Eccentric Exercise IGF1 & Athlete's Heart; Long or Short Intervals, Both Improve Arterial Stiffness. Plus: Exercise Heals Wounds & Makes You Rust Proof Within One Year!

Controlled exhaustion = positive adaptation; continuous exhaustion = wear and tear = one out of 57,002 who suffer from cardiac arrest during a marathon (data based on Webner. 2012)

As announced on Saturday, already this is a "special edition" of the On Short Notice series, focusing exclusively on exercise related studies. With

• two studies on heart health, 
• one on wound healing and the last one on the 
• bullet proof endogenous anti-oxidant system of trained athletes, 

this installment of the "Exercise News Roundup" and two studies on different HIIT, it does however have both a health, as well as a HIIT focus.

I know that does not sound as sexy as being big and buffed, but what's the use of that if you don't fit the coffin, you're about to need, when your looks are more important to you than your health?

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IGF-Response to exercise implicated in "athletes heart" A group of polish researchers describes in their latest paper that's been published ahead of print in the International Journal of Sports Medicine, how the differential IGF-1 response to eccentric (ECC) and concentric (CON) arm exercise in 10 trained strength athletes (1.5-2.0 h on 3-5 days weekly) and 10 age-matched healthy non-trained subjects could explain the differences in the degree of left ventricular hypertrophy, the scientists had measure via M-mode and 2D Doppler echocardiography beforehand (Zebrowska. 2012).

IGF1 and left ventricular hypertrophy (LVH): The correlation stands out of question, but what about the implications? Is this a causative relationship? And what's more: How dangerous are LVH  and having an athlete's heart, at all?

The athletes with LVH did not only have higher IGF-1 levels at baseline (52±5 nM vs. 46±7 nM for controls, p<0.05), they also showed a significantly more pronounced IGF-1 response during the eccentric (ECC) exercise test, with athletes with LVH exhibiting 30% higher and athletes without LVH 15% higher IGF-1 levels than untrained controls (54±6 nM). Moreover, both CON and ECC exercise resulted in higher serum IGFBP-3 levels in LVH athletes compared to controls (242±57 and 274±58, athletes, vs. 215±63 and 244±67, controls, nM, p<0.05), while no differences in other hormones were found between groups. Yet though the scientists' conclusion that these findings would "suggest a role of IGF-1, possibly released from contracting muscle, in stimulating LV hypertrophy in resistance training" is certainly right, we would be ill-advised to jump to any conclusions, hastily by simply (and faultily) equating correlation and causation, here.

Moreover, we should acknowledge that the previously accepted paradigm that LVH, per se, is a bad thing that has to be avoided at all costs is actually not supported by empirical evidence, or as Florescu et al. have it "'Supranormal' cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo-arterial coupling; athlete's heart is purely a physiological phenomenon, associated with 'supranormal' cardiac function, and there are no markers of myocardial fibrosis." (Florescu. 2010)... in short: in the absence of myocardial fibrosis, a big heart is nothing you will die from - how IGF-1 could actually prevent the latter, i.e. the occurrence of fibrotic structures due to uncompensated growth of the heart muscle, would yet be the topic for another quite lengthy blogpost ;-)

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This image shows a study participant of another study during a VO2 max test on the exact same bike Rakobowchuk et al. used (WSCU.edu). Wrt to the protocols the researchers remark "the protocols involved an identical total training volume and time commitment but differed regarding metabolic stress" With the HIIT trial inducing greater metabolic stress due to the longer periods at supra-amaximal workloads (cf. Turner. 2006).

Heavy or moderate interval training equally heart healthy - at least if you take their effect on arterial stiffness and heart rate dynamics as a measure. That's the message of an article that was published ahead of print in the European Journal of Applied Physiology at then end of last week. During a six-week experiment, Mark Rakobowchuk and his colleagues from the University of Essex and the University of Leeds investigated which of the following protocols (all performed three times per week, for a total of 18 session; 2min warm-up for each; cf. Rakobowchuk. 2012),

• MIIT - moderate intensity interval training consisting of 10s : 20s cycles at 120% of the pretraining max. workrate : 20W for 30, 35 and 40min (bi-weekly progression), or
• HIIT - high intensity interval training consisting of 30s : 60s cycles at 120% of the pretraining max. workrate : 20W for 30, 35 and 40min (bi-weekly progression),

would elicit more favorable changes in carotid artery stiffness, blood pressure, and heart rate variability in a group of 20 healthy, previously untrained young men and women (n = 7 men and 13 women; age 23.5y; BMI 23).

