Acute ingestion of Ibuprofen does not influence the release of IL-6 or improve self-paced exercise in the heat despite altering cortical activity.

The present study tested the hypothesis that ingesting 800 mg Ibuprofen prior to self-paced cycling at a fixed rating of perceived exertion (RPE) improves performance by attenuating the release of Interleukin (IL)-6 and its signalling molecules, whilst simultaneously modulating cortical activity and cerebral oxygenation to the brain. Eight healthy, recreationally active males ingested 800 mg Ibuprofen or a placebo ~ 1 h prior to performing fixed RPE cycling for 60 min in 35 °C and 60% relative humidity at an intensity of hard to very hard (RPE = 16) with intermittent maximal (RPE = 20) sprints every 10 min. Power output (PO), core and mean skin temperatures (Tc, Tsk), respectively, and heart rate (HR) were measured continuously. Electroencephalography (EEG) recordings at the frontal (Fz), motor (Cz) and Parietal (Pz) areas (90 s) were collected every 5 min. IL-6, soluble glycoprotein receptor (sgp130) and IL-6 receptor (R) were collected at pre-, 30 min and immediately post-exercise. Mean PO, HR, Tc and Tsk, and RPE were not different between trials (P ≥ 0.33). At end-exercise, the change in IL-6, sgp130 and sIL-6R was not different between trials (P ≥ 0.12). The increase in α and ß activity did not differ in any cortices between trials (P ≥ 0.07); however, there was a significant reduction in α/ß activity in the Ibuprofen compared to placebo trials at all sites (P ≤ 0.05). Ingesting a maximal, over-the-counter dose of Ibuprofen prior to exercise in the heat does not attenuate the release of IL-6, nor improve performance, but may influence cortical activity evidenced by a greater reduction in α/ß activity.

Impacts of Climate Change on Work Health and Safety in Australia: A Scoping Literature Review.

This scoping review explores the extant literature on climate change impacts on Workplace Health and Safety (WHS) in Australia. It maps the coverage of climate hazards, occupations at risk, and health and socio-economic impacts with the aim of identifying climate change impacts on WHS in Australia and associated knowledge gaps. We used a scoping review approach to identify and investigate 41 scholarly works at the nexus between climate change and WHS in Australia. Thematic template analysis and the NVivo software helped us identify and structure the main themes and systematically document the analysis process. The review highlighted a research focus on the impacts on WHS of heat and extreme weather events resulting from climate change. Agriculture and construction emerged as the most examined occupations, emphasising climate-related diseases and productivity loss. Other climate-related hazards, occupations, and health and socio-economic impacts were largely overlooked in the included research literature. The analysis revealed there is scope for further research relating to climate change impacts on occupational hazards (e.g., air pollution), occupations (e.g., indoor settings at risk), worker health (e.g., injuries), and socio-economic impacts (e.g., change in social practice). Furthermore, the results highlight that the main themes (hazards, occupations, health, and productivity) are interconnected, and the impacts of climate change can be 'cascading', adding complexity and severity. Hence, it is important to look at WHS as a multifaceted phenomenon in a holistic way to understand the risks and support required.

Serum brain-derived neurotrophic factor (BDNF) and self-paced time-trial performance in older untrained men.

PURPOSE: This study examined the effect of 12 weeks of concurrent aerobic and resistance training on brain derived neurotrophic factor (BDNF) levels, neuromuscular performance and cerebral oxygenation on self-paced cycling exercise in previously untrained older men. METHODS: Eight untrained healthy males aged 53-64 years performed a familiarisation and a pre-training self-paced cycling time trial before 12 weeks of exercise training which combined aerobic and resistance exercise. The self-paced cycling time trial comprised a 30 s maximal effort sprint for every 4.5 min of lower intensity pace for a total of 25 min. Upon completion of 12 weeks of training, a comparison of the pre-training trial analysed for serum BDNF, neuromuscular performance, and cerebral oxygenation was undertaken. RESULTS: Serum BDNF decreased significantly from 10.02 ± 4.63 to 6.96 ± 3.56 ng/ml after 12 weeks of training. There was also attenuated physiological strain for a comparable self-paced cycling performance. Despite positive physiological responses during the time trial pacing strategy was not altered compared with pre training. CONCLUSION: BDNF decreases following 12 weeks of concurrent training and might reflect neuroplasticity for this type of training stimulus. Exercise training in previously sedentary older men can result in a multitude of physical benefits, which may also confer a neuroprotective effect. However, specific training is required to improve pacing strategies in previously untrained older males. CLINICAL TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry number ACTRN12622001477718.

