Friday, 1 February 2013

Diet - Carbs in the evening| Muscle & Strength

Revamp Your Routine With Whole Body Training And A New Diet | Muscle & Strength

 Diet - Carbs in the evening

Looking to re vamp your diet for weight loss/maintenance? Low carbohydrate dieting is becoming increasingly popular thanks to its quick onset of weight loss for bodybuilders and recreational lifter a like. Some of the most common struggles with low carbohydrate diets are centered on a lack of energy and compliance to limiting daily intake of carbohydrates.

Recent research by Israeli scientists on obese police officers confirmed that consuming carbohydrates in the evening increased dietary compliance and subsequently weight loss. How is this possible? It has always been assumed that consuming carbohydrates in the evening would lead to an increase in fat stores.

The reasoning behind this is based on the fact that there is less potential for energy expenditure in the evenings and because leptin levels (signal satiation) work through circadian rhythms throughout the day, and they are highest in the evening. Although this is true, what must be remembered when it comes to weight loss is that the two factors that supersede nutrient timing are the total number of macronutrients consumed in a day and most importantly: the total number of calories consumed in a day.

If you were on a very low carbohydrate diet of only 100 grams of carbs a day and you consumed that quantity at night before going to sleep, do you believe that would halt weight loss? While it wouldn’t be ideal, your body would still have to metabolize more fat for fuel when the sum of the low carbohydrate days are added together.

Noticeable fat loss doesn’t happen in a day, you can’t eat healthy for one or two days and expect a change; fat loss occurs when a sum of calorie/macronutrient restricted days are put together. With that in mind, consider this: consuming carbohydrates in the evening does spike insulin, however the large spike in leptin levels increases satiation and thus compliance with a dietary regimen the following day.
So don’t be afraid of consuming carbohydrates at dinner time while on a low carb diet, as long as you’re not surpassing your total daily carbohydrate limits, this strategy will actually work to increase diet compliance.

Dustin Elliott is the Head Formulator for Betancourt Nutrition.

Capacity for Moderate Exercise in Obese Subjects after Adaptation to a Hypocaloric, Ketogenic Diet


Logo of jcinvestThe Journal of Clinical InvestigationCurrent IssueArchiveSubscriptionAbout the Journal
J Clin Invest. 1980 November; 66(5): 1152–1161.
PMCID: PMC371554

Capacity for Moderate Exercise in Obese Subjects after Adaptation to a Hypocaloric, Ketogenic Diet

The Journal of Clinical Investigation 

Abstract

To study the capacity for moderate endurance exercise and change in metabolic fuel utilization during adaptation to a ketogenic diet, six moderately obese, untrained subjects were fed a eucaloric, balanced diet (base line) for 2 wk, followed by 6 wk of a protein-supplemented fast (PSF), which provided 1.2 g of protein/kg ideal body wt, supplemented with minerals and vitamins. The mean weight loss was 10.6 kg.

The duration of treadmill exercise to subjective exhaustion was 80% of base line after 1 wk of the PSF, but increased to 155% after 6 wk. Despite adjusting up to base line, with a backpack, the subjects' exercise weight after 6 wk of dieting, the final exercise test was performed at a mean of 60% of maximum aerobic capacity, whereas the base-line level was 76%. Resting vastus lateralis glycogen content fell to 57% of base line after 1 wk of the PSF, but rose to 69% after 6 wk, at which time no decrement in muscle glycogen was measured after >4 h of uphill walking. The respiratory quotient (RQ) during steady-state exercise was 0.76 during base line, and fell progressively to 0.66 after 6 wk of the PSF. Blood glucose was well maintained during exercise in ketosis. The sum of acetoacetate and beta hydroxybutyrate rose from 3.28 to 5.03 mM during exercise after 6 wk of the PSF, explaining in part the low exercise RQ.

The low RQ and the fact that blood glucose and muscle glycogen were maintained during exhausting exercise after 6 wk of a PSF suggest that prolonged ketosis results in an adaptation, after which lipid becomes the major metabolic fuel, and net carbohydrate utilization is markedly reduced during moderate but ultimately exhausting exercise.

Full text

Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.6M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References.

What is respiratory exchange ratio (RER)? What is respiratory quotient (RQ)?

