To fast, or not to fast? That is the question

Is exercising in a fasted state detrimental on muscle growth? Does it increase fat loss? This is a controversial topic to the average gym goer, and I always here wildly different opinions on the matter. The general consensus I hear is that training while fasted will deplete muscle glycogen, decrease performance, but will increase fast loss. While training after a meal will increase performance but not maximize fat loss. I decided to look at some of the data to get the facts on these claims. This 2011 study showed that when moderate endurance exercise is done to lose body fat, fasting before exercise does not enhance lipid utilization and that physical activity after a light meal is advisable (Paoli et al.) So training while fasted is not as effective for loss, but what about muscle performance? Neufer et al. showed in 1987 that total work produced was increased in subjects fed carbohydrates before training vs. fasted subjects, also confirming what I usually hear among gym goers. So it seems it's obvious that eating before training is optimal, right? Not so fast, this 1980 study compared liver and muscle glycogen levels in carbohydrate fed and fasted rats after exercise and found that the fasted rats showed depletion of liver glycogen with an increase in muscle glycogen, while the carbohydrate fed rats showed about the same increase in muscle glycogen but with also a large increase in liver glycogen (Fell at al.). Nieman et al. confirmed this preservation of muscle glycogen after exercising in a fasted state, and also contradict the Paoli et al. study showing that lipid oxidation in fact is increased in fasted subjects vs. fed subjects. The data I presented is just the tip of the ice berg. There is plenty of literature that will contradict these studies I presented, and literature that will contradict those studies. Thus, the debates in the gym continues. One potential benefit of fasting may be on its affects on behavior, rather than the quantified data of muscle glycogen and work output measured in the other studies. Bhutani et al. showed that regular fasting contributed to positive behavioral changes such as decreased uncontrolled eating, decreased likeliness to cheat on diet, and increased satisfaction after eating. The behavioral impacts from fasting could certainly impact weight loss completely separate from the glycogen levels and work produced observed in the other studies. So with all the conflicting data on whether to fast or feed before training, I think one should focus on personal preference and trial and error until the literature can finally reach a definite conclusion. Personally, I prefer to train fasted because I do not see any decrease in performance, it takes an extra step out of my morning routine, and I do see an improvement in my appearance. What are your opinions on the topic and personal preferences when it comes to eating before training and why? Is breakfast really the most important meal of the day?


Bhutani, S., Klempel, M. C., Kroeger, C. M., Aggour, E., Calvo, Y., Trepanowski, J. F., . . . Varady, K. A. (2013). Effect of exercising while fasting on eating behaviors and food intake. Journal of the International Society of Sports Nutrition,10(1), 50. doi:10.1186/1550-2783-10-50

Fell, R. D., Mclane, J. A., Winder, W. W., & Holloszy, J. O. (1980). Preferential resynthesis of muscle glycogen in fasting rats after exhausting exercise. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology,238(5). doi:10.1152/ajpregu.1980.238.5.r328

Neufer, P. D., Costill, D. L., Flynn, M. G., Kirwan, J. P., Mitchell, J. B., & Houmard, J. (1987). Improvements in exercise performance: Effects of carbohydrate feedings and diet. Journal of Applied Physiology,62(3), 983-988. doi:10.1152/jappl.1987.62.3.983

Nieman, D. (2009). Effect of training in the fasted state on metabolic responses during exercise with carbohydrate intake. Yearbook of Sports Medicine,2009, 140-141. doi:10.1016/s0162-0908(08)79366-8

Paoli, A., Marcolin, G., Zonin, F., Neri, M., Sivieri, A., & Pacelli, Q. F. (2011). Exercising Fasting or Fed to Enhance Fat Loss? Influence of Food Intake on Respiratory Ratio and Excess Postexercise Oxygen Consumption after a Bout of Endurance Training. International Journal of Sport Nutrition and Exercise Metabolism,21(1), 48-54. doi:10.1123/ijsnem.21.1.48

What if there was a way to improve performance under hypoxic conditions? A pill that could help climbers improve their exercise tolerance?

A study listed in the Annals of Internal Medicine have tested the pill, sildenafil, on participants in hypoxic environments. For those who may not know, sildenafil is also known as Viagra, which is usually used to treat erectile dysfunction and help lower blood pressure. Sildenafil is known as a phosphodiesterase type 5 inhibitor, meaning it blocks the action of cGMP-specific phosphodiesterase on cyclic GMP in smooth muscle (such as the blood vessels) leading to vasodilation.

With the help of sildenafil, participants in the study had a significant increase in their oxygen saturation and maximum workload during exercise compared to those who only had a placebo pill. Sildenafil also reduced hypoxic pulmonary hypertension at rest and during exercise, and overall increased exercise capacity during hypoxia. So, next time you plan on climbing a tall mountain, get some sildenafil to bring with you.

Ghofrani HA, Reichenberger F, Kohstall MG, Mrosek EH, Seeger T, Olschewski H, et al. Sildenafil Increased Exercise Capacity during Hypoxia at Low Altitudes and at Mount Everest Base Camp: A Randomized, Double-Blind, Placebo-Controlled Crossover Trial. Ann Intern Med. ;141:169–177. doi: 10.7326/0003-4819-141-3-200408030-00005

Does your doctor's gender matter?

