Home Posts tagged "Rugged Magazine" (Page 2)

Ask EC: Installment 1

By Eric Cressey

Q: I know that you're a proponent of DB Isometric Split Squats for extended periods of time. I can only manage 15 seconds on both legs with no weights. I feel that this is pretty pathetic in light of my performance on other exercises, which tends to be quite good. So, to get that time up more and to start using weights, should I simply hold the position as long as I can and look to get up to 60 seconds? Or would I be better off doing ski-squats against the wall more often until the hold strength builds up?

Also, when I'm doing the exercise, I feel the exercise more in the elevated leg in the quads. It's not up that high ,but I am sinking pretty low to get the required angle. I'm 6' 2". A: Definitely stick with the Bulgarian EQIs; your endurance will pick up in no time. Remember, although muscular endurance is an added bonus of the exercises, this is more about working on active flexibility. I work with several guys each week that are 7-feet tall or very close to it, and they can all get it done; at 6-2, you shouldn't have a problem once you find the right position. You should feel it in your hip flexors on the elevated leg; if you're feeling it in the quad of that leg, it means that you're exerting too much force on the foot on the bench instead of allowing your hips to sink down while keep the back leg extended (or close to it). Drive your front heel into the ground and contract your glutes hard, pulling the chest up and shoulder blades back and down. Make sure that your knee is directly above your foot and your weight is on the heel. Q: Thanks to your advice on taking care of primary subacromial impingement, my pain is gone and I'm ready to get back to work on my pressing strength. I'm not sure how to reintegrate benching and overhead pressing. I definitely don't want to reaggravate the injury; any suggestions? A: You're correct that it isn't a good idea to jump right back into things with full range of motion and loading. I favor the following progession (although slight medications in rapidity of progression are always made based on symptoms): Body Weight Push-up > Weighted Push-up > Cable Crossover from Low Pulley > Cable Crossover from Hip Height > Neutral Grip DB Floor Press > Neutral Grip Decline DB Press > Pronated Grip Decline DB Press > Barbell Floor Press > Decline Barbell Press > Flat DB Press > Incline DB Press > Barbell Bench Press > Barbell Incline Press > DB Military Press > Barbell Military Press/Push Press > Behind the Neck Presses Note: Some trainees don't even need to go as far as the end, as the cost:benefit ratio for loaded behind-the-neck exercises is way out of whack for some people post-injury. The rationale for these progressions are: a) The scapular and humeral stabilizers are most effective in closed chain positions.(justifying the push up). b) Impingement symptoms are most likely to be aggravated with flexion and/or abduction of the humerus beyond 90-degrees. c) Traction (pulling the humeral head away from the glenoid fossa, as with a cable crossover) is less traumatic to the previously injured muscles than approximation (forcing the humeral head into the fossa). d) Internal rotation (as seen with pronated grips) mechanically decreases the subacromial space, increasing the risk of re-injury.

With this progression, I like to start recovering trainees off with long eccentrics in the 6-8 rep ranges. In many cases, high-speed movements like speed benches and push jerks can be the most problematic, so I avoid these early on. It's important to pay attention to not only how the shoulder feels during the exercise, but also what you feel in the 12 or so hours afterward. If you're hurting, you've likely jumped the gun on your rehabilitation. During this time, keep up working hard to strengthen your scapular retractors and depressors and the external rotators of your humerus. In fact, your volume on these exercises should still be greater than that of internal rotations and protractions. Ice post-exercise and don't do too much too soon, and you'll be back on track in no time. Q: I'm working my back from a shoulder injury, and wanted to know if you think it would be feasible to do a little external rotation and scapular retraction work each day? While I'm not feeling any pain, I can still tell that my stabilizers are pretty weak. I have been alternating between rowing movements and face pulls each day as of late along with doing some sort of RC work each day (external rotations, 90 degree prone rotations, prone trap raises, band work, etc). Is this too much in your opinion or is it fine? I'm talking like 3x15 of rowing/face pulls and maybe 3 exercises of 3-4x15 of RC work