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Some butter on top of the broccoli would allow for the assimilation of the absorption of the 101.6?g vitamin K 623IU vitamin A (various).

There are a handful of very basic questions in nutrition science, no one appears to have an answer to. One of these questions, which is directly related to the  well-known fact that the vitamins A, D, E & K are "lipid soluble". This means that they are "solved" and thus made absorbable by fats and oils. The general assumption is thus that the vitamins A, i.e. the retinol and carotenoids, all forms of vitamin D, the tocopherols and -trienols (vitamins E) and the two major forms of vitamin K, i.e. phylloquinone (K1) and menaquinone (K2) will only be absorbed, if you consume them with a sufficient amount of dietary fat. Now, the questions obviously are (a) is this correct and (b) how much is sufficient.
In view of the fact that the answers to (a) and be are not necessarily identical for all four vitamins of interest, it appears sensible to tackle them one after the other.


Starting with vitamin A and the various forms of carotenoids, we can already confirm that (a), i.e. the assumption that we need dietary fats to optimally absorb vitamin A is correct. As Karin van het Hof and her colleagues point out, the "amount of dietary fat required to ensure carotenoid absorption [does yet] seem low (?3–5 g per meal), although it depends on the physicochemical characteristics of the carotenoids ingested." (van het Hof. 2000) In spite of the fact that 5g of fat are not exactly much, the classic uncooked vegetarian orthorexic salad often comes with a total of only 5g of fat of which 95% remain at the bottom of the salad bowl. If that sounds like your favorite dish, you should be aware that you are risking that all the good  beta- and other carotenoids in the salad will pass right through.

Figure 1: Changes in hepatic vitamin A (retinol) and carotenoid stores in gerbils after 14 days on high fat (30%) vs. low fat (10%) diet (Deming. 2000)

In that, the concomitant presence of both dietary fat and carotenoids in a meal is a necessary prerequisite for the absorption of vitamin A, also because the fatty acids will trigger the conversion of of beta-carotene into vitamin A and its subsequent absorption via the lymphatic system (Ribaya?Mercado. 2002). It is thus not surprising that animal studies by Lakshman et al. (1996) and Deming et al. (2000; see Figure 1) suggest that low fat diet can lead to a depletion of the vitamin A tissue stores even if the serum levels remain constant. The amount of fiber in the diet, on the other, has no influence the absorption of vitamin A (Mills. 2009).

Interestingly enough, the provision of the fat blocker Orlistat reduces the absorption of vitamin A only insignificantly, as a 1996 paper by Angela T. Melia, Susan G. Koss?Twardy, and Jianguo Zhi would suggest (Melia. 1996).

Which takes us right to vitamin E, the absoprtion which is - in spite of being "blocked" by the fat blocker orlistat (Melia. 1996) - less susceptible to the absence of dietary fat than you may think. Annet JC Roodenburg, Rianne Leenen, Karin H van het Hof,  Jan A Weststrate, and Lilian BM Tijburg do in fact argue that the optimal intake of vitamin E requires only "a limited amount" of dietary fat (Roodenburg. 2000).

Figure 2: Vitamin E serum levels after 7 days on control (low fat, 3g) or high(er) fat (36g) diet with and without supplemental vitamin E (Roodenburg. 2000)

As you can see in Figure 2. A minimum intake of only 3g per day was sufficient to keep the vitamin E levels stable. The short study period of 7-days (each) and the absence of measures of tissue concentration of vitamin E do yet reduce the practical relevance of the data, Roodenburg et al. present in their Y2k paper in the American Journal of Clinical Nutrition.
If you take a look at the high prevalence of vitamin E dieficiency among the fat (and PUFA) "loving", or at least eating, majority of Americans, it does yet become obvious that a lack of dietary fat is not just theoretically, but also practically not exactly the #1 reason you may become deficient in tocopherols and -trienols. That the latter is an increased demand due to chronic inflammation and the (over-)consumption of exactly those PUFAs that come with a shitload of vitamin E in nature, for a reason would yet be a topic for another SuppVersity article and thus something we will skip to fast forward to ...

...Vitamin K, obviously. Vitamin K is a relative newcomer to the publics understanding of the alphabet soup. Aside from being it a good tool to rip customers vitamin K, or rather K1 (plant sources) and K2 (animal sources) are thus also the only fat soluble vitamins not everyone knows. The fact that the amount of phylloquinone (K1) that makes it into your blood stream is ~70% reduced if you eat your spinach without fat (Gijsbers. 1996).

