Objectives To assess physical activity (PA), mental health and well-being of adults in the UK, Ireland, New Zealand and Australia during the initial stages of National governments’ Coronavirus disease (COVID-19) containment responses. Design Observational, cross-sectional. Methods An online survey was disseminated to adults (n = 8,425; 44.5 ± 14.8y) residing in the UK, Ireland, New Zealand and Australia within the first 2-6 weeks of government-mandated COVID-19 restrictions. Main outcome measures included: Stages of Change scale for exercise behaviour change; International Physical Activity Questionnaire (short-form); World Health Organisation-5 Well-being Index; and the Depression Anxiety and Stress Scale-9. Results Participants who reported a negative change in exercise behaviour between pre-initial COVID-19 restrictions and during initial COVID-19 restrictions demonstrated poorer mental health and well-being compared to those demonstrating either a positive-or no change in their exercise behaviour ( p < 0.001). Whilst women reported more positive changes in exercise behaviour, young people (18-29y) reported more negative changes (both p < 0.001). Individuals who had more positive exercise behaviours reported better mental health and well-being ( p < 0.001). Although there were no differences in PA between countries, individuals in New Zealand reported better mental health and well-being ( p < 0.001). Conclusion The initial COVID-19 restrictions have differentially impacted upon PA habits of individuals based upon their age and sex, and therefore have important implications for international policy and guideline recommendations. Public health interventions that encourage PA should target specific groups (e.g., men, young adults) who are most vulnerable to the negative effects of physical distancing and/or self-isolation.

This study explored the relationship between serum ferritin and hepcidin in athletes. Baseline serum ferritin levels of 54 athletes from the control trial of five investigations conducted in our laboratory were considered; athletes were grouped according to values <30 μg/L (SF<30), 30–50 μg/L (SF30–50), 50–100 μg/L (SF50–100), or >100 μg/L (SF>100). Data pooling resulted in each athlete completing one of five running sessions: (1) 8×3 min at 85% vVO2peak; (2) 5×4 min at 90% vVO2peak; (3) 90 min continuous at 75% vVO2peak; (4) 40 min continuous at 75% vVO2peak; (5) 40 min continuous at 65% vVO2peak. Athletes from each running session were represented amongst all four groups; hence, the mean exercise duration and intensity were not different (p>0.05). Venous blood samples were collected pre-, post- and 3 h post-exercise, and were analysed for serum ferritin, iron, interleukin-6 (IL-6) and hepcidin-25. Baseline and post-exercise serum ferritin levels were different between groups (p<0.05). There were no group differences for pre- or post-exercise serum iron or IL-6 (p>0.05). Post-exercise IL-6 was significantly elevated compared to baseline within each group (p<0.05). Pre- and 3 h post-exercise hepcidin-25 was sequentially greater as the groups baseline serum ferritin levels increased (p<0.05). However, post-exercise hepcidin levels were only significantly elevated in three groups (SF30–50, SF50–100, and SF>100; p<0.05). An athlete's iron stores may dictate the baseline hepcidin levels and the magnitude of post-exercise hepcidin response. Low iron stores suppressed post-exercise hepcidin, seemingly overriding any inflammatory-driven increases.

Caffeine use is widespread among athletes following its removal from the World Anti-Doping Agency banned list, with approximately 75% of competitive athletes using caffeine. While literature supports that caffeine has a small positive ergogenic effect for most forms of sports and exercise, there exists a significant amount of inter-individual difference in the response to caffeine ingestion and the subsequent effect on exercise performance. In this narrative review, we discuss some of the potential mechanisms and focus on the role that genetics has in these differences. CYP1A2 and ADORA2A are two of the genes which are thought to have the largest impact on the ergogenicity of caffeine. CYP1A2 is responsible for the majority of the metabolism of caffeine, and ADORA2A has been linked to caffeine-induced anxiety. The effects of CYP1A2 and ADORA2A genes on responses to caffeine will be discussed in detail and an overview of the current literature will be presented. The role of these two genes may explain a large portion of the inter-individual variance reported by studies following caffeine ingestion. Elucidating the extent to which these genes moderate responses to caffeine during exercise will ensure caffeine supplementation programs can be tailored to individual athletes in order to maximize the potential ergogenic effect.

Twenty-four hours of controlled low carbohydrate intake resulted in higher baseline hepcidin levels and post-exercise IL-6 responses than a high carbohydrate intake. Such hormone increases may be induced by gluconeogenic signaling of the liver, and may negatively impact an athlete's iron metabolism.

The current study investigated whether ambient heat augments the inflammatory and post-exercise hepcidin response in women, and if menstrual phase and/or self-pacing modulate these physiological effects. Eight trained females (age: 37±7 y; VO2max: 46±7 mL∙kg-1∙min-1; peak power output: 4.5±0.8 W∙kg-1) underwent 20 min of fixed-intensity cycling (100 and 125 W) followed by a 30-min work trial (≈75% VO2max) in a moderate (MOD: 20±1 °C, 53±8% relative humidity) and warm-humid (WARM: 32±0 °C, 75±3% relative humidity) environment in both their early follicular (days 5±2) and mid-luteal (days 21±3) phases. Mean power output was 5±4 W higher in MOD than in WARM (p=0.02) such that the difference in core temperature rise was limited between environments (-0.29±0.18 °C in MOD, p<0.01). IL-6 and hepcidin both increased post-exercise (198% and 38%, respectively), however, neither were affected by ambient temperature or menstrual phase (all p>0.15). Multiple regression analysis demonstrated that the IL-6 response to exercise was explained by leukocyte and platelet count (r2=0.72, p<0.01) and the hepcidin response to exercise was explained by serum iron and ferritin (r2=0.62, p<0.01). During exercise participants almost matched their fluid loss (0.48±0.18 kg·h-1) with water intake (0.35±0.15 L·h-1) such that changes in body mass (-0.3±0.3%) and serum osmolality (0.5±2.0 mOsm·kg-1) were minimal or negligible, indicating a behavioral fluid-regulatory response. These results indicate that trained, iron sufficient women suffer no detriment to their iron regulation in response to exercise with acute ambient heat stress or between menstrual phases on account of a performance-physiological trade-off.