Trainees who want to increase their VO2max should still do HIIT, because only the subjects in the HIIT training group achieved statistically significant increases with respect to this outcome measure (+14% in HIIT vs. +3% VO2 max in MIIT).

Just as the scientists had speculated, their hypothesis that irrespective of the metabolic stress, which would be higher in the HIIT vs. the MIIT trial, the total volume, which was identical would determine the overall adaptive response. For them it was therefore not surprising that all measured parameters of  heart health, i.e.blood pressure, heart rate dynamics and carotid arterial stiffness, improved without significant inter-group differences. Most notably, though, those with the highest arterial stiffness before the trial saw the greatest reductions!

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Figure 2: Additional exercise sped up the wound healing process only in the obese rodents, not the lean ones (Pence. 2012)

Exercise speeds healing of subcutaneous wounds in obesity. This was allegedly observed only in obese rodents, but since the underlying mechanism was neither mediated by gene or protein expression of proinflammatory cytokines interleukin-1A and tumor necrosis factor-alpha or the anti-inflammatory cytokine interleukin-10 in the wounds, I felt it was still worth mentioning, also because it is, as the scientists point out,

"the first report of an exercise effect on wound healing that is unrelated to alterations in wound site inflammation." (Pence. 2012) 

Future trials will have to elucidate whether clotting and homeostasis, which occur in the earliest stage of wound healing, approximately 30 min after the trauma may be involved in this phenomenon.

In this context, some of you will probably remember my recent post on the "Antithrombotic effects of caffeine blunt platelet activity in response to interval training" that exercise increases the tendency of your blood to clot - a tendency that does obviously come handy, when you are bleeding. That the increase in coagulation factors came into effect only in the obese, yet not in the normal weight control, in turn, could be related to the presence of existing hemostastic imbalances due to obesity which would have been corrected by the 30min of treadmill running the rodents in the exercise groups performed at a pace of 12 m/min on a 5% incline for the final 30 min of the light period (0930–1000 h), three days before until five days after the wounding.

A bunch of maggots on a diabetic wound.

Be that as it may, there are more than enough sedentary, "SAD dieting" (and the standard high fat diet rodents are fed in studies like this is nothing but a clone of the S-tandard A-merican D-diet) full-blown or pre-diabetic obese human beings who could likewise benefit from as little as 30min of daily aerobic activity. I mean think about it, if you could thus avoid having 50-100 maggots being placed on those nasty diabetic wounds (see picture on the right) that would never heal without those tiny critters secreting their salivary juices onto the wound to liquefy and subsequently ingest and further degrade the dead tissue in their gut, you can hardly argue that this is too much to ask for, can you?

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"Rust proof" athletes don't need vitamin pills with copious amounts of anti-oxidants and don't have to be afraid of fruit with their synergistic blend of small, but highly effective and synergistic amounts of vitamins and polyphenols, either.

Oxidation proof after 1 year+ of regular aerobic + anaerobic training. According to a paper that's soon going to be published in Medicine & Science in Sports & Exercise trained athletes between the ages of 21 and 35yrs who had been participating in a structured exercise training program (including both aerobic and anaerobic) for the past 12 months, with each session lasting no less than 45 min per session, as well as no less than three sessions per week, are virtually "rust proof".

That's at least my allegedly nonchalant interpretation of the non-existent increases in serum markers of oxidation the scientists from the University of Memphis observed in their 12 male subjects (BMI 25kg/m², body fat 12.8%; VO2Max 20 ml/kg/min) in response to four training sessions separated by 1 wk.

