12/05/2009 2:01am, #281
And more on fat loss...
To determine whether trained individuals rely more on fat than untrained persons during high-intensity exercise, six endurance-trained men and six untrained men were studied during 30 minutes of exercise at 75% to 80% maximal oxygen consumption (VO2max). The rates of appearance (Ra) and disappearance (Rd) of glycerol and free fatty acids (FFAs) were determined using [1,1,2,3,3-2H]glycerol and [1-13C]palmitate, respectively, whereas the overall rate of fatty acid oxidation was determined using indirect calorimetry. During exercise, the whole-body rate of lipolysis (ie, glycerol Ra) was higher in the trained group (7.1 +/- 1.2 v 4.5 +/- 0.7 micromol x min(-1) x kg(-1), P < .05), as was the Ra (approximately Rd) of FFA (9.0 +/- 0.9 v 5.0 +/- 1.0 micromol x min(-1) x kg(-1), P < .001). FFA utilization was higher in trained subjects even when expressed as a percentage of total energy expenditure (10% +/- 1% v 7% +/- 1%, P < .05).
In other words: Trained people can generate more power from their fat reserves when working at high intensities.
Whole body lipid kinetics were evaluated during basal resting conditions, 4 h of treadmill exercise eliciting an oxygen uptake of 20 ml.kg-1.min-1, and 1 h of recovery in five untrained and five endurance-trained men. Glycerol and free fatty acid (FFA) rate of appearance (Ra) values in plasma were determined by infusing [2H5]glycerol and [1-13C]palmitate, respectively, and lipid oxidation was determined by indirect calorimetry. The lipolytic response to 4 h of exercise, expressed as the average glycerol and FFA Ra values, was similar in both trained (9.85 +/- 1.02 and 24.64 +/- 3.76 mumol.kg-1.min-1, respectively) and untrained subjects (11.29 +/- 0.99 and 24.13 +/- 0.39 mumol.kg-1.min-1, respectively). However, mean triglyceride oxidation was greater during exercise in the trained than in the untrained group (7.51 +/- 0.26 and 5.67 +/- 0.51 mumol.kg-1.min-1, respectively; P < 0.001).
Summary: As above, but for low intensities too.
In biopsies from m. vastus lateralis, the activity of the enzymes citrate synthase, β-hydroxy acyl CoA dehydrogenase (HAD), and hormone sensitive lipase was higher in the ET subjects. The HAD activity correlated significantly with fat oxidation at moderate and high intensities. We conclude that the ET women had a higher fat oxidation at moderate- and high-exercise intensities both at same relative and at absolute intensity compared with the UT women.
Summary: The trained women had greater HAD enzyme activity, resulting in more fat burning.
And for a dietary tie-in:
This study was conducted to obtain additional information about the adaptations after 12 wk of high-fat diet (HFD) per se or HFD combined with endurance training in the rat using a two [diet: carbohydrate (CHO) or HFD] by two (training: sedentary or trained) by two (condition at death: rested or exercised) factorial design. Adaptation to prolonged HFD increases maximal O2 uptake (VO2max; 13%, P less than 0.05) and submaximal running endurance (+64%, P less than 0.05). This enhancement in exercise capacity could be attributed to 1) an increase in skeletal muscle aerobic enzyme activities (3-hydroxyacyl-CoA dehydrogenase and citrate synthase in soleus and red quadriceps) or 2) a decrease in liver glycogen breakdown in response to 1 h exercise at 80% VO2max. When training is superimposed to HFD, the most prominent finding provided by this study is that the diet-induced effects are cumulative with the well-known training effect on VO2max, exercise endurance, oxidative capacity of red muscle, and metabolic responses to exercise, with a further reduction in liver glycogen breakdown.
Summary: The increased fat metabolism (thanks to HAD again) from both training and a high-fat diet are complementary, at least in rats.
Edit: I just can't help myself. I'm on a roll. From Phinney, "Ketogenic diets and physical performance"
Point #1: Low-carbohydrate diets will only destroy your endurance until you've adapted to them (given adequate sodium and potassium intake).
Both observational and prospectively designed studies support the conclusion that submaximal endurance performance can be sustained despite the virtual exclusion of carbohydrate from the human diet. Clearly this result does not automatically follow the casual implementation of dietary carbohydrate restriction, however, as careful attention to time for keto-adaptation, mineral nutriture, and constraint of the daily protein dose is required.
the one caveat that anaerobic (ie, weight lifting or sprint) performance is limited by the low muscle glycogen levels induced by a ketogenic diet, and this would strongly discourage its use under most conditions of competitive athletics.
At the other end of the spectrum, higher protein intakes have the potential for negative side-effects if intake of this nutrient exceeds 25% of daily energy expenditure. One concern with higher levels of protein intake is the suppression of ketogenesis relative to an equi-caloric amount of fat (assuming that ketones are a beneficial adaptation to whole body fuel homeostasis).
