be elucidated. This review has implications for sporting, occupational, and recreational activities at terrestrial high altitude where cognitive performance is essential. Further studies are required to understand physiological mechanisms that determine cognitive performance when acute exercise is performed in hypoxia.

Partial-body cryotherapy (-135°C) and cold-water immersion (10°C) after muscle damage in females.

This randomized controlled trial examined the effects of cold-water immersion (CWI), partial-body cryotherapy (PBC), or a passive control (CON) on physiological and recovery variables following exercise-induced muscle damage (EIMD, 5 × 20 drop jumps) in females. Twenty-eight females were allocated to PBC (30 seconds at -60°C, 2 minutes at -135°C), CWI (10 minutes at 10°C), or CON (10 minutes resting). Muscle oxygen saturation (SmO2 ), cutaneous vascular conductance (CVC), mean arterial pressure (MAP), and local skin temperature were assessed at baseline and through 60 minutes (10-minute intervals), while delayed onset of muscle soreness (DOMS), muscle swelling, maximum voluntary isometric contraction (MVIC), and vertical jump performance (VJP) were assessed up to 72 hours (24-hour intervals) following treatments. SmO2 was lower in PBC (Δ-2.77 ± 13.08%) and CWI (Δ-5.91 ± 11.80%) compared with CON (Δ18.96 ± 1.46%) throughout the 60-minute follow-up period (P < .001). CVC was lower from PBC (92.7 ± 25.0%, 90.5 ± 23.4%) and CWI (90.3 ± 23.5%, 88.1 ± 22.9%) compared with CON (119.0 ± 5.1 and 116.1 ± 6.6%, respectively) between 20 and 30 minutes (P < .05). Mean skin temperature was lower from CWI vs PBC (between 10 and 40 minutes, P < .05). Mean skin temperature was higher in CON compared with CWI up to 60 minutes and compared with PBC up to 30 minutes (P < .05). DOMS was lower following both PBC and CWI compared with CON through 72-hour (P < .05), with no difference between groups. No main group differences for swelling, MVIC, and VJP were observed. In conclusion, CWI elicited generally greater physiological effects compared with PBC while both interventions were more effective than CON in reducing DOMS in females, but had no effect on functional measures or swelling.

The physiological effects of daily cold-water immersion on 5-day tournament performance in international standard youth field-hockey players.

PURPOSE: This study examined the effects of daily post-exercise cold-water immersion (CWI) on match performance, perceptual recovery, and biomarkers of muscle damage and metabolic load during a 5-day international tournament of elite youth field-hockey players. METHODS: The entire German under-18 national squad (n = 18) was randomly assigned to a daily CWI- (5-min at ~ 6 °C; excluding the head; n = 9) or passive recovery (CON; n = 9) intervention. Training and match performance were assessed using a GPS-tracking system and perceived exertion (RPE). Daily ratings of delayed onset muscle soreness (DOMS), perceived stress and recovery, quality of sleep, heart-rate recovery and serum creatine kinase (CK), lactate dehydrogenase, and urea nitrogen were also recorded. Repeated-sprint ability (RSA) and counter-movement jump (CMJ) were carried out on days 1 and 5. RESULTS: There was no significance between intervention differences in time-on pitch, total distance, velocity zones, and accelerometer-base parameters during match performance (all p > 0.05). DOMS (p < 0.01), RPE (p < 0.01), and CK (p < 0.01) were significantly elevated over the course of the tournament; however, no between-intervention effects were observed (all p > 0.05). Both groups were able to maintain RSA and CMJ (all p > 0.05). CONCLUSION: In conclusion, daily post-exercise CWI did not improve match performance, perceptual recovery, or biomarkers of muscle damage and metabolic load in elite youth field-hockey players.

Antioxidants for preventing and reducing muscle soreness after exercise: a Cochrane systematic review.

