Brent Holland

Why does exercise make us happy and calm? Almost everyone agrees that it generally does, a conclusion supported by research. A survey by Norwegian researchers published this month, for instance, found that those who engaged in any exercise, even a small amount, reported improved mental health compared with Norwegians who, despite the tempting nearness of mountains and fjords, never got out and exercised. A separate study, presented last month at the annual meeting of the American College of Sports Medicine, showed that six weeks of bicycle riding or weight training eased symptoms in women who’d received a diagnosis of anxiety disorder. The weight training was especially effective at reducing feelings of irritability, perhaps (and this is my own interpretation) because the women felt capable now of pounding whomever or whatever was irritating them.

But just how, at a deep, cellular level, exercise affects anxiety and other moods has been difficult to pin down. The brain is physically inaccessible and dauntingly complex. But a recent animal study from researchers at the National Institute of Mental Health provides some intriguing new clues into how exercise intertwines with emotions, along with the soothing message that it may not require much physical activity to provide lasting emotional resilience.

For the experiment, researchers at the institute gathered two types of male mice. Some were strong and aggressive; the others were less so. The alpha mice got private cages. Male mice in the wild are territorial loners. So when then the punier mice were later slipped into the same cages as the aggressive rodents, separated only by a clear partition, the big mice acted like thugs. They employed every animal intimidation technique and, during daily, five-minute periods when the partition was removed, had to be restrained from harming the smaller mice, which, in the face of such treatment, became predictably twitchy and submissive.

After two weeks of cohabitation, many of these weaker mice were nervous wrecks. When the researchers tested them in a series of stressful situations away from the cages, the mice responded with, as the scientists call it, “anxiety-like behavior.” They froze or ran for dark corners. Everything upset them. “We don’t use words like ‘depressed’ to describe the animals’ condition,” said Michael L. Lehmann, a postdoctoral fellow at the institute and lead author of the study. But in effect, those mice had responded to the repeated stress by becoming depressed.

But that was not true for a subgroup of mice that had been allowed access to running wheels and nifty, explorable tubes in their cages for several weeks before they were housed with the aggressive mice. These mice, although wisely submissive when confronted by the bullies, rallied nicely when away from them. They didn’t freeze or cling to dark spaces in unfamiliar situations. They explored. They appeared to be, Dr. Lehmann said, “stress-resistant.”

“In people, we know that repeated applications of stress can lead to anxiety disorders and depression,” Dr. Lehmann said. “But one of the mysteries” of mental illness “is why some people respond pathologically to stress and some seem to be stress-resistant.”

To discern what was different, physiologically, about the stress-resistant mice, the scientists looked at brain cells using stains and other techniques. They determined that neurons in part of the rodents’ medial prefrontal cortex, an area of the brain involved in emotional processing in animals and people, had been firing often and rapidly in recent weeks, as had neurons in other, linked parts of the brain, including the amygdala, which is known to handle feelings of fear and anxiety.

The animals that had not run before moving in with the mean mice showed much less neuronal activity in these portions of the brain.

Dr. Lehmann said that he believed that the running was key to the exercised animals’ ability to bounce back from their unpleasant housing conditions.

Of course, as we all know, mice are not people. But the scientists believe that this particular experiment is a fair representation of human interpersonal relations, Dr. Lehmann said. Hierarchies, marked by bullying and resulting stress,  are found among people all the time. Think of your own most dysfunctional office job. (Interestingly, the same experiment cannot be conducted on female mice, who like being housed together, Dr. Lehmann said, so he and his colleagues are testing a female-centric version, in which “cage mates are swapped out continuously,” to the consternation and grief of the female mice left behind.)

Perhaps best of all, Dr. Lehmann does not believe that hours of daily exercise are needed or desirable to achieve emotional resilience. The mice in his lab ran only when and for as long as they wished, over the course of several weeks. Other animal experiments have intimated that too much exercise could contribute to anxiety, and Dr. Lehmann agrees that that outcome is possible. Moderate levels of exercise seem to provide the most stress-relieving benefits, he said. Dr. Lehmann does not have a car and walks everywhere, and although he lives in Washington, a cauldron of stress induction, he describes himself as a “pretty calm guy.”

