By Austin Baraki
Sorry for the delay, folks! I’ve been busy graduating from medical school :). We’ve made it to the fourth, final, and most important article in our series. Before we begin, let’s briefly review what we’ve covered so far.
In our first article we defined sarcopenia as a loss of skeletal muscle mass and strength/performance, and discussed the mechanisms that contribute to muscle protein breakdown. In part II we showed how to stimulate muscle protein synthesis (MPS). We then looked at how this translates into muscle hypertrophy, and proved that “it’s never too late” – no matter how old! In part III we discussed the different factors that can affect muscle “quality” independent of muscle size. We also took a clinical perspective on diagnosing sarcopenia using validated measures of muscle mass, muscle strength, and muscle function.
Today we’ll look at the best ways to treat and prevent sarcopenia, and apply this understanding to provide practical recommendations.
We know that sarcopenia dramatically decreases mobility, functional activity, and increases risks of falls, injury, and death, so the next question is how should we treat and prevent it (1-4)? Most studies in biomedical research known mechanisms of disease to generate “therapeutic targets” for intervention. As we know from the prior articles in this series, these mechanisms include both an imbalance between muscle protein synthesis and breakdown, and a progressive decline in muscle quality/function. Logically, then, our interventions to treat or prevent sarcopenia should increase muscle protein synthesis relative to breakdown, and promote improvements in muscle quality/function. Simply put, to reverse sarcopenia (where muscles get small and weak) we should use the best interventions to make them big and strong! Of course, we place the most emphasis on increasing strength, since that is really what allows us to function in our world. Furthermore, in the clinical setting we’d like to know not just what works, but rather what works optimally, especially for patient-oriented outcomes like preventing falls and decreasing mortality. Let’s take a look at some of the best methods available for these purposes, including exercise, nutrition, supplements, and pharmacological treatments.
Exercise is the cheapest and most effective intervention available to prevent and treat sarcopenia. Unlike some pharmaceuticals, there are no non-responders to exercise with respect to improving the various metrics that define sarcopenia. In other words, it “works” for everyone, even very old individuals (>80-90 years) (5-7). It is this author’s opinion that the topic deserves a thorough discussion both because of its breadth, and because the vast majority of clinicians and patients are completely unaware of current exercise recommendations. This very likely includes your own doctor, who — like myself — received NO formal education on exercise in medical school (8).
One survey of primary care physicians showed that less than 12% were aware of the current exercise recommendations by the American College of Sports Medicine (ACSM) and American Heart Association (AHA) (9). Furthermore, of this 12% who were familiar with the recommendations, only half actually provided this specific information to their patients! These are abysmal statistics for such an inexpensive, potent, and side-effect free intervention. Admittedly, it can be very difficult (sometimes impossible) to motivate individuals to begin any kind of consistent, productive exercise program. But cynicism should never stop us from providing this information to patients and downplaying its significance by omission. In fact, the research suggests that despite all the perceived barriers to exercise, older patients in particular are more likely to follow physician recommendations because of increased respect and more frequent contact with their doctors (10). So let’s take a look at the current ACSM/AHA exercise recommendations for “apparently healthy adults,” which are summarized here (11-12):
- Cardio or Aerobic Exercise-Moderate-intensity cardiorespiratory exercise training for ≥30 min/day on ≥5 days/wk for a total of at least 150 min/wk, OR-Vigorous-intensity cardiorespiratory exercise training for ≥20 min/day on ≥3 days/wk for a total of at least≥75 min/wk, OR-A combination of moderate- and vigorous-intensity exercise to achieve a total energy expenditure of ≥500-1000 MET·min/wk. (MET = metabolic equivalents)
- Resistance exercise
-2-3 sessions per week for novice trainees
-Target all “major muscle groups”
-Use of concentric, eccentric, and isometric contractions
-Slow-to-moderate contraction velocities
-Unilateral and bilateral exercises, with emphasis on multi-joint, free-weight exercises
-May complement with machine-based exercises
-60-70% 1RM loads for novices
-Multiple sets per exercise
3. Flexibility exercise
-“completing a series of flexibility exercises for each the major muscle-tendon groups (a total of 60 seconds per exercise) on ≥2 days/wk” to “maintain joint range of movement”
Although most of these guidelines do have supporting evidence in the exercise science literature, let’s consider them critically and practically. In Part 1 of this series we showed that resistance training is unequivocally superior to endurance training for outcomes of MPS, muscle mass, strength, and improving muscle quality. Furthermore, high-intensity interval training (HIIT) augments these gainzZz™ with potent cardiometabolic and MPS effects. Short bouts of HIIT at least match and often outperform the effects of endurance exercise, despite lower training volume and significantly less time commitments (13-17). Interestingly, research has even shown that HIIT is perceived to be more enjoyable than moderate-intensity continuous exercise, despite feeling “harder” (18)! Finally, and perhaps most importantly, we know that muscular strength is independently associated with a reduced risk of death from all causes, even after adjusting for cardiorespiratory fitness (19).
