4/2018
vol. 19
Review paper
Physical activity, nutrition, and bone health
Human Movement 2018 vol. 19 (4), 1-10
Online publish date: 2018/09/24
Introduction
Bone tissue consists of specialized cells located in
a mineralized matrix containing collagen fibres. The
specific architecture and composition provides bone
with exceptional solidity and resistance to pressure
and traction. In spite of these characteristics and structural
functions, bone is a living tissue, continuously
changing during the phases of life. Bone remodelling
takes place thanks to the balance between the demolition
of the tissue by osteoclasts and its reconstruction
by osteoblasts [1]. This process varies with age: during
preadolescence, more than 50% of adult total bone mineral
content (BMC) is obtained [2]; with aging, the activity
of osteoblasts, producing new bone, can no longer
completely replace bone tissue destroyed by osteoclasts,
which leads to a loss of bone mass (i.e. osteopenia). When
this loss is accentuated, the normal skeletal function
becomes compromised, thus establishing a pathological
condition known as osteoporosis. Osteoporosis is
characterized by a decrease in the protein and mineral
component of bone, with consequent skeletal microstructure
alteration and fragility of bone, highly predisposed
to fractures [3]. In particular, bone not only
has the function of supporting and protecting the body,
but it also intervenes in the balance of minerals, in the
production of blood cells, and in numerous metabolic
processes [4]. Furthermore, owing to its ability to produce
osteocalcin, it can be defined as a true endocrine
organ [5–7]. Being considered a metabolically active
tissue, bone is in turn influenced by several factors
such as sex hormones, growth hormone, insulin, diet
(calcium, phosphate, vitamin D and A [8, 9]), and physical
activity [10–12].
This review outlines the involvement of physical
activity and nutrition in bone homeostasis.
Physical activity and bone
It is well established that many diseases can be prevented
through physical activity [13]. Physical activity
has a protective role against metabolic diseases, such
as diabetes; furthermore, it helps prevent cardiovascular
diseases (CVD) or manage hypertension [13]. Most
studies have verified the influence of exercise on CVD
mortality. Regarding bone metabolism, physical activity is also important to stimulate bone growth and help
maintain and restore adequate bone mineral density
(BMD), both in pathological and non-pathological conditions,
supporting the regeneration of bone tissue. Exercise
stimulates the production of electric fields in
the bone that activate osteoblasts, causing new bone
matrix synthetization [14]. Therefore, as it has been
demonstrated, moderate physical activity increases
bone mass [15] and can provide an important contribution
in cases of low BMD [16]. In turn, bone loss
results from the removal of mechanical loading [17],
caused by sedentary life [18], bed rest, low body weight
[17], or significant weight loss due to excessive physical
exercise without adequate nutrition. Therefore, mechanical
signals generated by exercise can prevent
a reduction in the musculoskeletal system, and exercise-
related improvement in cortical thickness can be
effective in increasing the bone mass of bone structure
sites, especially the trabecular and cortical sites [15].
Physical activity influences bone metabolism also
through hormone secretion and local factors [15]. Besides,
intestinal Ca++ absorption, energy metabolism,
and the volume of skeletal muscles improved as a result
of moderate exercise [19]. Therefore, the right amount
and intensity of exercise combined with proper nutrition
can be considered key factors to maintain adequate
BMD. Although physical activity produces both mechanical
and hormonal stimuli, the exact mechanisms
underlying the exercise-related effect on bone metabolism
are not clear.
How mechanical stress regulates
bone metabolism: a possible explanation
Regarding mechanical stimulation, recent studies
have shown that mechanical stress stimulates proliferation
and differentiation of osteoblasts (the key cells
involved in bone regulation) and inhibits the proliferation
and activity of osteoclasts (the cells that regulate
bone resorption and are essential for the balance
of bone metabolism), modulating the anabolic and anticatabolic
gene expression in bones, thus improving
bone metabolism [20–22]. The mechanical stimulus
provided by physical exercise seems to directly influence
microRNA (miRNA), an abundant class of short
non-coding RNA, molecules composed of about 22 nucleotides
[23]. MiRNA and protein translation are involved
in multiple biological processes including cell
proliferation, differentiation, survival, transposing silencing
[24], and self-renewal of stem cells [25]. MiRNA
has been shown to play a regulatory role in bone metabolism
[26, 27], in mesenchymal bone marrow stem
cells (BMSC) and in osteoblasts [28], which suggests
that miRNAs could be one of the main mechanisms
by which exercise or mechanical load regulate bone
metabolism and promote bone formation. MiRNAs
regulate the proliferation and differentiation of osteoblasts
and osteoclasts and, subsequently, bone metabolism
[29]. However, the numerous miRNAs can play
different and opposite roles: while some promote osteoblast
proliferation and differentiation, others have
been shown to inhibit osteoblast proliferation and differentiation
[30]. Lack of mechanical stimuli, as experienced
by patients bedridden or under microgravity
conditions, results in osteoporosis [17, 31, 32], although
miRNAs are not the only mechanism by which mechanical
stress regulates bone metabolism. However,
it is shown that they are influenced by mechanical
loading effects on bone formation by modulating the
expression of osteogenic factors or bone resorption
factors. The response of bone cells to a mechanical
stress stimulus is negatively affected when critical
miRNAs are lacking.