To view original article please visit www.nytimes.com

By 

John Kiefer

Published: November 7, 2011

When I look at the fat guy in the gym wasting his time on forearm curls to lose weight, I don’t feel sympathy. The big tough guy getting stapled to the bench by 365 pounds, when just a second ago he couldn’t even handle 315 pounds — nope, no sympathy there either. The girl who spends thirty minutes bouncing between the yes-no machines (abductor and adductor machines), who is going to have trouble walking the next day — I can’t muster even an iota of pathos. Nobody told them to do these things. But then I watch my friend, Jessica, running on the treadmill, day after day, year after year, running like a madwoman and going nowhere. Her body seems to get softer with every mile and the softer she gets the more she runs. I do feel pity for her because everybody, everywhere has convinced her that running is the way to stay slim and toned.

There’s a Jessica in every gym and spotting one is easy. The woman that runs for an hour or more every day on the treadmill, who every month or so sets a new distance or time goal. Maybe the goal encompasses the treadmill workouts; maybe it will be her fifth fund-raising marathon; or maybe she’s competing with runners in Finland via Nike®. The goal doesn’t matter, because years of seeing her on the treadmill exposes the results: she’s still — I’m not going to sugar coat this — fat. Or worse, she’s fatter.

I tried to rescue my Jessica from the clutches of the cardio contingent, but to no avail until a month ago when she called to tell me that a blood test had confirmed her doctor’s suspicion: she had hypothyroidism — her body no longer made enough thyroid hormone. Her metabolism slowed to a snail’s pace and the fat was accumulating. Now she had a culprit to blame, it wasn’t the cardio causing her problems, it was her body rebelling. When Jessica asked my advice, I told her to do two things: schedule a second test for two weeks later and until then, stop all the goddamn running.

Don’t assume I’m picking on women or making fun. There are men out there who do the same, thinking cardio wipes away the gut resulting from regular weekend beer binges, but they are, in comparison, rare. I am targeting women for three very good reasons:

1. They are often intensely recruited for fund-raisers like Team-In-Training, lured by the promise of slim, trim health resulting from the month of cardio training leading to a marathon in addition to helping the charity in question
2. Some physique coaches prescribe 20-plus hours per week of pre-contest cardio for women (that’s a part-time job)
3. Steady-state endurance activities like this devastate a woman’s metabolism. It will devastate a man’s too, but in different ways.

There’s not much I hate in the fitness world — well, that’s not true, I hate most things about its present state, but at the top of the list is over-prescribed cardio. I’m not talking about walking or even appropriate HIIT cardio, but the running, cycling, stair climbing or elliptical variety done for hours at or above 65 percent of max heart rate, actually anaerobic threshold is a better measure, but not practical for day-to-day use.

Trashing steady-state cardio is nothing new and the better of the physique gurus figured this out a long time ago, but even then, they only apply the no-steady-state-cardio rule to contest preparation. The non-cardio coaches fail to state the most detrimental effect, one that applies specifically to women and is a primary reason many first-time or second-time figure and bikini competitors explode in weight when returning to their normal diet. It’s the same reason the Jessicas of the world run for hours per week with negative results. Studies demonstrate beyond any doubt that in women, cardio chronically shuts down the production of the thyroid hormone, T3.^1-11

T3 is the body’s preeminent regulator of metabolism by throttling the efficiency of cells.^12-19 T3 acts in various ways to increase heat production.^20-21 As I pointed out, in Logic Does Not Apply: A Calorie Is A Calorie, this is one reason using static equations to perform calorie-in, calorie-out weight loss calculations doesn’t work—well, that’s why it’s stupid, actually. When T3 levels are normal, the body burns enough energy to stay warm and muscles function at moderate efficiency. Too much thyroid hormone (hyperthyroidism) and the body becomes inefficient making weight gain almost impossible. Too little T3 (hypothyroidism) and the body accumulates body fat with ease, almost regardless of physical activity level.

Women unknowingly put themselves into the hypothyroid condition because they perform so much steady-state cardio. In the quest to lose body fat, T3 levels can grant success or a miserable failure because of how it influences other fat-regulating hormones.^22-31 In addition, women get all the other negative effects, which I’ll get to. Don’t be surprised or aghast. It’s a simple, sensible adaption of the body, especially a body equipped to bear the full brunt of reproducing.

Think about it this way: the body is a responsive, adaptive machine evolved for survival. If running on a regular basis, the body senses excessive energy expenditure and adjusts to compensate. Remember, no matter what dreamy nonsense we invent about how we hope the body works, its endgame is always survival. Start wasting energy running and the body reacts by slowing the metabolism to conserve energy. Decreasing energy output is biologically savvy for the body: survive longer while doing this stressful, useless activity — as the body views it. Decreasing T3 production, increases efficiency and adjusts metabolism to preserves energy quickly.

