Friday, November 13, 2009

To Marathon or Sprint

I recently ran (no pun intended) across a great article on marathons and 10 reasons NOT to run in marathons.  There are so many reasons not to run long distances...ever!  We were not made to run long distances.  Our bodies combat running long distances in a variety of ways and will do anything to protect us from doing so.   Signals from our mind and bodies tell us to halt immediately.

Top Ten Reasons Not to Run Marathons, by Arthur De Vany

In light of the three deaths last week in Detroit and the two deaths the week before in marathons or half marathons, I am reposting this old post of mine on the dangers of marathoning. The readers of my private blog have known not to engage in this dangerous activity for some time. I put this post up with some sadness and take no pleasure whatsoever in these tragic and needless deaths. It is a measure of how poor the prevailing fitness advice is that so many needless deaths occur in the quest for health.

I was speaking with some of the participants in the St. George Marathon before the Senior Games. Most of them had chronic or recent injuries from their last event or from their training. There was a sense of pride among them as though they had done something to prove something about themselves. Perhaps, but there are other goals one could have that are more heathful and fulfilling. Not one of them looked really fit or healthy. Most said they had formerly been sedentary and wanted to get up and show they still had it. A few had been doing it for many years; they really looked bad, wrinkled and skinny with no muscle and poor posture. Only a few natural runners looked OK.

I told them of the risks versus benefits of marathoning and all were astonished and in total denial. I sent them to this site and told them to look for a reprise of this old post. So, here it is. Let the complaints begin.

With my apologies to David Letterman, here are the top ten reasons not to run marathons.

10. Marathon running damages the liver and gall bladder and alters biochemical markers adversely. HDL is lowered, LDL is increased, Red blood cell counts and white blood cell counts fall. The liver is damaged and gall bladder function is decreased. Testosterone decreases.

From Wu, Worl J Gastroenterol. 2004 Sep 15: 10 (18): 2711-4, “RESULTS: Total bilirubin (BIL-T), direct bilirubin (BIL-D), alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) increased statistically significantly (P<0.05) the race. Significant declines (P<0.05) in red blood cell (RBC), hemoglobin (Hb) and hematocrit (Hct) were detected two days and nine days d after the race. 2 d after the race, total protein (TP), concentration of albumin and globulin decreased significantly. While BIL, BIL-D and ALP recovered to their original levels. High-density lipoprotein cholesterol (HDL-C) remained unchanged immediately after the race, but it was significantly decreased on the second and ninth days after the race. CONCLUSION: Ultra-marathon running is associated with a wide range of significant changes in hematological parameters, several of which are injury related. To provide appropriate health care and intervention, the man who receives athletes on high frequent training program high intensity training programs must monitor their liver and gallbladder function.”

9. Marathon running causes acute and severe muscle damage. Repetitive injury causes infiltration of collagen (connective tissue) into muscle fibers.

From Warhol et al Am J Pathol. 1985 Feb: 118 (2): 331-9, “Muscle from runners showed post-race ultrastructural changes of focal fiber injury and repair: intra- and extracellular edema with endothelial injury; myofibrillar lysis, dilation and disruption of the T-tubule system, and focal mitochondrial degeneration without inflammatory infiltrate (1-3 days). The mitochondrial and myofibrillar damage showed progressive repair by 3-4 weeks. Late biopsies showed central nuclei and satellite cells characteristic of the regenerative response (8-12 weeks). Muscle from veteran runners showed intercellular collagen deposition suggestive of a fibrotic response to repetitive injury. Control tissue from nonrunners showed none of these findings.”
8. Marathon running induces kidney disfunction (renal abnormalities).

From Neyiackas and Bauer, South Med J. 1981 Dec; 74 (12): 1457-60, “All postrace urinalyses were grossly abnormal…We conclude that renal function abnormalities occur in marathon runners and that the severity of the abnormality is temperature-dependent.”

7. Marathon running causes acute microthrombosis in the vascular system.

From Fagerhol et al Scan J Clin Invest. 2005; 65 (3): 211-20, “During the marathon, half-marathon, the 30-km run, the ranger-training course and the VO2max exercise, calprotectin levels increased 96.3-fold, 13.3-fold, 20.1-fold, 7.5-fold and 3.4-fold, respectively. These changes may reflect damage to the tissues or vascular endothelium, causing microthrombi with subsequent activation of neutrophils.”
6. Marathon running elevates markers of cancer. S100beta is one of these markers. Tumor necrosis factor, TNF-alpha, is another.

From Deichmann et al in Melanoma Res. 2001 June; 11 (3): 291-6. “In metastatic melanoma S100beta as well as melanoma inhibitory activity (MIA) are elevated in the serum in the majority of patients. Elevation has been found to correlate with shorter survival, and changes in these parameters in the serum during therapy were recently reported to predict therapeutic outcome in advanced disease.”