Adequate physical activity
and bone metabolism
Although numerous studies report that trained subjects
have a greater BMD (osteogenic effect) compared
with untrained ones [33, 34], it is crucial to identify
the volume, intensity, and frequency of training suitable
for stimulating osteogenic activity. Below, some
of the different types of training responsible for the
osteogenic effect are described.
Resistance training vs. aerobic activities
Recent studies show that resistance training helps
maintain homeostasis and has numerous metabolic
effects [35].
Bone deformation during resistance training is associated
with higher improvement in BMD as compared
with exercise performed at a lower intensity, e.g. running
results in more mechanical stress than aerobic
activity [36–39]. As the magnitude of the stimulus
proved to be more important than its frequency [37–40],
a relationship between BMD and the level of muscular
strength could be hypothesized [39, 41, 42], although
the type of muscular contraction also plays a key role.
In particular, an eccentric contraction stimulates the
bone more than a concentric contraction [43, 44], and
it is therefore more effective in BMD increasing [45].
For example, comparing concentric and eccentric contractions
trainings for the knee extensors and flexors, Hawkins et al. [45] showed that only subjects who administered
eccentric training had a increase of 3.9%
in the femoral BMD. These results were confirmed in
a recent study [46] in which cyclic mechanical stretch
was shown to up-regulate the protein expression of
Runx2 and promote osteoblast proliferation, which
explains the biomolecular mechanisms in the bone
during the eccentric and elongation phase.
Osteoporosis prevention with physical activity
As strength training is an important form of exercise
for bone growth, there are other activities recommended
for the prevention of osteoporosis by health organizations
[47, 48]. Weight-bearing exercises, high impact
exercises such as jumping, plyometric training (jumping/
hopping), and weight lifting [49] have positive effects
on bone, regardless of age [50]. The subject’s age
is another important factor of physical exercise effect on
bone metabolism because the bone response to mechanical
stress changes during lifetime. In adolescence,
resistive exercise can increase bone strength [51],
whereas during middle age and after puberty it can
help to reduce loss of bone mass and density [50]. The
combination of high impact or weight-bearing and
aerobic training can prevent age-related bone loss [52]
but aerobic activities, such as cycling, walking, yoga,
and swimming, are not osteogenic [52]. Therefore, to
provide the magnitude of load necessary to maintain
bone mass and density, it is crucial to combine low-load
activities, such as aerobics, with resistance exercises.
Possible negative effects of excessive
physical activity on bone
Physical activity inadequate in volume and intensity
could have negative effects on bone metabolism,
leading to a loss of BMD up to osteoporosis when very
intense physical exercise is associated with inadequate
caloric intake (in particular, that of specific nutrients)
[53] and low starting BMD. Bone stress as a consequence
of high-intensity physical activity can be more easily
manifested in women. As female sex hormones (oestrogens)
play a key role in bone metabolism and their
concentration can be influenced by physical exercise
[54], high intensity of endurance training might lead
to an early bone loss due to an excessive decrease in
body fat. Therefore, low level of oestrogen synthesis
substrate and the effects of the female sexual hormones
on the bone homeostasis are altered [54]. Although
there is a bone strengthening effect of physical activities
with overload, intense training may cause low hormonal
production, with a negative effect on the axial
bone health, mainly in women. However, the bone loss
in this case occurs because of a caloric deficit, and
an appropriate nutritional diet could help avoid these
hormonal disturbances in female athletes [55–57].
Nutrition effects on physical activity
and bone. General considerations
for athletes’ nutrition
To guarantee the necessary energy for intense physical
activity and to help avoid the aforementioned problems,
adequate diet must include the right contribution
of all the main nutrients, as enumerated below.