OBJECTIVE: To determine whether antioxidant supplements and antioxidant-enriched foods can prevent or reduce delayed-onset muscle soreness after exercise. METHODS: We searched the Cochrane Bone, Joint and Muscle Trauma Group Specialised Register, the Cochrane Central Register of Controlled Trials, MEDLINE, Embase, SPORTDiscus, trial registers, reference lists of articles and conference proceedings up to February 2017. RESULTS: In total, 50 studies were included in this review which included a total of 1089 participants (961 were male and 128 were female) with an age range of 16-55 years. All studies used an antioxidant dosage higher than the recommended daily amount. The majority of trials (47) had design features that carried a high risk of bias due to selective reporting and poorly described allocation concealment, potentially limiting the reliability of their findings. We rescaled to a 0-10 cm scale in order to quantify the actual difference between groups and we found that the 95% CIs for all five follow-up times were all well below the minimal important difference of 1.4 cm: up to 6 hours (MD -0.52, 95% CI -0.95 to -0.08); at 24 hours (MD -0.17, 95% CI -0.42 to 0.07); at 48 hours (mean difference (MD) -0.41, 95% CI -0.69 to -0.12); at 72 hours (MD -0.29, 95% CI -0.59 to 0.02); and at 96 hours (MD -0.03, 95% CI -0.43 to 0.37). Thus, the effect sizes suggesting less muscle soreness with antioxidant supplementation were very unlikely to equate to meaningful or important differences in practice. CONCLUSIONS: There is moderate to low-quality evidence that high-dose antioxidant supplementation does not result in a clinically relevant reduction of muscle soreness after exercise of up to 6 hours or at 24, 48, 72 and 96 hours after exercise. There is no evidence available on subjective recovery and only limited evidence on the adverse effects of taking antioxidant supplements.

Infrared cameras overestimate skin temperature during rewarming from cold exposure.

OBJECTIVE: The primary aim of this study was to assess the accuracy of an infrared camera and that of a skin thermistor, both commercially available. The study aimed to assess the agreement over a wide range of skin temperatures following cold exposure. METHODS: Fifty-two males placed their right hand in a thin plastic bag and immersed it in 8 °C water for 30 min whilst seated in an air temperature of 30 °C. Following hand immersion, participants removed the bag and rested their hand at heart level for 10 min. Index finger skin temperature (Tsk) was measured with a thermistor, affixed to the finger pad, and an infrared camera measured 1 cm distally to the thermistor. Agreement between the infrared camera and thermistor was assessed by mean difference (infrared camera minus thermistor) and 95% limits of agreement analysis, accounting for the repeated measures over time. The clinically significant threshold for Tsk differences was set at ±0.5 °C and limits of agreement ±1 °C. RESULTS: As an average across all time points, the infrared camera recorded Tsk 1.80 (SD 1.16) °C warmer than the thermistor, with 95% limits of agreement ranging from -0.46 °C to 4.07 °C. CONCLUSION: Collectively, the results show the infrared camera overestimated Tsk at every time point following local cooling. Further, measurement of finger Tsk from the infrared camera consistently fell outside the acceptable level of agreement (i.e. mean difference exceeding ±0.5 °C). Considering these results, infrared cameras may overestimate peripheral Tsk following cold exposure and clinicians and practitioners should, therefore, adjust their risk/withdrawal criteria accordingly.

Whole-body cryotherapy (-110 °C) following high-intensity intermittent exercise does not alter hormonal, inflammatory or muscle damage biomarkers in trained males.

PURPOSE: This study examined the acute effects of a single session of Whole-body Cryotherapy (WBC) following severe intermittent running exercise on biomarkers of inflammation, muscle damage and stress. METHODS: Endurance-trained males (n = 11) were tested twice using a within-participant, balanced cross-over design that consisted of 5 × 5 min of high-intensity running (HIR) followed by either 3 min of WBC at -110 °C or a passive control condition (CON). Before the HIR and after 60 min of recovery a ramp-test was completed. At seven time points up to 24 hrs post exercise venous blood samples were analyzed for serum levels of interleukin 6 (IL-6), interleukin 10 (IL-10), c-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), myoglobin, cortisol, and testosterone. RESULTS: HIR induced significant increases in all biomarkers except sICAM-1 in both recovery conditions, respectively. Compared to the CON condition WBC did not attenuate exercise- induced changes in IL-6, IL-10, sICAM-1, myoglobin, cortisol, testosterone or their ratio. Increased levels of cortisol following exercise were negatively correlated with subsequent running performance in both conditions (WBC: r = -0.61, p = 0.04; CON: r = -0.64, p = 0.04). CONCLUSION: The results of this study suggest that the postulated physiological mechanisms by which WBC is proposed to improve recovery, i.e. reductions in inflammation and muscle damage, may not be accurate.