per day (light weight obviously). Or would it be better to just do everything 3-4 times per week. I just figured I would divide the volume up throughout the entire week. A: I think it would definitely be advantageous to do some every day, although your loading and set/rep parameters could use some revisions. Try loading the movements in the 6-10 rep range once a week, and then hitting them with lighter weights in the 12-15 rep range on another day. On the other five days, just do some work with the theraband and/or light dumbbells to get the blood flowing. These are really small muscles, so you have to go out of your way to promote bloodflow and, in turn, healing. It certainly won't hurt to get them "activated" so that they're firing on all cylinders when you get back to your compound movements down the road. Q: After reading your article in the October issue in Rugged, I have a question or two. In healthy individuals, are you saying you do NO "direct" local (deep) ab work. i.e. plank, "thin tummy?" It seems as if the trainee gets plenty of local ab work w/ exercises like the DL, squats etc, but I don't know if "direct" ab work is mandated. I am still confused about this, even know I've read countless articles relating to this topic. A: Be careful with your classification scheme; I wouldn't classify tummy sucking with plank exercises. The cues I give to my athletes on plank exercises are to brace as if someone is about to kick them in the stomach (much like you would push out when squatting and deadlifting). The training effect is markedly different with this approach than with sucking in the tummy. In short, bracing makes you strong, and tummy sucking makes you look and perform like a wanker. You are, however, correct in saying that I think attempting to isolate the TVA in healthy individuals is a bad idea from both a training economy and potential harm standpoint. This training time would be better spent on other things, most notably multi-joint exercises and mindlessly gawking at gorgeous women in sports bras and spandex shorts. Q: First of all, let me tell how much I enjoy your no-nonsense, information filled articles. It's great that people like you are writing about various posture related, biomechanics issues. I have a problem to which I have not been able to find a solution here in India. I have over-pronation in both feet, resulting in low reactive force output plus patello-femoral pain if I run long distances. Aside from getting orthotics, is there anything else I can do about this over pronation. A: It really depends on whether the cause is structural or functional. You state that you have over-pronation in both feet, but don't allude to whether the feet have been flat for your entire life or if it's something that's kicked in as a result of movement dysfunction. From a structural standpoint, orthotics are really your only bet; the structural abnormality will dictate how the orthotic is shaped. From a functional standpoint, you need to determine if you have weakness in a decelerator elsewhere that's forcing the extra pronation in order to compensation. The external rotators of the hip (especially the gluteus maximus) and quadriceps are notable possibilities. Don't forget the dorsiflexors, either.
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Adrenomedullary Enlightenment

Sometimes, you need to be smart just for the sake of being smart. With that in mind, I present to you the first paper I wrote as a graduate student. While it undoubtedly made me a more informed researcher and student, it's still one week of my life that I'll never, ever get back. Enjoy. Introduction The adrenal medulla is well known as a powerful modulator of the physiological response to both exercise and rest via the "Fight-Flight" response. However, in light of opioid peptide research over the past few decades, it is now quite clear that the adrenal medulla plays a more prominent role than was originally perceived. Now, the study of adrenal medullary secretory activity, which was once limited to the catecholamines epinephrine, norepinephrine, and dopamine, also encompasses the lesser understood proenkephalin family of opioid peptides. With that in mind, it is important to consider adrenal medullary response to exercise stress and subsequent recovery in a broader sense. The Catecholamines and Adrenomedullary Activity Before considering the widespread impacts of the catecholamines in relation to exercise, it is important to note the relative contributions of each. Norepinephrine secretion from the adrenal medulla is certainly a contributing factor to the overall sympathoadrenal-medullary response to exercise, as the plasma concentration of the hormone (which also acts as a neurotransmitter) can