Bone of contention: what endurance athletes should know about skeletal health

Although endurance exercise is great for improving overall health and longevity, new research suggests that it could actually be detrimental for bone health. Tom Whipple explains, and provides essential recommendations for skeletal health

Endurance exercise has long been recognised as a means to improve both quality and length of life. However, there is a paradox as many endurance athletes may experience accelerated skeletal aging and premature bone loss (reduced bone density, which can lead to osteoporosis – see box 1). Consider these conclusions from studies published in a number of scientific journals:

  • “Runners and swimmers demonstrated deficits in bone mineral density when compared to athletes in other sports”1.
  • “This study suggests that high-intensity cycle training may adversely affect bone mineral density”2.
  • “Bone mineral content at all measured sites correlated negatively with weekly running mileage” (ie the more miles run per week, the lower the bone density3.

Bone is a dynamic tissue that is constantly undergoing structural modification through a process known as ‘remodelling’. Two specialised bone cells (osteoclasts and osteoblasts) are responsible for skeletal degradation and synthesis, respectively. Osteoclasts dissolve (resorb) old or damaged bone and liberate free calcium from storage while osteoblasts form new bone. The unique actions are linked, but the overall balance of remodelling can be tipped in favour of either degradation or formation. Excessive resorption results in net bone loss; robust formation results in net bone gain. The good news is that skeletal remodelling is determined by factors that are within your control.

In normal human development, through the teenage and early adult years, there is a net gain in bone strength culminating in peak bone mass (figure 1). In the adult skeleton, bone loss and gain are relatively balanced. In late adult life however, bone strength tends to diminish as bone resorption accelerates and formation diminishes. Failing to achieve a large peak bone mass earlier in life, or having a steeper rate of bone loss later in life, increases the risk of fracture and/or osteoporosis.


BOX 1: OSTEOPOROSIS FACTS

In the UK alone, over 3 million people have osteoporosis, and 1 in 3 women and 1 in 12 men over the age of 50 years can expect to experience a bone fracture as a result of the condition. Translated literally, osteoporosis means ‘porous bones’ and is defined by the World Health Organisation (WHO) as ‘a progressive systemic skeletal disease characterised by low bone mineral density (BMD) and micro-architectural deterioration of bone tissue, with consequent increase in bone fragility and susceptibility of fracture”.

In simple terms, this means that as bone mass is lost, the mineral structure of the bone becomes progressively more porous, with microscopic gaps appearing in the structure that both weaken the bones and make them more brittle and less able to withstand knocks and shocks without damage. In short, bones that were once strong can break very easily. In severe cases for example, a simple stumble can result in a broken leg or hip. All bones can be affected by osteoporosis but fractures are most common in the wrist, spine and hip.

The pain and trauma of a broken bone is bad enough, but in older people (the age group most at risk of the disease), it can often lead to long-standing illness and incapacity. In fact it has been calculated that if you sustain a hip fracture after the age of 50, your chances of walking again unaided are halved, you’re twice as likely to have to move into a nursing environment in subsequent years, and worse still, are nearly three times more likely to die prematurely due to associated consequences.

Once we reach the age of 40, some degree of bone mass loss due to the aging process is inevitable (see figure 1). However, osteoporosis is a far more extreme condition, which is linked to a number of lifestyle factors including exercise habits and diet. Scientists now believe that large volumes of endurance training can increase the risk of osteoporosis.

FIGURE 1: BONE MASS CHANGES AND AGE*

Box 1: Words by Andrew Hamilton Figure 1: Graphic courtesy of Dr Felicity Kaplan


BOX 2: MEASURING BONE STRENGTH

Bone strength is typically defined by its density and measured by a DEXA (Dual Energy X-ray Absorptiometry) scan. A bone density test calculates the amount of bone mineral that is present within a certain area, and is reported as grams per square centimetre (g/ cm2). A T-score compares your bone density to those of healthy young adults while a Z-score compares your result to age-matched peers. If you have a positive T or Z-score, your bone mass density and strength is greater than average while negative values mean your bones are weaker than average. Low Z-scores, particularly in later life, may indicate the onset of osteoporotic bone formation (see figure 2).

FIGURE 2: NORMAL VS. OSTEOPOROTIC BONE

Osteoporotic bone is less dense than normal bone tissue. It’s weaker, more porous structure reduces its structural integrity.


Lifestyle and bone health

Understanding how training and lifestyle factors influence skeletal remodeling is the key to reducing the likelihood of undesirable consequences. Independent of your genetic makeup, the primary govenors of skeletal remodeling are your nutrition, hormone balance, and the amount/type of muscular activity you participate in. Other exercise-related factors known to negatively influence bone cell activity include perturbations in blood acid/base balance dehydration, a high sodium intake, and emotional distress. The most common causes of accelerated bone loss in endurance athletes include:

  1. Energy deficit (ie consuming too few calories for your activity level).
  2. Loss of muscle strength/power.
  3. A calcium/vitamin D insufficiency.