Nothing exemplifies this increasing efficiency better than how the body starts burning fuel. Training at a consistently plus-65 percent heart rate adapts the body to save as much body fat as possible. That’s right, after regular training, fat cells stop releasing fat during moderate-intensity activities like they once did.^32-33 Energy from body fat stores decreases by a whopping 30 percent. ^34-35 To this end, the body even sets into motion a series of reactions that make it difficult for muscle to burn fat at all.^36-41 Instead of burning body fat, the body is taking extraordinary measures to hold on to it. Still believe cardio is the fast track to fat loss?

But wait. By acting now, you too can lose muscle mass. That’s right. No more muscle because too much steady-state cardio triggers the loss of muscle.^42-45 This seems to be a two-fold mechanism, with heightened and sustained cortisol levels triggering muscle loss,^46-56 which upregulates myostatin, a potent destroyer of muscle tissue.⁵⁷ Oh yeah — say good bye to bone density too — it declines with the muscle mass and strength.^58-64 And long-term health? Out the window as well. The percentage of muscle mass is an independent indicator of health.⁶⁵ Lose muscle, lose bone, lose health—all in this nifty little package.

When sewn together, these phenomena coordinate a symphony of fat gain for most female competitors post-figure contest. After a month—or three—of cardio surpassing the 20 hours-per-week mark, fat-burning is at an astonishing low, and fat cells await an onslaught of calories to store.^66-72 The worst thing imaginable in this state would be to eat whatever you wanted as much as you wanted. The combination of elevated insulin and cortisol would not only make you fat, but creates new fat cells so that you can become fatter than ever.^73-80

I won’t name names, but I have seen amazing displays of gluttony from the smallest, trimmest women. Entire pizzas disappear leaving only the flotsam of toppings that fell during the feeding frenzy; appetizer, meal, cocktails, dessert—a paltry 4000 calories at The Cheesecake Factory vanish as the wait staff delivers each. A clean plate for each return to the buffet — hell with that, the only thing they’re taking to the food bar is a spoon and they’re not coming back. There are no leftovers; there are no crumbs. Some women catch it in time and stop the devastation, but others quickly swell and realize that the supposed off-season look has become their every-season look. And guess what they do to fix it: cardio for an hour every morning and another in the evening to hasten things…

The “cardio craze” — and it is a form of insanity — is on my hit list and I’m determined to kill it. I don’t know what else I can say. There are better ways to lose fat, be sexy and skinny for life, better ways to prepare for the stage. Women, you need to get off the damn treadmill; I don’t care what you’re preparing for. Stop thinking a bikini-body is at the end of the next marathon or on the other side of that stage. It’s not if you use steady-state cardio to get there — quite the opposite. The show may be over, the finish line might be crossed, but the damage to your metabolism is just starting.

Don’t want to stop running, fine. At the very least stop complaining about how the fat won’t come off the hips and thighs or the ass. You’re keeping it there.

What about Jessica, my friend who’s dilemma spawned this article? Luckily she took my suggestion and cut the cardio. Two weeks later, her T3 count was normal. Who would have guessed?

1.     Baylor LS, Hackney AC. Resting thyroid and leptin hormone changes in women following intense, prolonged exercise training. Eur J Appl Physiol. 2003 Jan;88(4-5):480-4.

2.     Boyden TW, Pamenter RW, Rotkis TC, Stanforth P, Wilmore JH. Thyroidal changes associated with endurance training in women. Med Sci Sports Exerc. 1984 Jun;16(3):243-6.

3.     Wesche MF, Wiersinga WM. Relation between lean body mass and thyroid volume in competition rowers before and during intensive physical training. Horm Metab Res. 2001 Jul;33(7):423-7.

4.     Tremblay A, Poehlman ET, Despres JP, Theriault G, Danforth E, Bouchard C. Endurance training with constant energy intake in identical twins: changes over time in energy expenditure and related hormones. Metabolism. 1997 May;46(5):499-503.

5.     Rone JK, Dons RF, Reed HL. The effect of endurance training on serum triiodothyronine kinetics in man: physical conditioning marked by enhanced thyroid hormone metabolism. Clin Endocrinol (Oxf). 1992 Oct;37(4):325-30.

