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. 2010 Jan 30;14(2):149–153. doi: 10.1007/s12603-009-0224-5

Potential of creatine supplementation for improving aging bone health

DG Candow 1,3,a, PD Chilibeck 2
PMCID: PMC12878991  PMID: 20126964

Abstract

Aging subsequently results in bone and muscle loss which has a negative effect on strength, agility, and balance leading to increased risks of falls, injuries, and fractures. Resistance training is an effective strategy for maintaining bone mass, possibly by increasing activity of cells involved in bone formation and reducing activity of cells involved in bone resorption. However, bone loss is still evident in older adults who have maintained resistance training for most of their life, suggesting that other factors such as nutrition may be involved in the aging bone process. Emerging evidence suggests that creatine supplementation, with and without resistance training, has the potential to influence bone biology. However, research investigating the longer-term effects of creatine supplementation and resistance training on aging bone is limited.

Key words: Resistance training, bone remodelling, nutrition

Introduction

Aging is associated with a reduction in bone mass (i.e. 0.5% per year after the age of 40) (1). The accompanying loss of muscle masss and strength (2) has a negative effect on agility and balance leading to increased risks of falls, injuries, and fractures. The mortailtiy rate for older adults in the first year after fracture is approximately 15-20% (1). Osteoporosis, defined as a skeletal disorder characterized by low bone mass and bone strength (3), is a major health concern with direct and indirect health costs in the billions of dollars (3). With the projected increase in life expectancy, the incidence of bone loss and fracture may rise and potentially drain the health care system, with greater need for hospitalization, treatment, and rehabilitation (4)

Despite an abundance of literature on aging bone, there remains a scarcity of information regarding the underlying mechanism(s) and adaptations of aging. Bone has a remarkable ability to respond and adapt to mechanical stress (i.e. resistance training) (5). Bone remodeling (i.e. bone resorption by osteoclasts followed by bone formation by osteoblasts) is necessary for repair of bone and maintenance of blood calcium levels; however, the bone remodeling cycle is most likely altered with aging. Normal bone remodeling is a tightly controlled process in which the rate of bone resorption is equal to the rate of bone formation (6). However, accelerated bone loss with aging may be the result of an imbalance between resorption and formation, favoring resorption (6, 7).

Although aging bone can be maintained or increased with pharmacologic therapy (i.e. hormone replacement therapy, bisphosphonates), physical activity (i.e. resistance training or exercise training with high-impact loading) is the only current strategy proven to increase bone mass and bone strength and reduce the risks of falls in older adults (1). However, individuals who have maintained resistance training for most of their life (i.e. master athletes) are still likely to experience bone loss with age, suggesting that other factors such as nutrition may be involved. Emerging evidence suggests that nutritional intervention with creatine monohydrate may affect bone biology possibly by increasing the metabolic (i.e. alkaline phosphatase) activity of osteoblast-like cells involved in bone formation (8) and decreasing cross linked N-telopeptides of Type I collagen, an indicator of osteoclast mediated bone resorption ( 9., 10., 11., 12.). However, the clinically significant effects of creatine supplementation alone, and in combination with resistance training, on properties of aging bone are relatively unknown.

Resistance training

It is well established that resistance training is a safe and effective strategy to increase whole-body muscle mass and strength in older adults (13). Potentially, the mechanical strain applied to bone via muscle hypertrophy may increase bone formation in proportion to resorption, leading to bone accretion over time in older adults. However, the effects of resistance training on properties of aging bone are inconsistent, with some showing an improvement in bone mineral density ( 14., 15., 16.) and bone mineral content (17) while others have not observed the same benefits ( 18., 19., 20., 21.). Accounting for this confusion, at least in part, are differences in resistance-exercise intensity, volume, and duration as 6-8 months of training is usually required to detect measurable changes in bone (1). For a summary of studies investigating resistance training and aging bone, see Table 1.

Table 1.

Summary of studies investigating the effects of resistance-training on properties of aging bone.