And if we take the results researchers from the Gifu University School of Medicine present in a 1996 paper in the Journal of Pharmacological Sciences, as a reference, the amount of fat you need to optimally absorb your K2 (menaquinones), is not exactly low.

Figure 3: For optimal absorption of K2, there has got to be a huge amount of fat in the meal - but who wonders. K2 comes with a high amount of fat (Uematsu. 1996)

Uematsu et al. had to supply their subjects, who consumed otherwise identical test meals with 8.8, 20.0 and 34.9g of fat in them with the maximal (i.e. 35g) of fat before the K2 absorption maxed out. In that the total area under the curve did not really differ between those subjects who consumed the K2 before and those who took it immediately after the test meal.

Thats a pity, cause a high intake of vitamin K (menaquinone from animal sources) has been associated with a 27% reduced risk of developing heart disease (Geleijnse. 2004), an ailment of which many still believe that it was brought about by the fat they need to optimally absorb their vitamin K.

For vitamin D, our last "V" on the list, things look differently. For one, everybody knows about this miracle vitamin and for two, it may be "fat soluble", but the amount of fat thats required to optimally absorb it turned out to be much lower than previously thought (see "A Fat D-Ficiency! Do You Really Need More Vitamin D or Simply More Fatty Foods? Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat. " | read more).
In fact, Niramitmahapanya et al. found in 2011 that its not necessarily a high amount, but rather the right type of fat that determines if and how much of the vitamin D you take in capsule form or find in comparably low amounts in your foods that determines how much of the vitamin D actually makes it into your bloodstream:

"The change in plasma 25OHD (nanograms per milliliter) during vitamin D supplementation was positively associated with MUFA, (? = 0.94; P = 0.016), negatively associated with PUFA, (? = ?0.93; P = 0.038), and positively associated with the MUFA/PUFA ratio (? = 6.46; P = 0.014)."

In plain English this means, that the "good" seed and vegetable oils with their high PUFA content will effectively inhibit the absorption of vitamin D - an observation that adds to the many reasons the modern sedentary, sun-avoiding, sun-screen using, soybean oil (MUFA:PUFA = 0.4) guzzling American is low in or  quasi devoid of vitamin D.

Figure 4: 25(OH)D levels of 30 healthy men and women after ingestion of 50.000IU vitamin D3 supplement in conjunction with a normal or low fat breakfast (Raimundo. 2011)

Against that background its not surprising that you will not find a conclusive answer to the question how much fat you actually need. In a study that used a fatty meal with soybean oil in it, the effect would be totally different from one in which the subjects consumed meals that were made with sunflower oil, an oil with a MUFA:PUFA ratio >1. In view of the results Gnadinger et al present in a recent appear it does still seem appropriate to consume at least some fat alongside your vitamin D supplements. As far as the food-borne vitamin D is concerned, you dont have to worry, anyways. Foods that are high in D3 usually come with all the fat you need to absorb it.

How much fat, exactly you would need to make the most of dietary and supplemental vitamin D, on the other hand, is still not known. The previously mentioned data from the study by Raimondo et al. (see Figure 4, to the right) I wrote about in "A Fat D-Ficiency" is obviously still valid. The extremely high amount of vitamin D (50,000IU!) could yet require a correspondingly high amount of fat to be optimally absorbed and the fact that the fat in the study came from a "vegetable margarine" with an undisclosed ratio of MUFA:PUFA does not make the real-world effects any more predictable.
References:

• Chitchumroonchokchai, Chureeporn, et al. "Dietary fats with increased ratio of unsaturated to saturated fatty acids enhance absorption of carotenoid and vitamin E by increasing both efficiency of micellarization and lipoprotein secretion." FASEB J 24 (2010): 539-3.
• Deming, Denise M., et al. "Amount of dietary fat and type of soluble fiber independently modulate postabsorptive conversion of ?-carotene to vitamin A in Mongolian gerbils." The Journal of nutrition 130.11 (2000): 2789-2796. 
• Geleijnse, Johanna M., et al. "Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study." The Journal of nutrition 134.11 (2004): 3100-3105.
• Gijsbers, Birgit LMG, Kon-Siong G. Jie, and Cees Vermeer. "Effect of food composition on vitamin K absorption in human volunteers." British Journal of Nutrition 76.02 (1996): 223-229.
• Goodman, Dew S., et al. "The intestinal absorption and metabolism of vitamin A and beta-carotene in man." Journal of Clinical Investigation 45.10 (1966): 1615.
• Jayarajan, P., Vinodini Reddy, and M. Mohanram. "Effect of dietary fat on absorption of ? carotene from green leafy vegetables in children." Indian journal of medical research 137.5 (2013).
• Kris-Etherton, P. M., et al. "Polyunsaturated fatty acids in the food chain in the United States." The American journal of clinical nutrition 71.1 (2000): 179S-188S.
• Lakshman, M. R., et al. "The effects of dietary taurocholate, fat, protein, and carbohydrate on the distribution and fate of dietary ??carotene in ferrets." (1996): 49-61.
• Melia, Angela T., Susan G. Koss?Twardy, and Jianguo Zhi. "The effect of orlistat, an inhibitor of dietary fat absorption, on the absorption of vitamins A and E in healthy volunteers." The Journal of Clinical Pharmacology 36.7 (1996): 647-653.
• van het Hof, Karin H., et al. "Dietary factors that affect the bioavailability of carotenoids." The Journal of nutrition 130.3 (2000): 503-506.
• Raimundo, Fabiana Viegas, et al. "Effect of high-versus low-fat meal on serum 25-hydroxyvitamin D levels after a single oral dose of vitamin D: a single-blind, parallel, randomized trial." International journal of endocrinology 2011 (2011).
• Ribaya?Mercado, Judy D. "Influence of Dietary Fat on ??Carotene Absorption and Bioconversion into Vitamin A." Nutrition reviews 60.4 (2002): 104-110.
• Roodenburg, Annet JC, et al. "Amount of fat in the diet affects bioavailability of lutein esters but not of ?-carotene, ?-carotene, and vitamin E in humans." The American journal of clinical nutrition 71.5 (2000): 1187-1193. 
• Uematsu, Toshihiko, et al. "Effect of dietary fat content on oral bioavailability of menatetrenone in humans." Journal of pharmaceutical sciences 85.9 (1996): 1012-1016.

Scientific evidence suggests: There is not one optimal protein to build muscle - its the mix of fast to slow proteins thats key.

For someone like yourself, whos making sure to get his daily dose of SuppVersity Science News, the results Reidy et al. present in their latest paper in the Journal of Applied Physiology can hardly be surprising. I have, after all, written about the superiority of whey + casein blends as potential muscle builders only recently ("When Whey & Casein Unite in the Spirit of True Physique Improvements, BCAAs & Glutamine Better Shut the F*** Up"  | (re-)read the article). It was thus only to be expected that a study in which the scientists from the University of Texas Medical Branch compared the effects of the prolonged hyperaminoacidemia thats associated with the ingestion of a blend of plant (25% soy) and dairy (50% casein, 25% whey) proteins (with varying digestion rates) to that of a pure rapidly digested whey would yield a definite points win for the "time-released" formula.
The reasons why its still well worth taking a closer look at the study results are (a) the fact that the f**** up supplement industry is still trying to tell you that protein blends would be inferior to overpriced isolates and (b) the educative value of the post-workout + post-supplementation serum amino acid profiles Reidy et al. observed the 16 healthy, young subjects (age range: 19 –30 yr) who participated in their double-blind, randomized clinical trial (with body fat levels of >24% those were certainly no physical culturists, though ;-)

Figure 1: Graphical overview of the study design (Reidy. 2014)

As you can see in Figure 1 the study protocol involved a standardized resistance training session in the course of which the subjects who had been kept on a diet containing 20% protein, 60% carbohydrate, and 20% fat at 12 kcal/kg for 72h, performed leg extensions on a Cybex-VR2 (Medway, MA), i.e. 8 sets of 10 repetitions at 55% (set 1), 60% (set 2), 65% (set 3), and 70% (sets 4 – 8) of the participants previously determined 1 RM with 3-min rest between sets, before they consumed the protein beverages (Whey or Blend) exactly 1 h postexercise.

Figure 2: Net phenylalanine enrichment (left) and inward and outward transport (right)

The ingestion of the beverages of which the blend and the whey protein contained of 20.1 g total protein (providing 1.9 g leucine, 1.0 g phenylalanine, 1.3 g valine, and 9.0 g EAA; 50% protein from sodium caseinate, 25% protein from whey protein isolate, and 25% protein from soy protein isolate) and 17.3 g of protein (providing 1.9 g leucine, 0.6 g phenylalanine, 1.1 g valine, and 8.7 g EAA; 100% whey protein isolate), respectively, lead to significant increases in amino acid transporter activity (2/SLC38A2, proton-assisted amino acid transporter 1/SLC36A1, cationic amino acid transporter 1/SLC7A1).