From Santos et al Life Sci. 2004 September: 75 (16): 1917:24, “After the test (a 30km run), athletes from the control group presented an increase in plasma CK (4.4-fold), LDH (43%), PGE2 6.6-fold) and TNF-alpha (2.34-fold) concentrations, indicating a high level of cell injury and inflammation.”

5. Marathon running damages your brain. The damage resembles acute brain trauma. Marathon runners have elevated S100beta, a marker of brain damage and blood brain barrier disfunction. There is S100beta again, a marker of cancer and of brain damage.
From Marchi, et al Restor Neurol Neurosci, 2003; 21 (3-4): 109-21, “S100beta in serum is an early marker of BBB openings that may precede neuronal damage and may influence therapeutic strategies. Secondary, massive elevations in S100beta are indicators of prior brain damage and bear clinical significance as predictors of poor outcome or diagnostic means to differentiate extensive damage from minor, transient impairment.”  Other studies indicate confusion in post-event marathon runners.
4. Marathons damage your heart.

From Whyte, et al Med Sci Sports Ecerc, 2001 May, 33 (5) 850-1, “Echocardiographic studies report cardiac dysfunction following ultra-endurance exercise in trained individuals. Ironman and half-Ironman competition resulted in reversible abnormalities in resting left ventricular diastolic and systolic function. Results suggest that myocardial damage may be, in part, responsible for cardiac dysfunction, although the mechanisms responsible for this cardiac damage remain to be fully elucidated.”
3. Endurance athletes have more spine degeneration.

From Schmitt et al Int J Sports Med. 2005 Jul; 26 (6): 457-63, “The aim of this study was to assess bone mineral density (BMD) and degenerative changes in the lumbar spine in male former elite athletes participating in different track and field disciplines and to determine the influence of body composition and degenerative changes on BMD. One hundred and fifty-nine former male elite athletes (40 throwers, 97 jumpers, 22 endurance athletes) were studied. …Throwers had a higher body mass index than jumpers and endurance athletes. Throwers and jumpers had higher BMD (T-LWS) than endurance athletes. Bivariate analysis revealed a negative correlation of BMD (T-score) with age and a positive correlation with BMD and Kellgren score (p < 0.05). Even after multiple adjustment for confounders lumbar spine BMD is significantly higher in throwers, pole vaulters, and long- and triple jumpers than in marathon athletes.”

The number two reason not to run marathons.

2. At least four particiants of the Boston Marathon have died of brain cancer in the past 10 years. Purely anecdotal, but consistent with the elevated S100beta counts and TKN-alpha measures. Perhaps also connected to the microthrombi of the endothelium found in marathoners. [Sterling Advice note: 15,000 cases per year in U.S. general population and 10,000 deaths (.0200%) .  4 deaths in Boston Marathoners per 20,000 participants (.0033%).]

And now ladies and gentlemen the number one reason not to run marathons,

1. The first marathon runner, Phidippides, collapsed and died at the finish of his race. [ Jaworski, Curr Sports Med Rep. 1005 June; 4 (3), 137-43.]

Now there is a recommendation for a healthy activity. The original participant died in the event. But, this is not quite so unusual; many of the running and nutritional gurus of the past decade or two died rather young. Pritikin, Sheehy, Fixx, and Atkins, among many other originators of “healthy” practices died at comparatively young ages. Jack LaLanne, the only well-known guru to advocate body building, will outlive us all.

This got me thinking...

Compare a marathoner to a sprinter.  What would you rather look like?  Would you rather look and be healthy and strong OR unhealthy and weak?

