Your muscles need energy in the form of ATP (adenosine triphosphate) to keep up with the physical demands of exercising. But those 60 minutes a day aren’t the only time your body is put to the test.
While strenuous exercise can increase muscle ATP demands 100-fold compared to resting needs, you also require ATP to complete tasks you usually don’t think about: energy to pump your heart, exchange gases in your lungs, digest food, regulate body temperature, control emotions, and more.
So next time you’re presenting at a board meeting, cheering at your kid’s soccer game, meal-prepping a week’s worth of nutritious foods, or hitting the gym for a few sets, ask yourself, “Is my body making enough energy, or could I be doing better?”
The basics of ATP production
The rod-shaped mitochondria of our cell produce energy in the form of ATP from carbohydrates, fats, and proteins in your body through reactions in the citric acid (or Krebs) cycle and the electron transport chain. Although this ATP production is essential for survival, it is limited based on the number of mitochondria in the cell, which in turn is determined by the cell’s metabolic needs.
This means that cells within specific tissues have vastly different numbers of mitochondria – ranging from zero to one to thousands. Red blood cells have none, whereas liver cells that require lots of energy have thousands.
When a cell or a muscle is low in ATP, then an enzyme called AMP-activated kinase (AMPK) is activated, which initiates a cascade of other processes.
Most notably, AMPK regulates mitochondrial biogenesis, the important process by which cells make new mitochondria, thus increasing the amount of ATP that can be produced.
AMPK sets in motion processes that can do two things: (1) increase ATP generation for immediate use, such as fatty-acid oxidation and glucose transport, and (2) decrease processes that consume ATP but are not required for survival, such as lipid or glycogen synthesis and cell growth or multiplication.
What can limit your ATP production?
ATP production is limited by the number and function of your mitochondria, and unfortunately, the “use it or lose it” rule also applies to the quality and quantity of mitochondria. There are both controllable and uncontrollable factors to consider.
1. Sedentary lifestyle
Muscles naturally undergo structural and functional change with age, which can result in sarcopenia, the loss of muscle mass. The lack of sufficient and appropriate exercise can result in a decline of mitochondrial number and function.
2. Chronic conditions
Diseases and chronic health conditions affect mitochondrial quantity and quality. The muscles of individuals with type 2 diabetes can experience reduced aerobic capacity, insulin resistance, and inadequate mitochondrial biogenesis. Furthermore, insufficient mitochondrial biogenesis in the heart can predispose individuals to heart disease or metabolic syndrome.
Aging plays a large role when it comes to quantity and quality of mitochondria. Normal aging is accompanied by an accelerated rate of muscle loss – both in mass and strength.
Although muscle strength over a lifetime declines at an average rate of 1% per year, for those in their 70s the rate of decline can increase 2-4 times faster. Decreasing numbers and functionality, or increased levels of mitochondrial mutations, can predispose an individual to age-related diseases.
What can you do to make more mitochondria?
Fortunately, there are several things you can do to support mitochondrial biogenesis as you naturally age into mid-life or older.
All muscles should contain the highest amount of mitochondria to support the massive amounts of ATP needed for purposeful exercise and everyday physiological movement. Training intensity helps mitochondria function, whereas training volume helps with mitochondrial number. VO2 peak and mitochondrial efficiency positively correlate, meaning those who have a higher capacity to consume oxygen have a higher rate of mitochondrial enzymatic activity.
Make sure your workout program contains both – vary the types of exercises, duration and intensity of workouts, and rest periods between lifting sets and exercise bouts.
These exercise-induced mitochondrial changes require regular and consistent training, because similar to other training adaptations, these improvements can be reversed with even short periods of decreased training load/intensity or exercise cessation.
2. Explore nutritional supplements
NiaCel 400: A key component in the Krebs cycle and electron transport chain is nicotinamide adenine dinucleotide (NAD+). Research has demonstrated that nicotinamide riboside (NR), the active ingredient in NiaCel, is a direct precursor to NAD+.* Adequate amounts of NAD+ improve mitochondrial energetics in the heart and muscles, and boost production of energy-creating ATP, which provides support for endurance athletes and fatigued individuals.*
What can you expect?
You might or might not notice a difference, but your body will be better equipped to keep up with your physical energy demands. How exactly? ADP (adenosine diphosphate) moves from the cytosol into the mitochondrial matrix and indirectly influences the rate which molecules proceed through the glycolytic system, the energy system that supports short, quick, intense energy demands that only last 90 seconds or so.
Also, there are direct effects on the rate of breakdown of ATP to ADP – making more ADP available for oxidative phosphorylation – the system that supports energy demands lasting two minutes or longer.
Benefits attributed to an improvement in mitochondrial ADP sensitivity – due to the increase in mitochondrial content – include exercise performance improvements, muscle glycogen sparing, lactate production attenuation, and increased reliance on aerobic metabolism following training.
So think about how your current exercise regimen and nutritional supplements can be improved to support your day-to-day lifestyle – at work, at home, and in the gym.
- Bishop D, Granata C, Eynon N. Can we optimise the exercise training prescription to maximise improvements in mitochondria function and content? Biochim Biophys Acta 2014;1840(4):1266-1275.
- Nisoli E, Clementi E, Carruba M, Moncada S. Defective mitochondrial biogenesis: a hallmark of the high cardiovascular risk in the metabolic syndrome? Circ Res 2007;100(6):795-806.
- Richter E, Ruderman N. AMPK and the biochemistry of exercise: implications for human health and disease. Biochem J 2009;418(2):261-275.
- Ritov V, Menshikova E, He J, et al. Deficiency of subsarcolemmal mitochondria in obesity and type 2 diabetes. Diabetes 2005;54(1):8-14.
- Sun N, Youle R, Finkel T. The mitochondrial basis of aging. Mol Cell 2016;61(5):654-666.