Obesity and chronic alcohol consumption have been associated with an elevated risk of osteoarthritis (OA). We examined here whether the administration of metabolic stressors in the form of diet compromised cartilage morphology or biochemistry, and whether low intensity vibration could mitigate any of the degenerative effects observed. First, we investigated if high fat diet, in young mice, compromised the attainment of articular cartilage thickness. Further, we sought to determine if low intensity vibration (LIV) could enhance the formation of articular cartilage in a mouse model of diet induced obesity. Five-week-old, male, C57BL/6 mice were separated into 3 groups (n=10):​ Regular diet (RD), High fat diet (HF), and HF+LIV (HFv;​ 90Hz, 0.2g, 30 min/d, 5 d/w) with the diet administered for 8 weeks, and LIV for 6 weeks, which was considered short term diet and LIV administration. Additionally, an extended HF diet study was run for 6 months (LIV at 15m/d), and a separate short term HF diet study on older mice (17- weeks old C57BL/6 mice) to investigate the effects of short term diet and LIV on the mature knee joint. Lastly, we investigated the effects of chronic alcohol consumption on the young rat knee joint, and whether LIV could mitigate the degenerative effects observed. 19 four-weekold, female Wistar rats were separated into 3 groups (n=6-7/group):​ Control (C), Alcohol diet (A), or Alcohol +LIV, (A+LIV), with the diet and LIV administered for three weeks total. Articular cartilage and subchondral bone morphology, and sulfated GAG content were quantified using contrast agent enhanced µCT. For the young HF mouse study, gene expression within femoral condyles was quantified using real-time polymerase chain reaction, and histology was used to measure chondrocyte cell density within the articular cartilage. After short and long term HF administration, beginning in young mice, HF cartilage thickness was not statistically different from RD, however, HF had a lower cartilage thickness to body weight ratio when compared to RD. In contrast, LIV increased cartilage thickness compared to HF, yielding a cartilage thickness to weight ratio not different from RD. Further, long term HF diet resulted in subchondral bone thickening, compared to RD, providing early evidence of OA pathology—LIV suppressed the thickening, such that levels were not significantly different from RD. HF diet and LIV administration, beginning in older mice, did not result in significant changes in articular cartilage thickness to body weight ratio, with no changes in subchondral bone thickness, however, incorporation of a refractory period stimulated increased cartilage thickness compared to RD controls. Looking at a different metabolic stressor, chronic alcohol consumption in young rats did not result in significant changes in articular cartilage thickness or sulfated GAG content. These data suggest that articular cartilage thickness failed to scale with increased body mass in HF diet mice, when the diet was administered to the animals at a young age. Dynamic loading, via LIV, stimulated an increase in cartilage formation, resulting in joint surfaces better suited to the risks of greater loading that parallel obesity. The data from older mice indicate that the aged joint was not responsive to high fat diet, and was only responsive to LIV with the incorporation of a rest period between bouts. Chronic alcohol consumption, within the short term, did not induce detectable degenerative changes in the developing rat knee. The lack of a cartilage response in the alcohol consumption model may be the result of there not being a weight gain in these animals, potentially eliminating the need for an adaptation of cartilage thickness. Age and the type of metabolic stressor will be important when considering a patient for LIV treatment for promoting joint health.