Sprinting: An Examination, by Chris Clancey aka Loki

You don’t run against a bloody stop watch, do you hear? A runner runs against himself, against the best that’s in him. Not against a dead thing of wheels and pulleys. That’s the way to be great, running against yourself-- against all the rotten mess in the world; against God, if you’re good enough..." -Wlliam Persons
If you were to ask me to pick one form of exercise and say that—for as long as I lived, for the remainder of my days—I could do as much of it as I wanted, whenever I wanted, but could never work out any other way, why, I’d look you right in the face and say "sex." But then you’d probably say sex doesn’t count, and that it’s not a valid form of exercise, to which I’d probably reply "oh the hell it ain’t," and then we’d probably end up getting into a really long, heated argument about it. But—as a fictional hypothetical—let’s assume you win that dispute, and force me to pick again. Well if that were the case, it wouldn’t take me long to reply "sprinting," because—deep down—I’d know I made the right choice.
Of course I’m being slightly facetious, but I think I may have also piqued a few people’s interest. Especially those of you who typically scoff at HIIT, run six-day weight splits, and haven’t done cardio since the Presidential Physical Fitness Test’s timed mile back in middle school. Think about it. I, of all people, have one of the most unhealthy, obsessive fixations on being supra-physiologically ripped and cut. "And yet even in spite of this Loki," you ask, "you would be willing to leave the iron behind for all eternity?" Yup. Because if I knew I could sprint whenever and however it pleased me, I know I’d be juuuuuuust fine—maybe not all that big, but fine (perhaps even "damn-fine").
Sprinting: The Courvoisier of Cardio
When it comes to cutting you up and promoting a nutrient-partitioning milieu conducive to building and maintaining a lean, muscular physique, sprinting simply cannot be beat. A simple look at competitive athletics demonstrates this pretty clearly. And I am NOT even talking about PRO-athletics, a world rife with performance-enhancing-drug-using, one-and-a-million-gene-possessing individuals who are able to log hours of gym-time every day while being tended to by a virtual cadre of trainers, coaches, dieticians and sports-specialists. No, instead just think back to your high-school days (unless you were home-schooled, in which case may someone have mercy on your sad, coddled soul, because you’re just going to have to skip a few sentences).
Okay, now—mild genetic-selectivity aside—who were the most ripped (re: lowest amount of bodyfat relative to the amount of lean body mass carried) guys on your football team? The running backs, wide receivers and defensive backs, right? Track team? Jumpers and guys who ran events 400m and shorter. Basketball team guards? Almost none of the guys or girls whose athletic lively-hoods depended on their being able to sprint at maximal or near-maximal speed (causing them to thereby hone their anaerobic threshold in the process) ever had an appreciable amount of bodyfat on their frames during their playing days.

Most folks (while speeding by the track on the way to the weight-room) still mistakenly attribute this phenomenon to simple ‘ectomorphism.’ Well I, Loki, shall not tolerate it any longer, and that is why I have come to preach the gospel of "going really fast with your feet." The fact of the matter is, those kids’ physiques may have been influenced by ‘ectomorphism,’ but they were influenced a whole helluva’ lot more by "the big A’s" when it comes to nutrient-partitioning, fat oxidation, and physique-augmentation—5’-AMP-mediated protein kinase (AMPk), acetyl-CoA carboxylase (ACC), and ADP: ATP (adenosine di- and tri- phosphate, respectively) cellular ratios.

The fact of the matter is, unless you simply happen to be the most inept Google-user on God’s green Earth, if you’re reading this article, you care about exercise and how you look. And if you care about either (and hopefully both), then you should make sure you save some room in that split of yours for some sprint work. Because ‘booking it big-time’—be it on a track, in a park, in your yard, or from ‘the 5-0’—will do more to develop your aesthetic and anaerobic capacities than anything else out there.

Trying to lose fat? You should be sprinting. Trying to gain lean mass? You should be sprinting. Trying to defy conventional established wisdom and be really badass and do both simultaneously in an effort to ‘recomp?’ Then you damn-sure NEED to be sprinting. And a look at the physiological effects and adaptations elicited by consistent (and possibly even infrequent) sprint-sessions, which I shall now share with you… will make things abundantly clear.

Getting "Sciency & Shiznit" With Cellular Basics

By now, AMPk has pretty much been discussed to death around these parts. Nonetheless, for those needing a refresher or for anyone else out there who is still having trouble putting together all the pieces of the big picture, I’m going to break it down for you. But before we get to the current enzymatic "it-kinase" in the world of bodybuilding, let’s first lay some groundwork by examining how our (muscular) energy metabolism works during a maximal or near-maximal effort sprint; a scenario which creates a perpetual, unsustainably-intensive demand for anaerobic energy and substrate from start to finish.

Your sprint begins obviously when the little voice in your head communicates to you it’s time to move, which tells your muscle cells to begin to rapidly trigger muscle cell activity (contraction) following cellular "excitation." This is a process linked via the second-messenger signal coming from transferred calcium ions (Ca ++) (1). When you begin to run, you may think your legs are just "pushing off." But what’s simultaneously (or nearly-simultaneously) occurring in every muscle-fiber that the sprint is going to recruit, is a vast, intricate force-generating process taking place in your sarcomeres. Sarcomeres are the functional portions of a myofibril, the microscopic contractile protein which—when arranged alongside other myofibrils in ‘tubes’—forms the structural back-bone of your body’s skeletal muscle fibers (1, 2).

I know for a fact I just confused somebody out there, so allow me to run it back right quick: muscles are made of lots of muscle fibers, which, as cells in your body go, are generally ‘hyooge.’ I mean, we’re talking some inherently swole little cells here. So swole, in fact, that they are multinucleate (re: multiple nucleuses) and also jam-packed with their own cellular beefiness. These long, aligned tubes of myrofibrils house the sarcomeres that internally generate the molecular force that enables you to lift the barbells, hippies, and shirts off members of the opposite sex whom you encounter in your day-to-day life.