It has been well-documented that non-white patients are more likely to survive dangerous health conditions if they are treated by physicians of their race, which has spurred a push from hospitals to hire a more diverse team of physicians. A recent study in PNAS expanded these findings to gender, showing that among a sample of patients experiencing an acute myocardial infarction (AMI), female patients were more likely to survive when treated by a female ER physician.

The researchers used patient and physician data from Florida ED admissions between 1991 and 2010, because a patient admitted to the ER does not have a choice in which physician they see, resulting in a semi-random assignment of physician to patient. They divided the data into four groups: male doctors seeing male patients, male doctors seeing female patients, female doctors seeing male patients and female doctors seeing female patients, discarding all gender-neutral doctor names to avoid error. Survival rates after AMI were 2-3 times higher for female patients being treated by female physicians, even controlling for physician experience.

However, there were some attenuating factors. If a male doctor worked in a hospital with many female colleagues, or if he had treated a significantly higher number of female patients in the past, the difference in survival was improved. This may be because of knowledge “spillover” from his female colleagues or because hospitals with a commitment to even gender ratios may have policies that improve treatment gaps, or possibly mandate training to improve treatment of female patients.

 This study is of significant import to us as future providers. For maximum beneficence, male providers should keep the results in mind and seek out hospitals with a commitment to unbiased hiring practices to improve their skills and the survival of their patients. Female providers should look out for female patients that are being treated by male colleagues and share knowledge when appropriate. Medical schools should emphasize the different presentations of conditions like AMIs in men and women to avoid maleficence. And when possible and appropriate, patients should be given the autonomy to choose their doctor.

Maybe becoming hotter isn't as great as it sounds...

Since 1880, the global temperature has risen by 1.8 degrees Fahrenheit, with seventeen of the last eighteen warmest years on record occurring since 2001.  In addition to that, CO2 levels in the air are at their highest in 650,000 years, Earth's ice sheets are losing 413 gigatons of mass each year, and sea levels are rising by 3.2 millimeters each year (source).

I know what you're thinking.  "That's awful, and climate change is something we need to address."  Well, if you needed another reason to think that, did you know that climate change affects human health as well?

Climate change can affect human health mainly in two ways: first, it can change the severity or frequency of health issues already affected by climate, and second, it can create new problems in places where it hasn't happened previously.  For example, temperature extremes can exacerbate chronic conditions like cardiovascular and respiratory diseases, owing to the fact that increased CO2 promotes the growth of plants that release allergens that decrease air quality both outdoors and indoors (source).  It also increases the likelihood of water-related illness in humans, because increased temperature and precipitation/runoff affect the growth, survival, spread, and virulence of water-related pathogens.  These pathogens can get into our system though ingestion, inhalation, and consumption of contaminated fish (source).

One of the more interesting things I found was climate change's ability to negatively affect mental health.  Many people exposed to weather-related disasters experience a significant amount of stress (which we know affects health...I hope) and can even develop clinical disorders.  Additionally, those people already with mental illness are more at risk for poor physical health due to extreme heat, and people of lower socioeconomic status are more likely to experience these negative effects of climate change on mental health (source).

Microbes and Alzheimer's Disease

Alzheimer’s Disease (AD) affects many people worldwide but what if this disease was simply caused by an infection by a microbe. I came across an article while reading the news that supports this idea and how possibly we have been going in the wrong direction when treating this disease for many decades. The theory goes something like this, a person is infected leading to a metabolic waterfall effect, leading to a diseased brain and in response amyloid plaques (Davis, 2018). A Harvard neuroscientists, Dr. Tanzi,  believes that amyloid plaques are possibly part of our ancient immune system after finding that these plaques are lethal to microbes in a test tube (Davis, 2018). Dr. Tanzi believes the amyloid plaques are in response to an initial infection which then leads to build of plaques. This then leads to an inflamed state in the brain which then causes the actual damage known as Alzheimer’s. Dr. Tanzi says this may not be the only possible route that leads to Alzheimer’s but we should consider all possibilities when trying to reduce the prevalence and incidence of Alzheimer’s (Davis, 2018). After further literature review I found an article that names herpes simplex virus type 1 (HSV1) as a possible precursor infection that ultimately leads to Alzheimer’s. This article relates that many AD patients have microbes present in their brains and that HSV is known to cause herpes simplex encephalitis (HSE) an inflammatory response to the disease (Itzhakia et al., 2016). AD has long been known to have an inflammatory component that lends to the idea that AD is infection caused. Is it possible that we have been overlooking the microbe as a cause of Alzheimer’s Disease?

As future healthcare providers it is important that we always seek the answer and never get narrow minded about our practice. We must provide justice and beneficence to patients by always seeking out ways to better healthcare and provide the best outcome for them.

Davis, A. (2018). Could Alzheimer’s Be An Infectious Disease. Health News NPR.

Itzhakia, R. F., Lathe, R., Balin, B. J., Ball, M. J., Bearer, E. L., Bullido, M. J., Fulop, T.            (2016). Microbes and Alzheimer’s Disease. Journal of Alzheimer’s Disease. https://doi.org/10.3233/RNN-150534