Fat
Lipids (or fats) are organic compounds widely diffused
in nature, representing one of the four main
classes of organic compounds of biological interest, together
with carbohydrates, proteins, and nucleic acids.
They constitute an important energy reserve, especially
during long-term exercise, being the main sources of
skeletal muscle adenosine triphosphate (ATP) production
[58]. Chronic exercise training results in favourable
mitochondrial adaptations in adults, which
enhance lipid metabolism as well [59], although gender
differences in relative fat and carbohydrate oxidation
during exercise exist [60]. Dietary lipids are essential
for the absorption of vitamins and for sex hormones
homeostasis [61]. In terms of caloric requirements,
most sources recommend that lipid intake should be
limited to 25–30% of the total caloric intake. Nonetheless,
caloric demands are increased in athletes [62], and
lipids are important to produce hormones involved in
healthy growth, maturation, and bone metabolism [63].
Ingested lipids differ in the composition of the hydrocarbon
chain and this can affect the metabolism [64,
65]. In particular, monounsaturated fatty acids can
potentially have a favourable effect on body composition
[66]; fish oil and conjugated linoleic acid could exert
ergogenic and anabolic effects on exercise, being also
related to increased testosterone synthesis.
Protein
Proteins are biological macromolecules made up
of chains of amino acids linked to one another by a peptide
bond. Their functions are mainly structural and
synthesis-related, but they also play a role in energetic
processes, although in a lower percentage compared
with carbohydrates and fats, with a greater thermic effect [67]. Consequently, they are fundamental to guarantee
a good physical performance. The adequate protein
intake indicated by the American College of Sports
Medicine (ACSM) is 1.2–1.8 g/kg of body mass for
active adults [68, 69], with athletes requiring higher
protein intake to maintain protein synthesis [70]. In
particular, a recent study has shown that the ingestion
of 20 g of protein post-exercise helps maintain
positive protein balance following exercise [71].
Carbohydrate
Glucides or glycides are organic chemical compounds
formed of carbon, hydrogen, and oxygen atoms, constituting
the carbohydrate biomolecule class. On the basis
of their chemical structure, carbohydrates are classified
into simple and complex and some confusion exists
in athletes’ understanding of specific carbohydrate
needs. General carbohydrate intake recommendations
suggest adult athletes to consume 5–12 g of carbohydrate
per kilogram per day but this dependent on different
exercise/activity, its intensity, duration, and volume,
as well as the environmental conditions in which
physical activity takes place. Moreover, as men and
women are biologically different, they react differently
to physical exercise and consequently the caloric intake,
especially from carbohydrates, should be adapted
to their needs [72]. It is therefore difficult to suggest
the exact carbohydrate intake necessary for an athlete
during particular activities. However, Burke et al. [72]
suggested that carbohydrate ingestion during activities
lasting 45 minutes or longer provides an ergogenic
effect with doses varying from small ones up to 90 g/
hour, whereas ACSM recommends that athletes should
ingest simple sugars at the rate of 30–60 g/hour for
exercise lasting longer than 60 minutes. Additionally,
Amato et al. [69] showed that gymnastics performance
improved after eating a carbohydrate snack compared
with a different pre-exercise meal.
Micronutrients
Micronutrients, subdivided into vitamins and minerals,
are ingested substances whose main function is
not directly related to energy production and growth.
Among vitamins most important for homeostasis, vitamin
A is involved in immune function, vision, reproduction,
and cellular communication [73–75], also supporting
cell growth and differentiation [76], whereas
vitamin B12 helps keep the nerve and blood cells healthy
and supports DNA synthesis, also preventing megaloblastic
anaemia, which makes people tired and weak
[77]. Furthermore, being important in the cross-linking
of collagen fibres in bone [77], vitamin C (ascorbic
acid) is a cofactor in the hydroxylation of lysine and
proline, whereas vitamin K is a cofactor in the gammacarboxylation
of glutamic acid, important in the production
of osteocalcin [78, 79].
One of the most important minerals for homeostasis
is magnesium, involved in bone and mineral homeostasis,
crucial for bone crystal growth and stabilization.
Magnesium, along with other nutrients found in
fruit and vegetables, contributes to an alkaline environment
and may promote bone health through a variety
of mechanisms, therefore it is difficult to examine
the effects of magnesium alone. The recommended
dietary allowances (RD As) for magnesium are 400–
420 mg daily for males and 300–320 mg daily for females
[80].