So we’ve established that your muscles have received the "run, muf[*#$&*#!]a’!!!" signal from your brain, and its time for your sarcomeres to show the goods and begin powering your muscles. Now how this actually occurs is via a reaction that incorporates two different types of cellular filaments (‘thick’ myosins and ‘thin’ actins) which are going to bind to one other in a process called cross-bridging, where the head of the myosin binds to the actin and the filaments pull across each other (1). Movement, tension, force, bingo—your muscles are now open for business.

And really, in essence, at the molecular-basis-of-motion-core of muscle contractions, it’s really just thousands upon thousands of these two tiny filaments binding and pulling inside your sarcomeres which end up getting the ball (and your entire body shortly thereafter) rolling (2). Yeah, there’s more to it. Trust me—if you don't already have it, you should still have a solid enough grasp of the basics to be able to follow me through the rest of the article. In fact, you can start rocking your thinking caps with a trucker-tilt for all I care, because we’re about to jump back into familiar territory…

Love Don’t Cost a Thing, But Anaerobic Expenditure Sure Does…

"Houston, we have cross-bridging." Since each cycle of myosin-actin binding (and subsequent filament ‘bump-n’-grind’ that follows) involves the hydrolysis (re: breakdown) of one molecule of our good ole’ anaerobic fuel-friend ATP (adenosine tri-phosphate), this also now means that we gon’ be expending some energy. As most of you are already aware, hydrolysis is a process that results in the cleaving (off) of a phosphate, which produces ADP+Pi (adenosine di-phosphate and an additional, high-energy ‘free’ phosphate group) (3). Here is another important thing to keep in mind: despite the fact that ATP availability is essentially the rate-limiting factor for muscle contraction, the actual amount of ATP that your muscles naturally store is relatively modest (hence the reason why creatine is such a good training adjunct) (3).

It’s All About Gettin’ AMPed Up

Sprinting, however—due to the extreme nature of the muscular recruitment and activity needed to power it—takes these energy-currency transactions that are occurring in your muscles even further. By going from a resting state to full-blown, maximal anaerobic exertion in a mere second or two, the cellular demand for ATP & phosphates skyrockets, not only causing ATP molecules to become hydrolyzed into ADP, but also causing a high number of ADP molecules to become further hydrolyzed into AMP (+Pi ) molecules with only a single phosphate left over (4). Once again, due to the massive "about-face" your system has just undergone, neither glycogen nor oxidative phosphorylation can provide enough phosphates to get you off and sprinting without leaving AMP levels ramped way the hell high.

As a result, the first several seconds of every full-out sprint are going to have a tremendously significant effect on the cellular energy environment in the vast majority of your skeletal muscle, a milieu which your body detects, and (shout out to Charles Darwin) has evolved adaptive response mechanisms. One of the most critical of these mechanisms, especially when it comes to actually shifting a large portion of the activity in your body involving glucose and fatty-acid metabolism, is AMPk. Aaaaaching!!! [Authors note: Justin, please cue gratuitously inappropriate imaginary cash-register sound…now.]

It should hopefully be evident by this point that since AMPk is activated in an intensity-dependent manner in response to increased cellular creatine hosphocreatine (PCr) and AMP:ATP ratios, in terms of effectively achieving significant and systemic AMPk activation, sprinting really is king in spades [Author’s note: for those who have recently suffered an injury and/or regularly experience joint and ligament problems, both high-intensity swimming and iron or clean cardio can be utilized as serviceable HII alternates to replace sprint work in your split that will achieve similar effects on cellular energy state signaling](5,). It’s also the adaptive nature of AMPk-activity that makes it such a potent phenotype-augmenting force. While it generally remains inactive as a substrate-source shifter during periods of high intensity exercise due to the spikes and dips in cellular Ph that accompany rapid PCr/ATP turnover, during the post-workout period this little kinase immediately begins to pull every enzymatic trick up its sleeve. It does this in an attempt to simultaneously replenish, bolster, AND protect your muscle cells so that they’ll be better able to respond to future situations that require similarly high degrees of rapid fuel and substrate turnover (7).
If You’re Consistently on the Track, You’re on Track; It’s Just That Simple…

It’s my firm belief that if your primary motivation for training is to optimize your aesthetic appearance and you’re still shirking sprint-work, you’re doing yourself and your split a disservice. Even with all the research that has emerged recently regarding the positive effects of AMPK on GLUT-4 translocation, mitochondrial size and density, and fatty acid metabolism, a large percentage of bodybuilders still cling to the misconceived notion that HIIT is detrimental to anabolism or outright catabolic. Or that simply lifting regularly will bestow the same adaptive benefits as sprint-work, making it an unnecessary and awkward component to try to fit into a multiple-session per week training split.

But the fact of the matter is, unless you repeatedly incorporate Olympic lifts, extended drop-sets, incomplete rest intervals, and/or rest-pause sets in the gym, you are simply NOT getting the same immeasurably positive adaptive benefits as you could be reaping if from HIIT. But what if you are one of "those" lifters, a 100% pure branded beef barbell buster who can stay classically-chiseled like Adonis just doing swiss-ball crunches, and yet still insists on bracketing strip-set power snatches with power cleans? Okay, fair enough. If that’s the case, I’m willing to grant you the ever-coveted "Kansas school-board exemption," so you can ignore my dangerous thinking.