increase twenty-fold with high-intensity exercise (1). However, sympathetic nerve endings also directly secrete norepinephrine to target tissues; during exercise, roughly 50% of total norepinephrine secretion occurs in the active muscles (2). Dopamine is the first catecholamine formed after the conversion of tyrosine to dihydroxyphenylalanine (dopa), the common chemical precursor for the three catecholamines. Norepinephrine and epinephrine are formed thereafter from this same pathway (3-5). Dopamine is present in the adrenal medulla and cortex, kidneys, peripheral nerves, carotid body, and sympathetic ganglia (6). In fact, it is the most abundant catecholamine in human plasma (5). However, only 2% exists in the free form; the remainder consists of biologically inactive metabolites (5,6). And, though the plasma free form dopamine concentration rivals that of epinephrine (and 20% of norepinephrine), it is not capable of the magnitude of physiological effects seen with epinephrine and norepinephrine (6). As such, although dopamine certainly plays a role in the adrenomedullary cascade of events in response to exercise, it is a less utilized measure of adrenomedullary activity during exercise and in recovery. Although dopamine is the most abundant catecholamine in the blood, epinephrine constitutes the vast majority of adrenal-medullary catecholamine release. Shah et al. proposed that those tissues outside of the CNS that produce catecholamines be labeled the "sympathochromaffin system," and be divided into two components: the sympathetic nervous system (neurotransmitter norepinephrine from postganglionic neurons) and the chromaffin cells (which secrete epinephrine, norepinephrine, and/or dopamine) (7). In short, plasma norepinephrine concentrations best quantifies sympathetic neuronal activity, whereas plasma epinephrine concentration is the optimal index of adrenomedullary secretions of catecholamines (7). With all these factors in mind, one can surmise that changes in plasma free epinephrine concentrations serve as the measure of choice in the discussion of the adrenomedullary catecholamine response to exercise and subsequent recovery. Catecholamine Response to Exercise Various intensities, durations, and modes of exercise serve as powerful stimuli to the adrenal medulla to initiate the Fight-Flight response. Numerous studies have found that epinephrine and norepinephrine secretions increase as exercise intensity increases. For instance, Kraemer et al. found that plasma epinephrine (Figure 1) and norepinephrine steadily increased during graded exercise on a bicycle ergometer from 54% to 83% and 100% of maximum oxygen consumption (VO2 max) in both trained and untrained subjects (8). Others have verified this relationship between plasma catecholamines and intensity during graded exercise sessions regardless of training status (9-12). Designation of a specific exercise intensity at which the adrenomedullary activity becomes significant is yet to occur, as catecholamines are always at work in the body. Unloaded cycling at approximately 10% VO2 max did not increase plasma catecholamines above resting values in young men (13). Likewise, as demonstrated in Figure 1, graded exercise on a bicycle ergometer did not increase plasma epinephrine above baseline at 54% VO2 max (8). However, Greiwe et al. demonstrated that norepinephrine and epinephrine (Figure 2) both increased with each 5% increment from 60% to 85% VO2 max before and after ten weeks of endurance training (14). Figure 1: Plasma epinephrine (Epi) concentrations at rest and after 15 min of exercise at the same relative exercise intensity before and after 10 wk of endurance exercise training. Greiwe et al. J Appl Physiol 1999. Designation of a specific exercise intensity at which the adrenomedullary activity becomes significant is yet to occur, as catecholamines are always at work in the body. Unloaded cycling at approximately 10% VO2 max did not increase plasma catecholamines above resting values in young men (13). Likewise, as demonstrated in Figure 1, graded exercise on a bicycle ergometer did not increase plasma epinephrine above baseline at 54% VO2 max (8). However, Greiwe et al. demonstrated that norepinephrine and epinephrine (Figure 2) both increased with each 5% increment from 60% to 85% VO2 max before and after ten weeks of endurance training (14). Figure 1: Plasma epinephrine (Epi) concentrations at rest and after 15 min of exercise at the same relative exercise intensity before and after 10 wk of endurance exercise training. Greiwe et al. J Appl Physiol 1999. (PICTURE)

As such, it appears that the cutoff point for significant adrenomedullary stimulation during endurance exercise is in the 55-60% VO2 max range.

