“…Come to me, all who labor and are heavy laden, and I will give you rest. Take my yoke upon you, and learn from me, for I am gentle and lowly in heart, and you will find rest for your souls. For my yoke is easy, and my burden is light.”
Why Sleep is More Important Than Training: Part II
Sleep is absolutely critical to a successful weight-loss/fitness program. It can be summed up as simply as this – less sleep equates to performance degradation, potential weight gain, and poor recovery. Yes, it’s a bit more complicated than that, but that’s the long and short of it. Additionally, a lack of sleep is also associated with several negative physiological consequences (Taheri, Lin, Austin, Young & Mignot, 2004), which includes its affects on two key hormones involved with hunger and fat storage. Enter: Leptin and Ghrelin.
Leptin is a hormone found in our adipose tissue (fat cells). You can think of leptin as the master gatekeeper of our energy levels. Superfluous amounts of leptin in the body relay to your brain two things: first and foremost that you’re not starving and secondly that because you’re not starving it’s ok to burn your existing fat stores for fuel. What are the two most crucial things that regulate leptin levels you ask – fat (dietary fat) and you guessed it, sleep!
When you consume sufficient amounts of good dietary fat this notifies your brain it’s ok to burn its fat stores for fuel. This is why low-fat diets DO NOT work! Conversely, if you are not consistently getting enough quality sleep (like the majority of Americans) this also lowers your leptin levels a significant amount (Taheri, et al 2004). Insufficient stores of leptin trigger natural body warnings, to which your brain then relays to the body, “You are starving! Take action!” Your body will then hold onto its existing fat stores, refusing to burn them for energy, for fear of starvation. Since your brain now believes you are in a survival situation, it then sets in motion an increased desire to consume more calories. Furthermore, these additional consumed calories are more likely to be stored as fat, rather than burned, because of the perceived “emergency situation” your brain is experiencing. Less sleep = less fat burning and more fat storage.
Ghrelin is a hormone that is primarily secreted in the stomach. Its job is to either increase or decrease our appetite. As we get hungry our ghrelin levels rise, when we finally eat they decrease. A lack of sleep causes ghrelin levels to rise. This in turn causes us to become hungrier and can incite us to consume more (Doheny, 2010). In this account, less sleep = a greater sense of being hungry.
Another major health consequence involving the lack sleep is insulin resistance, a precursor to type II diabetes (Meisinger, Heir & Loewel, 2010). Insulin resistance means that your body is becoming inefficient at utilizing the nutrition you do consume. In particular, blood sugar spikes caused by sugar and simple carbohydrate ingestion are harder for your body to regulate and handle efficiently (Meisinger, et al 2010).
As you can see the consistent lack of good quality sleep has a powerful snowball effect. Inconsistent sleep or sleep deficit inhibits several delicate systems within our bodies, with these affects combining to negatively affect mood, performance, recovery, and stress level. To sum it up, a lack of sleep makes you hungrier and turns you into a fat storing machine. So sleep hard!
Doheny, K. (2010, June 22). Hormone ghrelin raises desire for high-calorie foods. Retrieved from http://www.webmd.com/diet/news/20100622/hormone-ghrelin-ups-desire-for-high-calorie-foods
Meisinger, C., Heir, M., & Loewel, H. (2010). Sleep disturbance as a predictor of type 2 diabetes mellitus in men and women from the general population. Retrieved from http://www.springerlink.com/content/gy2c4r23v3u2v83b/
Taheri, S., Lin, L., Austin, D., Young, T., & Mignot, E. (2004, December 07). Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. Retrieved from http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0010062