"However, the ingestion of the protein blend resulted in a prolonged and positive net phenylalanine balance during postexercise recovery compared with whey protein (P 0.05)." (Reidy)

In view of identical postexercise myofibrillar protein synthesis in both groups this difference may appear negligible. If youve been following my articles about the often oversimplified protein synthesis and increases in skeletal muscle mass, you should be aware that net retention and not fractional synthesis is the term you have to look for, when youre analyzing corresponding studies.
Reference: 

• Reidy, Paul T., et al. "Soy-dairy protein blend and whey protein ingestion after resistance exercise increases amino acid transport and transporter expression in human skeletal muscle." Journal of Applied Physiology 116.11 (2014): 1353-1364.

Compared to liquid beverages, gels have the advantage of causing lower GI stress, when significant quantities of CHOs are consumed during exercise. Bars, can be held in the cheek pouch and chewed during critical phases of a race.

The headline gives it away. Todays SuppVersity article is a brief review of the (mostly sponsored) literature on Gatora.... ah, I mean carbohydrate supplementation during exercise. The headline also implies that the usefulness and efficacy of carbohydrate supplements depends on exercise duration and the type of exercise.

As a seasoned student of the SuppVersity you will know that certain paradox involved with regard to the duration / type of exercise. Short exercise durations, for example, shouldnt require large CHO boluses, long duration exercise, on the other hand, is fueled mostly by fat - so why should you supplement with carbohydrates, anyway?
I promise to answer this and other questions in the following paragraphs, but before I do so, I would like to point out that there is as of now no evidence that the much-praised "fat adaptation" increases the exercise performance to an "Olympia" level. Carbohydrate supplements, on the other hand, are still part of the regular supplementation regimen for the 99% of the top athletes.

That being said, the human physiology dictates that the use of carbohydrate supplements during aerobic workouts that last less than 60 minutes is useless, because muscle glycogen is generally not limiting to performance when exercise durations are less than ~60 minutes.

It should not work for short duration exercise, but it still does

Interestingly, 16 out of 23 studies, Trent Stellingwerff and Gregory R. Cox from the Canadian Sport Institute-Pacific and the Australian Institute of Sport reviewed for their recent paper in Applied Physiology have found that carbohydrate supplementation and/or oral (mouth) exposure to carbohydrate can improve performance of tasks less than 1 hour in duration:

You wont fully deplete your muscular glyocogen levels during short duration resistance training (Haff. 2003)

"In 2004 a seminal paper was published showing that a carbohydrate mouth-wash (swirling 25ml of a 6% CHO beverage (only ~1.5g of CHO in 25ml [6.4% maltodextrin solution (CHO)]) around in the mouth for ~10 sec, every 7.5min) significantly improved time trial (TT) performance [in seven male and two female endurance cyclists] by ~3% (Carter et al. 2004a)." (Stellingwerff & Cox. 2014)

This effect of CHO mouth-washing to improve performance in events from 30-60min has now been replicated in several other performance studies (10 of 13 studies) using both cycling and running interventions and with both sweet (sucrose) and non-sweet (maltodextrin) caloric CHO sources,as compared to 5 non-caloric artificial sweetener placebo trials showing no performance enhancing effects.

Figure 1: Hard to believe, but true - In 2010 Pottier et al. observed that CHO mouth-rinsing, but not CHO ingestion increases the 1h high intensity time-trial performance in trained subjects.

 "All these findings have been mechanistically supported with a functional magnetic resonance brain imaging study showing that CHO mouth-washing from both sweet tasting glucose and non-sweet maltodextrin can stimulate the brain areas of the insula/frontal operculum, orbitofrontal cortex and striatum, which are involved with brain centers responsible for reward and motor control (Chambers et al. 2009). Interestingly, if the mouth (oral receptors) and GI tract is by-passed by CHO infusion straight into the blood stream then 1h cycling TT performance was unaltered as compared to no CHO supplementation (Carter et al. 2004b)." (Stellingwerff & Cox. 2014)

Studies evaluating the effects on perceived exertion (Fares et al. 2011) found similar benefits all of which support the idea that the effect does not occur in the musculature, but rather in the head.
It should be obvious that the physiological, or rater intra-muscular benefits of carbohydrate supplements increases with the exercise duration.