12/05/2009 8:31am, #282“Most people do not do, but take refuge in theory and talk, thinking that they will become good in this way” -- Aristotle, Nicomachean Ethics, II.4
12/05/2009 5:44pm, #283
1) I brought this up with a kinesiology lecturer I know, and she took an interesting angle on it. Her reply reminded me of u1ysses's point about bias against social scientists in their own fields.
I wonder if perhaps there's some illusory sense of superiority of endocrinology over kinesiology, where an endocrinologist can "condescend" to doing a kin study without feeling obliged to check if the kin folk (sorry) know something he doesn't.
2) We still don't have a mechanism for elevated post-workout energy consumption (I don't even know what to call it, FFS), do we? I mean, there's EPOC (excess post-exercise oxygen consumption), but my understanding is that this more closely corresponds to accumulated oxygen debt than energy consumption.
Sitting here just now, an idea struck me:
-The energy sources that the body taps to generate high levels of power (physics definition) are faster (peak joules-per-second).
-Their substrates are also bulkier (grams per joule).
-What if they are also less efficient (joules of work:joules of waste energy)?
I think I managed to find an example in the Cori cycle:
(Edit: Sorry, the image doesn't show up well on black - see the Wiki article)
If this is what we're looking at, elevated post-workout energy consumption is compensating for the inefficiency of anaerobic glycolysis during exercise (for those reading along, inefficiency here is a good thing - it means greater caloric expenditure).
In order to examine the factors governing the timing and flexibility of skeletal muscle switching between fat and carbohydrate oxidation, Ukropcova et al. studied the effect of glucose and fatty acid availability on the preference for fat oxidation in myocytes cultured from human male quadriceps muscle taken from subjects with varied BMI, fat mass, and insulin sensitivity. The authors found that in vivo insulin sensitivity was related to a higher in vitro capacity for fat oxidation. These findings support the concept that the capacity of skeletal muscle to oxidize fat under appropriate physiological conditions is related to leanness, aerobic fitness, and insulin sensitivity.
I've been thinking a lot lately about the rate-limiting steps in fat oxidation. After all, we know how to increase oxygen supply (Tabatas, EPO/CERA, etc). If we can open the floodgates holding back lipid oxidation, the benefits to long-term endurance would be... Biblical.
they will run and not grow weary
they will walk and not be faint
Edit #2: I thought it was odd that the lactate/pyruvate transitions there didn't show any usage of energy. It seems to be bound to a NAD+ <--> NADH transition. I'm really fuzzy on this, but (cheating off page 107-108 of Bugg's "An introduction to enzyme and coenzyme chemistry"):
NAD+ + H+ + 2e- -> NADH
redox potential = -0.32V
Pyruvate + 2H+ + 2e- -> Lactate
redox potential = -0.19V
Pyruvate + NADH -> Lactate + NAD+
redox potential = +0.13V
Seems that NADH to NAD+ is energetically favourable and is driving the pyruvate to lactate conversion?
ΔG = − n (23.062 kcal) (ΔE)
n=2, ΔE=-0.19V -> ΔG = 8.76 kcal/mol
From Wiki, ATP->ADP = -30.5 kJ/mol, so that's about another quarter-ATP of inefficiency in the cycle.
12/06/2009 11:13pm, #284So as I may (or may not) have mentioned earlier, I've been mixing ~20g of flaxseed oil into my pre-bed shakes (along with olive oil, guar gum and milk protein isolate). Obviously I haven't been doing any training to speak of that would require anti-inflammatory effects, but...Many things we do naturally become difficult only when we try to make them intellectual subjects. It is possible to know so much about a subject that you become totally ignorant.
-Mentat Text Two (dicto)
12/06/2009 11:57pm, #285
Or in plain language: milk and booze? Gross!
(In happier news, my re-up of milk protein isolate should be here early this week...)
Oh, and as far as what it is, it's basically a mixture of slow-digesting stuff. The fats (olive and flaxseed oil) sit in the stomach (IIRC) for a while and slow gastric dumping. Casein (this is what most of the protein in milk is) takes a while to break down. Guar turns into a vaseline-like gel upon mixing with water, and slows down the movement of stuff through the digestive tract.
In a way, steak and cheese would probably do the same thing, but my mixture has one advantage - guar is a soluble fiber, so constipation isn't an issue.
12/07/2009 12:18am, #286
Oh, and as far as what it is, it's basically a mixture of slow-digesting stuff. The fats (olive and flaxseed oil) sit in the stomach (IIRC) for a while and slow gastric dumping. Casein (this is what most of the protein in milk is) takes a while to break down. Guar turns into a vaseline-like gel upon mixing with water, and slows down the movement of stuff through the digestive tract.Many things we do naturally become difficult only when we try to make them intellectual subjects. It is possible to know so much about a subject that you become totally ignorant.