Given this information we logically conclude that, given a limited amount of time and energy to dedicate to an exercise program, endurance training is a significantly inferior use of time and effort for both healthy and sarcopenic individuals, and therefore progressive resistance training is the optimal first-line intervention in terms of efficiency and outcomes, followed by the addition of HIIT if possible.
So how do we optimize a resistance training program for a goal of increasing strength? Since you’re at BarbellMedicine.com, it should come as no surprise that our ideal plan would involve a simple program using barbell-based multi-joint movements under the supervision of a competent coach. These exercises should engage the greatest amount of muscle mass through the longest effective range of motion, using heavy weights that allow us to get strong. We only require a few exercises because, when used correctly, barbells allow us to safely and efficiently administer a potent systemic stress in a controlled, incrementally increasable fashion (more on this here). We would use the squat, overhead press, deadlift, and bench press, i.e. movements that utilize concentric, eccentric, and isometric muscular contractions in all major muscle groups, which conveniently fulfill the ACSM recommendations.
Now, if the individual is sarcopenic or simply too weak to perform these movements at the start, individualized progressions can be applied based on their starting abilities (e.g. machine-based movements, bodyweight movement, lighter barbells, or even manual resistance training if critically ill or immobile) to develop the requisite strength for our ultimate goal. (Skeptics: see here, here or here). By aiming to train whole-body compound movements, we are left with little need for additional unilateral or machine-based movements. We also eliminate the need for any separate balance/coordination exercises, because it turns out that the simple act of not falling over with progressively heavier weights in your hands or on your back requires (and therefore improves) balance and coordination! This simple strength-focused plan also adequately stimulates a degree of muscular hypertrophy, power development, and conditioning for our purposes. In addition to this resistance training regimen, we might add an effective interval training modality added such as the Prowler sled (or a lighter version of a sled as seen here), or a cycling-based method (e.g. Wingate/stationary bike) for an additional stimulus.
Recall that in order to overcome age-related “anabolic resistance,” this stimulus must be of sufficient intensity to induce an MPS response. For resistance training, this means using adequate workloads: typically 70-90% of 1-repetition maximum (1RM) loads, or lighter loads performed to muscular failure (20). Performing repetitions to muscular failure causes dramatic soreness and increases injury risk as technique degrades over the course of a long set, so we opt for the former choice. In contrast, the use of heavier loads for fewer repetitions improves absolute strength far better than using light loads, and if we had to choose between “strength” versus “size” in the aging individual, we will always opt for strength (more on this here) (21). Therefore the ACSM recommendation of 60-70% of 1RM is suboptimal for our goals of MPS, muscle mass, and muscle strength, although starting “lighter” with a novice is also understandable depending on the individual.
Our desired approach would instead have a novice trainee work up to a challenging set of 5 reps that can be performed with strict technique. This workload will typically lie somewhere in the 80% their baseline 1RM range, but note that never test a baseline 1RM measurement, as this is unreliable and potentially dangerous for untrained novices. We would use this baseline training weight and progress it over time, with the coach maintaining a careful balance between overcoming anabolic resistance, avoiding overtraining, and sustaining progress. It should be noted that resistance training in older individuals causes greater adaptations in terms of muscle quality (e.g. intramuscular fat content, neurologic innervation, etc.) rather than muscular hypertrophy (5). Regardless, resistance training has shown dramatic improvements in strength and functional ability (e.g. gait speed, chair rise, etc.) in all age groups, despite the suboptimal training modalities used in most research studies (5-7)!
The skeptics among our readers might be asking, “This doesn’t sound safe — aren’t there situations where we shouldn’t apply these methods?” To consider this, let’s take a look at a few of the most common diseases in the USA.