Hypohydration alters pre-frontal cortex haemodynamics, but does not impair motor learning.

It is unknown how hypohydration influences fine motor performance training and motor learning. Here, 30 participants (aged 19-46 years) were randomly assigned to a hypohydration (HYPO) or control (CON) group (both n = 15). Moderate hypohydration (~ 2.4% loss in body mass) was produced in HYPO via active dehydration before a 46 min fluid restricted rest period was undertaken. The conclusion of rest coincided with when CON attended the facilities. Both groups undertook a discrete sequence production task consisting of 6 training blocks, and returned ~ 300 min later to complete a delayed retention and transfer test while euhydrated. Bilateral pre-frontal cortex (PFC) haemodynamics were assessed using functional near-infrared spectroscopy throughout training and delayed learning assessments. Response time improved across training (P < 0.01) and was similar between the groups (both P = 0.22). Analysis of training PFC haemodynamics revealed a significant group by block interaction for oxygenated (O2Hb; P < 0.01), but not deoxygenated haemoglobin (P = 0.77). In training block 1, bilateral O2Hb was higher in HYPO (P = 0.02), while bilateral O2Hb increased in CON between blocks 2-3 and 5-6 (both P ≤ 0.03). During the delayed retention and transfer test, no group differences or interactions were found in response time, response error, or PFC haemodynamics (all P ≥ 0.27). Moderate hypohydration does increase PFC activation during motor skill learning, however, this appears to be transient and of little consequence to training or delayed retention or transfer performance.

The evolution of human fatigue resistance.

Humans differ from African great apes in numerous respects, but the chief initial difference setting hominins on their unique evolutionary trajectory was habitual bipedalism. The two most widely supported selective forces for this adaptation are increased efficiency of locomotion and improved ability to feed in upright contexts. By 4 million years ago, hominins had evolved the ability to walk long distances but extreme selection for endurance capabilities likely occurred later in the genus Homo to help them forage, power scavenge and persistence hunt in hot, arid conditions. In this review we explore the hypothesis that to be effective long-distance walkers and especially runners, there would also have been a strong selective benefit among Homo to resist fatigue. Our hypothesis is that since fatigue is an important factor that limits the ability to perform endurance-based activities, fatigue resistance was likely an important target for selection during human evolution for improved endurance capabilities. We review the trade-offs between strength, power, and stamina in apes and Homo and discuss three biological systems that we hypothesize humans evolved adaptations for fatigue resistance: neurological, metabolic and thermoregulatory. We conclude that the evolution of endurance at the cost of strength and power likely also involved the evolution of mechanisms to resist fatigue.

The exercise-induced inflammatory response in inflammatory bowel disease: A systematic review and meta-analysis.

BACKGROUND: This study investigated selected inflammatory responses to acute and chronic exercise in individuals with inflammatory bowel disease (IBD). METHODS: A systematic review and meta-analysis was conducted on all relevant exercise-based intervention publications with IBD participants. The study included articles that utilised a broad range of acute and chronic exercise interventions, with inflammatory biomarkers measured and symptoms documented, both pre- and post-exercise for those with IBD. The search was limited to studies published in English, the use of human participants, and primary studies, with no restrictions on date of publication or participant's age. Articles were retrieved through the electronic databases: PubMed, SPORTDiscus, and Scopus. This study adhered to Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. RESULTS: Six inflammatory markers were included in the meta-analysis which consisted of five studies. Exercise interventions resulted in no significant difference in IL-6 (SMD = -0.09; 95% CI = -0.49, 0.30; P = 0.64), TNF-α (SMD = 0.08; 95% CI = -0.31, 0.48; P = 0.68), CRP (SMD = -0.04; 95% CI = -0.58, 0.50; P = 0.89), IL-17 (SMD = 0.15; 95% CI = -0.45, 0.76; P = 0.62), leukocytes (SMD = 0.40; 95% CI = -0.53, 1.33; P = 0.40) or lymphocytes (SMD = 0.32; 95% CI = -0.33, 0.97; P = 0.33), thus, indicating exercise may have no effect on inflammatory markers in IBD. Bowel symptoms improved following regular moderate exercise that incorporated stress management. CONCLUSION: Heterogeneity among the identified literature may have led to exercise interventions being ineffective in reducing inflammation. Although the limited number of eligible studies may reduce the reliability of results, it emphasises the need for additional research in this domain. Importantly, no adverse symptomatic responses to exercise indicate that exercise is safe for IBD patients.