The Sessions were counterbalanced and included either a no-exercise condition (subjects simply rested for the entire period) or one of the these three:

• MISS - moderate intensity + duration steady state: 70% HR reserve for 60min; total time: 60min with 60min of actual work
• HIIT - high intensity + moderate duration interval sprints: 5x60s at 100% + 225s recovery yielding a 1:3.75 work-to-rest ratio ("Within each interval, subjects were instructed to pedal between 80 and 100 rpm for the first 45 s, and then for the final 15 s, subjects were instructed to pedal as fast as possible"); total time: 20 min with 300s of actual work
• MaxIIT - maximal intensity + short duration interval: 10x15s at a wattage of 200% of VO2max, followed by 116s of recovery (1:7.7 work-to-rest ratio); total time: 20 min with 150s of actual work

All exercise bouts were performed on the same cycle ergometer used for the GXT, and subjects reported to the laboratory in the morning (0600–0900 h) after a minimum 10-h overnight fast. The HR was continuously monitored via Polar (TM) HR monitors and blood was drawn at the end of the 20-min rest period  (corresponding to the immediate postexercise blood samples) and 30 and 60 min after the 20-min rest period (corresponding to the postexercise blood samples).

Figure 3: Total antioxidant capacity (TEAC), SOD, CAT and GPx values immediately (0min), 30min and 60min after the respective exercise bouts (data based on Farney. 2012)

The respective total work performed during the trials was 461.1kJ, 96.9kJ, 96.9kJ for the MISS, HIIT and MaxIIT trials, respectively, the perceived exertion was highest in the MaxIIT trial (16.7 vs. 15.6 for HIIT and 13.5 for MISS), while the maximal heart rate 171.7bpm was achieved in the HIIT trial. Still,

"No differences were noted in malondialdehyde, H2O2, advanced oxidation protein product, or NOx between conditions or across time (P > 0.05) [while the a]ntioxidant capacity was generally highest at 30 and 60 min after exercise and lowest at 0 min after exercise." (Farney. 2012; my emphases)

If you will, you could even go one step further and argue that the total antioxidant capacity increases in well-rested, well conditioned athletes in response to exhaustive exercise bouts. Though, this increase reaches statistical significance in the MaxIIT trial only (see figure 3).

Hungry for more news? Visit the SuppVersity on Facebook!

That's it for today, ... but only as far as SuppVersity posts go. In about 2h at 1PM (EST), to be precise you can - if you want - listen to me on Super Human Radio. I am going to pick up on the topic of the first hour which is "Moderate Alcohol Consumption how (Un-)Healthy is it really" and do my best to provide some insights into the discrepancy that exists between reliable scientific evidence, the media coverage on the topic and Mr Average Joe's interpretation of the latter. And if you ain't into booze, just work out ;-) [update: download the podcast]

References:

• Farney TM, McCarthy CG, Canale RE, Schilling BK, Whitehead PN, Bloomer RJ. Absence of blood oxidative stress in trained men after strenuous exercise. Med Sci Sports Exerc. 2012 Oct;44(10):1855-63.
• Pence BD, Dipietro LA, Woods JA. Exercise Speeds Cutaneous Wound Healing in High-Fat Diet-Induced Obese Mice. Med Sci Sports Exerc. 2012 Oct;44(10):1846-1854.
• Rakobowchuk M, Harris E, Taylor A, Cubbon RM, Birch KM. Moderate and heavy metabolic stress interval training improve arterial stiffness and heart rate dynamics in humans. Eur J Appl Physiol. 2012 Sep 16.
• Turner AP, Cathcart AJ, Parker ME, Butterworth C, Wilson J, Ward SA (2006) Oxygen uptake and muscle desaturation kinetics during intermittent cycling. Med Sci Sports Exerc 38:492–503.
• Webner D, Duprey KM, Drezner JA, Cronholm P, Roberts WO. Sudden cardiac arrest and death in United States marathons. Med Sci Sports Exerc. 2012 Oct;44(10):1843-5.
• Zebrowska A, Waśkiewicz Z, Zając A, Gąsior Z, Galbo H, Langfort J. IGF-1 Response to Arm Exercise with Eccentric and Concentric Muscle Contractions in Resistance-Trained Athletes with Left Ventricular Hypertrophy. Int J Sports Med. 2012 Sep 7.