HOWEVER, for all you who have chosen to remain card-carrying members of the HIIT Haters Club because "Siff never really mentioned sprinting," I strongly urge you to reconsider your stance. If not from the substrate usage-shifting angle, perhaps you should reconsider it from a simple volume and recovery one. Yeah, I admit: I'm biased. I was a track kid in high-school. In fact, track is the sport that got me lifting weights to begin with. As a result, sprinting and strength-training have long remained closely-linked in my mind. Now, my hope is that I can forge a similar sort of associative intimacy in yours.

Try as you might, unless your God-given physical and neural recovery abilities far exceed that of 99.9% of healthy, fit individuals or you’re willing to perpetually run massive doses of steroidal and non-steroidal supplemental ancillaries, you really should only be doing 3-4 strength-training sessions per week (note: there are exceptions to this of course, but as a subjective generalization I find that this contention holds up quite well in vivo). Too much more volume than that and chances are, you’re unnecessarily taxing your CNS—if not your basic energy and recovery reserves themselves. And it’s here where I feel HIIT really shines, because sprint-workouts can be added to a three/four day split to augment anabolism and nutrient partitioning without leaving a trainee overly drained or unable to recover in between workouts (assuming proper pre- and post-workout nutritional principles are adhered to, of course).

Furthermore, sprinting likely has the potential to induce enough mild muscular-hypertrophy across nearly all lower and upper-body muscle-groups that—provided one is in a state of positive energy-balance—it can further stimulate skeletal muscular anabolism without overly (and adversely) influencing mTOR-mediated protein synthesis or creating the same type of DOMS after-effects that most conventional weight-oriented hypertrophy programs will (8). And all these numerous boons can be reaped from a workout that need not span any more than twenty or thirty minutes—most of which will be taken up by low-impact, low-exertion recovery intervals in between sprints.

Finally, sprinting is also tremendously effective at simultaneously improving one’s aerobic and anaerobic cardiovascular (to differing degrees, depending on the type of sprint(s) used and format of the workout) capacities. This may also be able to improve weight-workout performance by increasing a trainee’s respiratory VO2 uptake (and subsequent ability of his/her mitochondria to draw in greater amounts of oxygen on the cellular level) during periods of exertion. This in turn enables his/her muscles to work more efficiently even in the face of high blood lactate (re: acidic) levels (9,10).

Let the Laundry-Listing of Benefits Begin!!!

I know I dragged you through a lot just now, and I apologize. Nonetheless, all of this only goes to show just how silly-useful HIIT training can be for the bodybuilder, especially when you consider the fact that even my overly-verbose ass and sesquipedalian semantics can’t adequately summarize all the positive effects of sprinting even when given several pages to do so. So, without further adieu here’s how sprinting will definitively aid your bodybuilding and athletic efforts:

1. Harmer et al. demonstrated that seven weeks of sprint training (3 sessions per/week) enhanced maximal sprint-peak power, lengthened time to exhaustion at maximal sprint-exertion, lowered blood-pressure, and increased incremental VO2 peak during exertion in healthy male subjects as a result of increased glycolytic and oxidative enzyme activity (11)

2. Sprint-training directly augments full-body glycogen storage-potential via cellular and enzymatic mechanisms while increasing GLUT4 translocation (and subsequently insulin-stimulated glucose transport) in large systems of both lower and upper-body skeletal muscle (12,13). In addition, repeated bouts of sprint-like exertion will generate higher levels of nuclear respiratory factor-1 (NRF-1) synthesis in muscle too (14). All told, sprint-training literally makes you more carb-sensitive in regards to your daily glucose intake, ensuring that more of carbs will be partitioned and stored in your muscles.

3. In fact, sprinting is quite likely the single most effective form of exercise in terms of increasing NRF-1 binding activity in skeletal muscle (5, 6, 14, and 15). What’s so great about NRF-1 (or maybe it’s just "what the hell is NRF-1")? Allow me to explain then. Essentially, NRF-1 is a transcription factor protein that acts on nuclear genes by encoding respiratory subunits and creating components of the cellular machinery that actually transcribe and replicate mitochondria (14, 15).

[/list]NRF-1, in conjunction with NRF-2 and peroxisome proliferator activated receptor co-activator 1alpha (PCG-1) basically work together to provide your muscles with the stimuli for adaptive cellular overhauls in response to exercise by promoting mitochondrial biogenesis so that your skeletal muscle contains not only more mitochondria, but also larger mitochondria (16). This obviously has tremendous ramifications for nutrient partitioning. First and foremost is the fact that larger mitochondrial surface area means more CPT availability. Another is that increased PCG-1 activity means that PPAR activation in the peroxisomes is also being positively augmented (17).