CHO supplementation during exercise that lasts 60 minutes or longer

In view of the fact that it is 100% logical and well established by studies by Coyle et al. (Coyle 1992a; Coyle 1992b) that the intake of carbohydrate (glucose alone, and glucose + fructose blends) can significantly improve prolonged endurance capacity and performance (>60min of exercise (Jeukendrup 2010)).

Figure 2: Overview of the performance increases in the 50 studies Stellingwerff & Cox reviewed (2014)

Against that background I will not bother you with another overview of the results, but focus on the efficacy of different carbohydrate supplementation strategies and types of carbohydrate supplements for exercise durations beyond the "magical" hour.

Glucose + fructose - the combination advantage

As a SuppVersity reader youve previously heard about the benefits of combining glucose and fructose in your intra-workout beverage. It is thus only logical that most commercially available formulas are mixtures  glucose + fructose (GLU:FRU) or maltodextrin + fructose - so-called "multi-transportable CHOs". The advantage of using both glucose and fructose is that the carbohydrates will be absorbed via SGLT1 and GLUT5 intestinal transporters.

Specifically during long(er) duration exercise, when the carbohydrate consumption can exceed 60g/h there is a significant performance increase with multi- vs. single source carbohydrate supplements (Stellingwerff & Cox. 2014)

An advantage that has been scientifically established among others by Jeukendrup et al. (2010) who found that this pattern of CHO ingestion results in ~20 to 50% higher CHO oxidation rates compared to the ingestion of a drink that contains nothing but glucose or maltodextrin.


Now an increase in carbohydrate oxidation alone does not sound like something you would aim for as an endurance athlete. In practice, increases in carbohydrate oxidation have yet been shown to increase the performance during prolonged exercise bouts compared to isocaloric glucose-only beverages. (Currell et al. 2008; Triplett et al. 2010; OBrien et al. 2011; OBrien et al. 2013).
Needless to say that there is still research to be done with respect to individual influencing variables of carbohydrate requirements. The currently available evidence, for example, is largely based on results from runners and cyclists. Two other factors / issues that come to mind are...

• the dose-response relationship, which appears to be capped at 75g/h - at least according to a large-scale multi-center study by Smith et al. (Smith. 2013) who found that their subjects, endurance trained cyclists or triathletes experienced significant performance increases, with increasing amounts of carbohydrates (0, 10, 20, 30, 40, 50, 60, 70, 80, 90, 100, 110 and 120g of CHO/h) during a 2h constant load ride.
  
  

  Figure 3: Mean log time to complete time trial (natural) as function of CHO treatment condition with fitted quadratic curve (with 95% CI of mean curves). Differences 100 represent percent change in performance. The quadratic function relating CHO ingestion rate to time complete time trial for 43% (95% CI = 11%–75%,P= 0.059) of the variation in mean performance score (Smith. 2013)

  The CHO given was a 1:1:1 glucose:maltodextrin:fructose blend. Results indicated incremental performance improvements of 1.0%, 2.0%, 3.0%, 4.0%, and 4.7% at 9, 19, 31, 48, and 78g CHO/h, respectively, with diminishing performance enhancement seen at CHO levels >78g/h.
  
  The optimal amount for performance (+4.7%) was 78g/h, with a range of 68 to 88g/h. However, even at 10g/h, a 1.0% increase in performance was observed, showing even a small amount of carbohydrate has the potential to positively impact performance. 
• the optimal mix of glucose, dextrose, fructose, maltodextrin or other "special" carbohydrates  - needless to say that waxy maize, hydroxypropyl distarches (learn more) or the expensive fast absorbing highly insulinogenic patented carbohydrate source Vitargo come to mind, when we are talking about finding the optimal mix of different carbohydrate sources - a mix, by the way, of which you can safely assume that it will differ according to the physiological demands of the workout and the exercise duration.
  
  One thing we shouldnt forget, though, is that next to optimal performance, optimal GI tolerance, i.e. the absence of bloating, diarrhea & co would be an important criteria the "optimal" carbohydrate blend would have to meet.