Energy deficit

There is now abundant scientific evidence that nutritional shortcomings are the prime culprit in the genesis of both stress fractures and exercise-induced osteoporosis. ‘Energy deficit’ is the term used to describe an imbalance that results when calories expended during exercise exceed those consumed through food and drink. Many scientific investigations have revealed that endurance athletes train in a chronic 15-30 percent calorie deficit. In other words, the total calories consumed in the diet are insufficient to fuel exercise and properly support all the other functional requirements for good health. This disturbing finding is especially common in those athletes attempting to reduce body weight for performance gain and/or those that favour carbohydrates and shun fat. A study on this subject found that when recreational runners were allowed to eat as much as they desired from a carbohydrate-rich meal plan, an energy deficit promptly developed. However, when these subjects increased their intake of fat from 17% to 31% (re-establishing energy balance) their running performance was improved by an impressive 18%4. In another study, bone remodelling cells of eight well trained runners were studied after they ran on a treadmill for 60 minutes under two different conditions of energy availability: deficient by 50% and balanced5. When the runners were in an energy deficit state, blood markers of bone formation were significantly decreased. Conversely, when their intake/expenditure was balanced, bone remodelling was undisturbed. When Hippocrates said, “Let your food be your medicine and medicine be your food” he may have been speaking specifically about bone!

An acute or chronic energy deficit induces bone loss through pathways involving both reproductive and stress hormones known to govern bone cell activity. ‘Calorie-challenged’ athletes have reduced levels of the hormones estrogen and testosterone, while cortisol (a stress hormone) levels are elevated. In addition to the loss of bone health, other symptoms associated with inadequate energy intake may also be present, including soft-tissue injuries that are slow to heal, frequent illness and infections, ‘heavy’ legs (or arms), fatigue, irritability, and decreased performance.

Countering energy deficit

To counter an energy deficit, an athlete needs to reduce his or her training load, consume more calories, or do a bit of both. An increased calorie count can be accomplished by increasing portion sizes, adding snacks, or increasing the proportion of dietary fat. Fats from cold-water fish (sardines, herring, salmon) and nuts or nut butters (eg almond or peanut butter) are especially good choices for endurance athletes as they are known to exert favourable effects on bone strength and improve endurance performance (see table 1)6 7.

TABLE 1: A SAMPLE DAILY INTAKE OF FAT-RICH FOODS FOR AN ATHLETE CONSUMING APPROXIMATELY 3,500 KCALS/DAY

Two whole eggs
A quarter cup of walnuts
Six ounces of canned salmon with bone
Three tablespoons of olive oil
Two teaspoons of cocount oil
Half an avocado
Two tablespoons of almond butter

Loss of strength/power

Muscle contractions and ground-reaction (landing) forces are the leading mechanical governors of bone strength. As a consequence of habitual loading, bone remodels in a manner that is consistent with mechanical force. The forces acting on the skeleton during endurance exercise are small relative to those encountered in other sports such as court sports (tennis, basketball etc), gymnastics, and weight lifting. As such, in tests of strength and power most endurance athletes score well below average. Interestingly, the low level of muscular strength exhibited by endurance athletes seems to be an adaptation to training rather than an innate trait – ask any top notch Olympic weight lifter what would happen to his explosive strength after he jogs or cycles for an hour! To maximise bone strength and reduce the progressive loss of maximal strength associated with endurance training, it is absolutely imperative to engage in some regular low-volume, high-intensity strength training. Recent editions of Peak Performance have provided you with exercises and programmes that will yield improvements in both bone strength and sport performance (Ed – see issues 357 and 366).

TABLE 2: PORTIONS OF CALCIUM-RICH FOODS

One cup of milk or yogurt
Two cups of broccoli
One cup of greens (collard, turnip)
Three cups of kale
Four ounces of canned salmon with bone
Three ounces of sardines with bone
Eight ounces of tofu
A quarter of a cup of sesame seeds

Calcium/Vitamin D insufficiency

Calcium is the most abundant mineral in the human body with the majority being stored in the skeleton. Beyond its structural role, calcium is involved in muscle contraction, blood pressure regulation, nerve transmission, glycogen mobilisation, and maintenance of normal pH balance in the body. When dietary intake falls short of needs, the skeleton undergoes immediate and accelerated demineralisation in order to liberate free calcium for functional requirements. Unfortunately, researchers continue to report that calcium remains one of the most frequently deficient nutrients in the diets of endurance athletes. As an example, a 1994 study reported that out of 17 nutrients examined in the diets of female runners, only calcium levels were indadequate8. Researchers have consistently demonstrated that low calcium intake is one of the strongest predictors of stress fracture risk. How strong you ask? Well, one study reported that compared to subjects consuming the highest amounts of dietary calcium, stress fractures were 12 times more likely in those with the lowest calcium intakes9!