Exercise News Round-Up: The Latest on Weight Lifting, Steady State, HIIT, Pyramid Training & Co, Their Effects on Body Composition, Leptin, Muscle Morphology & More

Running may be the "original exercise", but there is more to physical culture than that - irrespective of your gender, by the way; HIIT would be one thing, weight lifting the other that must not be missing from your regimen which can yet still benefit from one or another classic cardio session (img womanshealthmag.com).

I must admit that I am a bit lazy today and not really in the mood of writing a lengthy post on circadian rhythms. The weather is awesome and I think I'd better spend the time in the sun recharging the batteries of my circadian clock, than sitting in front of a computer screen.

Since I do know that the former, i.e. the good weather won't apply to all of you and that reading these posts does not take anywhere as long as writing them, I will yet put together the promised post on "exercise news" - and I can tell you there is half a dozen of them, such as

• liver health, aerobics and strength training
• no leg-based cardio on leg day
• aerobics alone won't cut it
• intramuscular arguments in favor of HIIT 
• reverse or classic pyramid about equally effective
• intense exercise has leptin plummeting

You see, more than enough for one day, so we better get right down and dirty... ah, I mean, sweaty - yeah, sweaty ;-)

• Putting weights into the equation squeezes the fat out of your liver and belly In a recently conducted study into the effects of long-term exercise on the weight and fat loss in post-pubertal overweight adolescent with non-alcoholic fatty liver disease, the combination of aerobic and resistance training was "more effective in significantly improving noninvasive biomarkers of NAFLD that are associated with the highest risk of disease progression in the pediatric population" (de Piano. 2012). The main facts about the program
  

  

  Figure 1: Only combined aerobic and resistance training offers the body recompositioning effect we are all looking for: more muscle, less fat - and that works optimally, only, if your liver is still fully functional (de Piano. 2012)

  • one-year intervention + dietary counseling
  • 60min of personalized aerobic training, or
  • 30min aerobic + 30min resistance training
  • performed three times a week

  In the abstract of their study the scientists unfortunately fail to point out that the additional resistance training, which consisted of a standardized, progressive full-body training with 3 sets of 6-20 reps (depending on exercise) had the extra bonus of building more muscle and cutting more body fat than the less versatile three times pe -week 60min aerobics program.
  Moreover, the fact that only the participants in non-NAFLD, "just obese" control group were able to increase their muscle mass, goes to to show you, how important an optimally functioning liver actually is, when it comes to building muscle, losing weight and staying healthy.

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  Image 2: If you train legs with a similar volume as Arnold & Franco did, back in the day, you don't want to and probably also don't have to do any additional cardio before or after your workouts.

  Doing 30min of cardio on the elliptical reduces the number of reps you will be able to perform on a subsequent leg workout, but the bench press performance won't suffer. That's the very unsurprising result of a hitherto unpublished dissertation by Jeremy Tan from the University of California in Fullerton (Tan. 2012).
  Tan had recruited twelve young men who had completed four trials in random order. In two of those trials the guys performed 30min on the elliptical machine at 70% of their age-predicted (not measured!) HRmax followed by either 3 sets of back squats or bench presses performed to failure at 75% of their predetermined 1RM - not exactly an "Arnold-esque training volume, anyway, right (see image 2)?
  Bottom line: Better don't do a lengthy cardio workout before your leg training - but also: Don't believe the bro-scientific myth that 30min of cardio were so exhausting (systemically) that you could not train a body part that was not heavily involved in the cardio session (in this case the upper body), afterwards.

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  Figure 2: Cardio alone won't change your body for the better and the changes in CRP and leptin are not statistically significant (data expr. rel. to baseline; based on Bijeh. 2012)