-Mentat Text Two (dicto)
12/07/2009 1:33am, #287
12/07/2009 2:02am, #288
Looks like I fucked up.
On steroids athletes generally become less susceptible to fatigue, which allows longer, more frequent, and harder training sessions. Injuries to muscles, tendons, and ligaments occur less often in weight training, and when they do occur they heal more quickly than usual.
And is there experimental evidence to support these claims of testosterone's effects on connective tissue? There is, after a fashion:
Detailed studies dealing with the biological and metabolic effects of testosterone on the periodontium revealed that the sex steroid increased the proliferation of osteoblasts, as well as the formation of osteoid in the alveolar bone and the proliferation of cementoblasts on the tooth root surface. This hormone also increased the degree of cellularity in the periodontal ligament, and the formation of NaCl soluble collagen and the synthesis of glycosaminoglycans and hyaluronic acid.
Sorry, guys. I'll do better next time.
12/08/2009 12:23am, #289
The kids have been asking about hypertrophy lately.
We applied K-means cluster analysis to test the hypothesis that muscle-specific factors known to modulate protein synthesis and satellite cell activity would be differentially expressed during progressive resistance training (PRT, 16 wk) in 66 human subjects experiencing extreme, modest, and failed myofiber hypertrophy. Muscle mRNA expression of IGF-I isoform Ea (IGF-IEa), mechanogrowth factor (MGF, IGF-IEc), myogenin, and MyoD were assessed in muscle biopsies collected at baseline (T1) and 24 h after the first (T2) and last (T3) loading bouts from previously untrained subjects clustered as extreme responders (Xtr, n = 17), modest responders (Mod, n = 32), and nonresponders (Non, n = 17) based on mean myofiber hypertrophy. Myofiber growth averaged 2,475 µm2 in Xtr, 1,111 µm2 in Mod, and –16 µm2 in Non. Main training effects revealed increases in all transcripts (46–83%, P < 0.005). For the entire cohort, IGF-IEa, MGF, and myogenin mRNAs were upregulated by T2 (P < 0.05), while MyoD did not increase significantly until T3 (P < 0.001). Within clusters, MGF and myogenin upregulation was robust in Xtr (126% and 65%) and Mod (73% and 41%) vs. no changes in Non. While significant in all clusters by T3, IGF-IEa increased most in Xtr (105%) and least in Non (44%). Although MyoD expression increased overall, no changes within clusters were detected. We reveal for the first time that MGF and myogenin transcripts are differentially expressed in subjects experiencing varying degrees of PRT-mediated myofiber hypertrophy. The data strongly suggest the load-mediated induction of these genes may initiate important actions necessary to promote myofiber growth during PRT, while the role of MyoD is less clear.
I don't know that the experiment is especially important from my perspective (no offense intended to the authors), but the introduction is fascinating.
1) Lift heavy weights*
3) Gene expression
4) Muscle growth
In case anyone else was wondering what #2 was, you're not alone. Here's a juicy tidbit:
There have been some developments in understanding mechanotransduction mechanisms which result in electrical signals. The patch clamp technique has revealed that mechanosensitive channels exist, for example stretch activated Ca2+ channels in muscle. When looking for factors that activate gene expression,
the influx of anions or cations, particularly calcium and nitric oxide, have to be considered. However, as far as muscle is concerned extensive studies on cardiac myocytes by Izumo and coworkers
indicate that stretch induced hypertrophy of cardiac myocytes involves the production of autocrine growth factors (Sadoshima & Izumo, 1997). There is evidence that other cell systems also produce autocrine growth factors and the morphological basis of the mechanism involves the cytoskeleton and the extracellular matrix, the deformation of which leads to the activation of certain enzymes which result in the rapid production of signalling molecules (Ingebar, 1997). These in turn presumably induce a cascade of events and the
expression of transcriptional factors that activate the structural genes required for the repair and adaption of the individual cells.
* Actually, if you were following along carefully, you noticed that it's not lifting the weights (concentric), it's lowering them (eccentric) that seems to induce hypertrophy. Or, in the words of Dante "Doggcrapp" Trudel:
I try so hard to get the weight up only for the sole reason I can lower it slowly
Therefore for adaptation for sprinting short intensive bouts of
exercise are required as these result in increase in mass without the upregulation of slow myosin.
12/08/2009 1:28am, #290
so the women who are bitching at the WOD's about "getting too big" I can just tell "drop the weight quickly!"? interesting, seems totally intuitive...beyond that gobbeldy-****^Many things we do naturally become difficult only when we try to make them intellectual subjects. It is possible to know so much about a subject that you become totally ignorant.
-Mentat Text Two (dicto)