Why Your Workouts May Not Be Building Stronger Bones - A Guide to Bone Density and Osteoporosis Prevention

You've been showing up to the gym for years. You eat reasonably well. You thought you were doing everything right. Then a DEXA scan comes back and the numbers surprise you.  Suddenly you're wondering how this happened.  You can't assume that if they work out consistently, your bones are covered. Bone is not built by movement alone. It is built by a specific kind of mechanical signal, and many otherwise healthy exercise routines never deliver enough of that signal to meaningfully improve bone strength or bone mineral density (BMD).

The natural progression of your bones

Bone is living tissue, and it changes across the lifespan. During childhood, adolescence, and early adulthood, the body is in a net bone-building phase, laying down more bone than it removes and steadily increasing bone mass until peak bone mass is reached, typically in the early 20s and sometimes up to about age 25 to 30.

An easy way to understand this is to think of bone like a bank account. The more bone deposited during those early years, the larger the reserve available later in life when withdrawals begin to outpace deposits.

After peak bone mass is reached, bone density tends to plateau for a period and then gradually declines with age. In women, that decline often speeds up around menopause because estrogen falls, and estrogen plays an important role in slowing bone breakdown. This is one reason bone loss can seem to accelerate in the midlife years even when exercise habits have not changed.

Sometimes bone loss has a clear culprit. More often, it's a quiet accumulation of factors, some we chose, many we didn't. Common contributors include:

• Low calcium intake: consistently below about 1,000 mg per day for most adults, or below 1,200 mg per day for many postmenopausal women and older adults.

• Low vitamin D: a blood 25(OH)D level below about 20 ng/mL is commonly considered deficient, and levels between about 20 to 30 ng/mL are often considered insufficient.

• Low body weight: a BMI below 18.5 is underweight, and bone risk is especially concerning when low weight is paired with weight loss, low muscle mass, or under-fueling.

• Low energy availability: eating too little for training demands, even without obvious weight loss, especially when periods become irregular or stop.

• Menopause and aging

• Long-term glucocorticoid use: daily or frequent prednisone-equivalent use for 3 months or longer is a common threshold for meaningful bone risk.

• Low physical loading: mostly sedentary activity, or exercise that rarely includes enough resistance, impact, or progression to challenge bone.

• Low bone mass on DEXA: a T-score between -1.0 and -2.5 is osteopenia, and -2.5 or lower is osteoporosis.

• Smoking and higher alcohol intake

• Family history of osteoporosis or fracture, and personal history of a fragility fracture

• Medical conditions such as hyperthyroidism, hyperparathyroidism, malabsorption, inflammatory disease, and some cancer-related conditions

• Medications such as some breast cancer therapies, and other drugs associated with bone loss

  
  

How bone is built and broken down

To understand why certain workouts help bone and others do not, it helps to know that bone is constantly being remodeled. Two cell types drive this process: osteoclasts break down old bone in a process called bone resorption, and osteoblasts build new bone in a process called bone formation. It takes 7-10 years for bone to renew.

When these two processes stay balanced, bone can remain stable over time. But when bone resorption outpaces bone formation, bone mass declines and the internal structure of bone becomes weaker, which raises fracture risk.

Mechanical loading matters because bone adapts to strain. When the skeleton experiences a force large enough to challenge it, the body interprets that strain as a signal to strengthen the tissue in the direction of the load. That is the foundation for later sections on exercise, DEXA, and treatment: bone is dynamic, and it responds to the forces and hormonal environment around it.

What builds bone and how

Bone-building exercise is not just about lifting the heaviest weight possible. Bone responds to mechanical strain, and that strain depends on more than load alone. It also depends on the direction of force, the rate at which force is applied, the novelty of the movement, the part of the skeleton being loaded, and whether the challenge is high enough for the individual.  It’s a bit overwhelming to think about.

Knowing that bone is formed in response to the direction of the force placed on it helps explain why certain exercises are more useful than others for the spine, hips, or wrists.

For example, you may perform many repetitions with light weights and get a muscular endurance benefit without meaningfully challenging bone. Another person may use a heavier but well-controlled load in a squat, step-up, deadlift, overhead press, or impact drill and create a more useful osteogenic stimulus because the skeleton is receiving a stronger, more specific mechanical signal.