4. Hopefully, even those of you with no intellectual ambitions when it comes to cellular biology can see from the above that sprint-training has tremendously positive ramifications for fat-burning, both directly and indirectly. For one, AMPk activation promotes fatty-acid oxidation by inhibiting acetyl-CoA carboxylase (ACC) levels which is a key enzymatic player when it comes to synthesizing malonyl-CoA, the coenzyme which deactivates CPT in the mitochondria (18,19,20). So through sprint-training, we basically create a metabolic scenario allowing us to "run the gamut" on fat-oxidation.

[/list]We activate AMPk to reduce ACC activity in order to naturally optimize CPT-assisted mitochondrial FFA-oxidation as best we can, while simultaneously stimulating mitochondrial biogenesis, which gives us more mitochondria with more CPT to work with, allowing for an even greater rate of FFA-oxidation. But wait, it gets even better. As I just mentioned a few sentences back, sprinting also provides us with that spike in PCG-1 activity which—although relatively transient—will further potentiate glucose and FFA oxidation in the peroxisomes (17).

At the same time, it is highly probable that sprinting-evoked, systemic AMPk activation simultaneously curtails an individual’s natural genetic propensity for fat-storage as well. This is because, in response to the rapid ATP-depletion prompted by those repeated, maximal-intensity bouts of anaerobic expenditure, AMPk also works to curtail Acyl-coenzyme A: diacylglycerol acyltransferase (DGAT1) activity and glucose uptake into adipocytes. This saves ATP for energy repletion rather than having it be "misallocated" to synthesize new triacylglycerol (TAG) in your adipocytes (21, 22, 23). I desperately want to write something witty here, but—to be perfectly honest—the above dynamic still strikes me as so miraculous that it generally tends to leave me at a loss for words whenever I go back and re-conceptualize it. But, trust me, it’s "pretty good" to have this going on, which just goes to show how potent a physique-shaping force sprinting can be when it comes to furthering your bodybuilding goals.
Unfortunately, due to space constraints, that’s going to have to do it for this installment of sprinting examined "Avant-style." In next issue’s Part II, I’ll be returning to take a look at sprint technique and methodology, different strategies for incorporating sprint-work into your lifting split, and also harkening on emerging aesthetic trends in the realm of contemporary bonsai-gardening. Or maybe I’ll just throw in a few supplement recommendations. I don’t know; I’m still a little undecided on that last part. But until then, I’m off to the races, off with the hope that you’ll all soon follow. Cheers all.

Part II

"The trouble with jogging is that the ice falls out of your glass" - Martin Mull

Admit it. It’s kind of refreshing isn’t it? The wind whipping against you as each muscle group works in swift synergy while you power along like some kid who just knocked off a 7-11. Sure, there’s the burn deep down in your lungs and the inevitable fatigue that even the best of us occasionally succumb to during our more difficult roadwork sessions, but there’s also quite a bit of gain to be derived from that pain, especially when you really start getting it all shored down—the integrated, sprint-incorporating split, the proper form and technique, and the right strategies and techniques for reaping the most out of your sprint sessions.

So what am I, Loki, going to contribute to the vast wealth of sprint savvy, sagacity, and know-how already out and about in various training circles, methodologies, and programs? Yeah. So…how ‘bout them Sox? But with all seriousness, what I’m looking to do with this sequel of sorts is incorporate several different proximate bodies of theory involving sprinting and sprint-training into a single, comprehensive ‘Sprinting how-to’ for the bodybuilder and/or fitness-minded reader. So without further ado, let’s get this bad-boy off and running.

Finding Your Ying Yang with tha’ Sprint Thang

Now this is where it gets tricky. On one hand, improving mobility, flexibility, and anaerobic endurance threshold will obviously improve one’s sprinting. However, since we’re using sprinting as one of several different interrelated means to an end, we need to strike a delicate balance between honing our sprinting abilities in said specific mean without diminishing ourselves in other areas which might ultimately hinder our progression toward that oh-so-money end (re: “being swole”).

But as I said before, there’s a little more to it than simply going out, hauling ass ‘til hyperventilation sets in, and then stopping for a bit to breath into a paper baggy. So let’s break it down.

Sprinting with an Emphasis on Fat Loss

As I demonstrated in Part I, pretty much any form of consistent sprint training will result in adaptive modifications to skeletal muscular metabolism which will promote fatty-acid oxidation and favorable nutrient partitioning. Yeah, “sprinting good for fat loss”—big surprise, I know. So we’re going to mold a little meat onto the maxim, because honestly, we know a bit more than that—and we can do better.

First off, different diets and training regimens work for different people, with each offering its own benefits and shortcomings. Unfortunately, this also means I really can’t make ‘blanket’ recommendations regarding sprint training, because a drug-free carb cycling dieter and a steroid using HST dieter have far different parameters and potential for incorporating sprint work into their split. Even two ‘regular dieters’ would have far different capacities for sprint work if one was doing a ketogenic diet and the second a high carb, low fat diet.

