Bone metabolism is a process in which osteoclasts continuously clear old bone and osteoblasts form osteoid and mineralization within basic multicellular units, which are in a dynamic balance. The process of bone metabolism is affected by many factors, including diet. Reasonable dietary patterns play a vital role in the prevention and treatment of bone-related diseases. In recent years, dietary patterns have changed dramatically. With the continuous improvement in the quality of life, high amounts of sugar, fat and protein have become a part of people’s daily diets. However, people have gradually realized the importance of a healthy diet, intermittent fasting, calorie restriction, a vegetarian diet, and moderate exercise. Although these dietary patterns have traditionally been considered healthy, their true impact on bone health are still unclear. Studies have found that caloric restriction and a vegetarian diet can reduce bone mass, the negative impact of a high-sugar and high-fat dietary (HSFD) pattern on bone health is far greater than the positive impact of the mechanical load, and the relationship between a high-protein diet (HPD) and bone health remains controversial. Calcium, vitamin D, and dairy products play an important role in preventing bone loss. In this article, we further explore the relationship between different dietary patterns and bone health, and provide a reference for how to choose the appropriate dietary pattern in the future and for how to prevent bone loss caused by long-term poor dietary patterns in children, adolescents, and the elderly. In addition, this review provides dietary references for the clinical treatment of bone-related diseases and suggests that health policy makers should consider dietary measures to prevent and treat bone loss.

Bone tissue is an important load-bearing organ of the human body. Moderate exercise enhances bone mass through mechanical loading, while high-intensity exercise may suppress it. Infrared therapy improves circulation, reduces pain/inflammation, and aids tissue repair. This paper presents a protocol to elucidate the modulatory effects of infrared therapy on high-intensity exercise-induced skeletal metabolic disorders and their molecular mechanisms. In this study, 24 6-week-old mice were randomly divided into control (CTR, N = 8), high-intensity treadmill exercise training (HIT, N = 8), and infrared therapy after high-intensity treadmill exercise (IRT, N = 8) groups. The latter two groups were trained for 8 weeks. In the first week, the mice underwent treadmill acclimation training. In the second week, the mice exercised at the rate of 24 m/min for 50 min, which increased at the rate of 1 m/min and 10 min every week until it reached 28 m/min for 80 min, with a gradient of 5° for 6 days. At the fifth week, HIT group mice were subjected to whole-body infrared therapy intervention, with the temperature controlled between 42 °C and 45 °C. The whole treatment process lasted ~40 min, 3x a week. Results showed that in the HIT group compared with those in the CTR group, the bone volume/total volume and trabecular number were significantly decreased, the trabecular separation was significantly increased, the osteogenic-related genes of Atf4, Runx2, and Ocn were downregulated, and the osteoclast-related genes of Ctsk and Mmp9 were upregulated. The micro-CT results of the IRT group mice showed no significant difference, but the osteogenesis-related genes Alp, Atf4, Runx2, Ocn, and Osx were upregulated in the femur. In addition, the osteoclast-related gene Ctsk was downregulated. Long-term high-intensity treadmill exercise may reduce bone mass. While infrared therapy does not affect bone mineral density, it may improve bone metabolism.

Bone tissue is an important load-bearing organ of the human body. Moderate exercise enhances bone mass through mechanical loading, while high-intensity exercise may suppress it. Infrared therapy improves circulation, reduces pain/inflammation, and aids tissue repair. This paper presents a protocol to elucidate the modulatory effects of infrared therapy on high-intensity exercise-induced skeletal metabolic disorders and their molecular mechanisms. In this study, 24 6-week-old mice were randomly divided into control (CTR, N = 8), high-intensity treadmill exercise training (HIT, N = 8), and infrared therapy after high-intensity treadmill exercise (IRT, N = 8) groups. The latter two groups were trained for 8 weeks. In the first week, the mice underwent treadmill acclimation training. In the second week, the mice exercised at the rate of 24 m/min for 50 min, which increased at the rate of 1 m/min and 10 min every week until it reached 28 m/min for 80 min, with a gradient of 5° for 6 days. At the fifth week, HIT group mice were subjected to whole-body infrared therapy intervention, with the temperature controlled between 42 °C and 45 °C. The whole treatment process lasted ~40 min, 3x a week. Results showed that in the HIT group compared with those in the CTR group, the bone volume/total volume and trabecular number were significantly decreased, the trabecular separation was significantly increased, the osteogenic-related genes of Atf4, Runx2, and Ocn were downregulated, and the osteoclast-related genes of Ctsk and Mmp9 were upregulated. The micro-CT results of the IRT group mice showed no significant difference, but the osteogenesis-related genes Alp, Atf4, Runx2, Ocn, and Osx were upregulated in the femur. In addition, the osteoclast-related gene Ctsk was downregulated. Long-term high-intensity treadmill exercise may reduce bone mass. While infrared therapy does not affect bone mineral density, it may improve bone metabolism.