- Hypertension (HTN) and Cardiovascular Disease (CVD): the American Heart Association (and many others) have published numerous studies and clinical practice guidelines promoting resistance exercise as safe and effective in patients with hypertension and cardiovascular disease (even if considered “high-risk” or even post-heart attack) (22-25). Interestingly, HIIT has also shown superior results compared to moderate-intensity continuous exercise in the cardiac rehabilitation setting (26).
- Heart Failure (HF) is a highly burdensome condition that occurs when the diseased heart is no longer able to pump blood as efficiently. For many years exercise, and particularly resistance exercise, was thought to be risky by potentially increasing the risk of “decompensation” and disease progression. Many trials of exercise have now established that both aerobic and resistance training are safe, effective, and beneficial (i.e. reduce mortality) from heart failure (27-31).
- Chronic Obstructive Pulmonary Disease (COPD), a chronic lung disease typically related to smoking, is yet another condition that has been proven to benefit from progressive resistance training. These patients improve strength, physical capacity (e.g. 6-minute walk distance), quality of life and self-reported health perceptions from exercise training, without increased risk of acute exacerbations of their disease (32-35).
- Chronic Kidney Disease (CKD) is another highly burdensome disease, often progressive and requiring onerous procedures and dialysis schedules. These patients are often malnourished and prone to muscle wasting and sarcopenia; furthermore, CKD directly contributes to cardiovascular disease, depression, and a dramatically increased risk of death (36). Not surprisingly, resistance training has proven benefits – it reduces chronic inflammation, improves nutritional status, reverses muscle wasting, and improves functional status without any increased risk of disease progression (37-40).
The above discussion covers a vast number of patients and shows that they may safely engage in productive training modalities. However, there are a few conditions where more concern might be warranted, such as patients with uncorrected valvular heart disease, aortic dissection, or aortic aneurysms, in which cases there simply isn’t enough quality research evaluating the safety of resistance training in these populations. The studies are starting to be done, for example evaluating exercise training in patients with abdominal aortic aneurysm, with some promising initial results (41). I imagine such study proposals must be quite difficult to get through an IRB approval committee, however.
Again note that the vast majority of research has demonstrated positive effects of resistance exercise despite the common problems of poor training prescriptions (e.g. high-rep, low-intensity isolation machine-based exercises) and short study durations! Remember that the adaptations to resistance training (building new muscle, bone, and connective tissue) take time to occur. Imagine what the results might show if the resistance training protocols in these studies were correctly designed to optimally increase strength, and the subjects followed for 6-12 months of training rather than 6-12 weeks! Hopefully THIS project will one day give us our answer.
Nutrition is another critically important piece of the treatment/prevention puzzle that deserves a detailed discussion due to its breadth. As discussed in part 1, the physiologic “anorexia of aging” decreases intake of total calories and protein, resulting in muscle atrophy due to an increased rate of protein breakdown relative to protein synthesis (43). Chronic diseases like cancer, kidney/liver failure, and AIDS exacerbate this loss of appetite, resulting in a syndrome known as “cachexia” that dramatically worsens prognosis. Jordan has already written a good article here on how to optimize protein intake for the average individual, but we’ll cover the basics once more (with more science!).
Recall from part II the significance of dietary protein, particularly the branched-chain amino acid (BCAA) Leucine. Elevated blood levels of leucine and other Essential Amino Acids (EAAs) directly stimulate MPS, and when combined with resistance exercise result in an even more powerful synergistic effect. According to the Institute of Medicine’s (IOM) 2010 recommendations, the US Recommended Dietary Intake (RDI) is 0.8 grams of protein per kilogram of body weight (44). These recommended values were determined as the minimum amount needed to “meet the needs” of 97% of the population, which is defined as preventing a negative nitrogen balance. Unfortunately, the data supporting this claim came entirely from studies in college-aged males and relied on measurements of nitrogen balance rather than more relevant physiologic endpoints (44). There are multiple problems with using nitrogen balance as a marker of muscle protein changes, most notably that all tissues are made of protein and thus have significant nitrogen content such that changes in any tissue’s mass, skeletal muscle or not, will effect “net nitrogen balance”. A better study is to look at tagged amino acids and see if they are being incorporated into skeletal muscle mass with any appreciable increases or, conversely, being lost from the skeletal muscle mass at a significant rate. We have the technology to do so, however this methodology has not been used to establish protein needs and thus, optimal protein recommendations with respect to skeletal muscle mass have to be extrapolated from a number of studies. In sum, it should be obvious that the recommendation of 0.8g/kg of protein may or may not the amount that optimizes health or any specific parameter depending on a host of factors, but likely not for anyone in the elderly population!