Study Subjects Age (Ave) Training Program Duration Bone Measurements
Bocalini (22) Postmenopausal 70 yrs RT 3 sets 3x/wk ↔ LS BMD, FN BMD
Females (n=23) 0 reps 24 wks
Bemben (23) Postmenopausal 50 yrs RT 1-3 sets 3x/wk ↔ LS BMD, FN BMD, trocanter BMI
Females (n=17) 8 reps 24 wks Ward’s triangle BMD
↔ osteocalcin
Candow (9) Males (n=10) 65 yrs RT 3 sets 3x/wk ↔ Ntx
10 reps 12 wks
Candow (24) Males (n=12) 64 yrs RT 3 sets 3x/wk ↔ Ntx
10 reps 10 wks
Chilibeck (17) Males (n=13) 71 yrs RT 3 sets 3x/wk ↑ 0.5 whole-body BMD
10 reps 2 wks ↑ 1.1% leg BMD
Chilibeck (18) Postmenopausal 57 yrs RT 2 sets 3x/wk ↔ whole-body BMD, LS BMD
Females (n=10) 8-10 reps 52 wks FN BMD, Ward’s triangle BMD
Kerr (14) Postmenopausal RT 3 sets 2x/wk ↑ 1.7% TH BMD
Females (n=56) 8 reps 12 wks ↑ 1.5%ITHBMD
↑ 2.3% Ward’s triangle BMD
↑ 2.4% URS BMD
Kohrt (25) Females (n=13) 65 yrs RT 2-3 sets 3x/wk ↑ 1.6% whole-body BMD
8-12 reps 44 wks
Kukuljan (26) Males (n=89) 60 yrs RT 2 sets 3x/wk ↑ 1.5% LS BMD, ↑ 1.8% FN BMD
8-12 reps 12 wks ↑1.5%LSBMD,
↑ 5.1% Ward’s triangle BMD
Liu-Ambrose (27) Females (n=32) 80 yrs RT 2 sets 2x/wk ↑ 1.4% cortical BMD
6-8 reps 24 wks
Maddalozzo (28) Male/Females 55 yrs RT 3 sets 3x/wk ↑ 1.9% LS BMD, ↑ 1.3-2.0% GT
(n=54) 2-13 reps 24 wks BMD
Menkes (29) Males (n=11) 59 yrs RT 1-2 sets 3x/wk ↑ 2.0% LS BMD, ↑ 3.8% FN BMD
15 reps 16 wks
Nelson (30) Postmenopausal 60 yrs RT 3 sets 2x/wk ↑ 1.0% LS BMD, ↑ 1% FN BMD
Females (n=20) 8 reps 52 wks
Pruitt (21) Postmenopausal 53 yrs RT 1 set 3x/wk ↑1.6%LSBMD
Females (n=17) 10-15 reps 36 wks
Ryan (31) Postmenopausal 62 yrs RT 2 sets 3x/wk ↔ BMD, osteocalcin, ALP, NTx
Females (n=27) 10-15 reps 16 wks
Stewart (32) Male/Females 65 yrs RT 2 sets 3x/wk ↔ LS BMD, FN BMD, GT BMD
(n=57) 10-15 reps 24 wks
Verschueren (33) Postmenopausal 65 yrs RT 1-3 sets 3x/wk ↔ Hip BMD, osteocalcin, NTx
Females (n=22) 10-15 reps 24 wks
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ALP= alkaline phosphatase, Ave= average, BMD= bone mineral density, FN= femoral neck, GT=greater trocanter, ITH= intertrochanteric hip, LS= lumbar spine, NTx= n-telopeptides, PF= proximal femur, reps= repetitions, RT= resistance training, TH= trochanter hip, URA= ultraradistal radial site, wk= week.

Creatine

Creatine (C4H9N302) is a nitrogen-containing compound naturally produced in the liver, pancreas and kidneys (i.e. 1-2g/day) from reactions involving the amino acids glycine, arginine, and methionine and is also consumed in the diet (i.e. 1-2g/day) primarily from red meat and seafood (34). Creatine is a component of the high-energy phosphate, phosphocreatine (PCr), which is needed to resynthesize adenosine diphosphate (ADP) to maintain adenosine triphosphate (ATP) during intense muscle contraction (i.e. PCr + ADP ↔ATP + Cr). In addition, creatine may potentially increase muscle accretion and strength by enhancing satellite cell activity (35), cellular hydration status (36) anabolic hormone production (37), and myogenic transcription factors leading to greater myofibrillar protein content (38) and by reducing protein catabolism (9) and oxidative stress (39). While resistance training typically results in an 8% increase in muscle strength, the addition of creatine to resistance training further augments these gains by an additional 12% (40).