  Aerobics alone won't really cut it and this goes not just for advanced male athletes, but even for middle aged (42y) women (BMI 25-27) who have never trained before. At least this is what the results of Bijeh, Hosseini and Hejazi from the University of Mashhad (Iran) would suggest, because even after 6 months with 3x 60 minutes (55-65 HRmax) none of those body composition parameters women are usually trying to improve, when they are taking up an exercise regimen did come about (Bijeh. 2012): Other than a minimally, but statistically non-significant reduction of body fat a prominent but not significantly different (P=0.2 for the variation) increase in leptin levels in the exercise group were the only "beneficial" changes the "workouts" brought about.
  Plus, in how far the increase  in leptin actually is a good thing does still remain to be seen, also because the CRP levels (inflammatory marker) in the training group increased (likewise not statistically different) and the allegedly statistically significant difference in the waist to-hip ratio (-0.01 in the aerobics group vs. no change in the sedentary control) of the women is so small against the standard deviations of the respective value that I am not sure about how significant it really is - regardless of what ANOVA, a program that's often used to do the statistics on data like that, say.
  Bottom line: If for whatever reason you can only do light "classic cardio" there is no way it will make a difference if you don't combine it with a sound dietary regimen.
• HIIT and classic endurance training equally effective in increasing muscle microvascular density The latest study from the UK shows that HIIT is more and more being accepted by researchers as a viable alternative to the classic aerobic training programs. In a 6-week intervention, Cox et al. assigned 16 young previously sedentary men (age 21±0.7 yrs, BMI 23.8±0.7 kg/m²) randomly to either 40-60 min cycling at ~65% VO_2peak, 5 times per week (ET), or a much less time-consuming HIIT protocol that comprised 4-6 Wingate tests, 3 times per week (HIIT).

  

  Image 3: While the study used the classic wingate test protocol with a stationary bike you can also do 30s all-out sprints, use a spinning bike or whatever else allows for maximal efforts and temporary exhaustion without you hurting yourself or the equipment breaking down (or both ;-)

  Other than most of their colleagues the scientists were yet less interested in the beneficial effects this exercise would have on VO2Max, let alone simple weight loss, but analyzed muscle samples for their microvascular endothelial eNOS and NOX2 content (indicative of the vascularization) and the actual morphological capillarization of the muscle by quantitative immunofluorescence microscopy. Whole body insulin sensitivity, arterial stiffness, and blood pressure were also assessed.
  The results showed that both protocols were equally effective in inducing the adaptive changes in microvascular capillarization and NOX2 expression, while the short intense exercise bouts during the HIIT protocol yielded 12% greater increases in eNOS content (ET 14%; P<0.05, HIIT 36%; difference p < 0.05).
  Now, eNOS is actually better known for its preventive role in CVD (and hypertension), but its negative correlation with body fat levels (higher eNOS <> lower body fat - note: this is almost certainly not a causal relationship(!); cf. Hickner. 2006), its central role in the maintenance of exercise capacity (Lee-Young. 2009) and its putative role the maintenance of mitochondrial function and integrity into the old age (Chanséaume. 2009) it should be obvious that time-efficiency is not the only thing that speaks in favor of HIIT, here. 

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  Figure 3: Strength gains (no idea what the scientists mean by "compression", just think about it as the effect size) of 6 weeks, 18 lifting sessions, employing a classic or reverse pyramid loading scheme on chest (bench press), quads (leg extension) and biceps (curl) strength (adapted from Bostani. 2012)

  No statistical significant differences in strength gains between classic and reverse pyramid While Bostani and Shariati did in fact not find statistically significant differences between the strength gains of their physically active, but "non-athlete" (sic!) study participants (N=10 for the two active and the control arm) a closer look at the data in figure 3 to the right does still reveal that it could make a difference, whether increase the weight from set to set (regular pyramid) or decrease it from set to set (reverse pyramid) - at least for your extremities, with the quads responding more favorable to the reverse pyramid and the biceps to the classic pyramid training.
  If the study was not so hilariously poorly described and the translation so sloppy, I would love to use these insights for a recommendation on how to train.
  In the absence of set number, reps and everything else that would be necessary, I can yet just say that this appears to confirm my personal experience, which tells me that you have to hammer your legs to grow and get stronger, while the classic pyramid with it's generally lower overall volume matches the "hit it hard and short" approach that appears to work best for biceps, in the longer run.