What is respiratory exchange ratio (RER)? What is respiratory quotient (RQ)?


E-mail Print PDF
Prepared by Dr Ma Hon Ming, SMO TPH (M&EC) and Dr Lo Ho Yin, MO AHNH (Med)
RER is the ratio of carbon dioxide output to oxygen uptake (VCO2 / VO2) measured at the mouth ie external respiration whereas RQ is the ratio of CO2 production to O2 consumption through tissue metabolism (mCO2 / mO2) ie cellular respiration. RER approximates RQ only at steady state conditions when VO2 = m02 and VC02= mCO2 (eg at rest or after 3-4 min steady state exercise at constant workload). In clinical practice, RER is more readily obtained by measuring VCO2 and VO2. In steady states, RQ = RER. In non-steady states, dynamic RER values reflects active coupling of external respiration to cellular respiration.

In metabolic assessments by indirect calorimetry (either open circuit using canopy or close circuit for patients on ventilator), VCO2, VO2 and RER are obtained. RQ = RER in steady state. Based on known values of RQ (carbohydrate 1.0, protein 0.82, fat 0.71, mixed diet 0.85, ketosis 0.67 to 0.7, lipogenesis 1.0-1.2) and urinary nitrogen excretion of patients, we can assess their caloric and metabolic status. The goals are to ensure adequate caloric intake, to optimise nutritional formula and avoid overfeeding to prevent excessive CO2 production that escalates ventilatory demands. Dietary manipulation may change RQ. Physical fitness & endurance training can also change RQ through increased energy utilisation from fatty acid metabolism at a given workload.

In cardiopulmonary exercise testing, RER is derived from breath by breath O2 and CO2 flow measurements at the mouth. RER at rest stays ~ 0.8 (Westernised food). However, subjects who are anxious or hyperventilating for various reasons often have RER> I. Thus, VE and EtCO2 should be taken into consideration when interpreting RER values. During exercise, changes in cellular respiration needed to increase energy output are closely linked to external respiration through the circulation.

Studies on VCO2- VO2 relationship (V-slope) gave us valuable insights into our body wisdom. During exercise with cycle ergometer at increasing work rates (ramp), a steady state for VCO2 & VO2 is achieved at 3 to 4 min at work rates not causing increase in arterial lactate. This is the lower 'aerobic' component slope SI (RER ~ 0.95 corresponding to increase carbohydrate utilization during exercise). With glycogen depletion study (fasting and vigorous exercise on preceding day), SI falls to 0.79-0.81, showing that SI in V-slope plot below anaerobic threshold (AT) represented muscle substrate RQ.

With progressive increase in work rates, capillary PO2 reaches a 'critical' level below which mitochondria cannot consume oxygen (N~ l4mmHg, chronic stable heart failure~ 22mmHg) and lactate rises significantly. VO2 continues to increase at a rate proportional to the rise in lactate but VCO2 further diverges from VO2 increase due to extra CO2 release from cells as HCO3- buffered lactic acid. This is the steeper, upper 'anaerobic' component slope S2. This CO2 rise and HCO3- consumption shifts the O2 dissociation to the right (Bohr effect). Thus lactic acidosis serves to facilitate O2 dissociation and O2 transport to muscle cells without further reduction in end-capillary PO2. From this stage onward, RER is > 1.

AT occurs around a normal subject's mid-work capacity, not at V02 max. RER continues to increase as exercise progresses, up to > 1.6 in short duration, high work rate testing. During cool down, RER returns rapidly to baseline levels with occasional shoot-ups from hyperventilation. RER at peak exercise> 1 (eg RER >1.15 in some computerised ramp protocol) is often taken as indicator that a subject has made good effort. This contrasts with those with 'functional' impairment whose RER always stays < 1 with very high breathing and heart rate reserve even at 'peak' exercise.

