Obesity in pregnant women presents a risk to fetal health, leading to numerous metabolic syndromes and chronic inflammation risks. Previously, physical exercise was considered to be one of the primary treatments for obesity. However, the effect of fat consumption throughout the life cycle on physical endurance capacity remains unknown. A total of two groups of female mice (age, 6 weeks; C57BL/6J) were fed with a normal chow diet and a moderate high fat diet (MHFD), during pregnancy and lactation (8 weeks), with the offspring receiving the same diet as the mother. When filial mice were 8, 16 and 24 weeks old, they were tested for endurance, blood pressure (BP) and glucose tolerance, as well as adipose tissue infiltration and macrophage subtype. Compared with the control group, filial mice in MHFD groups exhibited increased BP and glucose levels and larger adipose cells (~4‑fold). During adolescence, the obese filial mice demonstrated increased endurance compared with controls. Endurance declines in middle and old age; the endurance of aged obese mice was 29% that of lean ones. In addition, body coordination and movement memory did not notably change. The expression of cluster of differentiation 68, one of the most reliable markers of macrophages, increased by 2.48‑fold, demonstrating that macrophages were recruited and underwent infiltration. In addition, increased tumor necrosis factor‑α and decreased interleukin‑10 expression demonstrated that infiltrated macrophages are polarized to the M1 state, which weakens physical endurance and resists type M2 macrophages, which exhibit repairing functions. In conclusion, hereditary MHFD weakens physical endurance and alters the metabolic characteristics of C57BL/6 offspring.