The correct exercise dose is always individual. What is heavy enough to stimulate bone in one person may be too easy, too advanced, or unsafe for someone else, especially if osteopenia, osteoporosis, pain, balance limitations, or prior fracture are already present. If you have osteoporosis or a high risk of fracture, weighted forward flexion or rotation of the spine is not advised.  It’s best to work with a qualified trainer or instructor with anatomy training and ideally osteoporosis health.

DEXA, BMD, and FRAX

A DEXA scan, also written DXA for dual-energy X-ray absorptiometry, is the standard imaging test used to assess bone mineral density, or BMD. BMD is the amount of mineral content in bone, and it gives a practical estimate of bone strength and fracture risk when interpreted alongside the rest of a person’s history.

DEXA commonly measures BMD at the lumbar spine and hip, and sometimes the forearm when needed. The report usually includes the BMD, a T-score, and a Z-score.

The T-score compares a person’s BMD with that of a healthy young adult reference population. In general:

• A T-score of -1.0 or above is considered normal.

• A T-score between -1.0 and -2.5 is classified as osteopenia, meaning low bone mass.

• A T-score of -2.5 or below is classified as osteoporosis

  
  

The Z-score compares BMD with people of the same age and sex. This can be useful when the result seems unexpectedly low for age and prompts a search for secondary causes of bone loss.

The key takeaway from a DEXA report is not just the label. The most relevant questions are where bone loss is happening, whether the numbers are changing over time, and how those findings fit with fracture history, family history, menopause status, medications, and other clinical risks.

FRAX adds another layer. FRAX is a fracture risk calculator that estimates the 10-year probability of a major osteoporotic fracture and hip fracture using clinical risk factors, with or without BMD entered into the model. In widely used U.S. treatment thresholds, a hip fracture risk of 3 percent or more, or a major osteoporotic fracture risk of 20 percent or more, can support treatment even when the T-score falls in the osteopenia range rather than osteoporosis. Here is the link to calculate the FRAX score:  https://frax.shef.ac.uk/FRAX/tool.aspx?country=9

When treatment for bone is recommended

Treatment decisions are based on more than one number. Major guidelines generally support treatment for people with a prior hip or vertebral fragility fracture, a T-score in the osteoporosis range, or osteopenia with sufficiently elevated fracture risk based on FRAX or similar clinical assessment.

That means osteopenia is not always “mild” or harmless. If a person has already fractured, has rapidly declining BMD, or has a high 10-year fracture risk, medical treatment may be given even before the T-score reaches -2.5.

Medications used for bone loss

Several medication classes are used to reduce fracture risk. Treatment tend to depend on severity, fracture history, kidney function, menopausal status, treatment goals, and tolerance.

Medication class	Examples	What it does	Common side effects or cautions
Bisphosphonates	Alendronate (Fosamax), risedronate (Actonel), ibandronate (Boneva), zoledronic acid (Reclast)	Slow bone resorption by reducing osteoclast activity, which helps preserve bone and lower fracture risk. Can take up to 3 months to see improvements.  Shows better improvement in spine than hip.	Oral forms can cause reflux or other GI irritation; muscle or joint pain may occur; rare long-term risks include osteonecrosis of the jaw and atypical femur fracture.
RANKL inhibitor	Denosumab (Prolia)	Potently slows bone breakdown and lowers fracture risk while treatment continues. Patients are often prescribed for period of time then move to Reclast so improvements are maintained.	Can cause hypocalcemia and rare ONJ or atypical femur fracture; stopping without follow-on therapy can lead to rapid bone loss and rebound vertebral fractures.
Anabolic parathyroid receptor agonists	Teriparatide (Forteo), abaloparatide (Tymlos)	Stimulate new bone formation, making them useful in higher-risk patients or those with severe osteoporosis	Possible dizziness, nausea, leg cramps, and limited duration of use; usually followed by an antiresorptive medication to help maintain gains.
Sclerostin inhibitor	Romosozumab (Evenity)	Both increases bone formation and decreases bone resorption, which can improve BMD relatively quickly in high-risk patients	Can cause joint pain or headache and carries cardiovascular warning considerations in some patients
Selective estrogen receptor modulator	Raloxifene (Evista)	Reduces bone loss, particularly at the spine, and may be considered in selected postmenopausal women	Can increase hot flashes and risk of venous thromboembolism

Bone biomarkers

Bone biomarkers, also called bone turnover markers, are blood or urine markers that reflect how actively bone is being broken down and rebuilt at a given point in time. They are not used to diagnose osteoporosis on their own and are not used in FRAX calculations, but physicians may use them to understand bone remodeling activity, look for unusually high turnover, and monitor whether a medication is having its expected effect.