(Food for thoughts or exams! - 1) RQ differences: male vs female, obese vs lean, hyperthyroid vs euthyroid, changes with age and pregnancy. 2) RER changes during exercise in COPD. Answers can befound in the references below)


References
1. Pulmonary Function Testing and Cardiopulmonary Stress Testing/Vincent C. Madama. Delmar Publishers lnc 1993.
2. Clinical Exercise Testing I Norman L. Jones- 4thed. WB Saunders Co. 1997.
3. Manual of Pulmonary Function Testing I Gregg L. Ruppel- ih ed. Mosby 1998.
4. Nutritional Aspects of Lung Disease. Michael Donahoe, Robert M. Rogers. Ch 11, vol. 16. Current Pulmonologyl Donald F. Tierney. Mosby 1995.
5. Critical Care Handbook of the Massachusettes General Hospital I editors, William E. Hurford,DeanHess- 3rded. LW&W 2000.
6. Manual of Clinical Problems in Pulmonary Medicine I Richard A. Bordow, Andrew L. Ries, Timothy A. Morris- 5thed. 2001.
7. Role of Cardiopulmonary Exercise Testing in Rehabilitation Medicine. Ma HM. Rehabilitation Medicine Dissertation HKCP Jan 2000.
8. Substrate utilisation during endurance exercise in men and women after endurance training. Carter SL et al. Am L Physiol Endocrinol Metab 2001 Jun ; 280(6) : E898-907
9. Carbohydrate metabolism during exercise in females: effect of reduced fat availability. Howlett KF et al. Metabolism 2001 Apr; 50(4):481-487.
10. The effect of an increased free fatty acid concentration on thermogenesis and substrate oxidation in obese and lean men. Schiffelers SL et al. lnt J Obes Relat Metab Disord 2001 Jan; 25(1):33-38.
11. Critical capillary PO2 and the role of lactate production in oxyhemoglobin dissociation during exercise. Wasserman K. Adv Exp Med BioI 1999; 471:321-323.
12. Diagnosing cardiovascular and lung pathophysiology from exercise gas exchange Wasserman K. Chest 1997 Oct; 112(4):1091-1101.
13. Ventilation during exercise in chronic heart failure. Wasserman K. et al. Basic Res Cardioll996; 91 Suppll:l-l1.
14. Lactic acidosis as a facilitator of oxyhemoglobin dissociation during exercise. StringerW et al. J Appl Physiol1994 Apr; 76(4):1462-1467.
15. The bioenergetic and gas exchange basis of exercise testing. Whipp BJ. Clin Chest Med 1994 Jun; 15(2):173-192.
16. Coupling of external to cellular respiration during exercise: the wisdom of the body revisited. Wassserman K. Am J Physiol1994 Apr; 266 :E519-539.
17. Comparison of gas exchange, lactate and lactic acidosis thresholds in patients with chronic obstructive pulmonary disease. Patessio A et al. Am Rev Respir Dis 1993 Sep; 148(3):622-626.
18. Factors affecting the components of the alveolar CO2 output-O2 uptake relationship during incremental exercise in man. Cooper CB et al. Exp Physiol1992 Jan; 77 (I): 51-64.
19. Gas exchange theory and the lactic acidosis (anaerobic) threshold. Wasserman K. etal. Circulation 1990Jan; 81( 1 Suppl ):114-30.
20. A new perspective in pulmonary rehabilitation: anaerobic threshold as a discriminant in training. Cassaburi R et al. Eur Respir J Suppl 1989 Jul; 618s-623s.
21. Effect of altering the proportion of dietary fat and carbohydrate on exercise gas exchange in normal subjects. Sue CY et al. Am Rev Respir Dis 1989 Jun; 139(6):1430-4.
22. Metabolic acidosis during exercise in patients with chronic obstructive pulmonary disease. Use of the V-slope method for anaerobic threshold determination. Sue DY et al. Chest 1988Nov; 94(5);931-938.
23. The anaerobic threshold: definition, physiological significance and identification. Wasserman K. Adv Cardiol1986; 351-23.
24. A new method for detecting anaerobic threshold by gas exchange. Beaver WL et al. J Appl Physiol1986 Jun; 60(6):2020-2027.
25. The anaerobic threshold measurement to evaluate exercise performance. Wasserman K. Am Rev Respir Dis 1984 Feb; 129:S35-40.
26. The anaerobic threshold measurement in exercise testing. Wasserman K. Clin Chest Med 1984 Mar; 5(1) :77-88.
27. Ventilatory and gas exchange kinetics during exercise in chronic airways obstruction. Nery LE et al. J Appl Physiol1982 Dec; 53(6):1594-1602.
28. Anaerobic threshold alterations caused by endurance training in middle-aged men Davis JA et al. J Appl Physiol1979 Jun; 46(6): 1039-1046.