• Figure 4: CHO suppl. ameliorates  testosterone reductions in 800m runners (de Sousa. 2010)

  the impact of carbohydrate supplementation on hormonal changes during and in response exercise - several human studies suggest that CHO supplementation attenuates the suppression of the hypothalamic-pituitary-gonadal axis and the rise in stress hormones during periods of intense training; a recent rodent study shows that the provision of carbohydrate supple- ments can prevent / reverse exercise-associated menstrual dysfunction (de Sousa. 2010; Zhao. 2014)

I guess, I could come up with additional research gabs, but in the end, a list of "gaps" is not exactly useful for you. Much in contrast to a conclusion, which I am about to formulate in the bottom line, now.
References:

• Carter,  J.,  Jeukendrup,  A.E.,  Mundel,  T.,  and  Jones,  D.A.  (2003).  Carbohydrate  supplementation  improves moderate and high-intensity exercise in the heat. Pflügers Archiv : European journal of physiology446: 211-9.
• Carter, J.M., Jeukendrup, A.E., and Jones, D.A. (2004a). The effect of carbohydrate mouth rinse on 1-h cycle time trial performance. Medicine and science in sports and exercise36: 2107-11.
• Carter, J.M., Jeukendrup, A.E.,  Mann, C.H., and  Jones, D.A. (2004b). The effect of glucose infusion on glucose kinetics during a 1-h time trial. Medicine and science in sports and exercise36: 1543-50. 
• Chambers,  E.S.,  Bridge,  M.W.,  and  Jones,  D.A.  (2009). Carbohydrate  sensing  in  the  human  mouth:  effects  on exercise performance and brain activity. The Journal of physiology587: 1779-94. 
• de Sousa, Maysa Vieira, et al. (2010). Effects of carbohydrate supplementation on competitive runners undergoing overload training followed by a session of intermittent exercise." European journal of applied physiology 109.3: 507-516.
• Fares, E.J. and Kayser, B. (2011). Carbohydrate mouthrinse effects on exercise capacity in pre- and postprandial States. J Nutr Metab2011: 385962.   
• Pottier, Andries, et al. (2010). Mouth rinse but not ingestion of a carbohydrate solution improves 1?h cycle time trial performance" Scandinavian journal of medicine & science in sports 20.1: 105-111.
• Sawka,  M.N.,  Burke,  L.M.,  Eichner,  E.R.,  Maughan,  R.J.,  Montain,  S.J.,  and  Stachenfeld,  N.S. (2007).  American College of Sports Medicine position stand. Exerciseand fluid replacement. Medicine and science in sports and exercise39: 377-90.
• Smith, JohnEric W., et al. (2013). Curvilinear dose-response relationship of carbohydrate (0-120 g/h) and performance." Med Sci Sports Exerc 45.2: 336-341. 
• Stellingwerff, T., & Cox, G. R. (2014). Systematic Review: Carbohydrate Supplementation on Exercise Performance or Capacity of Varying Durations. Applied Physiology, Nutrition, and Metabolism (2014). Ahead of Print. 
• Zhao, Can, et al. (2014). Effects of carbohydrate supplements on exercise-induced menstrual dysfunction and ovarian subcellular structural changes in rats." Journal of Sport and Health Science 3.3: 189-195.

Are you training for nothing, if you are "too old" (whatever that may be)? Find out in todays SuppVersity Article!

"The older we get, the weaker we are." Thats something most normal men accept as a given truth - according to the latest science, it does yet appear as if it was more of a self-fulfilling prophecy.

Researchers from the Department of Biology of Physical Activity and Neuromuscular research Center at the University of Jyväskylä in Finland have recently conducted a study to verify the common sense assumption that older men are having a much harder time to to maintain / increase their muscle strength than young ones.

To find out, whether this would also be true for those, who are willing to succumb to a high volume, medium load “hypertrophic” resistance training, the Häkkinen et al. recruited young (28 ± 5 yr, 179 ± 6 cm, 77 ± 12 kg, 21 ± 8 percent fat) and older (65 ± 4 yr, 177 ± 6 cm, 80 ± 10 kg, 23 ± 6 percent fat) men via an advertisement in a local newspaper.
The experimental groups consisted of 23 young and 26 older men (training groups) and the non training control groups consisted of 10 young and 11 older men. The goal was to achieve maximum strength, muscle mass and muscle activation of the lower limbs in both groups.

Table 1:  Resistance training program of the young and older experimental groups (performed with resistance machines)

To this ends, both groups performed 10 weeks of whole-body resistance training twice per week with the emphasis on lower limb exercises. The training program consisted of high volume, medium intensity exercise with short inter-set rest intervals, as it is typically performed by bodybuilders (i.e. 2-5 sets of 8-14 repetitions, 1-2 min rest).