Metabolic and inflammatory health in SARS-CoV-2 and the potential role for habitual exercise in reducing disease severity.

INTRODUCTION: The rapid emergence and spread of SARS-CoV-2 in late 2019 has infected millions of people worldwide with significant morbidity and mortality with various responses from health authorities to limit the spread of the virus. Although population-wide inoculation is preferred, currently, there is large variation and disparity in the acquisition, development, and deployment of vaccination programs in many countries. Even with availability of a vaccine, achieving herd immunity does not guarantee against reinfection from SARS-CoV-2. Emerging evidence indicates that vaccines do not eliminate infection but protect against severe disease and potential hospitalisation. Therefore, additional strategies which strengthen the immune system should be strongly considered to assist in reducing the overall health care burden and stem the rate of infection. There is now substantial evidence that SARS-CoV-2 disease severity and death are linked to existing comorbidities such as cardiovascular disease, obesity, and metabolic disorders. PURPOSE: In this review, we discuss the potential medium-to-long-term strategy of habitual exercise and its relationship to targeted comorbidities and underlying inflammation as a protective mechanism against SARS-CoV-2 disease severity. CONCLUSION: We conclude that engagement in habitual physical activity and exercise could be a strategy to mitigate the development of comorbidities and improve the response of the immune system, potentially reducing the risk of symptoms and life-threatening complications if infected.

Inflammatory Status and Cardio-metabolic Risk Stratification of Rotational Shift Work.

OBJECTIVES: To investigate the physiological effects of rotational shift work on measures of cardio-metabolic function. METHODS: Sedentary, healthy men (n = 87; age 37 ± 9 years; body mass index: 30.7 ± 5.1 kg m2) were recruited and categorized via occupation. SHIFT group: currently employed in rotational shift work defined by 8-12 h morning, afternoon, and night rotations; or NSHIFT: working fixed daytime hours. Testing procedures included baseline objective sleep assessment and laboratory testing, conducted between 0600 and 0900 h to assess body composition, cardiorespiratory fitness (VO2peak), inflammatory status [C-reactive protein, interleukin (IL)-6, and tumour necrosis factor-alpha (TNF-α)], glucose metabolism, heart rate variability (HRV), and self-reported leisure time physical activity (PA). RESULTS: SHIFT reported significantly less leisure time PA (P = 0.019), reduced VO2peak (P = 0.007), higher body fat percentage (BF%) (P = 0.021), increase response time to oral glucose tolerance test (P = 0.016), and higher IL-6 values (P = 0.008) compared with NSHIFT. A significant difference was observed in actigraphy measured total sleep time, with SHIFT recording reduced sleep following a night shift (P = 0.001). No group difference was observed in HRV or average sleep parameters (P > 0.05). Linear regression identified a significant association between occupation and inflammatory status (P = 0.006). CONCLUSIONS: Rotational shift work is associated with increased risk factors for cardio-metabolic disorders, despite no differences in sleep quality and quantity. The results suggest rotational shift work has a detrimental effect on the health and wellbeing of employees; with homeostatic desynchronization identified as potential pathogenic mechanisms.

Prefrontal Cortex Activation During Motor Sequence Learning Under Interleaved and Repetitive Practice: A Two-Channel Near-Infrared Spectroscopy Study.