Exercise duration is also of appreciable significance in determining the adrenomedullary response to exercise. Galbo et al. found that although plasma epinephrine increased steadily with prolonged treadmill exercise to exhaustion at 76% VO2 max, graded exercise in the same subjects at 44, 77, and 100% of VO2 max yielded greater increases (9). Others have verified the trend of increasing plasma epinephrine with longer duration exercise (15,16). Clearly, there is an appreciable lag time between the onset of exercise and increases in plasma catecholamine concentrations. In bicycle ergometer exercise to exhaustion at 36, 55, 73, and 100% of maximal leg power (the equivalent of 115, 175, 230, and 318% VO2 max, respectively), significant immediate post-exercise increases in plasma epinephrine were only observed at 36 and 55% of maximal leg power. The mean duration of exercise at these two intensities were 3.31 and 0.781 minutes, respectively. At maximal leg power, mean duration was approximately six seconds, and the significant increase in epinephrine was not seen until 15 minutes post-exercise (17). Jezova et al. examined the differential responses of two bicycle ergometer tests of the same total work output but different duration and intensities. The researchers concluded that the overall catecholamine response is more dependent on exercise intensity than duration or total work output (18). Resistance training also has a profound impact on adrenomedullary activity. Bush et al noted significant increases in plasma epinephrine following two different resistance exercise protocols –one high force and the other high power – of the same total work. There was not, however, a significant difference in adrenomedullary activity between the two (19). In another study comparing body builders with powerlifters, Kraemer et al. found that a ten station resistance training session (comprising 30 total sets at 10 repetition maximum for various exercises) with short rest periods increased plasma epinephrine, norepinephrine, and dopamine significantly over pre-exercise values. No difference was noted between body builders and powerlifters on these measures (20). Pullinen et al. noted that although plasma epinephrine increased significantly with knee extensions to exhaustion at 20, 40, 60, and 80% of 1 repetition maximum (RM), the strongest stimulus to epinephrine, 20%, did not yield a significantly greater plasma epinephrine increase than the other three intensities (21). In contrast, Guezennec et al. observed that six sets of eight bench presses at 70% of 1RM yielded less of a plasma epinephrine and norepinephrine response than six sets of maximal repetitions at the same load (22). Therefore, intensity again appears to be paramount in determining the adrenomedullary response to exercise. Catecholamine Response to Recovery Several studies have noted abrupt drops in epinephrine values in the 5-15 minutes after the cessation of endurance, graded exercise, and resistance training sessions (8,17,19,23). In light of the aforementioned lag between the onset of exercise and increases in plasma catecholamine concentrations, one should note that epinephrine levels continue to increase for 15 minutes or more after very short duration, high-intensity exercise (e.g. sprints) (17,24). Additionally, 15 minutes following a 1000km ultra-marathon, free epinephrine concentrations remained well above pre-exercise values; clearly, the extensive nature of this duration appeared to be sufficient to elicit prolonged adrenomedullary activity (25). Chronic catecholamine adaptations to training have also been noted. Kjaer and Glabo found that endurance trained athletes demonstrated a greater ability than untrained subjects to secrete epinephrine in response to infusion of glucagon and acute hypercapnia and hypobaric hypoxia (26). This finding is significant, as Kjaer et al. had found previously (via epinephrine infusions in resting and cycling subjects) that plasma epinephrine concentration changes during exercise signify enhanced secretion rather than reduced clearance (27). In other words, endurance training appears to increase secretory capacity of the adrenal medulla. Lehmann et al. verified this phenomenon in finding that trained cyclists demonstrated lower plasma epinephrine concentrations than untrained subjects at the same relative oxygen uptake (28). The Opioid Peptides and Adrenomedullary Activity Since its discovery in the 1970s, the proenkephalin family of opioid peptides has become a recognized secretory product of the adrenomedullary chromaffin cells. Nonetheless, research regarding the opioid peptide response to exercise is limited (8,17,19). Perhaps the most studied member of the opioid peptide family is proenkephalin peptide F, which has responded to similar stimuli as epinephrine in previous studies (8,17,29).

Kraemer et al. noted differential peptide F responses during graded bicycle ergometer exercise in trained and untrained subjects. As Figure 2 demonstrates, in untrained subjects, peptide F increased similarly to epinephrine, whereas it peaked at 54% VO2 max and began to decline in trained subjects as exercise intensity increases to 83 and 100% VO2 max (8).

Figure 2: Plasma Epinephrine and Peptide F as a function of exercise intensity Kraemer et al. Proc Natl Acad Sci U S A. 1985 Note: squares indicate Trained group; triangles indicate untrained group. (PICTURE 2)

In a separate study, the differential responses between trained and untrained subjects were once again readily apparent when fit women had significantly higher plasma peptide F concentrations than their unfit counterparts at 80% VO2 max cycling (30).