There is research showing a positive effect from creatine supplementation on muscle mass in the aging population (41, 42). Since muscle mass is a strong predictor of bone mass with aging, the increase in muscle from creatine supplementation and resistance training may also have a favorable affect on bone. Subsequently, creatine could be categorized with conjugated linoleic acid (43) and milk-based proteins (44) as potential adjuncts to resistance training for improving properties of both muscle and bone.

Creatine and bone biology

Mechanistically, creatine may have a favorable effect on the bone remodeling process. Creatine supplementation (2% wet weight) given to growing rats (5 weeks of age; n=16) for 8 weeks significantly increased lumbar bone mineral density and femur bone strength over placebo, with a trend for greater bone mineral density of the distal femur (45). The authors speculate that creatine may have influenced bone metabolism and bone microarchitecture by increasing the development of trabeculae during endochondral bone formation through hypertrophy of chondrocytes and by increasing the ability of osteoblasts to form more bone tissue (45). Furthermore, Gerber et al. (8) found that creatine supplementation added to low serum cell culture medium increased metabolic activity and differentiation and mineralization of osteoblast-like cells. In addition to increasing bone formation, stimulating osteoblast activity may increase the production of osteoprotegerin, a cytokine which inhibits osteoclast differentiation and reduces bone resorption (46). This could help explain the decrease in markers of resorption (i.e. N-telopeptides) found in several studies ( 9., 10., 11., 12.).

Review of research involving creatine and bone

A PubMed literature search using the key search terms ‘creatine’ and ‘bone’ resulted in 12 peer-refereed publications (4 involving healthy older adults, 3 involving healthy younger adults, 2 involving young boys with muscular dystrophy, 2 involving rodents, and 1 involving a cell-culture medium). To compare relevant results across studies, we determined the magnitude of the treatment (i.e. creatine) or effect size on bone and compared this to placebo (control). Effect sizes (ES: mean 1-mean 2/standard deviation) were classified as small (<0.5), moderate (0.5-0.8), or large (>0.8) according to Cohen (47). For summary of studies showing a beneficial effect from creatine on properties of human bone, see Table 2.

Table 2.

Summary of studies showing a beneficial effect from creatine supplementation on human bone

Study Subjects Creatine Dosage Study Duration Exercise Program Frequency Bone Measurements ES
Candow (9) 23 male (66 yrs) 0.1g•kg-1 10 wk RT
3 sets, 10 reps
8 exercises		 3x/wk ↓ 30% N-telopeptides* 2.0
Chilibeck (17) 29 male
(71 yrs)		 0.3g•kg-1 (5 days)
0.07g•kg-1 (79 days)		 12 wk RT
3 sets. 10 reps
12 exercises		 3x/wk ↑ 3.2% BMC* 0.2
Cornish (10) 41 male
6 female
(23 yrs)		 9g/day 5 wk RT
4-5 sets
6-12 reps		 6x/wk ↓ 4% N-telopepetides† 0.4
Louis (11) 12 boys 3g/day 12 wk None ↑ 2% whole-body BMD* 0.8
(DMD) ↑ 3% lumbar spine BMD* 0.4
↓ 56% N-telopepetides* 3.1
Tarnopolsky (12) 30 boys
(DMD)		 0.1g•kg-1 16 wk None ↓ 22% N-telopepetides* NA
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BMD= bone mineral density, BMC= bone mineral content, DMD= Duchenne muscular dystrophy, ES= effect size; RT= resistance training, Wk=weeks, Yrs= years of age. NA= not available; * Significantly greater compared to placebo (p<0.05). † Significant decrease compared to an increase for individuals ingesting protein alone.

