Monday, September 24, 2012

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?

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 ;-)

This image shows a study participant of another study during a VO2 max test on the exact same bike Rakobowchuk et al. used ( 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!

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?

"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).
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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]

  • 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.