Interpreting the peptide F response to varying exercise intensities proves to be challenging. Peptide F increased significantly during high intensity cycle exercise at 36% maximal leg power (roughly 115% VO2 max), but not at three greater intensities with shorter durations (17). Another study found that plasma peptide F increased significantly with graded exercise at 75 and 100% VO2 max (31). Conversely, recall that the aforementioned Kraemer study noted a drop-off point in plasma peptide F at 54% VO2 max in trained subjects (8). In support of this drop-off point, exercise at 80-85% VO2 max did not yield a significant increase in plasma peptide F (32). Likewise, when strength-trained men took part in separate high force and high power resistance training protocols, plasma peptide F was significantly decreased from baseline values at the end of the exercise sessions. Meanwhile, epinephrine increased dramatically as expected. The researchers hypothesized that epinephrine increases are made possible by decreases in enkephalin-containing polypeptides in the adrenal medulla (19). This theory is supported by research by Angelopoulos et al., who asserted that the opioid peptides have an inhibitory effect on the release of catecholamines during intense exercise (33). On a related note, in a study involving purposeful resistance exercise overtraining of trained subjects, peptide F concentrations were not significantly different between the overtrained and control groups. This similarity was present in spite of the protocol's previously demonstrated propensity to induce dramatic increases in epinephrine (29). The fact that chronic training increases adrenomedullary secretory capacity for epinephrine certainly supports this inverse relationship and helps to elucidate the question of why trained and untrained subjects have different peptide F responses during exercise. Opioid Peptides Response to Recovery Perhaps the most intriguing aspect of the opioid peptides as they relate to exercise is the recovery period response. Increases in plasma peptide F have been noted not only in the first 5-15 minutes of the post-exercise period (9,17,19), but also at 240 minutes after resistance training sessions, when the mean concentration was more than 80% above the mean pre-exercise value (19). Researchers hypothesize that this post-exercise proenkephalin surge is indicative of the opioid peptides' crucial role in recovery (9,17,19,29,34). Additionally, enkephalin-containing polypeptides appear to play an essential role in the immune response through mechanisms such as neutrophil activation, natural killer cell modulation, and coagulation facilitation (29, 35). Given the negative impact of the catecholamines on overall immunity, the opioid peptides may serve as a means for the adrenal medulla to counteract immunosuppression during and after exercise (29). Conclusions The adrenal medulla is stimulated to secrete catecholamines by a variety of exercise intensities, durations, and modes, with a minimum intensity of 55-60% VO2 max likely being the most requisite factor. Generally speaking, as exercise intensity and duration increase, so does catecholamine secretion (most notably epinephrine) by the adrenal medulla. In untrained subjects, increases in plasma proenkephalin-containing peptides parallel increases in catecholamines. At the cessation of exercise, free catecholamine concentrations in the plasma decline sharply. Simultaneously, in trained subjects, concentrations of opioid peptides, which were relatively unaffected by exercise above 54% VO2 max, increase to values well above baseline. As the potentially immunosuppressive catecholamines (which are secreted at higher rates in trained individuals) dissipate, the enkephalin-containing peptides can begin to enhance recovery from exercise while enhancing the immune response. In spite of this theoretical paradigm, more research is clearly warranted in order to fully understand the causes of the differential opioid peptide response to exercise in trained and untrained subjects. Furthermore, the exact interaction scheme of the opioid peptides and the catecholamines remains to be definitively agreed upon.