Lower limb exercises, i.e. leg press, knee extension and knee flexion, were performed before upper body exercises. At least 48 h rest was required between training sessions. Maximum dynamic and isometric neuromuscular performance, as well as lean leg and muscle mass were examined before and after the training period. The changes in body composition were assessed 3-4 d and neuromuscular measurements were performed 7 d after the last training session.

Before participating in the study at hand, the "subjects were physically active but unaccustomed to resistance training for the previous 6 months." Training and testing took place throughout the day (9am-7pm), but young and older subjects were pair-matched to avoid any time-of-day effects on neuromuscular performance measurements. All subjects were given nutritional advice in an attempt to maximize muscle hypertrophy, however, no direct nutritional intervention was performed in the present study.
The resistance training program consisted of . Briefly, leg exercises (bilateral leg press, knee extension, and knee flexion) were performad before upper body and torso exercises; bench press, pulldown, shoulder press, seated row, triceps pushdown, biceps curl, abdominal crunches and back raises.

"The subjects performed medium intensity, high volume training consisting of 2–3 sets and 12–14 reps (60–70% 1RM) per exercise (weeks 1–4), then 2–3 sets and 10–12 reps (70–80% 1RM) per exercise (weeks 5–7), and 3–4 sets per exercise and 8–10 reps (75–85% 1RM) per exercise (weeks 8–10). One min rest was given between sets during weeks 1–4, and then 2 min rest was given between sets during the remaining weeks 5–10. One set was performed to failure during each training session." (Häkinnen. 2014)

As youve probably recognized by now this is a more or less classic linear periodization; a very conservative periodization technique with a lot of back up that it works (learn more about periodization).

Figure 1: Pre- and post values for 1RM and isometric leg strength (Häkkinen. 2014)

If you look at the results, youll see that this protocol led to significant increases in one repetition maximum (1RM) leg press performance in both training groups (young: 13 ± 7 %, P < 0.001; older: 14 ± 9 %, P < 0.001).

Interestingly, said performance improvements were accompanied by increased muscle activation, assessed by voluntary activation level (29 ± 51%, P < 0.05) and electromyography amplitude (35 ± 51 %, P < 0.01) in older men only. Unfortunately, only the young men showed significantly increased lower limb lean mass (2.4 ± 2.5 %, P < 0.01), which were furthermore significantly related to the strength increments (r = 0.524, P = 0.01, n = 23).
References:

• Häkinnen, et al. "Similar increases in strength after short-term resistance training due to different neuromuscular adaptations in young and older men." Journal of Strength and Conditioning Research (2014). Publish Ahead of Print.

Maximal protein synthesis requires protein, but how much exactly you need will depend on your age - the older you are the more PWO protein youll need.

Scientists from the University of Auckland were fed up with the lack of information about the differential response in protein synthesis in response to the ingestion of various amounts of protein. Accordingly, Randall F. D’Souza et al. conducted a study to characterize the changes in intramuscular levels of EAAs and BCAAs and the expression of the "protein pump" p70S6K at Thr389, a marker of protein synthesis, in response to resistance exercise and graded ingestion of whey protein in older men.

As a regular SuppVersity reader you will probably already think: "Where is the actual measurement of the fractional protein synthesis?" The unfortunate answer: Its not there.
Previous research had show that the ingestion of graded amounts of high-quality protein such as whey after resistance will maximize with "only" 20g of egg protein (Moore. 2009) or whey (Witard. 2014) in young men. Multiple studies in older adults (>60 years), on the other hand, suggest that they exhibit a lower anabolic signaling and MPS response to protein feeding, resistance exercise, and the combination of feeding and exercise when compared to young men (Cuthbertson. 2005; Fry. 2011; Burd. 2013). Scientists call this phenomenon age-related "anabolic resistance" (Yang. 2012b).

Figure 1: In contrast to the fractional protein synthesis in the elderly, which increases with increasing amounts of protein, the FSR of young men shows a ceiling effect at 20g+ whey protein (Yang. 2012a; Moore. 2009)

As you can see in Figure 1 from a 2012 study by Yang, the same 20g of extra-whey (total dose 40g) that was useless in young men, lead to a significant increase in protein anabolism in elderly men. Compared to young men, the MPS response to feeding 40 g of protein was yet still slightly lower in older vs. count men (Yang. 2012a; Churchward Venne. 2013b).