Recall that anabolic resistance progressively decreases one’s sensitivity to anabolic stimuli, so 20 grams of protein for a 19 year old will have a much greater effect than the same dose in a 75 year old (45) ! In fact, there is evidence suggesting that the recommended intake for healthy older individuals is inadequate to even maintain lean body mass (46)! The fact that the IOM recommendations treat 19-year olds and 75-year olds as identical from the standpoint of dietary protein needs is likely inadequate based on the current literature. Fortunately, the accumulating evidence is starting to push recommendations for elderly upwards into the range of 1.2-1.5 (and as high as 2.0) grams of protein per kilogram of bodyweight (47-49). So with that said, let’s take a look at the details of what we know about dietary protein and use this to build some practical recommendations:
There is a minimum “threshold” dose of leucine required to trigger an MPS response (50-53). Aging and physical inactivity increase the minimum threshold dose (anabolic resistance), but fortunately resistance training can acutely restore some anabolic “sensitivity”. Because of these variables, generalized threshold values are hard to pinpoint, but we know that maximal MPS is reliably stimulated in the range of 2.0 to 3.5 grams of leucine (depending on individual sensitivity). Saturation of this effect typically occurs at doses greater than 4-5 grams, above which there is no further increase in MPS response in most individuals.
The threshold dose maximally stimulates MPS if absorbed relatively rapidly, because the MPS effect depends on bloodstream EAA concentration (54). Thus, the use of fast-digesting protein sources (e.g. whey) is therefore superior to “slower” sources (e.g. casein), and we would prefer to use single, larger doses (boluses) over smaller intermittent doses (50).
A single meal-driven MPS episode typically peaks at 90 minutes after eating and lasts about 2-3 hours total regardless of continued nutrient availability in the bloodstream. It is then followed by an approximately 3-hour “refractory period” before another bout can be stimulated (20, 55-58). Interestingly, this refractory period persists if continued feeding occurs. Conversely, when doses (5-10 grams) of free-form BCAAs (like a supplement) are given in the hours between meals can overcome the refractory period and extend maximal MPS duration beyond the typical 2-3 hour limit (57-58)! This allows us to further tilt the balance between muscle protein synthesis and muscle protein breakdown in a favorable direction, especially in aging or sarcopenic individuals. Interestingly, additional BCAAs can also improve symptoms of muscle soreness from resistance exercise – bonus (59-60)!
Next, the evidence overwhelmingly supports whey protein as a superior anabolic driver compared to equal-calorie amounts of other protein sources (e.g. casein, soy, rice, pea, wheat etc.) due to its higher quantity and quality EAA content, as well as it’s faster rate of digestion and absorption (50, 61-66). This means that in order to elicit anywhere near the same anabolic effects as whey, you would need greater amounts of these other protein sources, which also means a higher total calorie intake). This means the other sources are LESS EFFICIENT, and therefore suboptimal choices for our purposes. Whey also has numerous other beneficial bioactive peptides that are unfortunately far beyond the scope of this article (see ref. 67 for details).
As we’ve discussed before, exercise and in particular, resistance training, have a synergistic effect on MPS. That is, EAA and resistance training together evoke a more prolonged and robust MPS response than either can individually (20,53,68). This is an especially important tool in the “anabolically resistant” population. Resistance training will also cause the body to retain a greater proportion of this newly synthesized protein rather than breaking it back down later in the diurnal cycle (69).
Now, once again for the skeptical readers – are there situations where these recommendations should not be applied? Let’s briefly look at a few of the common fears you might hear associated with increased dietary protein intake, especially: loss of bone mineral density, cancer, and kidney or liver disease.
- Fears that higher dietary protein intakes result in “acidification,” calcium loss, or osteoporosis are all unfounded, as well-controlled studies show no adverse effects on calcium retention (47,70-73). Additionally, those with the highest dietary protein intake tend to have higher bone mineral densities than lower protein folks (see here and here). Moreover, dietary changes have no significant effect on the pH of your body or your blood, which is tightly regulated by your kidneys. These claims have already been thoroughly debunked many times and honestly doesn’t even deserve further discussion.