Muscular dystrophy is a genetic disease which leads to muscle atrophy (48) and bone loss, characteristics resembling the aging process in muscle (i.e. sarcopenia) and bone (i.e. osteoporosis). Louis et al. (11) investigated the potential effects of creatine supplementation (3 grams/day) without structured exercise training in young boys with Duchenne (n=12) and Becker (n=3) muscular dystrophy. Patients were randomly assigned (double blind) to supplement with creatine or placebo for 3 months (cross-over design, 2 month washout period). Creatine supplementation decreased the urinary excretion of cross-linked N-telopeptides of Type I collagen, an indicator of bone resorption in 5 boys who were independent of a wheel chair compared to a 6% increase for placebo (creatine: pre 1365±245 mmol bone collagen equivalents [BCE]/mmol creatinine, post 599±154 mmol BCE/mmol creatinine or -56%, ES: 3.1; placebo: pre 1144±204 mmol BCE/mmol creatinine, post 1325±264 mmol BCE/mmol creatinine or +6%, ES: 0.8; p<0.01). Creatine also increased whole-body bone mineral density (creatine: pre 0.776±0.02g.cm-2, post 0.792±0.02g.cm-2 or +2.0%, ES: 0.8; placebo: pre 0.776±0.025g.cm-2, post 0.781±0.02g.cm-2 or 0.6%; ES: 0.2, p<0.05) and lumbar spine bone mineral dens ity in thes e young boys (creatine: pre 0.60±0.05g.cm-2, post 0.62±0.05g.cm-2 or +3.3%, ES: 0.4; placebo: pre 0.60±0.04g.cm-2, post 0.60±0.04g.cm-2 or 0%; ES: 0.0, p<0.05). It is important to note that creatine supplementation also increased maximal voluntary contraction of the elbow flexors (creatine: pre 5.4±2.1N.m, post 6.1±2.2±2.1N.m or +13%, ES: 0.3; placebo: pre 5.0±1.5N.m, post 4.9±1.6N.m or -2,0%; ES: 0.06, p<0.05) and exercise time to fatigue (creatine: pre 4.1±1.3 s, post 7.2±1.4s or +75%, ES: 2.4; placebo: pre 4.9±1.8s, post 4.2±1.2s or -14%; ES: 0.4, p<0.01). Using a randomized, double-blind, placebo-controlled, cross-over design, Tarnopolsky et al. (12) investigated the effects of creatine supplementation (0.1 g.kg-1) in young boys (n=30) with Duchenne muscular dystrophy for 4 months. Creatine supplementation did not have a favorable effect on whole-body bone mineral density or content but did attenuate the increase in urinary excretion of cross-linked N-telopeptides of Type I collagen by 22% compared to placebo (creatine: 220 nM BCE/mmol creatinine, placebo: 270 nM BCE/mmol creatinine, p<0.05), again indicating reduced bone resorption.

In addition to these two studies on creatine supplementation and muscular dystrophy, there are four published reports investigating the potential effects of creatine supplementation during structured exercise training on aging bone. In the most recent study, we found that creatine supplementation (0.1 g.kg-1) during supervised resistance training (8 whole-body machine-based exercises: leg press, chest press, lat pull-down, shoulder press, leg extension/curl, biceps curl, calf press; 3 sets of 10 repetitions to muscle fatigue, 1-2 minutes rest between sets, 3 days/week; 10 weeks) in healthy older males decreased bone resorption (cross-linked N-telopeptides of Type I collagen) by 30% compared to a non-significant 6% reduction in the placebo group (creatine: pre 57.1±8.5 mmol BCE/mmol creatinine, post 40.1±5.7 mmol BCE/mmol creatinine, ES: 2.0; placebo: pre 50.6±7.2 mmol BCE/mmol creatinine, post 47.4±10.3 mmol BCE/mmol creatinine, ES: 0.4, p<0.05) (9). These results support our previous findings that creatine supplementation (0.3 g.kg-1 for 5 days, 0.07 g.kg-1 for 79 days) during 12 weeks of supervised resistance training (12 whole-body machine-based exercises: leg press, chest press, lat-pulldown, shoulder press, leg extension/curl, biceps curl, hip flexion/extension/abduction/adduction, back extension, 3 sets of 10 repetitions to muscle fatigue, 2-minutes rest between sets, 3 days/week) in healthy older males increased upper-limb bone mineral content by 3.2% compared to a non-significant decrease (-1.0%) in the placebo group (creatine: pre 433±77 g, post 447±82 g, ES: 0.2; placebo: pre 405±97 g, post 401±98 g, ES: 0.04; p<0.05) (17). The increase in bone mineral content from creatine supplementation highly correlated with the increase in lean tissue mass (r=0.67, p<0.01); suggesting that the increase in muscle from creatine supplementation may have enhanced muscle pull and strain on bone, resulting in bone accretion.