How We Get Fat | BodyRecomposition - The Home of Lyle McDonald

How We Get Fat | BodyRecomposition - The Home of Lyle McDonald

How We Get Fat

Ok, this is going to be a bit ranty but, trust me, I write better when I’m upset.  If the Internet has proven anything to me over the years it’s this: basic literacy is sorely lacking.  Because the comments in response to the article I wrote on Tuesday, Excess Protein and Fat Storage – Q&A indicate that not only can people not understand rather basic concepts, they insist on reading things into what I am saying that I have never said.  I could rant about making uncritical inferences but I’ll spare everyone that.

In that piece I answered a very specific question with a very specific answer.  I made no implications of anything beyond the exact answer I gave to that specific question.  And somehow people managed to read all kinds of asinine stuff into it, things that I never said or even began to imply.  It’d amaze me if I hadn’t seen people do this consistently over the past 15 years.

The basic confusion in that article was that folks interpreted my saying that carbs and protein can’t be converted to fat as ‘Lyle says you can’t get fat overeating carbs and protein’.  Which I absolutely didn’t say.  But people inferred, incorrectly.  Basically, what I said and what they heard were not the same thing.

I’d note before continuing that if folks had taken 30 seconds to click on and read the article I linked Nutrient Intake, Oxidation and Storage, they would have realized the mistake they were making as I specifically said that overeating carbs can still make you fat, just not through direct conversion (rather through indirect mechanisms).  But in addition to a lack of basic literacy, laziness seems to be endemic on the net as well.  And for not taking a couple of minutes to read the piece that I specifically linked to, a bunch of people got confused and then aggro.

I’d also note that if folks reading the protein piece had taken time to read the, I dunno, 200+ other articles on the site, they’d realize that I am making no such claim that you can eat all the carbs you want (or that lowcarb diets are superior, or whatever nonsensical conclusions they reached).  Or that one specific dietary approach (e.g. lowcarbs) is automatically superior to another.


But rather than do that, they took a single article, addressing a single specific question, and ran with it.  That’s not a good thing to do, you can’t take a single answer to a single specific question out of context and take that to represent what I believe. Well you can but it’s stupid to do so.  That’s what a lot of people did.

But since they couldn’t do any of that, couldn’t take the time to even read the single linked article much less the rest of what’s on the site, rather than writing about something more interesting today, I’m going to clear it up once and for all.  And I still expect someone to read this completely wrong and go around the Internet mis-representing what I’m saying.  I’m used to it at this point.
.
How We Get Fat Part 1: Energy Intake Exceeds Energy Output


At a fundamental level, fat storage occurs when caloric intake exceeds caloric output, a topic I discussed in some detail in The Energy Balance Equation.  Now, I know that a lot of people claim that basic thermodynamics don’t hold for humans. Simply, they are wrong.  Invariably, the studies used to support this position are based on a faulty data set: to whit, they are drawing poor conclusions about what people SAY that they are eating.

For example, one popular book bases one of its many incorrect theses on a 1980 report suggesting that the obese ate the same number of calories as the lean.  Ergo, obesity was caused by something else.  The problem is this, the data set is wrong.  A fact we’ve known for nearly 30 years but that the author was somehow unable to become aware of in his ’5 years of dedicated research’.

Study after study after study over the past 30 years shows that the obese systematically under-report their food intake (by up to 30-50%) and over-report their activity (by about the same).  So when they say they are only eating 1800 calories per day, they may be eating 2400-3600 calories per day.  And their activity isn’t nearly what they think.

And when you put those same folks in controlled metabolic ward conditions and control their food intake and/or activity output…voila, the energy balance equation holds.  It’s only when you believe the (incorrect) self-reported data that it doesn’t.

And make no mistake I am NOT saying that the obese are lying about their intake, not consciously anyhow.  Most people simply suck at knowing how much they are actually eating.  Leave them to self-report it and they almost always screw it up.   If you’re mistaken enough to believe the self-reported values, you reach even more screwed up conclusions about things.

