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Plants exposed to hypoxic conditions have been suggested to produce more biologically active phytochemicals than those exposed to normal oxygen levels. Previously, we investigated 314 highland crop species and showed that the flavonoid kaempferol extracted from a highland quinoa grain markedly increased mitochondrial metabolism and ATP production in a hypoxic environment in vitro. Thus, we hypothesized that kaempferol would be effective during exercise under harsh conditions, in which anaerobic metabolism occurs. This study adopted a double‐blind, placebo‐controlled, crossover design to investigate the effect of a single oral dose of kaempferol (10 mg) on the athletic performance‐related indicators of 13 male university athletes (20.8 ± 0.7 years) who performed two consecutive 400‐m runs with the shortest 90‐min interval assuming qualifying and main races. Although no significant differences were observed in the 400‐m race times between the placebo and kaempferol groups, kaempferol intake markedly reduced the respiratory and heart rates during the second run (p < 0.05). In addition, kaempferol intake reduced the levels of muscle damage markers, myoglobin, and aspartate transaminase (p < 0.05). A single oral dose of kaempferol reduced the cardiopulmonary burden and muscle damage in individuals participating in 400‐m runs. Kaempferol may be a useful supplement for relieving the physical load, particularly in individuals performing strenuous exercises with high oxygen demand. Trial Registration: UMIN Clinical Trials Registry in Japan: UMIN000049588 [ABSTRACT FROM AUTHOR]

Prolonged intense exercise induces acute renal injury; however, the precise mechanism remains unclear. We investigated the effects of neutrophil depletion in male C57BL/6J mice. Male C57BL/6J mice were divided into four groups: sedentary with control antibody; sedentary with antineutrophil antibody; exhaustive exercise with control antibody; and exhaustive exercise with antineutrophil antibody. Antineutrophil (1A8) or control antibody was administered i.p. to the mice before they ran on a treadmill. Plasma levels of creatinine and blood urea nitrogen (BUN) were measured. Renal histology was assessed 24 h after exhaustive exercise, and the concentration of kidney injury molecule (KIM)‐1 was measured using an enzyme‐linked immunosorbent assay. The expression levels of inflammatory cytokines were measured using qRT‐PCR. Furthermore, NADPH oxidase activity and the hydrogen peroxide concentration in the kidney were measured. Immediately after exhaustive exercise, plasma BUN was significantly increased, but creatinine was not. The increase in BUN after exercise was suppressed by 1A8 treatment. The pathological changes manifested as congested and swollen glomeruli and nuclear infiltration after exhaustive exercise. These changes were suppressed by treatment with the 1A8 antibodies. The KIM‐1 concentration increased after exhaustive exercise but was reduced by the 1A8 antibodies. Treatment with the 1A8 antibody also decreased exhaustive exercise‐induced inflammation and reactive oxygen species levels in the kidney. These results suggest that neutrophils contribute to exercise‐induced acute renal injury by regulating inflammation and oxidative stress. What is the central question of this study?The popularity of endurance exercise events, such as marathon and triathlon races, is increasing, with some reports suggesting that the running population has increased by ∼50% in 2018 compared to 2008. The incidence of acute kidney injury after prolonged endurance exercise has been reported to range from 4 to 85%. However, the precise mechanism remains unclear.What is the main finding and its importance?In this study, we found that neutrophils contribute to the development of exercise‐induced renal injury. The data we have provided will lead to future research into preventive measures and treatments, such as nutritional supplements targeting oxidative stress and inflammation related to neutrophils. [ABSTRACT FROM AUTHOR]

Kaempferol (KMP) is an important flavonoid in many fruits and vegetables. Preclinical studies on KMP have reported its pharmacological effects, including antimicrobial, antioxidant, anti‐inflammatory, antitumor, antidiabetic, myocardial protective, and neuroprotective effects. Additionally, some epidemiological studies have revealed a negative association between the consumption of KMP‐containing foods and the risk of developing several disorders, such as cancer and cardiovascular diseases. Thus, although a large body of literature has demonstrated the benefits of KMP supplementation, there are no reports of clinical trials evaluating the safety of KMP aglycone administration or KMP aglycone‐rich food consumption. The purpose of this study was to evaluate the safety of a high dose of KMP aglycone by administrating KMP aglycone‐containing supplements to healthy adults. This study had a randomized, double‐blind, placebo‐controlled design and a 4‐week duration. Participants were randomly allocated to the KMP (n = 24) or placebo (n = 24) group. For 4 weeks, the KMP group received a capsule containing 50‐mg KMP daily, a dose approximately five times higher than the estimated human dietary intake. The placebo group received a capsule containing cornstarch‐based powder daily. The general toxicity parameters were evaluated by examining the characteristics of the participants, hematological and blood biochemical parameters, general urinalysis, qualitative urine tests, and adverse events. No clinical changes were observed in anthropometric and blood pressure measurements or blood and urine parameters in the KMP group compared to those in the placebo group. Furthermore, no adverse events owing to KMP aglycone administration occurred. The study results revealed that the consumption of 50‐mg KMP aglycone daily for 4 weeks is safe in healthy adults. [ABSTRACT FROM AUTHOR]

