In oestrogen-deficient mice, resistance training protected bone better than running
In short
Sixty-four ovariectomised (OVX) female C57BL/6J mice trained for eight weeks in either an aerobic (treadmill running) or a resistance (ladder climbing) protocol. Both raised osteoblast number and lowered osteoclast density versus sedentary controls (P<0.05) and reduced the RANKL/osteoprotegerin ratio (P<0.001). Resistance training went further, with higher osteocyte density (P<0.01), greater RUNX2 expression (P<0.001), larger muscle fibre cross-sectional area (P<0.05) and upregulated IGF-1 (P<0.01) and FNDC5 (P<0.05). Because this is a rodent model and not a human trial, it indicates a mechanism worth testing in people rather than a training prescription.
State the obvious first: the subjects here are mice, not women. Sixty-four female C57BL/6J mice had their ovaries removed to strip out oestrogen surgically, then trained for eight weeks. This is not a menopause clinical trial, so what comes out of it is a mechanism, not a prescription.
The mechanism is clear enough. After ovariectomy or sham surgery, animals were allocated to sedentary, aerobic (treadmill running) or resistance (ladder climbing) protocols for eight weeks, and the study measured femoral bone histology and histochemistry, skeletal muscle morphology, and gene expression in both bone and muscle tissue.
Both types of exercise slowed the bone loss
Running and ladder climbing alike increased osteoblast number and reduced osteoclast density in the OVX animals compared with sedentary controls (P<0.05) — more cells building bone, fewer removing it. The RANKL/osteoprotegerin ratio fell alongside it (P<0.001), and that ratio is effectively the switch controlling how many osteoclasts get made.
So both modalities mitigated the bone deterioration that oestrogen deficiency produced. That much lines up with human data. Which intensities and frequencies actually raised bone mineral density in postmenopausal women is covered, with human evidence, in strength training and bone density and the bone density training dose.
Where did the two diverge?
The resistance group's advantage was specific. It showed higher osteocyte density (P<0.01), greater expression of RUNX2 (P<0.001), the transcription factor that directs bone formation, and stronger suppression of osteoclastogenesis. Osteocytes are the cells that sense mechanical load on bone and convert it into signal, so a heavier-loading protocol thickening that layer is internally consistent.
Why muscle enters the story
The most interesting results are not in the bone at all. Only the resistance group significantly increased muscle fibre cross-sectional area (P<0.05) and upregulated IGF-1 (P<0.01) and FNDC5 (P<0.05) — both signals muscle secretes that act on bone.
That is why the authors frame it as muscle-bone crosstalk. In this data the resistance advantage is not simply that bone was pressed harder; the muscle that grew increased the signalling it sent to bone. The running group did not show that muscle-side rise.
The limits are large and obvious. Sixty-four mice, eight weeks, surgically induced oestrogen deficiency. Ladder climbing and treadmill running are not squats and jogging, and this study measured no clinical outcome such as fracture risk or bone mineral density. Do not change a human training plan on the strength of this paper. What it legitimately offers is a hypothesis for why the ‘resistance training is better for bone’ pattern keeps showing up in human research, and a next step: measure muscle-derived signals like IGF-1 and FNDC5 in people too.
What to actually log
Bone density is not something fairlift measures. But the variables this study points at — mechanical load reaching bone and the muscle mass generating it — are exactly what a Big 3 log tracks as a proxy. If your squat and deadlift are heavier than three months ago, the load reaching femur and spine went up too, and that axis is what moved bone-formation signalling in this experiment.
The inference this study does not support is worth stating just as plainly. A high strength score does not mean strong bones. Bone density is established by a scan, and around menopause the reference point should be that scan and a doctor's reading of it, not a training log.
Frequently asked questions
Is resistance training or cardio better for bone after menopause?
This particular study is an animal experiment: 64 ovariectomised mice trained for eight weeks. Under those conditions both running and ladder climbing raised osteoblast number and cut osteoclast density (P<0.05), but ladder climbing led on osteocyte density (P<0.01) and RUNX2 expression (P<0.001). It cannot be transferred directly to humans.
What does a lower RANKL/OPG ratio mean?
RANKL promotes osteoclast formation and osteoprotegerin blocks it. Both training groups showed a significantly lower ratio than sedentary controls (P<0.001), meaning the balance had tipped less far toward bone resorption.
Why do IGF-1 and FNDC5 matter here?
Both are muscle-expressed signals that act on bone. In this experiment only the resistance group showed increased muscle fibre cross-sectional area (P<0.05) together with upregulated IGF-1 (P<0.01) and FNDC5 (P<0.05), which the authors present as evidence of muscle-bone crosstalk.
Can these results be applied to people as they stand?
No. It is an eight-week model in 64 mice with oestrogen removed surgically, and it measured no clinical endpoint such as fracture or bone mineral density. Read it as a direction of mechanism and a hypothesis to test in humans.
So what should someone around menopause actually do for bone?
Follow the human evidence. The intensities and frequencies that raised bone mineral density in postmenopausal women have been studied in people directly, and decisions about bone density and fracture risk should rest on a scan and a doctor's advice.
Source: PubMed