In that vein, I have found that the chronically underweight “I can’t gain weight no matter what I do” are invariably vastly over-estimating what they are eating.  That is, they are eating far less than they think.  Other studies show that ‘health conscious people’ tend to under-report their true ‘junk food’ and dietary fat intake; to appear more healthy they conveniently forget or leave out that trip to the burger joint.

Put differently, this isn’t something that only occurs in the obese (so spare me accusations of ‘hating the obese’ or some nonsense).  Am I clear or are people going to misinterpret me some more in the comments and claim I said that fat people lie about their food intake?  Because I’m not saying anything of the sort.  Make no mistake, I’m sure some do lie about it; most are just clueless about how much they are actually eating.

Now let me make it clear that there is obviously a lot more going on here, hormones and all manners of other stuff impact on the energy balance equation.  For example, chronically elevated cortisol does a lot of nasty things in terms of reducing metabolic rate (reducing the energy out side of the equation) as well as negatively impacting on calorie partitioning (where calories go when you eat them as discussed in Calorie Partitioning Part 1 and Part 2).  But for the most part, a lot of that is outside of our control.  It’s relevant but you can’t do much with most of it.  So I’ll focus on calories.
.
How We Get Fat Part 2: Nutrient Intake, Oxidation and Storage Part Deux

The primary storage of fat in the body is in fat cells, duh.  Most of that is found in what is called subcutaneous fat, which is found under the skin.  There is also fat stored around the gut area called visceral fat (this surrounds the organs).  Fat can also be stored in ‘bad’ places like the liver and pancreas under certain conditions; this is called ectopic fat storage.

I’m going to focus here on subcutaneous fat.  There, whether or not fat is stored or removed comes down to a concept called fat balance, which I discuss in some detail in The Ultimate Diet 2.0.   You can think of fat balance as the fat specific equivalent of energy balance.  That is
Net Change in Fat Stores = Fat Stored – Fat Burned

I’d note that the same nutrient balance holds for protein, carbohydrates and alcohol (which I’m not going to talk about today).  That is, the net effect on bodily stores, whether protein or carbohydrate stores in the body increases, decreases or stays the same comes down to the balance of protein/carb stored vs. protein or carbs/burned.

So at a fundamental level, fat gain occurs when fat storage exceeds fat burning (technically oxidation).  And fat loss occurs when fat oxidation exceeds fat storage.  I’d note that both processes take place in some amounts throughout the day, controlled by a host of processes I’m not going to talk about.  Just recognize that what happens over time in terms of your fat stores comes down to the relationship between those two processes: fat storage – fat oxidation.
So what determines fat oxidation and fat storage rates?
.
How We Get Fat Part 3: Back to Nutrient Intake, Oxidation and Storage

Now, here’s where people got confused by Excess Protein Intake and Fat Storage – Q&A, and where they would have been unconfused by clicking the linked article on Nutrient Intake, Oxidation and Storage.  In fact, I’d suggest you go read it right now, it’s not that long and since I’m not going to retype all of it here (that’s why I wrote it the first time), it’d be a good idea.  I’ll wait.

However, since I know most of you will have just ignored my suggestion to actually read that piece, I’m going to summarize a few points from it (as well as from the Q&A):
  1. Carbs are rarely converted to fat and stored as such
  2. When you eat more carbs you burn more carbs and less fat; eat less carbs and you burn less carbs and more fat
  3. Protein is basically never going to be converted to fat and stored as such
  4. When you eat more protein, you burn more protein (and by extension, less carbs and less fat); eat less protein and you burn less protein (and by extension, more carbs and more fat)
  5. Ingested dietary fat is primarily stored, eating more of it doesn’t impact on fat oxidation to a significant degree
Let’s work through this backwards.  When you eat dietary fat, it’s primary fate is storage as its intake has very little impact on fat oxidation (and don’t ask me a bunch of questions about “But people say you have to eat fat to burn fat?” in the comments.  That idea is fundamentally wrong but would take an entire article to address).  It also doesn’t impact greatly on the oxidation of the protein or carbohydrates.

