It has long been hypothesized that “excessive” protein consumption can lead to impaired kidney function. Jose Antonio disproves this idea with a two-year case study on 5 well-trained body builders recently published here in the Official Research Journal of the American Society of Exercise Physiologists.
- “The general recommendations for optimal protein intake for building and maintaining skeletal muscle mass is 1.4 to 2.0 g/kg/day according to the Position Stands of the International Society of Sports Nutrition (8,10).” Individuals reported upon were asked to maintain a diet of > 2.2 g/kg/day.
- The subjects were analyzed using BodPod technology and blood panels every six months for two years.
- “The mean values for all of the parameters (group data) showed no harmful effects of protein consumption.”
- “When the individual data were examined, a few of the clinical values were slightly outside of the normal range. However, there was no consistent pattern.” Two markers of interest were creatinine and blood urea nitrogen. Creatinine is a waste product from the normal breakdown of muscle tissue. It’s filtered through the kidneys and excreted in urine. The liver produces urea in the urea cycle as a waste product of the digestion of protein, which is also excreted as urine.
- “It is clear from our investigations and others that the consumption of a high-protein diet, particularly in healthy exercise trained individuals has no harmful effect on renal function (13,7,15,16).
- Body composition changes were relatively inconsistent among the subjects.
- “Perhaps, in the short term, changes in exercise energy expenditure and, perhaps, non-exercise activity thermogenesis (NEAT) might account in part for the greater changes in body composition in those that consume large quantities of protein (14,18).”
- “According to Levine et al. (14), NEAT can vary between individuals by as much as 2000 kcals daily. Therefore, one might speculate that the more advanced training status of the high protein group might lend itself to greater NEAT. Protein has a thermic effect of feeding (TEF) of 19 to 23% in both obese and lean individuals. On the other hand, carbohydrate is approximately 12 to 14% (17). We would speculate that the primary effect of protein overfeeding is in the effect on NEAT.”
- Limitations exist in a variety of areas with this study. First, this paper looked at well-trained individuals and kidney function with a high protein diet. There may be a threshold in protein quantity which may yield different results. Secondly, the training age of these individuals should be recognized. Though the training programs are not controlled, we may assume that these individuals are training at higher loads, volumes, and frequencies than most college-aged males. Lastly, more may not be better- meaning that in caloric excess, a certain amount of protein may be secreted as waste or stored as fat regardless of kidney function.
- None-the-less, there are no grounds to be fearful that high protein diets of >2.2g/kg/day would impose any damage to kidney or liver function.
A colleague of mine sent me this paper on the topic of neuroplasticity and neurotrophic behavior. This is a highly marketed phrase today, but understand the general idea is to improve the efficiency of the brain by using numerous synapses to more effectively link neurons. Particularly, most folks are referring to synaptic plasticity- which are changes in the connections between neurons (new synapses). Imagine you have a muscle with thousands of fibers, but you are only able to tap into one or two fibers during a task. Neuroplasticity is the concept of using more synapses within the brain matter, as well as using the existing synapses more efficiently, which will in turn improve cognitive function. Turns out, there is an increasing amount of evidence this can be achieved via physical training, just as well as cognitive training.
- “Over the past decade, a number of studies on humans have shown the benefits of exercise on brain health and function, particularly in aging populations. Exercise participation has consistently emerged as a key indicator of improved cognitive function [, 3., 4., 5.].”
- This study, chose to focus on “brain-derived neurotrophic factor (BDNF) because it supports the survival and growth of many neuronal subtypes, including glutamatergic neurons [15., 16.]”. Also, previous literature has shown that “…BDNF emerged as a key mediator of synaptic efficacy, neuronal connectivity and use-dependent plasticity [17., 18., 19., 20.].”
- After seven days of rodents performing wheel-running, at their leisure, the findings were that “….several days of voluntary wheel-running increased levels of BDNF mRNA in the hippocampus , a highly plastic structure that is normally associated with higher cognitive function rather than motor activity.” Congruently, they were “…paralleled by increased amounts of BDNF protein ( 2)”.
- These are results we may have hypothesized, but where it gets more interesting is it seems that “…IGF-1 might be an upstream mediator of BDNF gene regulation, neurogenesis and the ability of exercise to protect the brain from injury [9., 52.].” Insulin-like growth factor-1 (IGF-1) is a potent anabolic hormone secreted by the pituitary gland which is vital for growth, development and anabolism throughout maturation.
- “IGF-1 levels increase in both the periphery  and brain  after exercise, and at least part of the increase in the brain reflects increased transport from the periphery across the blood–brain barrier .”
- “Interestingly, peripheral IGF-1 appears to participate in the neuroprotective effect of exercise, as peripheral infusion of IGF-1-blocking antibodies before an injury reduces the protection .”
- “These data suggest that peripheral IGF-1 initiates growth-factor cascades in the brain that can alter ongoing plasticity mechanisms.”
Take home point: regular activity, in this case locomotion, may increase levels of IGF-1 which will not only promote musculoskeletal enhanced health but also neurotrophic adaptions improving cognitive function.
Zach Even-Esh recently did a podcast with Dana Santas, aka the Mobility Maker. She practices yoga-like movement with a variety of sports teams in the NFL, MLB, NHL, and NBA. There is a segment that spoke to me about thirty-five minutes in, from which I would like to highlight a few points that resonated.
- Proactive approaches will always trump passive approaches to pain. Proactive modalities include movement and training corrections while passive modalities are medication, rest, etc.
- Pain is a sign something may be work improperly, which requires a fix- not a mask. The pain may not be issue- a spinal herniation is often not the issue but muscular strength and firing patterns are, which then lead to the exacerbation of issues.
- It doesn’t get more proximal than the diaphragm. Start with breathing and proximal muscular function, then work into distal patterns.
- The diaphragm attaches to the rib cage and the lumbar spine. In the lumbar spine attachment, there is a break in the tissues where the psoas major passes through very intricately. If the psoas is tight and inhibited, the diaphragm most likely is as well.
- The right side’s attachment to the lumbar spine is longer and thicker, sometimes up to two vertebrae lower.
- Rib flare is a result of externally rotated lower ribs. This would mean that the diaphragm is kept in a semi-contracted state at all times. This is very inefficient from unnecessary high muscular tone.
- Chronic non-specific lower back pain is more commonly right sided. We could make a case that more pulling to the ride side is a result of the increased muscle mass and poor contribution from the left side.
- Exhalation should drive the lower ribs downward, not necessarily the belly inward.
- Proper exhalation can help diminish upper trapezius, pectoralis minor, sternocleidomastoid, and intercoastal tone, which is a result of forced inhalation when the diaphragm cannot fully expand and contract.
- The diaphragm dictates rib and lumbar positioning. Forced inhalation often provokes anterior pelvic tilt and inhibited thoracic extension.
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