The daily requirement for calcium set by the US National Academy of Science’s Food and Nutrition Board is in the range of 1000-1300 mg/day. This can be achieved by eating a combination of whole foods, calcium fortified foods, and/or calcium supplements. The list in table 2 is composed of foods and serving sizes that will provide approximately 300mgs of calcium. An endurance athlete of average size would need 3-5 of these selections to satisfy the minimal calcium requirement for bone health and performance.

Some researchers believe that in order to prevent stress fractures and bone loss, athletes should consume significantly more calcium than is currently recommended. In a landmark study of 5,000 female US Navy recruits, stress fractures were reduced by 21% in an experimental group that consumed 2,000 mg of calcium and 800 IU of vitamin D per day (see box 1)10.

Vitamin D – also known as the ‘sunshine vitamin’ (see box 3) – helps to regulate calcium levels in the blood by promoting absorption in the intestine and re-absorption in the kidneys. It also may act independently on bone through the development of stronger muscle contractions. The current recommendation for vitamin D supplementation and consequential blood levels is an area of intense debate among scientists and medical professionals. The typical recommendations for daily supplementation range quite widely from 6004,000 international unit (IU) per day. A blood test may be necessary in order to define your specific supplemental needs. Sports medicine professionals recommend that athletes achieve a vitamin D blood level of at least 50 nmol/L.

Compromised vitamn D levels can influence an athlete’s overall health and ability to train and recover by affecting the immune system and inflammatory pathways. Insuficient levels have been linked to stress fractures, osteoporosis, cancer, coronary disease, diabetes, and degenerative diseases of the nervous system. Vitamin D requirements can be met through a combination of sun exposure, diet, and supplements:

  • 15 minutes of daily sun exposure
  • Fatty fish (salmon, herring, mackerel)
  • Cod liver oil
  • Supplemental capsules

BOX  3: CALCIUM AND VITAMIN D STUDY


BOX 4: SUNSHINE AND VITAMIN D

Vitamin D can be synthesised from a natural substance in the body (derived from cholesterol and called 7-dehydrocholesterol) when skin is exposed to sunlight. However, it’s important to note that it’s the UVB rays in sunshine that are needed for this reaction to occur. When the sun is high in the sky, for example during summer months or all year round in the tropics, the sunlight contains sufficient UVB to enable the synthesis of vitamin D. However, when the sun is low in the sky, its rays have to pass through a greater volume of atmosphere to reach the surface, significantly attenuating the UVB content.

Indeed, studies have shown that from November through to February, when human skin is exposed to sunlight on clear sunny days at latitudes of around 42o N (the same latitude as cities such as Boston, Rome and Marseilles), the UVB content of that sunshine is so low that no vitamin D can be synthesised even around midday when the sun is highest in the sky. Move up to around 52o N (for example London, Amsterdam and Berlin) and vitamin D synthesis in the skin becomes impossible from October right through to March!


Summary

Endurance athletes are at risk of stress fractures and osteoporosis due to several related factors that are ammenable to modification. Energy deficit, often resulting from undereating, alters the ratio of bone cell remodeling in a manner that favours bone loss. Progressive loss of peak muscle strength is also common in endurance athletes. Bone tissue remodels in a manner that is consistent with habitual muscle loading. Thus, in order to maintain peak bone mass, peak muscle strength must be maintained or improved. By re-establishing energy balance and ensuring adequate calcium and vitamin D levels, bone demineralisation can be prevented and the substates for new bone formation will be available. High-load, low-volume strength training provides the appropriate stimulus to maximise both muscle and bone strength as well as improve endurance performance!

See also:

 

References

  1. Barry D. J Bone Miner Res. 2008;23(4):484-91
  2. Mudd, LM. J Athl Train. 2007;42(3):403-408
  3. Hetland M. Clin Endocrin Met. 1993;77:770-775
  4. Horvath P, et al. J Am Col Nutr. 2000;19(1):42-51,52-60
  5. Zanker CL. Eur J Appl Phys. 2000;83:434-440
  6. Yi M. Int Soc Sports Nutr. 2014;11;11:18eCollection
  7. Mickleborough T. Am J Resp Crit Care Med. 2003;168(10):1181-1189
  8. Estok P. Health Care for Wom Int. 1994;15(5):435-451
  9. Myburgh K. Annals Int Med. 1990;113:754-759
  10. Lappe J. J Bone Min Res. 2008;23(5):741-749
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