6.     Loucks AB, Callister R. Induction and prevention of low-T3 syndrome in exercising women. Am J Physiol. 1993 May;264(5 Pt 2):R924-30.

7.     Loucks AB, Heath EM. Induction of low-T3 syndrome in exercising women occurs at a threshold of energy availability. Am J Physiol. 1994 Mar;266(3 Pt 2):R817-23.

8.     Rosolowska-Huszcz D. The effect of exercise training intensity on thyroid activity at rest. J Physiol Pharmacol. 1998 Sep;49(3):457-66.

9.     Wirth A, Holm G, Lindstedt G, Lundberg PA, Bjorntorp P. Thyroid hormones and lipolysis in physically trained rats. Metabolism. 1981 Mar;30(3):237-41.

10.  Opstad PK, Falch D, Oktedalen O, Fonnum F, Wergeland R. The thyroid function in young men during prolonged exercise and the effect of energy and sleep deprivation. Clin Endocrinol (Oxf). 1984 Jun;20(6):657-69.

11.  Hohtari H, Pakarinen A, Kauppila A. Serum concentrations of thyrotropin, thyroxine, triiodothyronine and thyroxine binding globulin in female endurance runners and joggers. Acta Endocrinol (Copenh). 1987 Jan;114(1):41-6.

12.  Lanni A, Moreno M, Lombardi A, Goglia F. Thyroid hormone and uncoupling proteins. FEBS Lett. 2003 May 22;543(1-3):5-10. Review.

13.  Leijendekker WJ, van Hardeveld C, Elzinga G. Heat production during contraction in skeletal muscle of hypothyroid mice. Am J Physiol. 1987 Aug;253(2 Pt 1):E214-20.

14.  Silva JE. Thyroid hormone control of thermogenesis and energy balance. Thyroid. 1995 Dec;5(6):481-92. Review.

15.  Argyropoulos G, Harper ME. Uncoupling proteins and thermoregulation. J Appl Physiol. 2002 May;92(5):2187-98. Review.

16.  Rolfe DF, Brown GC. Cellular energy utilization and molecular origin of standard metabolic rate in mammals. Physiol Rev. 1997 Jul;77(3):731-58. Review.

17.  Danforth E Jr, Burger A. The role of thyroid hormones in the control of energy expenditure. Clin Endocrinol Metab. 1984 Nov;13(3):581-95. Review.

18.  Schrauwen P, Hesselink M. UCP2 and UCP3 in muscle controlling body metabolism. J Exp Biol. 2002 Aug;205(Pt 15):2275-85. Review.

19.  Silva JE. The multiple contributions of thyroid hormone to heat production. J Clin Invest. 2001 Jul;108(1):35-7.

20.  Goglia F, Silvestri E, Lanni A. Thyroid hormones and mitochondria. Biosci Rep. 2002 Feb;22(1):17-32. Review.

21.  Goglia F, Moreno M, Lanni A. Action of thyroid hormones at the cellular level: the mitochondrial target. FEBS Lett. 1999 Jun 11;452(3):115-20. Review.

22.  Ribeiro MO, Carvalho SD, Schultz JJ, Chiellini G, Scanlan TS, Bianco AC, Brent GA. Thyroid hormone–sympathetic interaction and adaptive thermogenesis are thyroid hormone receptor isoform–specific. J Clin Invest. 2001 Jul;108(1):97-105.

23.  Beylot M, Riou JP, Bienvenu F, Mornex R. Increased ketonaemia in hyperthyroidism. Evidence for a beta-adrenergic mechanism. Diabetologia. 1980;19(6):505-10.

24.  Ostman J, Arner P, Bolinder J, Engfeldt P, Wennlund A. Regulation of lipolysis in hyperthyroidism. Int J Obes. 1981;5(6):665-70.

25.  Collins S, Cao W, Daniel KW, Dixon TM, Medvedev AV, Onuma H, Surwit R. Adrenoceptors, uncoupling proteins, and energy expenditure. Exp Biol Med (Maywood). 2001 Dec;226(11):982-90.

26.  Williams LT, Lefkowitz RJ, Watanabe AM, Hathaway DR, Besch HR Jr. Thyroid hormone regulation of beta-adrenergic receptor number. J Biol Chem. 1977 Apr 25;252(8):2787-9.

