Using an experimental model of extreme heat exposure that incorporates brief periods of light physical activity to simulate activities of daily living, the extent of thermal strain reported herein more accurately represents what would occur during actual heatwave conditions. Despite matching metabolic heat generation and environmental conditions, we show that older adults have augmented core temperature responses, likely due to age-related reductions in heat dissipating mechanisms.

Scientists rely upon an accurate scientific literature in order to build and test new theories about the natural world. In the past decade, observational studies of the scientific literature have indicated that numerous questionable research practices and poor reporting practices may be hindering scientific progress. In particular, 3 recent studies have indicated an implausibly high rate of studies with positive (i.e., hypothesis confirming) results. In sports medicine, a field closely related to kinesiology, studies that tested a hypothesis indicated support for their primary hypothesis ~70% of the time. However, a study of journals that cover the entire field of kinesiology has yet to be completed, and the quality of other reporting practices, such as clinical trial registration, has not been evaluated. In this study we retrospectively evaluated 300 original research articles from the flagship journals of North America (Medicine and Science in Sports and Exercise), Europe (European Journal of Sport Science), and Australia (Journal of Science and Medicine in Sport). The hypothesis testing rate (~64%) and positive result rate (~81%) were much lower than what has been reported in other fields (e.g., psychology), and there was only weak evidence for our hypothesis that the positive result rate exceeded 80%. However, the positive result rate is still considered unreasonably high. Additionally, most studies did not report trial registration, and rarely included accessible data indicating rather poor reporting practices. The majority of studies relied upon significance testing (~92%), but it was more concerning that a majority of studies (~82%) without a stated hypothesis still relied upon significance testing. Overall, the positive result rate in kinesiology is unacceptably high, despite being lower than other fields such as psychology, and most published manuscripts demonstrated subpar reporting practices

The purpose of our field study was to investigate the effects of running the Boston Marathon on acute kidney injury (AKI) biomarkers. We hypothesized that biomarker values would be elevated immediately post-marathon but would resolve in the 24-h post-marathon. Secondarily, we sought to identify sex differences related to renal stress. Participants were 65 runners who completed the Boston Marathon (46 ± 9 years, 65.4 ± 10.8 kg). Urine samples were collected at three different time points (pre-marathon, post-marathon, and 24-h post-marathon). Blood samples were collected post-marathon and 24-h post-marathon. Urine specific gravity (USG) and AKI biomarkers were evaluated. Pre-marathon USG (1.012 ± 0.007) was significantly less than post-marathon (1.018 ± 0.008) and 24-h post-marathon (1.020 ± 0.009; P < 0.001). Male USG (1.024 ± 0.009) was significantly greater 24-h post-marathon than females (1.017 ± 0.008; P = 0.019). Urinary neutrophil gelatinase-associated lipocalin values were significantly greater over time (P < 0.001), and there was a main effect of sex with female urinary creatinine (_UCr) greater than males at all three time points (P = 0.040). Post-marathon_UCr (366.24 ± 295.16 mg/dl) was significantly greater than pre-marathon (206.65 ± 145.28.56 mg/dl; p < 0.001) and 24-h post-marathon was significantly lower than other time-points (93.90 ± 125.07 mg/dl; P < 0.001). Female_UCr values were significantly greater than males 24-h post-marathon (P < 0.001). There was no difference in serum cystatin C (_SCys) values post- or 24-h post-marathon (P = 0.178). Serum creatinine (_SCr) significantly decreased between post-marathon and 24-h post-marathon, (P < 0.001). We can infer that the characteristics unique to the Boston Marathon may have attributed to prolonged elevations in AKI biomarkers. Sex differences were observed during the Boston Marathon warranting further investigation.

We tested whether older adults, compared with young adults, exhibit greater gastrointestinal permeability and kidney injury during heat stress. Nine young (32 ± 3 years) and nine older (72 ± 3 years) participants were heated using a model of controlled hyperthermia (increasing core temperature by 2°C via a water‐perfused suit). Gastrointestinal permeability was assessed using a multi‐sugar drink test containing lactulose, sucrose and rhamnose. Blood and urine samples were assayed for markers of intestinal barrier injury [plasma intestinal fatty acid binding protein (I‐FABP), plasma lipopolysaccharide binding protein (LBP) and plasma soluble cluster of differentiation 14 (sCD14)], inflammation (serum cytokines), kidney function (plasma creatinine and cystatin C) and kidney injury [urine arithmetic product of IGFBP7 and TIMP‐2 (TIMP‐2 × IGFBP7), neutrophil gelatinase‐associated lipocalin and kidney injury molecule‐1]. The lactulose‐to‐rhamnose ratio was increased in both young and older adults (group‐wide: Δ0.11 ± 0.11), but the excretion of sucrose was increased only in older adults (Δ1.7 ± 1.5). Young and older adults showed similar increases in plasma LBP (group‐wide: Δ0.65 ± 0.89 µg/mL), but no changes were observed for I‐FABP or sCD14. Heat stress caused similar increases in plasma creatinine (group‐wide: Δ0.08 ± 0.07 mg/dL), cystatin C (group‐wide: Δ0.16 ± 0.18 mg/L) and urinary IGFBP7 × TIMP‐2 [group‐wide: Δ0.64 ± 0.95 (pg/min)²] in young and older adults. Thus, the level of heat stress used herein caused modest increases in gastrointestinal permeability, resulting in a mild inflammatory response in young and older adults. Furthermore, our data indicate that older adults might be more at risk for increases in gastroduodenal permeability, as evidenced by the larger increases in sucrose excretion in response to heat stress. Finally, our findings show that heat stress impairs kidney function and elevates markers of kidney injury; however, these responses are not modulated by age.

Profound heat stress can damage the gastrointestinal barrier, leading to microbial translocation from the gut and subsequent systemic inflammation. Despite the greater vulnerability of older people to heat wave-related morbidity and mortality, it is unknown if age modulates gastrointestinal barrier damage and inflammation during heat stress. Therefore, the aim of this study was to determine if aging impacted enterocyte damage and systemic inflammatory responses to a 3-h exposure to very hot and dry (47 °C, 15% humidity) heat with accompanying activities of daily living (intermittent activity at 3 METS). Data from 16 young (age 21 to 39 years) and 16 older (age 65 to 76 years) humans were used to address this aim. In each group, log-transformed plasma concentrations of intestinal fatty acid binding protein (I-FABP_log), interleukin-8 (IL-8_log), and tissue factor (TF_log) were assessed as indices of enterocyte damage, systemic inflammation, and blood coagulation, respectively, before and after the 3-h heat exposure. In the younger cohort, I-FABP_log concentration did not increase from pre to post heat exposure (p = 0.264, d = 0.20), although it was elevated in the older group (p = 0.014, d = 0.67). The magnitude of the increase in I-FABP_log was greater in the older participants (p = 0.084, d = 0.55). Across all participants, there was no correlation between the change in core temperature and the change in IFABP_log. There was no change in IL-8_log in the younger group (p = 0.193, d = 0.23) following heat exposure, but we observed a decrease in IL-8_log in the older group (p = 0.047, d = 0.48). TF_log decreased in the younger group (p = 0.071, d = 0.41), but did not change in the older group (p = 0.193, d = 0.15). Our data indicate that I-FABP_log concentration (an index of enterocyte damage) is increased in older humans during a 3-h extreme heat exposure. Future studies should determine whether this marker reflects increased gastrointestinal barrier permeability in older individuals during heat exposure.