References 1. Silverberg AB, Shah SD, Haymond MW, Cryer PE. Norepinephrine: hormone and neurotransmitter in man. Am J Physiol. 1978 Mar;234(3):E252-6. 2. Savard GK, Richter EA, Strange S, Kiens B, Christensen NJ, Saltin B. Norepinephrine spillover from skeletal muscle during exercise in humans: role of muscle mass. Am J Physiol. 1989 Dec;257(6 Pt 2):H1812-8. 3. Kvetnansky R, Armando I, Weise VK, Holmes C, Fukuhara K, Deka-Starosta A, Kopin IJ, Goldstein DS. Plasma dopa responses during stress: dependence on sympathoneural activity and tyrosine hydroxylation. J Pharmacol Exp Ther. 1992 Jun;261(3):899-909. 4. Goldstein DS, Eisenhofer G, Kopin IJ. Sources and significance of plasma levels of catechols and their metabolites in humans. J Pharmacol Exp Ther. 2003 Jun;305(3):800-11. Epub 2003 Mar 20. 5. Miura Y, Watanabe T, Noshiro T, Shimizu K, Kusakari T, Akama H, Shibukawa S, Miura W, Ohzeki T, Takahashi M, et al. Plasma free dopamine: physiological variability and pathophysiological significance. Hypertens Res. 1995 Jun;18 Suppl 1:S65-72. 6. Van Loon GR. Plasma dopamine: regulation and significance. Fed Proc. 1983 Oct;42(13):3012-8. 7. Shah SD, Tse TF, Clutter WE, Cryer PE. The human sympathochromaffin system. Am J Physiol. 1984 Sep;247(3 Pt 1):E380-4. 8. Kraemer WJ, Noble B, Culver B, Lewis RV. Changes in plasma proenkephalin peptide F and catecholamine levels during graded exercise in men. Proc Natl Acad Sci U S A. 1985 Sep;82(18):6349-51. 9. Galbo H, Holst JJ, Christensen NJ. Glucagon and plasma catecholamine responses to graded and prolonged exercise in man. J Appl Physiol. 1975 Jan;38(1):70-6. 10. de Diego Acosta AM, Garcia JC, Fernandez-Pastor VJ, Peran S, Ruiz M, Guirado F. Influence of fitness on the integrated neuroendocrine response to aerobic exercise until exhaustion. J Physiol Biochem. 2001 Dec;57(4):313-20. 11. Kraemer WJ, Dziados JE, Gordon SE, Marchitelli LJ, Fry AC, Reynolds KL. The effects of graded exercise on plasma proenkephalin peptide F and catecholamine responses at sea level. Eur J Appl Physiol Occup Physiol. 1990;61(3-4):214-7. 12. McMurray RG, Forsythe WA, Mar MH, Hardy CJ. Exercise intensity-related responses of beta-endorphin and catecholamines. Med Sci Sports Exerc. 1987 Dec;19(6):570-4. 13. Krzeminski K, Kruk B, Nazar K, Ziemba AW, Cybulski G, Niewiadomski W. Cardiovascular, metabolic and plasma catecholamine responses to passive and active exercises. J Physiol Pharmacol. 2000 Jun;51(2):267-78. 14. Greiwe JS, Hickner RC, Shah SD, Cryer PE, Holloszy JO. Norepinephrine response to exercise at the same relative intensity before and after endurance exercise training. J Appl Physiol. 1999 Feb;86(2):531-5. 15. Sothmann MS, Blaney J, Woulfe T, Donahue-Fuhrman S, Lefever K, Gustafson AB, Murthy VS. Plasma free and sulfoconjugated catecholamines during sustained exercise. J Appl Physiol. 1990 Feb;68(2):452-6. 16. Rostrup M, Westheim A, Refsum HE, Holme I, Eide I. Arterial and venous plasma catecholamines during submaximal steady-state exercise. Clin Physiol. 1998 Mar;18(2):109-15. 17. Kraemer WJ, Patton JF, Knuttgen HG, Hannan CJ, Kettler T, Gordon SE, Dziados JE, Fry AC, Frykman PN, Harman EA. Effects of high-intensity cycle exercise on sympathoadrenal-medullary response patterns. J Appl Physiol. 1991 Jan;70(1):8-14. 18. Jezova D, Vigas M, Tatar P, Kvetnansky R, Nazar K, Kaciuba-Uscilko H, Kozlowski S. Plasma testosterone and catecholamine responses to physical exercise of different intensities in men. Eur J Appl Physiol Occup Physiol. 1985;54(1):62-6. 19. Bush JA, Kraemer WJ, Mastro AM, Triplett-McBride NT, Volek JS, Putukian M, Sebastianelli WJ, Knuttgen HG. Exercise and recovery responses of adrenal medullary neurohormones to heavy resistance exercise. Med Sci Sports Exerc. 1999 Apr;31(4):554-9. 20. Kraemer WJ, Noble BJ, Clark MJ, Culver BW. Physiologic responses to heavy-resistance exercise with very short rest periods. Int J Sports Med. 1987 Aug;8(4):247-52. 21. Pullinen T, Nicol C, MacDonald E, Komi PV. Plasma catecholamine responses to four resistance exercise tests in men and women. Eur J Appl Physiol Occup Physiol. 1999 Jul;80(2):125-31. 22. Guezennec Y, Leger L, Lhoste F, Aymonod M, Pesquies PC. Hormone and metabolite response to weight-lifting training sessions. Int J Sports Med. 1986 Apr;7(2):100-5. 23. Ferrari R, Ceconi C, Rodella A, De Giuli F, Panzali A, Harris P. Temporal relations of the endocrine response to exercise. Cardioscience. 1991 Jun;2(2):131-9. 24. Harmer AR, McKenna MJ, Sutton JR, Snow RJ, Ruell PA, Booth J, Thompson MW, Mackay NA, Stathis CG, Crameri RM, Carey MF, Eager DM. Skeletal muscle metabolic and ionic adaptations during intense exercise following sprint training in humans. J Appl Physiol. 2000 Nov;89(5):1793-803. 25. Pestell RG, Hurley DM, Vandongen R. Biochemical and hormonal changes during a 1000 km ultramarathon. Clin Exp Pharmacol Physiol. 