Cognitive performance is associated with cerebral oxygenation and peripheral oxygen saturation, but not plasma catecholamines, during graded normobaric hypoxia.

NEW FINDINGS: What is the central question of this study? What are the mechanisms responsible for the decline in cognitive performance following exposure to acute normobaric hypoxia? What are the main findings and their importance? We found that (1) performance of a complex central executive task (n-back) was reduced at FIO2 0.12; (2) there was a strong correlation between performance of the n-back task and reductions in SpO2 and cerebral oxygenation; and (3) plasma adrenaline, noradrenaline, cortisol and copeptin were not correlated with cognitive performance. ABSTRACT: It is well established that hypoxia impairs cognitive function; however, the physiological mechanisms responsible for these effects have received relatively little attention. This study examined the effects of graded reductions in fraction of inspired oxygen ( FIO2 ) on oxygen saturation ( SpO2 ), cerebral oxygenation, cardiorespiratory variables, activity of the sympathoadrenal system (adrenaline, noradrenaline) and hypothalamic-pituitary-adrenal axis (cortisol, copeptin), and cognitive performance. Twelve healthy males [mean (SD), age: 22 (4) years, height: 178 (5) cm, mass: 75 (9) kg, FEV1 /FVC ratio: 85 (5)%] completed a four-task battery of cognitive tests to examine inhibition, selective attention (Eriksen flanker), executive function (n-back) and simple and choice reaction time (Deary-Liewald). Tests were completed before and following 60 min of exposure to FIO2 0.2093, 0.17, 0.145 and 0.12. Following 60 min of exposure, response accuracy in the n-back task was significantly reduced in FIO2 0.12 compared to baseline [82 (9) vs. 93 (5)%; P < 0.001] and compared to all other conditions at the same time point [ FIO2 0.2093: 92 (3)%; FIO2 0.17: 91 (6)%; FIO2 0.145: 85 (10)%; FIO2 12: 82 (9)%; all P < 0.05]. The performance of the other tasks was maintained. Δaccuracy and Δreaction time of the n-back task was correlated with both Δ SpO2 [r(9) = 0.66, P < 0.001 and r(9) = -0.36, P = 0.037, respectively] and Δcerebral oxygenation [r(7) = 0.55, P < 0.001 and r(7) = -0.38, P = 0.045, respectively]. Plasma adrenaline, noradrenaline, cortisol and copeptin were not significantly elevated in any condition or correlated with any of the tests of cognitive performance. These findings suggest that reductions in peripheral oxygen saturation and cerebral oxygenation, and not increased activity of the sympathoadrenal system and hypothalamic-pituitary-adrenal axis, as previously speculated, are responsible for a decrease in cognitive performance during normobaric hypoxia.

Effects of acute or chronic heat exposure, exercise and dehydration on plasma cortisol, IL-6 and CRP levels in trained males.

This study examined the acute and chronic effects of euhydrated and hypohydrated heat exposure, on biomarkers of stress and inflammation. Eight trained males [mean (SD) age: 21 (3) y; mass: 77.30 (4.88) kg; V̇O2max: 56.9 (7.2) mL kg-1 min-1] undertook two heat acclimation programmes (balanced cross-over design), once drinking to maintain euhydration and once with restricted fluid-intake (permissive dehydration). Days 1, 6, and 11 were 60 min euhydrated exercise-heat stress tests (40 °C; 50% RH, 35% peak power output), days 2-5 and 7-10 were 90 min, isothermal-strain (target rectal temperature: 38.5 °C) exercise-heat sessions. Plasma was obtained pre- and post- exercise on day 1, 2, and 11 and analysed for cortisol, interleukin-6 (IL-6), and C-reactive protein (CRP). Cortisol and CRP were also assessed on day 6. IL-6 was elevated following the initial (acute) 90 min isothermal heat strain exercise-heat exposure (day 2) with permissive dehydration ((pre exercise: 1.0 pg mL-1 [0.9], post-exercise: 1.8 pg mL-1 [1.0], P = .032) and when euhydrated (pre-exercise: 1.0 pg mL-1 [1.4], post-exercise: 1.6 pg mL-1 [2.1], P = .048). Plasma cortisol levels were also elevated but only during permissive dehydration (P = .032). Body mass loss was strongly correlated with Δcortisol (r = -0.688, P = .003). Although there was a trend for post-exercise cortisol to be decreased following both heat acclimation programmes (chronic effects), there were no within or between intervention differences in IL-6 or CRP. In conclusion, acute exercise in the heat increased IL-6 and cortisol only when fluid-intake is restricted. There were no chronic effects of either intervention on biomarkers of inflammation as evidenced by IL-6 and CRP returning to basal level at the end of heat acclimation.