Training under high interference conditions through interleaved practice (IP) results in performance suppression during training but enhances long-term performance relative to repetitive practice (RP) involving low interference. Previous neuroimaging work addressing this contextual interference effect of motor learning has relied heavily on the blood-oxygen-level-dependent (BOLD) response using functional magnetic resonance imaging (fMRI) methodology resulting in mixed reports of prefrontal cortex (PFC) recruitment under IP and RP conditions. We sought to clarify these equivocal findings by imaging bilateral PFC recruitment using functional near-infrared spectroscopy (fNIRS) while discrete key pressing sequences were trained under IP and RP schedules and subsequently tested following a 24-h delay. An advantage of fNIRS over the fMRI BOLD response is that the former measures oxygenated and deoxygenated hemoglobin changes independently allowing for assessment of cortical hemodynamics even when there is neurovascular decoupling. Despite slower sequence performance durations under IP, bilateral PFC oxygenated and deoxygenated hemoglobin values did not differ between practice conditions. During test, however, slower performance from those previously trained under RP coincided with hemispheric asymmetry in PFC recruitment. Specifically, following RP, test deoxygenated hemoglobin values were significantly lower in the right PFC. The present findings contrast with previous behavioral demonstrations of increased cognitive demand under IP to illustrate a more complex involvement of the PFC in the contextual interference effect. IP and RP incur similar levels of bilateral PFC recruitment, but the processes underlying the recruitment are dissimilar. PFC recruitment during IP supports action reconstruction and memory elaboration while RP relies on PFC recruitment to maintain task variation information in working memory from trial to trial. While PFC recruitment under RP serves to enhance immediate performance, it does not support long-term performance.

A preliminary investigation of the effects of short-duration, vigorous exercise following sleep restriction, fragmentation and extension on appetite and mood in inactive, middle-aged men.

This preliminary study aimed to investigate the effect of exercise on appetite and mood following multiple days of sleep disruption (restriction [RES], fragmentation [FRAG]) or sleep extension (EXT), compared to normal sleep (CONT) in inactive, middle-aged men. Nine men completed four randomised trials initiated by 3 nights (day 1-3) of CONT (6.5-8 hr), RES (4 hr), FRAG (6.5-8 hr, interrupted at 2-hr intervals) or EXT (10 hr). On day 4 between 08:30 and 11:00 hours, perceived appetite, food cravings, appetite-related hormones (acylated ghrelin, leptin, peptide tyrosine-tyrosine [PYY]total ), glucose, mood states and wellness (stress, fatigue, soreness, and mood) were assessed before (post-sleep manipulation [SM]) and after (post-exercise [EX]) a 20-min vigorous cycling bout (rating of perceived exertion: 15). There was no effect of sleep manipulation or exercise on perceived appetite (p = .34-.62). Some aspects of food craving were altered after RES and EXT, with vigorous exercise attenuating the desire for sweet foods in RES (p = .12). PYYtotal was lower after RES compared to EXT and FRAG (p = .03), but was unaltered by exercise (p = .03). Ghrelin was higher for RES and EXT compared to CONT and FRAG after exercise (p = .001-.03). Total wellness was reduced and total mood disturbance (TMD) was higher after RES and FRAG compared to CONT and EXT (p ≤ .05). However, vigorous exercise countered these changes, with wellness and TMD remaining significantly impaired for FRAG compared to EXT only at this time (p = .02-.03). Vigorous exercise mitigates some aspects of food cravings and counters the impaired mood states that exist after multiple days of restricted and fragmented sleep.

Thirst perception exacerbates objective mental fatigue.

Thirst is represented within the anterior cingulate and insular cortices, and may share some common neuroanatomical structures that are implicated with the regulation of mental fatigue. This novel study investigated whether thirst might modulate the subjective, behavioural, or neurophysiological representations of mental fatigue. In a crossover design, thirst was monitored in 15 males during 60 min of cycling in normothermic conditions. Participants either consumed water to the dictates of their thirst (sated), or fluid was withheld and replaced with periodic salt water mouth rinses (thirst). Following either satiety or thirst, a 60 min modified Stroop task was completed to evoke mental fatigue. Prefrontal cortex (PFC) haemodynamics were monitored throughout the prolonged task, and subjective perceptions of fatigue were reported through a visual analogue scale. Behavioural performance was quantified as the total number of Stroop task iterations completed in the mentally fatiguing task, and by collating response time and accuracy into the inverse efficiency score (IES) for each 5 min interval throughout the task. During thirst, fewer iterations were completed and poorer IES performance was evident toward the latter portion of the mentally fatiguing task. Compensatory elevations in PFC oxyhaemoglobin were produced in each condition, however, differed temporally, and were premature during thirst. A diminished capacity to sustain cognitive performance is likely the product of an inability to preserve the distribution of resources within the prefrontal cortex, due to heightened activation about thirst regulatory centres. These data provide novel insight into the relationship between thirst and mental fatigue, and suggest that drinking to the dictates of thirst may be a pertinent strategy to sustain prolonged cognitive performance.