Carbohydrates are rarely converted to fat (a process called de novo lipogenesis) under normal dietary conditions. There are exceptions when this occurs.  One is with massive chronic overfeeding of carbs.  I’m talking 700-900 grams of carbs per day for multiple days.  Under those conditions, carbs max out glycogen stores, are in excess of total daily energy requirements and you see the conversion of carbohydrate to fat for storage.  But this is not a normal dietary situation for most people.

A few very stupid studies have shown that glucose INFUSION at levels of 1.5 total daily energy expenditure can cause DNL to occur but this is equally non-physiological.  There is also some evidence that DNL may be increased in individuals with hyperinsulinemia (often secondary to obesity).  There’s one final exception that I’ll use to finish this piece.

But when you eat more carbs, you burn more carbs and burn less fat.  And that’s why even if carbs aren’t directly converted to fat and stored as such, excess carbs can STILL MAKE YOU FAT.  Basically, by inhibiting fat oxidation, excess carbs cause you to store all the fat you’re eating without burning any of it off.  Did you get that?  Let me repeat it again.

Carbs don’t make you fat via direct conversion and storage to fat; but excess carbs can still make you fat by blunting out the normal daily fat oxidation so that all of the fat you’re eating is stored.  Which is why a 500 cal surplus of fat and a 500 cal surplus of carbs can both make you fat; they just do it for different reasons through different mechanisms.  The 500 calories of excess fat is simply stored; the excess 500 calories of carbs ensure that all the fat you’re eating is stored because carb oxidation goes up and fat oxidation goes down.  Got it?  If not, re-read this paragraph until it sinks in.

Oh yeah, the same holds for protein. Protein isn’t going to be converted to and stored as fat.  But eat excess protein and the body will burn more protein for energy (and less carbs and fat).  Which means that the other nutrients have to get stored.  Which means that excess protein can still make you fat, just not by direct conversion.  Rather, it does it by ensuring that the fat you’re eating gets stored.

Of course protein also has the highest thermic effect, more of the incoming calories are burned off.  So excess protein tends to have the least odds of making you fat under any conditions; but excess protein can make you fat.  Just not by direct conversion to fat; rather it’s indirectly by decreasing the oxidation of other nutrients.

Ok, is the above clear enough? Because I can’t really explain it any simpler but will try one last time using bullet points and an example.  Let’s assume someone is eating at exactly maintenance calories.  Neither gaining nor losing fat.  Here’s what happens with excess calories.  Assume that all three conditions represent identical increases in caloric intake, just from each of the different macros.  Here’s what happens mechanistically and why all three still make you fat:
  1. Excess dietary fat is directly stored as fat
  2. Excess dietary carbs increases carb oxidation, impairing fat oxidation; more of your daily fat intake is stored as fat
  3. Excess dietary protein increases protein oxidation, impairing fat oxidation; more of your daily fat intake is stored as fat
Got it?  All three situations make you fat, just through different mechanisms.  Fat is directly stored and carbs and protein cause you to store the fat you’re eating by decreasing fat oxidation.

And I’d note again, since someone will invariably misread this that that doesn’t mean that a low-carb and/or low-protein diet is therefore superior for fat loss.  I’m not saying that and don’t think that I am.  Because in such a situation, while you may be burning more fat, you’re also eating more dietary fat.  So net fat balance can be unchanged despite the dicking around with macronutrient content.  It still comes down to the deficit.
.
The Obvious Question: Why Not Just Eat Zero Dietary Fat?

And now I’ll answer the question that I know every person who has read (and hopefully understood) the above is asking: so if carbs and protein are rarely converted to and stored as fat, and make you fat by decreasing fat oxidation and causing all ingested dietary fat to get stored as fat, can’t I eat as much as I want of protein and carbs so long as my dietary fat intake is zero?

And the asnswer is still no.  Remember how I teased you above with one other exception, when carbs are converted to fat for storage?    That exception is when dietary fat is below about 10% of total daily calories.  Under that condition, the body ramps up de novo lipogenesis.  So you still get fat.

Because the body is usually smarter than we are.  Under conditions where dietary fat intake is ‘adequate’ (meaning 10% of total calories or more), the primary fate of that fat is storage and protein and carbs are used for other things.  And when dietary fat is too low, the body will start converting ingested carbs (and probably protein, though it would still be rare) to fat for storage.