Inter-individual variation in the adaptive response to heat acclimation.

AIM: To investigate inter-individual variance in adaptive responses to heat acclimation (HA). METHODS: 17 males (VO2max=58.8(8.4) mL·kg-1·min-1) undertook 10-days (exercise + heat-stress [40 °C, 50%RH]) HA. Adaptation was assessed by heat stress tests (HST; 60-minutes cycling, 35% peak power output) pre- and post-HA. RESULTS: Inter-individual variability was evident in adaptive responses e.g. mean(range) reduction in end-exercise Tre= -0.70(-0.20 to -1.32)°C, but, in the main, the variance in adaptation was unrelated across indices (thermal, sudomotor, cardiovascular, haematological), indicating independence between adaptation indices. Variance in adaptive responses was not correlated with aerobic capacity, history of previous HA, or the accrued thermal-dose. Some responses to the initial HST were related to the subsequent adaptations e.g. ∆T̅sk during the initial HST and the reduction in the within HST ΔTre after HA (r = -0.676), but responses to the initial HST may also have been influenced by HST design e.g. ΔTre correlated with metabolic heat production (r = 0.609). Metabolic heat production also correlated with the reduction in the within HST ΔTre after HA (r = -0.514). SUMMARY: HA indices are mainly independent; 'low', or 'high', responders on one index do not necessarily demonstrate similar response across other indices. Variance in HA responses was not related to aerobic capacity, previous HA, or thermal-dose. Thermo-physiological responses to a HST might identify individuals who will benefit from HA. However, some initial responses are influenced by HST design, which may also affect the scope for demonstrating adaption. CONCLUSION: Variance in the HA response remains largely unaccounted for and future studies should identify factors contributing to this variance.

The human ventilatory response to stress: rate or depth?

Many stressors cause an increase in ventilation in humans. This is predominantly reported as an increase in minute ventilation (V̇E). But, the same V̇E can be achieved by a wide variety of changes in the depth (tidal volume, VT ) and number of breaths (respiratory frequency, ƒR ). This review investigates the impact of stressors including: cold, heat, hypoxia, pain and panic on the contributions of ƒR and VT to V̇E to see if they differ with different stressors. Where possible we also consider the potential mechanisms that underpin the responses identified, and propose mechanisms by which differences in ƒR and VT are mediated. Our aim being to consider if there is an overall differential control of ƒR and VT that applies in a wide range of conditions. We consider moderating factors, including exercise, sex, intensity and duration of stimuli. For the stressors reviewed, as the stress becomes extreme V̇E generally becomes increased more by ƒR than VT . We also present some tentative evidence that the pattern of ƒR and VT could provide some useful diagnostic information for a variety of clinical conditions. In The Physiological Society's year of 'Making Sense of Stress', this review has wide-ranging implications that are not limited to one discipline, but are integrative and relevant for physiology, psychophysiology, neuroscience and pathophysiology.

Effects of 10 days of separate heat and hypoxic exposure on heat acclimation and temperate exercise performance.