Phosphorus is an essential bone-forming element
and, as in the case of calcium, an adequate supply of
phosphorus to bone is necessary throughout life. Both
calcium and phosphorus are required for an appropriate
mineralization of the skeleton, and a depletion
of serum phosphate leads to impaired bone mineralization,
compromising osteoblast function [81]. Furthermore,
a combined supplement of calcium, zinc, manganese,
and copper produced increases in BMD [82].
Finally, boron has effects on urinary calcium excretion
and associations with BMD have been reported [83].
As higher BMD has been associated with a higher
dietary potassium intake [80], the electrolytes of sodium
and potassium play an important role in the development
and prevention of osteoporosis. The adequate
intake for potassium is 4700 mg daily for males and
females [80].
Another essential component is iron, involved in
erythrocyte protein, haemoglobin, which transfers oxygen
from the lungs to the tissues [84]. It is also necessary
for growth, development, normal cellular functioning,
and synthesis of some hormones and connective
tissue [75, 85]. The RD As for iron are 8–11 mg daily
for males and 8–15 mg daily for females [75]. Athletes
will likely find additional benefit from including other
iron-rich foods, such as peanuts, dried fruit, and ironfortified
cereals as regular snacks. Furthermore, the
inclusion of foods higher in ascorbic acid with these
nonheme iron sources will improve iron absorption
from these snacks [85].
Athletes’ nutrition for bone health
Low energy availability due to exhausting physical
exercise linked with failure of diet intake of the above mentioned nutrients can impair bone health. In particular,
values below the minimum energy threshold
(30 kcal · kg lean body mass [LBM]–1 · d–1) [86] can alter
physiological mechanisms such as cell repair, thermoregulation,
immunity, growth, and bone turnover
through the distorted levels of metabolic hormones and
substrates, such as growth hormone, cortisol, fatty acids,
and glucose among the most important ones [87]. Under
this threshold, the levels of carboxyterminal propeptide
of type 1 procollagen (P1CP) and osteocalcin, the
matrix mineralization measure, were significantly reduced
[88]. The minimum energy threshold for athletes’
population has been identified as 45 kcal · kg LBM–1 · d–1
[86], depending on many factors, such as the different
types of physical activities, environmental conditions,
and physical characteristics of each athlete. As an example,
elite runners need 6 kcal · kg LBM–1 · d–1 [88], while
triathletes require 24–33 kcal · kg LBM–1 · d–1 [89].
Carbohydrate and protein intake
With a mixed meal, calcium, glucose, protein can
supresses bone resorption at rest [90]. Gastric inhibitory
polypeptide (GIP) and glucagon-like peptide-2
(GLP-2) are potential mediators of the post-prandial
regulation of bone turnover [91]. Henriksen et al. [90]
showed that only GLP-2 was secreted with glucose
and protein ingestion and was in parallel with the
suppression of beta C-terminal telopeptide ( -CTX).
The effects of carbohydrate supplementation during
intermittent running is bound with bone turnover
markers (a carbohydrate beverage including 1 g · kg
body mass [BM]–1 of maltodextrin reduced -CTX,
increased bone formation, and decreased resorption)
[92]. Another study demonstrated that a carbohydrate
drink (glucose) before, during, and after running exercise
at 70% VO2max attenuated procollagen type 1 amino-
terminal propeptide (P1NP) responses [93]. The
same author showed that a carbohydrate drink attenuated
the rise in the circulating interleukin 6 (IL-6),
an osteoclastogenesis activator associated with exercise.
Moreover, eating in close proximity to exercise
also suppresses bone resorption at rest but can cause
gastrointestinal discomfort, impairing performance
[94]. Simple carbohydrates and proteins are not likely
to cause gastrointestinal complaints as they contain
little fibre or fat, which means that digestion is quick
[95]. A carbohydrate + protein recovery drink consumed
immediately post-exercise is beneficial for endurance
athletes [96], in whom the ingestion of a carbohydrate
+ protein solution (containing 1.5 g · kg BM–1 of carbohydrate
and 0.5 g · kg BM–1 of protein) immediately
after an exhaustive run suppressed -CTX concentrations,
although a delayed ingestion of the carbohydrate
+ protein solution (2 hours post-exercise) also resulted
in a large suppression of -CTX concentrations.
Ca++ and vitamin D intake
Calcium is a key factor to keep human body homeostasis.
It is involved in many vital functions, such as
cellular processes including exocytosis, neurotransmitter
release, muscle contraction, and the proliferation
of action potentials through the cardiac muscle.
Bone is the largest reservoir of calcium in the body and
reductions in serum ionized calcium are therefore mitigated
by demineralization of bone, a process stimulated
by increases in the parathyroid hormone (PTH).