Biomarker	What it measures	How physicians use it
CTX or beta-CTX	A marker of bone resorption; it reflects collagen breakdown as osteoclasts break down bone. Can be a highly variable measurement.	Often used to monitor response and adherence to antiresorptive therapy because it usually falls within weeks to months when treatment is working.
NTX	Another marker of bone resorption derived from collagen breakdown.	Sometimes used similarly to CTX, though CTX is more commonly emphasized in current guidance.
P1NP or PINP	A marker of bone formation; it reflects new type I collagen synthesis by osteoblasts.	Commonly used to monitor treatment response, especially with anabolic therapy, because it often rises when bone formation is being stimulated.
Bone-specific alkaline phosphatase or BSAP/BAP	A marker of osteoblast activity and bone formation.	May be used when a formation marker is needed, including in some patients where renal issues complicate interpretation of other markers.
Osteocalcin	A marker associated with osteoblast activity and bone formation.	Less commonly used as a primary marker, but may be part of broader bone turnover assessment in some settings.

The most practical point for patients is that these tests are often most useful after treatment has started. Physicians may check them to see whether a bisphosphonate or denosumab is suppressing bone resorption as expected, or whether an anabolic drug such as teriparatide is stimulating bone formation.

Lab values to watch when concerned about bone

When bone loss is suspected, laboratory tests can help uncover secondary causes that may be driving low BMD or fractures. Here are some examples:

Lab value	What it can tell you
25-hydroxyvitamin D	Whether vitamin D status is adequate for calcium absorption and bone mineralization; low levels can contribute to bone loss.
Serum calcium	Helps identify calcium imbalance and can point toward parathyroid or other metabolic issues when abnormal.  Parathyroid regulates CA in bones.  If CA>10 then there may be parathyroid issues.
24-hour urine calcium	Can help show whether calcium losses are high or whether calcium handling is abnormal.
Parathyroid hormone or PTH	Elevated values may suggest hyperparathyroidism or a compensatory response to low calcium or low vitamin D.
Phosphate	Abnormal levels can suggest broader mineral or endocrine disturbances affecting bone.
Alkaline phosphatase or ALP	Can reflect increased bone turnover, though it is not bone-specific unless bone-specific ALP is measured.
Creatinine and kidney function	Kidney disease can affect mineral metabolism, vitamin D activation, medication choice, and bone health overall.
Thyroid-stimulating hormone or TSH	Helps screen for thyroid dysfunction, especially hyperthyroidism or overtreatment with thyroid hormone, both of which can accelerate bone loss.
Complete blood count or CBC	May help identify anemia, inflammation, or clues to systemic disease contributing to bone loss.
Liver function tests	Abnormal liver function can be associated with metabolic issues that affect bone.
Testosterone in men	Low testosterone can be a secondary cause of bone loss in men.
Celiac testing or other secondary workup when indicated	Used when symptoms, history, or low Z-score raise concern for malabsorption or another secondary cause.

The most important takeaway is that low bone density is sometimes the end result of a treatable upstream issue. That is why a thoughtful workup matters, especially in younger adults, men, people with unexpectedly low Z-scores, or anyone losing bone faster than expected.

Exercises that matter

Your workouts weren’t wasted.  They've done real things for your heart, your mind, your mood, your energy, and your resilience. Bone has a different ask, and most of us were never told what it was. The exercises most likely to support bone are the ones that create meaningful load through the skeleton, especially the spine and hips, and do so with enough progression over time. Broadly, the most evidence-based exercise categories are impact training, progressive resistance training, and weight-bearing movements that load bone from different angles. Keep in mind that your form matters.  You want to exercise while your body is in proper alignment.  Also, working with an experienced instructor can make a world of difference when using heavy weights.