Still, for the sake of this article not deforesting a small South American province every time somebody goes to print a copy, I’m essentially going to assume you are either:

A) Following a cyclical diet with periods of low or no carbs interspersed with infrequent, planned carbohydrate over-feedings, refeeds or carb-ups.

B) Following a traditional high-protein, moderate carb, roughly isocaloric, reduced calorie diet.

For a genetically average drug-free athlete looking to lose weight who is already strength training three to four times per week, you should really be performing two (perhaps only one; three if you’re really willing to push it) HIIT sessions in a given seven day split. Personally, I feel one session should involve shorter, repetitive interval sprinting at 90-95% intensity with a work : rest ratio of somewhere between 1:2 and 1:5, depending on trained state. This could be as simple as 10-15 second (or 80-100m) sprints performed 8-12 times, with walk or jog recovery. This weekly session will prompt high levels of AMPk activation (especially throughout the lower body) to optimize cellular and enzymatic activity conducive to fat-burning, and also stimulate more long-term augmentative adaptations in terms of mitochondrial biogenesis and glycogen-storage potential.

For our second session, we’re going to lengthen our intervals while slightly decreasing work intensity so that we’re performing our intervals at about 85%-90% of VO2max/perceived maximum potential exertion. These are anaerobic-glycolytic sprints, 200-400m in length. Aim to keep rest intervals between 1-2 minutes.

Note: I’m just going to come right out and say that 400m should be considered significantly superior in efficacy compared to 200m sprints, but be forewarned, doing 400m repeats is kind of like taking a caning to the lungs, so I’d much rather you train at your own initial fitness level rather than prefontaining yourself into the ER on the first day of your diet.

‘Wait,’ I’m sure some of you are asking; ‘didn’t you just say a few issues back that virtually all cellular AMPk signaling is triggered in response to the first few seconds of the sprint? Why in god’s name would I want to keep going for that long?’ Well mi amigo, the answer is quite simple. Sprint-induced AMPk activation triggers a lot of fat-burning; sprint-induced AMPk activation in glycogen depleted or semi glycogen depleted states triggers significantly more.

In fact, it has been conclusively demonstrated that systemic fat oxidation increases both at rest and during aerobic exercise when muscle glycogen stores (termed glucosyl units or GUs) dip below roughly 70 mmol/kg (1, 2). Now, average resting muscle glycogen stores in active individuals typically range from 100 to as high as 130 mmol/kg in elite athletes (1, 2). But if you’re sprint training—particularly while following a reduced carbohydrate diet, the sub-70 mmol/kg level can be reached and depleted quite quickly. And it’s here, with this readily available two-pronged anaerobic training punch, that we can really get lipolysis and FFA-oxidation soaring. This is achieved by getting both anaerobic energy-metabolism adaptation and widespread glycogen depletion in tandem.

There’s our window. Now let’s try to exploit it with some research and precision. Studies have looked at glycolysis rates in human skeletal muscle in response to moderate to high intensity sprint exercise (~95% of VO2Max). Those studies have basically established that the net or average glycogen breakdown in response to a moderate sprint is generally ~ 4.3 mmol/kg per minute of activity, which is roughly equivalent to running a single fast quarter mile (400m) (3).

Another study, this time using a group of hockey players, found that performing ten 60-second speed skating intervals at 120% of VO2Max resulted in the depletion of almost 60% of glycogen stored in the vastus lateralis portion of the quadriceps, with other leg muscles showing similar rates of depletion (4). The researchers who ran the study noted that the hockey players who performed the interval sessions showed levels of glycogen depletion that were highly analogous to levels of depletion seen in the leg muscles of cyclists who performed similar sprint intervals. Finally, a third study that examined quadriceps glycogen depletion patterns following 30 second maximal effort treadmill sprints found that a single, full-on sprint resulted in an on-average degradation of 24% of vastus lateralis glycogen stores (5).

Now obviously, sprinting hits the legs hardest, which means glycogen stores are going to be taxed disproportionately in the quadriceps, hamstrings, and calves in proportion to the degree of upper-body muscle recruitment. So for athletes looking to deplete glycogen stores below 70 mmol/kg, one option—albeit not a fun one—would be to substitute lower-body depletion lifting for the two above recommended sprint sessions. This would then allow for the athlete to reap the additional metabolic benefits of sprint training in addition to achieving the desired level of lower-body depletion.

Even if depletion isn’t your primary goal, as a dieter you should still be actively looking to get glycogen stores below that 70 mmol/kg threshold, as it will augment FFA oxidation levels on a twenty-four hour basis and amplify the amount of fat you can burn during your lower-intensity aerobic cardio sessions. Few things facilitate the above like sprint training. Now, couple this with all the adaptive cellular responses elicited by sprint work, and I think it’s clear why sprinting is the gold medal standard of fat-loss cardio.