Adaptations to heat and hypoxia are typically studied in isolation but are often encountered in combination. Whether the adaptive response to multiple stressors affords the same response as when examined in isolation is unclear. We examined 1) the influence of overnight moderate normobaric hypoxia on the time course and magnitude of adaptation to daily heat exposure and 2) whether heat acclimation (HA) was ergogenic and whether this was influenced by an additional hypoxic stimulus. Eight males [V̇o2max = 58.5 (8.3) ml·kg-1·min-1] undertook two 11-day HA programs (balanced-crossover design), once with overnight normobaric hypoxia (HAHyp): 8 (1) h per night for 10 nights [[Formula: see text] = 0.156; SpO2 = 91 (2)%] and once without (HACon). Days 1, 6, and 11 were exercise-heat stress tests [HST (40°C, 50% relative humidity, RH)]; days 2-5 and 7-10 were isothermal strain [target rectal temperature (Tre) ~38.5°C], exercise-heat sessions. A graded exercise test and 30-min cycle trial were undertaken pre-, post-, and 14 days after HA in temperate normoxia (22°C, 55% RH; FIO2 = 0.209). HA was evident on day 6 (e.g., reduced Tre, mean skin temperature (T̄sk), heart rate, and sweat [Na+], P < 0.05) with additional adaptations on day 11 (further reduced T̄sk and heart rate). HA increased plasma volume [+5.9 (7.3)%] and erythropoietin concentration [+1.8 (2.4) mIU/ml]; total hemoglobin mass was unchanged. Peak power output [+12 (20) W], lactate threshold [+15 (18) W] and work done [+12 (20) kJ] increased following HA. The additional hypoxic stressor did not affect these adaptations. In conclusion, a separate moderate overnight normobaric hypoxic stimulus does not affect the time course or magnitude of HA. Performance may be improved in temperate normoxia following HA, but this is unaffected by an additional hypoxic stressor.

Effects of dietary nitrate supplementation on the response to extremity cooling and endothelial function in individuals with cold sensitivity. A double blind, placebo controlled, crossover, randomised control trial.

Individuals with cold sensitivity have low peripheral skin blood flow and skin temperature possibly due to reduced nitric oxide (NO•) bioavailability. Beetroot has a high concentration of inorganic nitrate and may increase NO-mediated vasodilation. Using a placebo-controlled, double blind, randomised, crossover design, this study tested the hypotheses that acute beetroot supplementation would increase the rate of cutaneous rewarming following a local cold challenge and augment endothelium-dependent vasodilation in cold sensitive individuals. Thirteen cold sensitive participants completed foot and hand cooling (separately, in 15 °C water for 2 min) with spontaneous rewarming in 30 °C air whilst skin temperature and cutaneous vascular conductance (CVC) were measured (Baseline). On two further separate visits, participants consumed 140 ml of either concentrated beetroot juice (nitrate supplementation) or nitrate-depleted beetroot juice (Placebo) 90 min before resting seated blood pressure was measured. Endothelial function was assessed by measuring CVC at the forearm, finger and foot during iontophoresis of 1% w/v acetylcholine followed by foot and hand cooling as for Baseline. Plasma nitrite concentrations significantly increased in nitrate supplementation compared to Placebo and Baseline (502 ± 246 nmol L-1; 73 ± 45 nmol L-1; 74 ± 49 nmol L-1 respectively; n = 11; P < 0.001). Resting blood pressure and the response to foot and hand cooling did not differ between conditions (all P > 0.05). Nitrate supplementation did not alter endothelial function in the forearm, finger or foot (all P > 0.05) compared to Placebo. Despite a physiologically meaningful rise in plasma nitrite concentrations, acute nitrate supplementation does not alter extremity rewarming, endothelial function or blood pressure in individuals with cold sensitivity.

Antioxidants for preventing and reducing muscle soreness after exercise.