What is particularly relevant for the study at hand, and the previously criticized absence of actual MPS measurements is the fact that deficits in feeding induced p70S6K phosphorylation may at least partially underpin anabolic resistance in aged skeletal muscle (Cuthbertson. 2005), which is why measuring the p70S6K phosphorylation in older human subjects (mean age 71 years) in response to the graded ingestion of whey protein after a leg workout consisting of three sets of 8–10 repetitions of bilateral barbell smith rack squat, 45°leg press, and seated knee extensions at 80% of the subjects predetermined 1R is not as irrelevant at it may initially have seemed.

Workout + supplements, thats the "whey to go" ;-)

The exercises were performed in a circuit manner with 1 min rest between each exercise and 3 min rest between subsequent sets, the exercise protocol took approximately 20 min to complete. Following completion of the exercise protocol, subjects were immediately provided with a fixed-volume (350 mL) beverage, containing a flavored noncaloric placebo, or oneof the four doses of whey protein concentrate (10 g, 20 g, 30 g, or 40 g).

Figure 2: Intramuscular amino acids. This figure is a heat map which shows groups means fold changes from the resting fasted condition. Green represents a decrease in amino acid content, white represents no change, and red represents an increase in amino acid content (D’Souza. 2014)

Subjects were instructed to ingest the beverage within 2 min and were required to ingest the total volume provided. Following consumption of the supplements, subjects rested in a supine position throughout the 4 h of post-exercise recovery with additional muscle biopsy samples collected at 2 and 4 h post exercise.

Figure 3: Higher protein intake = higher increase in p70S6K phosphorylation (left graph). This increase is linearly associated with intramuscular leucine levels (right graph | both from D’Souza. 2014)

As you can see in Figure 3, there was a similar dose-dependent increase in p70S6K as it was observed previously for MPS in skeletal muscle of elderly subjects by Yang et al. (2012b). In fact, the fold change in the phosphorylation of p70S6K (Thr389) at 2 h post exercise was correlated with the dose of whey protein consumed (r =0.51,P<001) and was found to be significantly correlated with intramuscular leucine content (r =0.32,P=0.026).

Moreover, the intramuscular BCAAs, and leucine in particular, appear to be important regulators of anabolic signaling in aged human muscle during post-exercise recovery via reversal of exercise-induced declines in intramuscular BCAAs.
References:

• Burd, N. A., S. H. Gorissen, and L. J. van Loon. 2013.  Anabolic resistance of muscle protein synthesis with aging. Exerc. Sport Sci. Rev. 41:169–173.
• Churchward-Venne, T. A., N. A. Burd, C. J. Mitchell, D. W. West, A. Philp, G. R. Marcotte, et al. 2012. Supplementation of a suboptimal protein dose with leucine or essential amino acids: effects on myofibrillar protein synthesis at rest and following resistance exercise in men. J. Physiol. 590:2751–2765.
• DSouza, Randall F., et al. 2014. Dose?dependent increases in p70S6K phosphorylation and intramuscular branched?chain amino acids in older men following resistance exercise and protein intake. Physiological Reports 2.8: e12112.
• Churchward-Venne, T. A., L. Breen, and S. M. Phillips. 2013a. Alterations in human muscle protein metabolism with aging: protein and exercise as countermeasures to offset sarcopenia. BioFactors 40:199–205.
• Churchward-Venne, T. A., C. H. Murphy, T. M. Longland, and S. M. Phillips. 2013b. Role of protein and amino acids in promoting lean mass accretion with resistance exercise
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• West, D. W., and K. Baar. 2013. May the Force move you: TSC-ing the mechanical activation of mTOR. J. Physiol. 591:4369–4370.
• West, D. W., N. A. Burd, J. E. Tang, D. R. Moore, A. W. Staples, A. M. Holwerda, et al. 2009a. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. J. Appl. Physiol. 108:60–67 .
• West, D. W., G. W. Kujbida, D. R. Moore, P. Atherton, N. A. Burd, J. P. Padzik, et al. 2009b. Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men. J. Physiol. 587:5239–5247.
• Witard, O. C., S. R. Jackman, L. Breen, K. Smith, A. Selby, and K. D. Tipton. 2014. Myofibrillar muscle protein synthesis rates subsequent to a meal in response to increasing doses of whey protein at rest and after resistance exercise. Am. J. Clin. Nutr. 99:86–95
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• Yang, Y., T. A. Churchward-Venne, N. A. Burd, L. Breen, M. A. Tarnopolsky, and S. M. Phillips. 2012b. Myofibrillar protein synthesis following ingestion of soy protein isolate at rest and after resistance exercise in elderly men. Nutr. Metab. 9:57.