More specific examples include:

• Progressive lower-body strength work such as squats, deadlifts, split squats, lunges, step-ups, and loaded sit-to-stands, when appropriate for the individual.

• Upper-body and trunk loading such as overhead press variations, carries, rows, and resistance exercises that challenge posture and transmit force through the spine and upper extremities.

• Impact or higher-rate loading such as hops, skips, jumps, heel drops, or bounding progressions when safe and tolerated, because bone responds not only to force magnitude but also to the speed at which force is applied.

• Multi-directional weight-bearing tasks rather than only straight-plane repetitive movement, because varied loading can stimulate different regions of bone.

• Balance and fall-prevention work, which may not directly build large amounts of bone but is essential for lowering fracture risk.

  
  

What usually falls short is the exercise that improves fitness without creating enough skeletal strain. Steady-state cardio, walking at an easy pace, very light weights, and low-load movement sessions may be beneficial for cardiovascular health, mobility, and mood, but they often do not provide enough osteogenic stimulus to significantly improve BMD on their own.

Pilates can play an important role as it has the potential to improve posture, balance, trunk strength, movement quality, and body awareness, all of which matter for confidence, fall prevention, and the ability to perform more targeted loading safely. There is not enough evidence to say exactly how much Pilates alone can improve BMD, and existing studies are limited and mixed.  

Diet and lifestyle changes that can improve bone

Exercise matters, but it is only one part of the bone equation. Bone also depends on enough raw material, enough recovery, and daily habits that support remodeling rather than quietly undermining it.

The most useful diet and lifestyle changes often include:

• Meeting calcium needs consistently through food first when possible, and supplementing when dietary intake is not enough.  Before menopause CA should be at least 1000 mg/day and after menopause 1200-1500 mg/day.

• Correcting low vitamin D when present so calcium can be absorbed and used appropriately.

• Eating enough total calories and enough protein to support tissue repair, muscle mass, and bone formation rather than chronically under-fueling.  Here is a calculator for this:  https://www.calculator.net/protein-calculator.html

• If there is a gluten sensitivity, this can cause bone loss if eaten, even in moderation.

• Building a program that combines bone-targeted resistance and impact exercise with balance training and gradual progression.

• Stopping smoking or vaping, both of which are associated with weaker bone.

• Reducing excess alcohol intake, which can harm bone directly and also increase fall risk.

• Supporting sleep, stress regulation, and long-term consistency, because bone health is shaped by repeated habits over time rather than one perfect week.

Maybe you’ve noticed as you’ve entered midlife how the hardest part is not knowing that these changes matter. It is figuring out how to make them realistic, personalized, and sustainable. Bone health isn't a crisis to manage. It's a conversation you can start having with your body at any age. The information exists. The tools exist. And you don't have to figure it out alone.  Reforming You offers coaching support to help clients improve nutrition, exercise habits, recovery, and lifestyle choices in a way that supports stronger bones and better long-term health.  A new program will be offered soon that is created from literature to improve bone.  Visit us here at: www.reformingyou.com.

References

• Bone Health and Osteoporosis Foundation. The Clinician’s Guide to Prevention and Treatment of Osteoporosis.

• International Society for Clinical Densitometry. 2023 ISCD Official Positions Adult.

• National Osteoporosis Guideline Group. Full Guideline.

• Mayo Clinic. Laboratory Testing of Bone Turnover Markers.

• NIH / PMC. Osteoporosis: Investigations and Monitoring.

• Royal Osteoporosis Society. Are there any foods I should avoid?.

• Mayo Clinic. Keep Your Bones Healthy.

• PubMed. The effects of clinical Pilates exercises on bone mineral density, physical performance, and quality of life in postmenopausal osteoporosis.

• PubMed. Skeletal structural adaptations to mechanical usage (SATMU).

• AAFP. Osteoporosis Treatment: Updated Guidelines From ACOG.

• AAFP. Osteoporosis: Common Questions and Answers.

• PubMed. The association between plasma homocysteine levels and bone mineral density.

• PubMed. The association between the serum C-peptide level and bone mineral density.