1989 May;16(5):353-61. 26. Kjaer M, Galbo H. Effect of physical training on the capacity to secrete epinephrine. J Appl Physiol. 1988 Jan;64(1):11-6. 27. Kjaer M, Christensen NJ, Sonne B, Richter EA, Galbo H. Effect of exercise on epinephrine turnover in trained and untrained male subjects. J Appl Physiol. 1985 Oct;59(4):1061-7. 28. Lehmann M, Keul J, Huber G, Da Prada M. Plasma catecholamines in trained and untrained volunteers during graduated exercise. Int J Sports Med. 1981 Aug;2(3):143-7. 29. Fry AC, Kraemer WJ, Ramsey LT. Pituitary-adrenal-gonadal responses to high-intensity resistance exercise overtraining. J Appl Physiol. 1998 Dec;85(6):2352-9. 30. Triplett-McBride NT, Mastro AM, McBride JM, Bush JA, Putukian M, Sebastianelli WJ, Kraemer WJ. Plasma proenkephalin peptide F and human B cell responses to exercise stress in fit and unfit women. Peptides. 1998;19(4):731-8. 31. Kraemer WJ, Dziados JE, Gordon SE, Marchitelli LJ, Fry AC, Reynolds KL. The effects of graded exercise on plasma proenkephalin peptide F and catecholamine responses at sea level. Eur J Appl Physiol Occup Physiol. 1990;61(3-4):214-7. 32. Kraemer WJ, Rock PB, Fulco CS, Gordon SE, Bonner JP, Cruthirds CD, Marchitelli LJ, Trad L, Cymerman A. Influence of altitude and caffeine during rest and exercise on plasma levels of proenkephalin peptide F. Peptides. 1988 Sep-Oct;9(5):1115-9. 33. Angelopoulos TJ, Denys BG, Weikart C, Dasilva SG, Michael TJ, Robertson RJ. Endogenous opioids may modulate catecholamine secretion during high intensity exercise. Eur J Appl Physiol Occup Physiol. 1995;70(3):195-9. 34. Kraemer W, Noble B, Robertson K, Lewis RV. Response of plasma proenkephalin peptide F to exercise. Peptides. 1985;6 Suppl 2:167-9. 35. Hiddinga HJ, Isaak DD, Lewis RV. Enkephalin-containing peptides processed from proenkephalin significantly enhance the antibody-forming cell responses to antigens. J Immunol. 1994 Apr 15;152(8):3748-59.
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A Silly Split

The more I write, the more weird emails I receive. I'm always very accommodating in answering people's questions even if they're rude and critical of my work; in fact, I enjoy defending my assertions. I'm a firm believer that there must be a rhyme and a reason for everything a coach or writer recommends; what better way to prove it than to defend those recommendations in the face of criticism. Just recently, I had one such opportunity when I received an email criticizing me for writing a four-days-per-week training program that didn't "adhere" to the Mo-Tu-Th-Fr training split. Apparently, my actions constituted a serious program design faux pas, so I felt it necessary to justify my recommendation with an entire article on the very topic. In short, I'm not a big fan. It's a split designed for convenience. Unfortunately, there isn't much about the iron game that is inherently "convenient." Loading hundreds of pounds onto barbells and then lifting them isn't convenient, nor is sprinting, or preparing healthy meals, for that matter. Yeah, so you want the weekends off; who doesn't? Speaking anecdotally, I don't think that most trainees inflict enough damage to warrant two days of complete rest (and, for many, complete gluttony in front of a TV screen for college and NFL football games). And, to those who insist that the two days is enough for supercompensation to occur, I don't think you really even understand what supercompensation is; it take a lot longer than two days. I don't necessarily include MWF splits in this category, however, as they tend to be full-body training sessions that complement other training (e.g. sport-specific conditioning, cardiovascular activity, team practices, extra assistance sessions). First, let's consider why I don't like it from a logical perspective. You should know to prioritize work for your specific weaknesses by placing it on a "fresh" day (immediately after a rest day). Now, the Mo-Tu-Th-Fr training split allows for two fresh days, whereas a Mo-Tu-Th-Sa split, for example, allows for three. This might not seem like a big difference, but consider that it means trading roughly 50 pseudo-depleted sessions for 50 fresh sessions over the course of the year. In my mind, this corresponds to significant gains over the course of a training career; take a look at the template advocated by the lifters at Westside Barbell Club, which follows such a structural template, and you'll see that the proof