Exhaustive exercise is known to induce acute renal damage. However, the precise mechanisms remain unclear. We investigated the effects of macrophage depletion on exhaustive exercise-induced acute renal damage. Male C57BL/6 J mice were divided into four groups: sedentary with control liposome (n=8), sedentary with clodronate liposome (n=8), exhaustive exercise with control liposome (n=8), and exhaustive exercise with clodronate liposome (n=8). Mice were treated with clodronate liposomes or control liposomes intraperitoneally for 48 h before undergoing exhaustive exercise. Renal function and renal histology were tested at 24 h. The expression levels of kidney injury molecule (KIM)-1 and inflammatory cytokines in kidney tissues were measured by quantitative RT-PCR, and KIM-1 concentration was semi-quantified by immunostaining. As a result, exhaustive exercise increased macrophage infiltration into the kidney. However, clodronate reduced it. Although exhaustive exercise resulted in an increase in KIM-1 mRNA expression levels and concentration, injection of clodronate liposome reduced it. In addition, TUNEL positive apoptotic cells were increased after exercise, but significantly reduced by clodronate. Clodronate liposome treatment also decreased the mRNA expression levels of inflammatory cytokines (TNF-α, IL-1β, and IL-6) in the kidney after exhaustive exercise. These results suggest that macrophages play a critical role in increasing renal damage by regulating inflammation. [ABSTRACT FROM AUTHOR]

The innate immune system is associated with the development of local inflammation. Neutrophils play an essential role in the development of the adipose tissue ( AT) inflammation associated with obesity by producing elastase, which can promote the activation and infiltration of macrophages. Exercise training attenuates AT inflammation via suppression of macrophage infiltration. However, the mechanisms driving this phenomenon remains to be elucidated. Here, we evaluated the effects of exercise training on the infiltration of neutrophils and elastase expression in an obese mouse model. Four-week-old male C57 BL/6J mice were randomly assigned to one of three groups that either received a normal diet ( ND) plus sedentary activity ( n = 15), a high-fat diet ( HFD) plus sedentary activity ( n = 15), or a HFD plus exercise training ( n = 15). Mice were fed the ND or HFD from the age of 4 weeks until 20 weeks. Mice in the exercise group ran on a treadmill for 60 min/day, 5 days/week over the same experimental period. Mice fed with the HFD had increased content of macrophages in the AT and increased inflammatory cytokine mRNA levels, which were reduced by exercise training. Similarly, AT from the HFD sedentary mice contained more neutrophils than AT from the ND mice, and the amount of neutrophils in this tissue in HFD-fed mice was lowered by exercise training. The mRNA levels of neutrophil elastase in AT were lower in the HFD exercise-trained mice than those in the HFD sedentary mice. These results suggest that exercise training plays a critical role in reducing macrophage infiltration and AT inflammation by regulating the infiltration of neutrophils. [ABSTRACT FROM AUTHOR]

Although nonalcoholic steatohepatitis (NASH) is an important component of the metabolic syndrome, scavenger receptor CD36 also modulates NASH development. This study aimed to clarify whether exercise training suppresses CD36 expression in a mouse model of NASH. Male C57BL/6 mice were divided into four groups: normal diet (ND) sedentary, ND exercise, high‐fat diet and high‐fructose water (HFF) sedentary, and HFF exercise groups. The exercise groups were trained on a motorized treadmill at running speeds of 15–20 m/min for 60 min/day, 5 times/week for 16 weeks. CD36 cell surface expression of hepatic resident macrophages, peroxisome proliferator‐activated receptor (PPAR)‐γ protein, and mRNA levels in the liver were increased in HFF sedentary mice but were attenuated in HFF exercise mice. Hepatic resident macrophages were significantly lower in HFF exercise mice than in HFF sedentary mice. Our findings indicated that exercise training reduced macrophage quantity in the liver, and downregulated CD36 and PPAR‐γ expression in liver and macrophages. Exercise training attenuated cell surface expression of CD36 in hepatic resident macrophages in the NASH model mice. Exercise training‐induced reduction in CD36 expression might be regulated by the down‐regulation of PPAR‐gamma. [ABSTRACT FROM AUTHOR]