Thread: Calcium, Weight training and How bones react to stress.

So, let's use the example of weight training. You start strength training every day. Just how do the mechanical forces you experience cause a change in the cells' activities? It is a combination of three factors. First, increased activity means more calcium is needed for other tissues. So hormones adjust the activity of the osteoclasts. The hormone that stimulates osteoclasts is calcitonin. But, at the same time that osteoclasts are releasing calcium from your skeleton, the mechanical stress from weight training sends the message that you need more calcium so that you don't compromise the bones' density. In response to this message, another hormone called parathyroid hormone stimulates osteoblast activity, storing more calcium in the bones. So, the stress you put on your bones determines where remodeling will occur. In places with high stress, more calcium will be deposited and less taken away, while places with little stress are better candidates for resorption of calcium into circulation.


How does stress change bone density? One way involves the properties of the bone crystals, which are made from ions. All ions have electric charges. So when stress is exerted on the bone, tiny electrical fields are generated. These fields help the osteoblasts migrate to the site of stress to start laying down new matrix. In other words, the osteoblasts respond to electrical signals.

So what happens if these signals are not working properly and bones cannot respond adequately to stress? A homeostatic imbalance occurs. For example, if the bones don't get the calcium deposits they need, the body develops a condition called osteomalacia, also called "soft bones". The bones don't get enough calcium to harden correctly, causing pain when weight is put on them.

So ladies and gents, make sure your calcium intake is adequate.

I'd like to add how important calcium is for muscle contraction, as well.

Each muscle cell contains hundreds or even thousands of long, cylindrical structures called myofibrils. Myofibrils extend the length of the muscle cell as long, parallel tubes, like lengths of dried spaghetti inside of a canister. Each myofibril is divided into equal segments along its length called sarcomeres. Each sarcomere is packed full of small, fine protein strands called myofilaments. Myofilaments are the actual proteins involved in muscle contraction. These myofilaments may be either thick filaments, made of protein molecules called myosin, or thin filaments, made of a helix of proteins called actin.

In addition to actin and myosin, we need to discuss two regulatory proteins that play important roles in muscle contraction. The first one is called tropomyosin. It is an elongated protein that winds along the actin filaments. Its job is to prevent the myosin heads from binding to the active sites on the actin filament and causing contraction without the appropriate nerve signal. Tropomyosin is similar to a plastic child-protective cover on an electrical outlet. Until the cover is removed, you can't plug anything into the outlet. Similarly, in a muscle fiber, the myosin heads can't bind to the active sites until tropomyosin is removed.

Associated very closely with tropomyosin is a protein called troponin. Troponin is a small protein molecule that binds to tropomyosin to form the troponin-tropomyosin complex. Troponin has the job of moving the tropomyosin off the active sites once calcium ions bind to Troponin. In other words, troponin removes the child-protective cover--the tropomyosin--from the outlet--the active site on the actin filament--so that contraction can occur.