27.  Martin WH 3rd. Triiodothyronine, beta-adrenergic receptors, agonist responses, and exercise capacity. Ann Thorac Surg. 1993 Jul;56(1 Suppl):S24-34.

28.  Tsujimoto G, Hashimoto K, Hoffman BB. Effects of thyroid hormone on beta-adrenergic responsiveness of aging cardiovascular systems. Am J Physiol. 1987 Mar;252(3 Pt 2):H513-20.

29.  Richelsen B, Sorensen NS. Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism. Metabolism. 1987 Nov;36(11):1031-9.

30.  Wang JL, Chinookoswong N, Yin S, Shi ZQ. Calorigenic actions of leptin are additive to, but not dependent on, those of thyroid hormones. Am J Physiol Endocrinol Metab. 2000 Dec;279(6):E1278-85.

31.  Seidel A, Heldmaier G. Thyroid hormones affect the physiological availability of nonshivering thermogenesis. Pflugers Arch. 1982 May;393(3):283-5.

32.  Jones NL, Heigenhauser GJ, Kuksis A, Matsos CG, Sutton JR, Toews CJ. Fat metabolism in heavy exercise. Clin Sci (Lond). 1980 Dec;59(6):469-78.

33.  Romijn JA, Coyle EF, Sidossis LS, Zhang XJ, Wolfe RR. Relationship between fatty acid delivery and fatty acid oxidation during strenuous exercise. J Appl Physiol. 1995 Dec;79(6):1939-45.

34.  Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, Wolfe RR. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol Endocrinol Metab. 1993;265:E380-E391.

35.  Martin WH 3rd, Dalsky GP, Hurley BF, Matthews DE, Bier DM, Hagberg JM, Rogers MA, King DS, Holloszy JO.  Effect of endurance training on plasma free fatty acid turnover and oxidation during exercise. Am J Physiol. 1993;265:E708–14.

36.  Elayan IM, Winder WW. Effect of glucose infusion on muscle malonyl-CoA during exercise. J Appl Physiol. 1991 Apr;70(4):1495-9.

37.  Saddik M, Gamble J, Witters LA, Lopaschuk GD. Acetyl-CoA carboxylase regulation of fatty acid oxidation in the heart. J Biol Chem. 1993 Dec 5;268(34):25836-45.

38.  McGarry JD, Mannaerts GP, Foster DW. A possible role for malonyl-CoA in the regulation of hepatic fatty acid oxidation and ketogenesis. J Clin Invest. 1977 Jul;60(1):265-70.

39.  Robinson IN, Zammit VA. Sensitivity of carnitine acyltransferase I to malonly-CoA inhibition in isolated rat liver mitochondria is quantitatively related to hepatic malonyl-CoA concentration in vivo. Biochem J. 1982 Jul 15;206(1):177-9.

40.  McGarry JD, Mills SE, Long CS, Foster DW. Observations on the affinity for carnitine, and malonyl-CoA sensitivity, of carnitine palmitoyltransferase I in animal and human tissues. Demonstration of the presence of malonyl-CoA in non-hepatic tissues of the rat. Biochem J. 1983 Jul 15;214(1):21-8.

41.  Sidossis LS, Gastaldelli A, Klein S, Wolfe RR. Regulation of plasma fatty acid oxidation during low- and high-intensity exercise. Am J Physiol. 1997;272:E1065–70.

42.  Mertens DJ, Rhind S, Berkhoff F, Dugmore D, Shek PN, Shephard RJ. Nutritional, immunologic and psychological responses to a 7250 km run. J Sports Med Phys Fitness. 1996 Jun;36(2):132-8.

43.  Wesche MF, Wiersinga WM. Relation between lean body mass and thyroid volume in competition rowers before and during intensive physical training. Horm Metab Res. 2001 Jul;33(7):423-7.

44.  Eliakim A, Brasel JA, Mohan S, Barstow TJ, Berman N, Cooper DM. Physical fitness, endurance training, and the growth hormone-insulin-like growth factor I system in adolescent females. J Clin Endocrinol Metab. 1996 Nov;81(11):3986-92.

45.  Bisschop PH, Sauerwein HP, Endert E, Romijn JA. Isocaloric carbohydrate deprivation induces protein catabolism despite a low T3-syndrome in healthy men. Clin Endocrinol (Oxf). 2001 Jan;54(1):75-80.

46.  Essig DA, Alderson NL, Ferguson MA, Bartoli WP, Durstine JL. Delayed effects of exercise on the plasma leptin concentration. Metabolism. 2000 Mar;49(3):395-9.