The effect of cigarette smoking history on autonomic and cerebral oxygenation responses to an acute exercise bout in smokers.

The extent of smoking history is causally linked to adverse cerebro- and cardiovascular health outcomes, while conversely, exercise decreases this risk and associated mortality. However, the acute cerebro- and cardiovascular responses to exercise in smokers are unknown, and may provide insight to understand chronic adaptation. This study examined the acute heart rate (HR) variability (R-R intervals) and cerebral oxygenation responses to exercise in smokers compared to nonsmokers. Fifty-four males classified as smokers (n = 27) or nonsmokers (n = 27) were allocated into either younger (YSM, YNS) or middle-aged groups (MSM, MNS). Participants completed 40 min of stationary cycle ergometry at 50% of VO2peak. Cerebral oxygenation (near-infrared spectroscopy) and autonomic function (HR variability) were collected before, during, and after exercise at 0, 30 min, 1, and 4 hr postexercise. The nonsmoker cohort (MNS and YNS) demonstrated higher values for the standard deviation (SD) of the R-R interval (SDNN) and the root mean squared of the SD at 1 and 4 hr postexercise versus smokers (p < .05). The low frequency (LF) band in YSM was lower than in YNS at 1 hr (p < .05). However, LF and high frequency were higher for MNS compared to MSM at 1 hr (p < .05). Oxygenated hemoglobin during and following exercise were elevated in NS with values for MSM lower than YSM (p < .05). The findings show smoking history can affect cerebral oxygenation during and following an acute exercise bout. Further, following exercise, smokers may exhibit a delay or inhibition in parasympathetic activity.

The effect of active hypohydration on cognitive function: A systematic review and meta-analysis.

Hypohydration is generally considered to have a negative effect on cognitive function, despite several studies reporting comparable findings between hydration states. Recommendations to avoid moderate dehydration (≥ 2% loss in body mass) are commonly made to athletes, on the provision that this deficit may impair optimal cognitive performance. To determine whether cognitive function is impaired by hypohydration, and investigate the existence of the proposed critical water deficit of ≥2% loss in body mass purported to diminish cognitive performance, we conducted a systematic search of the literature and examined appropriate studies by meta-analysis. Overall, cognitive performance was not found to be impaired by hypohydration (g = -0.177; 95% CI = -0.532-0.179; P = .331). Nor were the underlying cognitive domains (complex attention, executive function, learning and memory) impaired (all P > .236), independent of the incurred fluid loss (less than or >2% loss in body mass), although results were not always homogenous (I2 ranging between 0% and 93%). Collectively, these results suggest that hypohydration may not compromise cognitive function, nor any of the investigated subdomains to a greater extent than if euhydration had been maintained. Furthermore, recommendations to avoid moderate hypohydration on the basis of maintaining optimal cognitive function are not substantiated by this meta-analysis.

Deception of cycling distance on pacing strategies, perceptual responses, and neural activity.

Pacing during exercise performance is well-established; however, little is known about the neural responses associated with changes in power output and the effect of exercise end-point knowledge. Therefore, the aim of this study was to examine the effect of deception of cycling distance on pacing, cerebral oxy- (O2Hb) and deoxy-haemoglobin concentrations, and alpha (α) wave activity. Ten well-trained male cyclists (23.7 ± 6.6 years) completed three cycling time trials (TT) on a stationary air-braked cycle ergometer and were informed the study was to examine the reliability of 3 × 30-km TT. Participants unknowingly completed three distances (24, 30, and 36 km) in a randomised order. Performance (power output; PO), physiological (heart rate; HR), perceptual (rating of perceived exertion; RPE), and neurological (O2Hb, HHb, and α activity) measures were recorded throughout each TT. Data were converted to a percentage relative to the total distance covered. At 100% completion, HR and PO were lower during the 36 km compared to the 30 km trial (P ≤ 0.01). Compared to the 24 km trial, α waves were reduced at 100% (effect size; ES = 1.01), while O2Hb was greater at 70% of completion in the 36 km trial (ES = 1.39). RPE was also higher for 36 km compared to 30-km trial at 80% and the 24-km trial at 10% and 40-100% of completion (P ≤ 0.02). We conclude that the increase in O2Hb and RPE during the 36-km trial, while a reduction in HR and PO is present, may indicate that the pre-frontal cortex may influence the regulation of exercise performance when deceived of the duration end-point by increasing perception of effort to reduce premature onset of physiological strain.