While these results across studies indicate potential benefits from creatine supplementation on bone, others have found no effect from creatine (Table 3). For example, Tarnopolsky et al. (49) investigated the combined effects of creatine monohydrate (5 grams/day) and conjugated linoleic acid (6 grams/day) supplementation in healthy older adults (65-85 years, 19 males, 20 females) during 6 months of structured resistance training (12 whole-body machine-based exercises: 3 sets of 12 repetitions for leg press, chest press, leg extension/curl, shoulder press, lat pull-down, seated row, calf raise, abdominal crunch, back extension, and 3 sets of 10 repetitions for biceps curl and triceps extension, 2 days/week). Creatine had no effect on bone mineral density (whole body: pre 1.02-1.20±0.11 g.cm-2, post 1.04-1.23±0.1 g.cm-2, ES: 0.2; hip: pre 0.83-0.94±0.1 g.cm-2, post 0.81-0.92±0.1 g.cm-2, ES: 0.2; lumbar spine: pre 0.94-1.19±0.12 g.cm-2, post 0.94-1.19±0.12 g.cm-2, ES: 0.0) or urinary excretion of cross-linked N-telopeptides of Type I collagen (creatine: pre 384±217 mmol BCE/mmol creatinine, post 494±434 mmol BCE/mmol creatinine, ES: 0.5; placebo: pre 367±283 mmol BCE/mmol creatinine, post 307±211 mmol BCE/mmol creatinine, ES: 0.2). In a previous investigation from the same laboratory, Brose et al. (50) used a double blind, placebo-controlled, repeated measures design to determine the effects of creatine supplementation (5 grams/day) during 1 4 weeks of resistance training (12 whole-body machine-based exercises: 4 lower-body, 8 upper-body, 3 sets of 10-12 repetitions, 3 days/week) in healthy older adults (n=14, 8 males, 6 females). The authors found no effect from creatine supplementation on serum osteocalcin (indicator of bone formation) over placebo (creatine: pre 16.0-17.1±4.8ng/ml, post 16.1-18.0±3.9ng/ml, ES: 0.1; placebo: 14.1-16.3±2.9ng/ml, post 14.1-16.6±2.7ng/ml, ES: 0.05). Based on these equivocal results across studies, it appears that creatine supplementation, independent of exercise, may have a small beneficial effect on bone mineral in healthy older adults. However, the effects of creatine on reducing bone resorption are much larger.

Table 3.

Summary of studies showing no effect from creatine supplementation on human bone

Study Subjects Creatine Dosage Study Duration Exercise Program Frequency Bone Measurement
Brose (50) 28 male/female 5g/day 14 wk 3 sets, 10-12 reps 3x/wk ↔ osteocalcin
(65 yrs) 12 exercises
Kerksick (51) 24 male/female 3g/day 12 wk 3 sets, 6-10 reps 3x/wk ↔ BMC
(18-45 yrs) 14 exercises
Kreider (52) 11 male 16g/day 4 wk 1-3 sets, 2-8 reps 4x/wk ↔ bone mass
(20 yrs) 13 exercises
Tarnopolsky (49) 19 male, 20 female 5g/day 24 wks 3 sets, 10-12 reps 3x/wk ↔whole-body BMD
(65 yrs) 12 exercises ↔ LS BMD
↔ hip BMD
↔ Ntx
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BMD= bone mineral density, BMC= bone mineral content, LS=lumbar spine, Ntx= n-telopeptides, yrs= years of age, reps= repetitions, wk=weeks.

Conclusions

Research involving creatine supplementation and bone biology is emerging. Based on the limited research thus far, there is potential for creatine to increase the metabolic activity of osteoblast-like cells involved in bone formation and decrease cross linked N-telopeptides of Type I collagen, an indicator of osteoclast mediated bone resorption. However, future research is needed using larger sample sizes of mixed gender, longer durations of resistance training, higher creatine dosage, and further evaluation of bone mineral, bone strength, and in vitro markers of bone metabolism (i.e. bone-specific alkaline phosphatase activity, osteoprotegerin, and hormones affecting bone such as calcitonin, parathyroid hormone, growth hormone, and insulin-growth factor-1) before consensus on the use of creatine for bone maintenance can be made.

Financial disclosure

None of the authors had any financial interest or support for this paper.

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