- Similarly, there is no convincing evidence from well-designed studies indicating that dietary protein intake has any specific effects on cancer incidence. In fact, some epidemiologic studies suggest that higher protein intake might improve survival in cancer patients (by this point in the article series, you should be able to hypothesize why this might occur…) (47)!
- The idea that a high dietary protein intake causes kidney damage in previously healthy human kidneys is completely false and has no scientific support whatsoever. There is no evidence that any level of dietary protein intake causes injury to non-diseased human kidneys, and indeed high protein diets often improve metabolic parameters and risk factors for chronic diseases like diabetes and high blood pressure (70-73). When looking at patients with pre-existing kidney disease, some of the literature suggests a very small beneficial effect of limiting dietary protein (~0.58 g/kg/day) on slowing progression of disease; however, other studies have shown no significant difference in disease progression, leaving no conclusive answer in the literature (47). Unfortunately, very few of these studies were randomized controlled trials, they were often too short in duration, and typically use serum creatinine measurements as indicators of disease progression (a parameter that, itself, can be affected by dietary intake and muscle mass). However, studies of very-low protein diets (<0.28 g/kg/day) have actually shown increased risks of death in these patients, possibly due to deterioration in nutritional status and progression to sarcopenia (74). In fact, there is evidence that dialysis patients require intakes as high as 1.4 g/kg/d just to maintain nitrogen balance on non-dialysis days (73).
- Finally, in patients with cirrhotic liver disease, although the nitrogen load from a high dietary protein intake might theoretically cause/exacerbate encephalopathy, there is no convincing evidence showing improved outcomes from low-protein diets (75,76). In fact, the research has continued to show that protein restriction in these patients is often inappropriate, results in worse nutritional status, and increases risk of death (77,78). BCAA supplementation has also been investigated, and appears to be well-tolerated and improves clinical outcomes without exacerbating the underlying disease (79,80).
Summary:In order to maximally stimulate MPS throughout the day we should consume leucine-rich sources of protein (e.g. whey, dairy, and/or animal proteins) in meals spaced at least 4 hours apart, targeting 1.2-1.5 g/kg/d for most aging individuals. This should ideally be coupled with progressive resistance training. Additional doses of BCAA (e.g. ~5-10 grams) can be used in between meals to further increase total daily MPS, but are a secondary priority compared to simply consuming adequate daily protein.
Next, supplementation is a controversial topic in the medical world, particularly because of the lack of regulation over the industry and lack of evidence supporting the use of most supplements. There are a select few exceptions to this, however, which we’ll discuss here.
Creatine is a molecule normally used by our body’s cells to rapidly generate usable energy in the form of ATP (note: this is a vast oversimplification for the sake of brevity). Our body produces some creatine on its own, and we can obtain some more by including meat in our diets. However, this is another situation where we must differentiate “just enough” from “optimal” intake. Creatine monohydrate is one of the most-studied dietary supplements; a dose of 5-10 grams taken daily has consistently proven benefits for skeletal muscle, including size, strength, and power, and it helps to prevent atrophy during disuse (5,81-84). It even appears to have beneficial effects for neurologic/psychiatric function as well by helping to ward off neurodegenerative disease and dysfunction (82,85).
In fact, congenital deficiency syndromes in humans result in mental retardation and developmental delays, and supplementation during pregnancy in rats decreases the risk of fetal hypoxic brain damage during the birthing process (an area ripe for study in humans) (86-88). These findings (among many others) are suggestive of creatine’s importance for proper neurological function. It has no significant short- or long-term risks, adverse effects, or contraindications when taken at a normal dose range (5-10 g/d), and is extremely cheap (typically $15-20 per kilogram) (84, 89). A more detailed discussion of creatine would at least double the length of this already lengthy series, so perhaps we’ll save that discussion for a future article. In the meantime, further information (supported by over 700 scientific citations) is available here at Examine.com and in ref. 84.
