Protein amount and type may matter regarding renal function alterations in healthy persons, both acutely (single meals) and chronically [8
]. These data appear inconsistent, however, and appear to depend on the population studied. Beyond study of chronically diseased persons or mixed groups of healthy persons, exercising populations should be studied specifically due to their known differences in renal function. Unfortunately, we simply do not know if these differences are helpful or harmful. Will biological differences among athletes lead to greater or less incidence in renal disease compared to the approximately 9% reported to develop among "normal healthy" persons [9
]? Some differences among athletes suggest increased vulnerability to renal damage and others suggest protection against it. For example, it has been estimated that splanchic and renal tissues receive 50% of resting cardiac output (approximately 3 L per minute) whereas these tissues receive under 5% of cardiac output (less than 1 L) during maximal exercise due largely to sympathetic vasoconstriction [10
]. Although exercisers adapt to some extent to this constriction, the relative ischemia may be detrimental to organ function [10
]. Indeed, research documents incidences of extreme muscle damage and renal failure (rhabdomyolysis) in various sports, including bodybuilding [11
]. Interestingly, protein intake may be a factor leading to associated creatine kinase elevations after resistance exercise [12
On the other hand, less severe exercise and the resulting reduction in blood flow and filtration [13
] may instead allow periods of "respite" for the kidneys. Periodic exercise sessions might reduce total renal work over time. Could this slow the normal age-related decline in glomerular filtration? It is not known. Data on exercise-related blood flow changes (sympathetic shunting) are largely animal based, leaving many unknowns among exercising humans.
The scientific community does know that exercising humans differ from non-exercisers in the amount of protein that can be found in their urine. Outside of the post-exercise period, both endurance trainers and resistance trainers exhibit lower microalbuminuria [14
]. The reduction in this "damage marker" does appear beneficial. As with sympathetic shunting of blood flow, however, the full significance of this difference is not clear. At times, exercisers actually exhibit increased
protein in their urine. The prevalence of proteinuria during and after exercise ranges from 18–100%, depending on exercise type and intensity – but not duration [15
]. Thus, there are periods in an exerciser's day where there is more, not less of this renal "damage marker". It should be noted that, unlike the proteinuria seen after a protein-rich meal, post-exercise proteinuria is not considered damaging [16
]. Still, the transient (~60 min half-time) post-exercise presence of protein in the urine [16
] is clearly different from what a healthy non-exerciser would exhibit. Again, the populations differ.
Even exercisers are not uniform in their renal-vascular physiology. Resistance trainers, for example, not only exhibit intense muscular activity but also vascular changes which are different from endurance athletes [17
]. Could large and repeated fluctuations in blood pressure, sympathetic activity, renal function, muscle microtrauma (creatine kinase concentrations), or even purposeful diet-induced hyper-insulinemia make this population different? Unfortunately, little to no research has compared renal function in groups of resistance trainers who have or have not sought ample dietary protein over a multi-year period. This absence of data is important because "education" provided to this population – which exhibits known differences in renal function – often involves concerned or dissuasive language [2
]. Given the known benefits of dietary protein foods/supplementation on protein synthesis, athletic recovery and potentially weight control (thermic effect, satiety), among other potential benefits such as accompanying nutrients, elevated antioxidant capacity, immune enhancement and overtraining amelioration,[18
] this "education" could be a mistake.
Two studies involving resistance trainers, specifically, are known to the authors of this review. These investigations will be examined in an effort to discern why their negative findings have not influenced educators' dissuasive language surrounding dietary protein. There will be a focus on population specificity and control variables as well as suggestions for future research.