The influence of thermal inputs on brain regulation of exercise: An evolutionary perspective.

The relationship between performance, heat load and the ability to withstand serious thermal insult is a key factor in understanding how endurance is regulated. The capacity to withstand high thermal loads is not unique to humans and is typical to all mammals. Thermoregulation is an evolutionary adaptation which is species specific and should be regarded as a survival strategy rather than purely a physiological response. The fact that mammals have selected ~37°C as a set point could be a key factor in understanding our endurance capabilities and strategy. Endurance presents a significant challenge to bodily homeostasis while our thermoregulatory strategy is able to cope exquisitely under the most unfavorable conditions. The ability of the CNS to regulate this strategy is key in athletic performance since the thermoregulatory center is located within the brain and receives input from multiple systems and deploys effector responses as needed. This chapter will discuss the evolution of thermoregulation in humans and propose that the brain is more than sufficiently capable of maintaining thermal-homeostasis because of its evolutionary path. As such, this is connected to our ability to modulate efferent drive during heat strain and in so doing provides us with the capability to pace during endurance events in the heat.

Cerebral responses to exercise and the influence of heat stress in human fatigue.

There are a number of mechanisms thought to be responsible for the onset of fatigue during exercise-induced hyperthermia. A greater understanding of the way in which fatigue develops during exercise could be gleaned from the studies which have examined the maintenance of cerebral blood flow through the process of cerebral autoregulation. Given that cerebral blood flow is a measure of the cerebral haemodynamics, and might reflect a level of brain activation, it is useful to understand the implications of this response during exercise and in the development of fatigue. It is known that cerebral blood flow is significantly altered under certain conditions such as altitude and exacerbated during exercise induced - hyperthermia. In this brief review we consider the processes of cerebral autoregulation predominantly through the measurement of cerebral blood flow and contrast these responses between exercise undertaken in normothermic versus heat stress conditions in order to draw some conclusions about the role cerebral blood flow might play in determining fatigue.

Similar mitochondrial signaling responses to a single bout of continuous or small-sided-games-based exercise in sedentary men.

This study assessed the mitochondrial related signaling responses to a single bout of noncontact, modified football (touch rugby), played as small-sided games (SSG), or cycling (CYC) exercise in sedentary, obese, middle-aged men. In a randomized, crossover design, nine middle-aged, sedentary, obese men completed two, 40-min exercise conditions (CYC and SSG) separated by a 21-day recovery period. Heart rate (HR) and ratings of perceived exertion (RPE) were collected during each bout. Needle biopsies from the vastus lateralis muscle were collected at rest and 30 and 240 min postexercise for analysis of protein content and phosphorylation (PGC-1α, SIRT1, p53, p53Ser15, AMPK, AMPKThr172, CAMKII, CAMKIIThr286, p38MAPK, and p38MAPKThr180/Tyr182) and mRNA expression (PGC-1α, p53, NRF1, NRF2, Tfam, and cytochrome c). A main effect of time effect for both conditions was evident for HR, RPE, and blood lactate (P < 0.05), with no condition by time interaction (P > 0.05). Both conditions increased PGC1-α protein and mRNA expression at 240 min (P < 0.05). AMPKThr172 increased 30 min post CYC (P < 0.05), with no change in SSG (P > 0.05). CYC increased p53 protein content at 240 min to a greater extent than SSG (P < 0.05). mRNA expression of NRF2 decreased in both conditions (P < 0.05). No condition by time interactions were evident for mRNA expression of Tfam, NRF1, cytochrome c, and p53. The similar PGC-1α response between intensity-matched conditions suggests both conditions are of similar benefit for stimulating mitochondrial biogenesis. Differences between conditions regarding fluctuation in exercise intensity and type of muscle contraction may explain the increase of p53 and AMPK within CYC and not SSG (noncontact, modified football).