Tremblay et al, in their 1994 study “Impact of exercise intensity on body fatness and skeletal muscle metabolism” noted that fifteen weeks of HIIT training resulted in a significantly more pronounced reduction in subcutaneous adiposity compared to the ET (‘endurance training’) control group despite its lower energy cost (6). In fact, “when corrected for the energy cost of training, the decrease in the sum of six subcutaneous skin folds induced by the HIIT program was nine fold greater than by the ET program” (6).

However, most dieters (especially those looking to lose weight without the assistance of anabolic and/or anti-catabolic drugs) need to keep in mind that leg training volume must[/i] be reduced to accommodate for potential sprint-induced wear-and-tear to the legs. I think a balanced max for leg volume is two intensive sprint sessions and two bouts of lower-body strength work (with weights heavy and working sets in the 3-6 rep range) per week. Yes, even a lot of you natural trainees could probably get away with more, but I see no need for them to.

Sprinting with an Emphasis on Nutrient Partitioning

Ah yes, the other side of the coin: the guy looking to pack on quality mass without tacking on a subcutaneous spare tire in the process. Fret not: the puissant partitioning benefits sprint training bestows can be of use to you as well. Feel free to ‘verbally Falluja’ me all the live-long day because I’m going to say it again: I strongly encourage natural bodybuilders on a mass phase to incorporate HIIT sprinting into their splits.

Last time I checked, being willing to include a few short, strategic sprint-sessions into your weekly training allotment while hypercaloric tends to lead to the development of a leaner, faster, and stronger athlete. Here, just as with cutting, it’s all about priorities. In this instance, we’re trying to foster anabolism, which means we don’twant an energy deficit. Quite the contrary. We want to pack in calories (and likely, in conjunction, carbohydrates) to provide enough energy to build on growth stimuli while keeping intramuscular glycogen stores relatively full. Yup, the tried-and-true recipe for growth.

But then let me ask all you ‘natural’ lifters out there: when was the last time you bulked and managed to build all of that bulk above the belt? Yeah, exactly—for a good 98% of you, some of that Weight gainer Uber-Zeros also ended up adding some size to your ass, which is why even you had to suck up a few weeks of eating salads and suffering the ignominy of having to make the walk of shame out of GNC with a shopping bag full of “new-and-improved HydroxyClenaphrine.”

Oh, but [*#$&*#!] sprinting. I mean, all it does is elevate intramuscular glycogen storage potential, increase insulin-stimulated glucose transport and carb tolerance. It also elevates FFA oxidation levels, partitions a higher percentage of ingested calories towards muscle, and curtails fat gain by downgrading DGAT1 activity and glucose uptake into adipocytes. This allows ATP to be saved for energy repletion rather than be “misallocated” to synthesize new triacylglycerol (TAG) in your adipocytes.

And I mean, what a joke: a few 100m repeat sprints with full recovery will only minimize anaerobic glycolysis, burn maybe two or three hundred calories max, and generate the AMPk activation that gets the ball rolling on all of the above, leaving you free the rest of your day off to eat and grow in the good places while your body tells your fat-deposits they’re going to “get nothing and like it.” Oh, and lest I forget to mention—unlike our poor cutter, we’ve got a caloric surplus going on, which means recovery from said sprint-session(s) is(/are) going to end up being heightened in addition to work capacity. Sure, I suppose that AMPk is going to result in a minor reduction in protein synthesis that might slow gains transiently. But I have still yet to see a well articulated argument as to why this isn’t an infinitely worthwhile tradeoff.

Look, you can scream ‘neural fatigue’ or ‘distended tendon’ all you want, but the fact of the matter is this: if you’re looking for convenient methods to significantly augment nutrient partitioning you can either a.) Use draconian nutrient manipulation schemes (oh, wait, I said ‘convenient,’ didn’t I. Whoops…), b.) Take drugs, or c.) Exercise more. Let’s go with option “C.” And nothing gives you the same kind of bang for your buck as sprinting. 10-20 minutes. You’re training your whole body. You’re training your body in ways that are almost impossible to duplicate in the weight room, no matter how much iron you try to hoist. Do I really need to keep saying this???

Bulkers, you want to keep your sprints and sprint volume short. 100m maximum in terms of distance; 10 intervals at most per session. Really, you should be doing 6-10 sprints with full recovery two to three times per week, using proper workout nutrition protocol. This is nothing new and this isn’t rocket science. If you cater to the above, you should have no problems with recovery, injury or overtraining.

There are as many reasons for running as there are days in the year, years in my life. But mostly I run because I am an animal and a child, an artist and a saint. So, too, are you. Find your own play, your own self-renewing compulsion, and you will become the person you are meant to be…" - George Sheehan


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