The first relevant study on athletes was performed in Belgium by Poortmans and Dellalieux in 2000 [19
]. This protocol detected no significant differences in renal function between higher and lower protein consumers. Despite being well controlled in most respects, there were a few issues of potential relevance to future study, particularly if it is to be longer-term. (Table .) Notably, the average-protein group was not from the same population as the higher-protein group. The average protein consumers were a collection of judoka, rowers and cyclists (skill and endurance-focused sports) while the group of higher protein consumers were bodybuilders (a strength and muscle mass-focused sport). Accordingly, the groups differed in 1.) Training stresses, 2.) Aerobic capacity, 3.) Body weight (presumably muscle mass) and 4.) Probably dietary practices. Over sufficient periods, could adaptations specific to heavy resistance training, such as vascular changes, affect study findings [17
]? Should other, diverging physical or lifestyle issues be addressed in future, needed, longer-term investigations? The following delineates how these four issues might affect results. Training stresses
: Mid-exercise differences such as blood flow variability, intra-abdominal pressures and extreme blood pressure changes occur among heavy lifting bodybuilders [21
]. Although transient, this may matter because "central pressures are more closely related to the pathophysiology of end-organ damage [23
]. Perhaps more importantly, arterial stiffness is exhibited by resistance trainers and this general condition has been associated with glomerular decline [17
]. Would a study of sufficient duration detect an emergence of renal damage among bodybuilders first? And might this be a natural consequence of their sport, irrespective of protein intake? Aerobic capacity
: Endurance athletes with high VO2
max can exhibit rhabdomyolysis just as bodybuilders do. Due to exercise-induced dehydration from long sessions or due to (arguably) possession of more muscle myoglobin, could endurance athletes be more likely to have myoglobin precipitate in their kidneys and harm renal function? Would a study of sufficient duration detect an emergence of renal damage among these
athletes first? 3.) Body weight/muscle mass
: The greater muscle mass of strength athletes may also affect findings over time. Lean body mass has been shown to influence serum creatinine concentrations and thus presumably renal "work" [19
]. Indeed, lean body mass has been shown to influence renal function [24
]. Muscle mass is also the primary recipient of blood glucose. Could intense exercise and repeated, whole-body eccentric muscle soreness (and thus transient insulin resistance) accelerate renal decline, due to associated hyperglycemia and hyperinsulinemia [25
]? Perhaps this is another reason for population-specificity in future study designs. 4.) Dietary practices
: In a population (bodybuilders) that already raises serum insulin with whey-carbohydrate drinks and large food intakes in general, any glycemic or insulinemic aberrations induced by muscle soreness may be particularly relevant. Hence, there are many physical activity and dietary parameters to consider [28
]. In all, an appreciation of the differences among athletes may be of greater importance if longer-term and/or observational studies are undertaken.
Methodological issues in existing protein-athlete investigations
The second relevant study on athletes was performed in Germany by Brandle and colleagues [29
]. The investigators found no correlation between albumin excretion rate (urinary albumin arguably being a damage variable) and gross protein intake (as assessed by nitrogen excretion rate). This investigation was also carefully done in many respects but left room for future research. (Table .) Again, the average-protein groups differed from the higher protein group, as opposed to being from the same population. The average protein consumers (comparison groups) were of different types: non-supplementing bodybuilders, vegetarians and normal healthy persons. These average-protein groups differed in weight, sex, serum creatinine, serum urea, and in two instances physical activity, from the higher-protein group. Perhaps most importantly, the subjects had been on their present diet for as little as four months. Although longer term than previous 1–4 week studies and long enough to see hormonal or perhaps structural changes in the kidney, it is not known whether longer durations would eventually reveal group differences. Finally, no dietary recording/analysis was performed, leaving confounding issues such as calorie intake [28
Thus, of the two known studies specific to strength athletes, neither was able to detect renal damage related to protein intake. Nonetheless, more evidence will be needed to address the concerns still present in educational materials. The totality of the literature appears to be a sum of 48 relatively-high-protein consuming strength athletes, compared to subjects unlike themselves, after fairly short (or unknown) periods of intake. Because strength athletes in particular routinely seek dietary protein [7
] and they differ in training stresses, muscle mass, and dietary practices, there is a need for longer term study exclusively on this population. Lastly, the existing studies were done in European cultures with subjects who may eat differently than American students and strength athletes (to whom much protein dissuasion is targeted). Cultural differences in protein sources (e.g. amino acid profile, accompanying nutrients) could affect renal results when studying free-living persons [8
]. Such potential cultural-dietary differences should be investigated among resistance trainers. We cannot assume that, when it comes to diet, "people are people". More homogeneous comparisons, still tighter experimental controls and longer study durations will help reduce the protein controversy currently in existence. Although not ideal from a cause: effect perspective, observational studies of long-time strength athletes would improve our understanding of the dietary protein-renal issue.