• 

  Figure 4: Eight weeks of intense exercise in the presence of a negative energy balance (as evidenced by the weight loss) take their toll on leptin levels, it is yet not sure for whom that's a bad thing (data based on Ferdosi. 2012)

  Intense exercise will make make your leptin levels drop and that irrespective of whether you do endurance training, strength training or both! That's the long and short of a study that has been published in the latest issue of Procedia - Social and Behavioral Sciences (Ferdosi. 2012), which did not even find a quantitative difference between the effects 8 weeks of 3 session of either 40 minutes (increasing from 25 in the first two, to 35min in weeks 3-6 and 40min in weeks 7-8) cycling at 75-85% HRmax (aerobic), a standard full-body workout (resistance) or both strength and aerobic training concomitantly (concomitant).
  It is thus obvious that done at a high enough intensity and in the presence of a negative energy balance, the same endurance exercise that elicited an increase in leptin in the Bijeh study (remember, this was more of a leisurely walk and without a build-in progression) will decrease leptin levels significantly.
  Now, that's great if you got a lot of fat to lose and are leptin resistant anyway, if you are yet lean already (with a BMI of 29kg/m² the healthy but untrained 48 male study participants, here, were not exactly ripped, but far from being obese) this can become a problem that could not just forestall fat loss, but could precipitate endocrine imbalances - and that's nothing that can only happen to women, in whom it usually manifest as amenorrhea (Christo. 2008)

That's it for today, but since I know you will be asking, yes, there I will catch up with the circadian rhythm series and yes I understand that the last item of today's installment has left at least some of you very dissatisfied. So, yes, I will finally address the issue of amenorrhea (but also hypogonadism in men) in an individual post, although I still don't have the clearcut "do this, don't do that" solution to the problem, I wanted to find before, I write the respective post... ah, and in case neither of those things does interest you, don't worry there will of course be other posts in the next days, as well ;-)

References:

• Bostani M, Shariati M. The Comparison of Between the Effects of Two Training Methods on Dynamic Strength of Non-Athletes Males Procedia - Social and Behavioral Sciences. 2012; 46: 417–420
• Bijeh N, Hosseini A, Hejazi K. The Effect of Aerobic Exercise on Serum C - Reactive Protein and Leptin Levels in Untrained Middle-Aged Women. Iranian J Publ Health. Sep 2012; 41(9).
• Chanséaume E, Morio B. Potential mechanisms of muscle mitochondrial dysfunction in aging and obesity and cellular consequences. Int J Mol Sci. 2009 Jan;10(1):306-24. Epub 2009 Jan 13. 
• Christo K, Cord J, Mendes N, Miller KK, Goldstein MA, Klibanski A, Misra M. Acylated ghrelin and leptin in adolescent athletes with amenorrhea, eumenorrheic athletes and controls: a cross-sectional study. Clin Endocrinol (Oxf). 2008 Oct;69(4):628-33. Epub 2008 Mar 10.
• Cocks M, Shaw CS, Shepherd SO, Fisher J, Ranasinghe AM, Barker TA, Tipton KD, Wagenmakers AJ. High intensity interval and endurance training are equally effective in increasing muscle microvascular density and eNOS content in sedentary males. J Physiol. 2012 Sep 3.
• de Piano A, de Mello MT, Sanches PD, da Silva PL, Campos RM, Carnier J, Corgosinho F, Foschini D, Masquio DL, Tock L, Oyama LM, Oller do Nascimento CM, Tufik S, Dâmaso AR. Long-term effects of aerobic plus resistance training on the  adipokines and neuropeptides in nonalcoholic fatty liver disease obese adolescents. Eur J Gastroenterol Hepatol. 2012 Aug 27.
• Ferdosi MH, Asad MR. The Effect of Endurance, Resistance and Concurrent Trainings on Plasma Leptin Levels of Non-Athlete Males. Procedia - Social and Behavioral Sciences. 2012; 46: 311–315.
• Hickner RC, Kemeny G, Stallings HW, Manning SM, McIver KL. Relationship between body composition and skeletal muscle eNOS. Int J Obes (Lond). 2006 Feb;30(2):308-12.
• Lee-Young RS, Ayala JE, Hunley CF, James FD, Bracy DP, Kang L, Wasserman DH. Endothelial nitric oxide synthase is central to skeletal muscle metabolic regulation and enzymatic signaling during exercise in vivo. Am J Physiol Regul Integr Comp Physiol. 2010 May;298(5):R1399-408. Epub 2010 Mar 3.
• Tan J. Acute effects of lower body aerobic exercise on lower body and upper body resistance training workshops. California State University. 2012. Publicatin no. 1513816.