BACKGROUND: Muscle soreness typically occurs after intense exercise, unaccustomed exercise or actions that involve eccentric contractions where the muscle lengthens while under tension. It peaks between 24 and 72 hours after the initial bout of exercise. Many people take antioxidant supplements or antioxidant-enriched foods before and after exercise in the belief that these will prevent or reduce muscle soreness after exercise. OBJECTIVES: To assess the effects (benefits and harms) of antioxidant supplements and antioxidant-enriched foods for preventing and reducing the severity and duration of delayed onset muscle soreness following exercise. SEARCH METHODS: We searched the Cochrane Bone, Joint and Muscle Trauma Group Specialised Register, the Cochrane Central Register of Controlled Trials, MEDLINE, Embase, SPORTDiscus, trial registers, reference lists of articles and conference proceedings up to February 2017. SELECTION CRITERIA: We included randomised and quasi-randomised controlled trials investigating the effects of all forms of antioxidant supplementation including specific antioxidant supplements (e.g. tablets, powders, concentrates) and antioxidant-enriched foods or diets on preventing or reducing delayed onset muscle soreness (DOMS). We excluded studies where antioxidant supplementation was combined with another supplement. DATA COLLECTION AND ANALYSIS: Two review authors independently screened search results, assessed risk of bias and extracted data from included trials using a pre-piloted form. Where appropriate, we pooled results of comparable trials, generally using the random-effects model. The outcomes selected for presentation in the 'Summary of findings' table were muscle soreness, collected at times up to 6 hours, 24, 48, 72 and 96 hours post-exercise, subjective recovery and adverse effects. We assessed the quality of the evidence using GRADE. MAIN RESULTS: Fifty randomised, placebo-controlled trials were included, 12 of which used a cross-over design. Of the 1089 participants, 961 (88.2%) were male and 128 (11.8%) were female. The age range for participants was between 16 and 55 years and training status varied from sedentary to moderately trained. The trials were heterogeneous, including the timing (pre-exercise or post-exercise), frequency, dose, duration and type of antioxidant supplementation, and the type of preceding exercise. All studies used an antioxidant dosage higher than the recommended daily amount. The majority of trials (47) had design features that carried a high risk of bias due to selective reporting and poorly described allocation concealment, potentially limiting the reliability of their findings.We tested only one comparison: antioxidant supplements versus control (placebo). No studies compared high-dose versus low-dose, where the low-dose supplementation was within normal or recommended levels for the antioxidant involved.Pooled results for muscle soreness indicated a small difference in favour of antioxidant supplementation after DOMS-inducing exercise at all main follow-ups: up to 6 hours (standardised mean difference (SMD) -0.30, 95% confidence interval (CI) -0.56 to -0.04; 525 participants, 21 studies; low-quality evidence); at 24 hours (SMD -0.13, 95% CI -0.27 to 0.00; 936 participants, 41 studies; moderate-quality evidence); at 48 hours (SMD -0.24, 95% CI -0.42 to -0.07; 1047 participants, 45 studies; low-quality evidence); at 72 hours (SMD -0.19, 95% CI -0.38 to -0.00; 657 participants, 28 studies; moderate-quality evidence), and little difference at 96 hours (SMD -0.05, 95% CI -0.29 to 0.19; 436 participants, 17 studies; low-quality evidence). When we rescaled to a 0 to 10 cm scale in order to quantify the actual difference between groups, we found that the 95% CIs for all five follow-up times were all well below the minimal important difference of 1.4 cm: up to 6 hours (MD -0.52, 95% CI -0.95 to -0.08); at 24 hours (MD -0.17, 95% CI -0.42 to 0.07); at 48 hours (MD -0.41, 95% CI -0.69 to -0.12); at 72 hours (MD -0.29, 95% CI -0.59 to 0.02); and at 96 hours (MD -0.03, 95% CI -0.43 to 0.37). Thus, the effect sizes suggesting less muscle soreness with antioxidant supplementation were very unlikely to equate to meaningful or important differences in practice. Neither of our subgroup analyses to examine for differences in effect according to type of DOMS-inducing exercise (mechanical versus whole body aerobic) or according to funding source confirmed subgroup differences. Sensitivity analyses excluding cross-over trials showed that their inclusion had no important impact on results.None of the 50 included trials measured subjective recovery (return to previous activities without signs or symptoms).There is very little evidence regarding the potential adverse effects of taking antioxidant supplements as this outcome was reported in only nine trials (216 participants). From the studies that did report adverse effects, two of the nine trials found adverse effects. All six participants in the antioxidant group of one trial had diarrhoea and four of these also had mild indigestion; these are well-known side effects of the particular antioxidant used in this trial. One of 26 participants in a second trial had mild gastrointestinal distress. AUTHORS' CONCLUSIONS: There is moderate to low-quality evidence that high dose antioxidant supplementation does not result in a clinically relevant reduction of muscle soreness after exercise at up to 6 hours or at 24, 48, 72 and 96 hours after exercise. There is no evidence available on subjective recovery and only limited evidence on the adverse effects of taking antioxidant supplements. The findings of, and messages from, this review provide an opportunity for researchers and other stakeholders to come together and consider what are the priorities, and underlying justifications, for future research in this area.