Bone diseases are usually caused by abnormal metabolism and death of cells in bones, including osteoblasts, osteoclasts, osteocytes, chondrocytes, and bone marrow mesenchymal stem cells. Mitochondrial dysfunction, as an important cause of abnormal cell metabolism, is widely involved in the occurrence and progression of multiple bone diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma. As selective mitochondrial autophagy for damaged or dysfunctional mitochondria, mitophagy is closely related to mitochondrial quality control and homeostasis. Accumulating evidence suggests that mitophagy plays an important regulatory role in bone disease, indicating that regulating the level of mitophagy may be a new strategy for bone-related diseases. Therefore, by reviewing the relevant literature in recent years, this paper reviews the potential mechanism of mitophagy in bone-related diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma, to provide a theoretical basis for the related research of mitophagy in bone diseases.

Studies seem to show that high-intensity interval training (HIIT) is a more time-efficient protocol for weight loss, compared with moderate-intensity continuous training (MICT). Our aim was to compare the acute effects of energy expenditure (EE) matched HIIT vs. MICT on excess post-exercise oxygen consumption (EPOC) and substrate metabolism in male college students with obesity. Twenty-one untrained male college students (age, 22 ± 3 years; body fat, 28.4 ± 4.5%) completed two acute interventions (~ 300 kcal) on a treadmill in a randomized order: (1) HIIT: 3 min bouts at 90% of maximal oxygen uptake (VO_2max) with 2 min of recovery at 25% of VO_2max; (2) MICT: 60% of VO_2max continuous training. EPOC and substrate metabolism were measured by indirect calorimetry during and 30 min after exercise. Results showed that EPOC was higher after HIIT (66.20 ± 14.36 kcal) compared to MICT (53.91 ± 12.63 kcal, p = 0.045), especially in the first 10 min after exercise (HIIT: 45.91 ± 9.64 kcal and MICT: 34.39 ± 7.22 kcal, p = 0.041). Lipid oxidation rate was higher after HIIT (1.01 ± 0.43 mg/kg/min) compared to MICT (0.76 ± 0.46 mg/kg/min, p = 0.003). Moreover, the percentage of energy from lipid was higher after HIIT (37.94 ± 14.21%) compared to MICT (30.09 ± 13.54%, p = 0.020). We conclude that HIIT results in greater total EE and EPOC, as well as higher percentage of energy from lipid during EPOC than EE matched MICT in male college students with obesity.