Oh yeah, the other question you’re going to ask in the comments “What about alcohol?”  That’s going to require a full article so be patient.  I know that’s another thing lacking on the Internet but so be it.
And I really hope that clears things up.  If it doesn’t, read this piece and the linked articles until it is.

Tuesday, 29 January 2013

A sixpack of kettlebell studies to remind trainers and trainees, alike, that there are more things you can lift than just dumbbells and barbells (various authors)

A sixpack of kettlebell studies to remind trainers and trainees, alike, that there are more things you can lift than just dumbbells and barbells (various authors)


I have never gotten hooked to kettlebells myself and would never agree to exchange my barbells and dumbbells for the finest set of kettlebells for more than one week, but if you take a look at some of the studies that have been published in the past 12 months or so, there is sufficient evidence to suggest that the incorporation of kettlebell workouts into your routine, as a means to provide new muscular and metabolic stimuli, could yield highly beneficial results:


Kettlebell swings restore
and enhance back health and function (McGill. 2012) On the basis of electromyography, ground reaction forces (GRFs), and 3D kinematic data the researchers determined that kettlebell swings create a "hip-hinge squat pattern characterized by rapid muscle activation-relaxation cycles of substantial magnitudes (∼50% of a maximal voluntary contraction [MVC] for the low back extensors and 80% MVC for the gluteal muscles with a 16-kg kettlebell) resulting in about 3,200 N of low back compression." The way the swings activate the abs and the unique loading patterns of the posterior shear of the L4 vertebra on L5, which is opposite in polarity to a traditional lift could make it a valuable tool in re- and prehab.

Kettlebell swing training improves maximal and explosive strength
(Lake 2012) 21 healthy men  were randomly assigned to either a kettlebell (KB) or jump squat (JS) training twice a week. The KB group performed 12-minute bouts of KB exercise (12 rounds of 30-second exercise, 30-second rest with 12 kg if lower than 70 kg or 16 kg if higher 70 kg). The JS group performed at least 4 sets of 3 JS with the load that maximized peak power—Training volume was altered to accommodate different training loads and ranged from 4 sets of 3 with the heaviest load (60% 1RM) to 8 sets of 6 with the lightest load (0% 1RM). The increase in maximum strength of 9.8%, as well as explosive strength (+19.8%) were identical in both groups

Kettlebell training has "
has potential for improving some components of MetS in middle-aged women." (Moreno. 2011): While the changes the author of the thesis observed in response to 10 weeks twice weekly kettlebell training did not reach statistically significance (probably due to the low subject size of N=6 physically inactive women, mean age (mean age 48.8y, BMI 31.8) the trends in " fasting glucose and body fat were encouraging and suggest that kettlebell training has potential for improving some components of MetS in middle-aged women."
Kettle bell workouts can decrease blood pressure (Douglass. 2012): Eight resistance trained pre-hypertensive and HTN males saw statistically and more importantly clinically significant declines in blood pressure (to normal levels!) in the course of a randomized cross-over designed study which included 12 minutes of continuous two-handed swings (THS), three sets of a 6 exercise circuit (CIR), and a resting control (CON).

Kettlebell training can improve strength, power and and endurance
(Mannocia. 2012):  23 subjects (age 18-72 years) were required to perform a10-week kettlebell training program that took place in a group setting two times per week. Post hoc pairwise comparisons of assessments barbell clean and jerk, barbell bench press, maximal vertical jump, and 450 back extensions performance revealed significant time x group interaction and a main effect (p < 0.05) for the bench press, a trend toward a time x group interaction and a significant main effect for clean and jerk. These observations suggest "that kettlebells may be an effective alternative tool to improve performance in weight- and powerlifting".
10 min of treadmill running may burn more more energy, than a short 10-min kettlebell drill, but pro-anabolic & strength edurance effects speak in favor of 'the bells' (McGill. 2012): Only those who still believe in santa... ah, I mean the calories in vs. out theory of weight loss, will probably care, whether they are burning 12.5 or 17.1kcal/min and therefore this "advantage" would hardly be important even if the participants had not been sprinting part of their 10min on the treadmill just to make sure to achieve the prescriped (identical) rates of perceived exertion. And as usual, there is no reason, why you could not switch back and forth from one "drill" to another.