The cross-linked C-telopeptide of type I collagen (CTX-I)
and, more recently, cross-linked C-telopeptide of type II
collagen (CTX-II) have been indicated as sensitive markers
of osteoclastic bone resorption, while the procollagen
I N-terminal propeptide (PINP) is determined as
a marker of osteoblastic bone formation [97]. Furthermore,
calcium absorption is dependent on adequate
levels of vitamin D [98]. Vitamin D is obtained either
from the diet or by synthesis in the skin under the action
of sunlight. The report on dietary reference intakes
for calcium and vitamin D by Ross et al. [98] shows
that all individuals meet their needs at RD As for vitamin
D, at 25-hydroxyvitamin D (25(OH)D) levels
of at least 20 ng/ml (50 nmol/l) even under conditions
of minimal sun exposure [98]. Associations have been
reported between plasma 25(OH)D and BMD in middle-
aged and older women [99, 100]. Supplementation
with calcium and vitamin D together resulted in
sizeable reductions BMD loss; bone loss was limited
to subjects with a daily calcium intake below 400 mg
[77, 101]. However, it is not clear what the pre-exercise
meal able to guarantee the right amount of calcium
to an athlete is, especially during long-lasting
and high-intensity sports, when there is a great sweat
calcium loss. For example, it has been observed that
~1000 mg calcium supplement pre- or post-exercise reduces
bone resorption markers levels [94, 102]. A recent
study by Haakonssen et al. [94] shows that a calciumrich
pre-exercise meal can maintain serum ionised
calcium and reduce post-exercise increase of PTH and
CTX-I, especially among endurance athletes.
Good foods and bad foods for bone health
The interaction between food supplementation, sport,
and bone health is complex. Recent studies show that in addition to the integration of ‘positive’ nutrients for
bone homeostasis, there are some foods that, on the
contrary, can be negatively related to BMD if taken in
excess. For athletes with chronic energy deficiency, an
excess of fibre, phytic and oxalic acids, isoflavones, and
vegetable proteins with an imbalance of other essential
macro- and micronutrients can be detrimental to
bone health [67]. Dietary fibre can influence the energy
availability and digestibility of complex foods. It
can interact with proteins and fats and decrease the
metabolizable energy of a diet, influencing the digestibility
of these components [103]. Because dietary fibre
increases most intestinal contents and accelerates calcium
and other minerals transit time in the intestine,
it causes loss of time to absorb these nutrients. Foods
rich in phytic acid, such as wheat bran, legumes, seeds,
nuts, and soy isolates, can reduce bioavailability and
thus prevent the beneficial effects of nutrients such as
calcium, magnesium, and protein on the bones [67].
Dietary fibre is inversely associated with the levels of
the luteinizing hormone, follicle-stimulating hormone,
oestradiol, and progesterone [104], and oestrogen plays
a significant defensive role in oxidative stress [105]
and attenuates bone endocortical reabsorption [106].
Moreover, it is already clear that reactive oxygen species
(RO S) induce the apoptosis of osteoblasts and
osteocytes; this inhibits osteogenesis, favouring osteoclastogenesis.
Antioxidants like polyphenols and
anthocyanins, the most abundant antioxidants in the
diet, counteract the action of oxidants, contributing to
the prevention of bone loss [107]. Specific nutritional
approaches suggest the antioxidant use to counteract
the resorption. Excess consumption of such foods is
predominant in sports in which aesthetics and the
maintenance of adequate weight are essential. However,
further studies are needed to provide understanding
of the recommended quantity of this type of food and
the athlete’s starting condition that can cause osteopenia.
Conclusion
The objective of this review was to point out how
nutrition and physical activity interact with each other
and how they affect bone metabolism. This issue is important
for the prevention of bone disease such as osteoporosis.
Bone health constitutes a crucial aspect for an
athlete. Bone metabolism is the basis of good musculoskeletal
system function and thus favourable performance,
which is in turn strongly related to the right
energy derived from nutrients intake. Recent studies
show how bone metabolism, diet, and training are interconnected
and crucial for elite athletes. Although
the purpose of this review was to clarify how these
elements interact with each other, further studies are
necessary to illustrate some other key elements, such
as adequate bone markers to be used to monitor bone
health, the exact quantity and quality of nutrients in
the diet, and the correct volume, frequency, and intensity
of training with the consideration of the biological
characteristics of an athlete.
Ethical approval
The conducted research is not related to either human
or animal use.
Disclosure statement
No author has any financial interest or received any
financial benefit from this research.
Conflict of interest
The authors state no conflict of interest.
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