is just as much in the numbers as it is in the logic. Next up, let's look at this from a pragmatic perspective. Are the gyms busier on weeknights or weekends? If you answered "weekends," you ought to just give up and take aerobics classes. Some of the best sessions of my training career have been on weekends simply because my mind was more clear of the all the nuisances of the "weekday world." Now, let's consider the Mo-Tu-Th-Fr split from a scientific perspective. Research has shown that following a resistance training session, skeletal muscle protein synthesis can be elevated for up to 48 hours (1). However, these researchers studied untrained subjects (2). MacDougall et al. (1995), on the other hand, found that in resistance trained subjects, protein synthesis had returned to baseline at 36 hours post-exercise (3). Keep in mind that I'm assuming that you're reading this site because you actually train, so we'll classify you with the latter group. If you don't train, why not head over to the Good Housekeeping forums? I'm sure that everyone will appreciate you sharing a few recipes while Martha Stewart is making license plates instead of quiches. To apply this protein synthesis data to you, we're going to calculate a thing I like to call "downtime." This is the time between training sessions minus 36 hours; basically, it gives you the amount of time in between sessions that you aren't above baseline in protein synthesis. We want to minimize this! Let's say that you're a Mo-Tu-Th-Fr evening lifter. Skeletal muscle protein synthesis is elevated rapidly, so we'll say that you stimulate it by 8PM on all days. From the time that you get the marked elevations on Friday to the time that protein synthesis is kickstarted on Monday, you're looking at 72 hours, the last two of which are essentially spent in a catabolic state during training (keep in mind that you'll be in a catabolic state all weekend if you're hopelessly intoxicated the entire time!). That leaves a full 36 hours of downtime (72 minus 36). Moreover, you get another 12 hours of downtime from 8AM to 8PM on Thursday; this is pretty much unavoidable, given your schedule. In all, theoretically speaking, that gives you two days per week (48 hours) that you aren't above baseline. Now let's consider what happens with the Mo-Tu-Th-Sa split and the same lifting times; assume once again that you're firing up protein synthesis around 8PM on all days. Because you took two rest days during the week and only one on the weekend instead of one during the week and two on the weekend, you have three 12-hour periods of downtime during the week (8AM-8PM on Monday, Thursday, and Saturday). Therefore, with the Mo-Tu-Th-Sa split, we have only 36 hours at baseline. A difference of twelve hours might not seem like much to you now, but over the course of a year, that works out to be an additional 26 days with protein synthesis elevated! If you don't buy into my scientific perspective, consider it from an anecdotal perspective by observing the outstanding results numerous trainees have experienced from programs that emphasize more frequent training (even if it means shorter sessions). While Bulgarian weightlifters have taken it to an extreme (albeit successfully) with several sessions per day, you can also read about the benefits of frequent training sessions in Joel Marion's Center Your Training; Ripped, Rugged, and Dense 2.0; and Sequential Development for Size. Conclusion The next time you write up your training program, ask yourself if it's based on logical, pragmatic, and scientific principles. Or, is it designed to make things convenient for you? If you find yourself answering yes to the latter question, chances are that you're sacrificing gains in both size and strength. Be sure to get your priorities straight before you determine how to break things up. With that said, let the angry email barrage commence! References 1. Phillips SM, Tipton KD, Aarsland A, Wolf SE, Wolfe RR. Mixed muscle protein synthesis and breakdown after resistance exercise in humans. Am J Physiol. 1997 Jul;273(1 Pt 1):E99-107. 2. Rasmussen BB, Phillips SM. Contractile and nutritional regulation of human muscle growth. Exerc Sport Sci Rev. 2003 Jul;31(3):127-31. 3. MacDougall JD, Gibala MJ, Tarnopolsky MA, MacDonald JR, Interisano SA, Yarasheski KE. The time course for elevated muscle protein synthesis following heavy resistance exercise. Can J Appl Physiol. 1995 Dec;20(4):480-6.
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