One final tidbit: in the body, creatine breaks down into a molecule called creatinine, which happens to be a commonly used biomarker to assess kidney function. People with lots of muscle mass or those who supplement with creatine may have an elevated serum creatinine measurement on bloodwork, potentially raising concern for kidney failure. Let’s be clear, creatine supplementation DOES NOT cause kidney damage of any kind, but has the potential to cause a “false-positive” test result (84,90-94). In fact, Jordan has a paper that will be published shortly in Annals of Emergency Medicine suggesting that creatine supplementation produces an isolated elevation in creatinine levels sufficient enough to garner the diagnosis of acute kidney injury without any evidence of an actual kidney injury. So if your doctor tells you that supplemental creatine is dangerous or might harm your kidneys, they are 100% wrong. Researchers have even tried giving patients with only one functioning kidney upwards of 20 grams of creatine daily (4 times the dose we’re recommending here) with no evidence of damage or decreased function (95). In short, everyone and their grandmother should be taking 5-10 grams of creatine monohydrate daily.
Vitamin D has been a popular, yet controversial supplement in recent years for a number of reasons. Again, a full discussion of vitamin D would dramatically increase length of this article, so we will keep things brief. Aging and chronic disease are associated with decreases in serum vitamin D levels, although correlative versus causative mechanisms have not been precisely worked out. Low vitamin D levels are associated with impaired muscle growth and strength, impaired nerve function, and increased risks of myopathy from statin medications, indicating that there is some relationship between vitamin D and neuromuscular tissue (which has been confirmed mechanistically) (81,96).
Overall, it appears that vitamin D replacement in patients with low serum levels increases muscle strength and function, decreases falls, and decreases mortality. In contrast, it is unclear whether individuals with normal serum levels derive any significant benefits. Despite a few conflicting studies, given its plausibility, low cost, and promising data so far, the majority of guidelines on aging and sarcopenia recommend checking patients’ serum levels and, for individuals with levels below 40 nmol/L, providing 700-1000 IU of oral vitamin D3 daily.
A variety of pharmacologic interventions have also been investigated and, in general, have limited potential for use in sarcopenia (97). Hormonal treatments such as ghrelin, estrogen, and DHEA have not shown beneficial effects on outcomes. ACE inhibitors (a class of blood pressure medication), Selective Androgen Receptor Modulators (SARMs), and Myostatin inhibitors are still under study, but have little hope for common clinical use in the future.
Of course, given our detailed discussion of the role of testosterone back in Part 2, it should make sense that exogenous testosterone might benefit sarcopenia by directly stimulating MPS, suppressing protein breakdown, supporting satellite cells and motor neurons, promoting growth of muscle cells and blocking fat cells. Testosterone is frequently used clinically to treat patients with hypogonadism (“Low T”), and has been studied for use in elderly sarcopenic patients. Not surprisingly, it consistently increases muscle mass and strength in these populations (98). However, there has long been concern that testosterone therapy increases the risk of prostate cancer and cardiovascular events (e.g. heart attacks and strokes). Both ideas have undergone dramatic shifts in recent years with emerging scientific evidence. The literature regarding prostate cancer risk remains conflicting at this time, but is starting to shift as there is no consistently demonstrated connection between serum testosterone and prostate cancer (98-100). As for cardiovascular disease, Testosterone therapy instead appears to have a strong beneficial effect on cardiovascular health in men “that is not widely understood” (per the Mayo Clinic’s own review) (101). However, the use of testosterone treatment will likely remain very controversial among urologists and endocrinologists for the foreseeable future.
So we’ve now essentially completed our discussion of sarcopenia, which was just one component of Dr. Sullivan’s “Sick Aging Phenotype” (SAP) of sarcopenia/frailty, metabolic syndrome, and polypharmacy/medical dependence. This triad drains a disproportionate share of healthcare resources, and each component is an independent risk factor for mortality. Fortunately, although our recommendations in this article focused on sarcopenia, they effectively address the other two SAP components as well. That is, by executing a proper resistance training program and implementing the discussed nutritional/supplementation interventions, metabolic syndrome can be significantly improved (or even reversed), and the need for medications and dependence on the healthcare system can be dramatically decreased as well. So if you’re young and healthy, put these recommendations into practice to prevent yourself from becoming sarcopenic with age, and if you know someone who is old or frail, spread the word and let’s get them stronger!
Austin Baraki is a 25 year old student just three months away from completing his M.D. degree. He came to the sport of powerlifting after 15 years of experience competing in and coaching competitive swimming through the collegiate level. Since transitioning to powerlifting he has achieved personal best lifts of a 480 lb squat, 365 lb bench press, and has deadlifted 550×2 at 5’10”/185 lbs. He is specializing in Internal Medicine and has a passion for coaching, teaching, preventive medicine, a nice rare steak, and making gainzZz™
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