47.  Kanaley JA, Weltman JY, Pieper KS, Weltman A, Hartman ML. Cortisol and growth hormone responses to exercise at different times of day. J Clin Endocrinol Metab. 2001 Jun;86(6):2881-9.

48.  Duclos M, Gouarne C, Bonnemaison D. Acute and chronic effects of exercise on tissue sensitivity to glucocorticoids. J Appl Physiol. 2003 Mar;94(3):869-75.

49.  Duclos M, Corcuff JB, Pehourcq F, Tabarin A. Decreased pituitary sensitivity to glucocorticoids in endurance-trained men. Eur J Endocrinol. 2001 Apr;144(4):363-8.

50.  Heitkamp HC, Schulz H, Rocker K, Dickhuth HH. Endurance training in females: changes in beta-endorphin and ACTH. Int J Sports Med. 1998 May;19(4):260-4.

51.  Duclos M, Corcuff JB, Arsac L, Moreau-Gaudry F, Rashedi M, Roger P, Tabarin A, Manier G. Corticotroph axis sensitivity after exercise in endurance-trained athletes. Clin Endocrinol (Oxf). 1998 Apr;48(4):493-501.

52.  Tyndall GL, Kobe RW, Houmard JA. Cortisol, testosterone, and insulin action during intense swimming training in humans. Eur J Appl Physiol Occup Physiol. 1996;73(1-2):61-5.

53.  Vasankari TJ, Kujala UM, Heinonen OJ, Huhtaniemi IT. Effects of endurance training on hormonal responses to prolonged physical exercise in males. Acta Endocrinol (Copenh). 1993 Aug;129(2):109-13.

54.  Hoogeveen AR, Zonderland ML. Relationships between testosterone, cortisol and performance in professional cyclists. Int J Sports Med. 1996 Aug;17(6):423-8.

55.  Seidman DS, Dolev E, Deuster PA, Burstein R, Arnon R, Epstein Y. Androgenic response to long-term physical training in male subjects. Int J Sports Med. 1990 Dec;11(6):421-4.

56.  Duclos, M, Corcuff JB, Rashedi M, Fougere V, and Manier G. Trained versus untrained: different hypothalamo-pituitary adrenal axis responses to exercise recovery. Eur J Appl Physiol 75: 343-350, 1997.

57.  Ma K, Mallidis C, Bhasin S, Mahabadi V, Artaza J, Gonzalez-Cadavid N, Arias J, Salehian B. Glucocorticoid-induced skeletal muscle atrophy is associated with upregulation of myostatin gene expression. Am J Physiol Endocrinol Metab. 2003 Aug;285(2):E363-71.

58.  Cvijetić S, Grazio S, Gomzi M, Krapac L, Nemcić T, Uremović M, Bobić J. Muscle strength and bone density in patients with different rheumatic conditions: cross-sectional study. Croat Med J. 2011 Apr 15;52(2):164-70.

59.  Dixon WG, Lunt M, Pye SR, Reeve J, Felsenberg D, Silman AJ, O’Neill TW; European Prospective Osteoporosis Study Group. Low grip strength is associated with bone mineral density and vertebral fracture in women. Rheumatology (Oxford). 2005 May;44(5):642-6.

60.  Lekamwasam S, Weerarathna T, Rodrigo M, Arachchi WK, Munidasa D. Association between bone mineral density, lean mass, and fat mass among healthy middle-aged premenopausal women: a cross-sectional study in southern Sri Lanka. J Bone Miner Metab. 2009;27(1):83-8.

61.  Li S, Wagner R, Holm K, Lehotsky J, Zinaman MJ. Relationship between soft tissue body composition and bone mass in perimenopausal women. Maturitas. 2004 Feb 20;47(2):99-105.

62.  Salamone LM, Glynn N, Black D, Epstein RS, Palermo L, Meilahn E, Kuller LH, Cauley JA. Body composition and bone mineral density in premenopausal and early perimenopausal women. J Bone Miner Res. 1995 Nov;10(11):1762-8.

63.  Winters KM, Snow CM. Body composition predicts bone mineral density and balance in premenopausal women. J Womens Health Gend Based Med. 2000 Oct;9(8):865-72.

64.  Witzke KA, Snow CM. Lean body mass and leg power best predict bone mineral density in adolescent girls. Med Sci Sports Exerc. 1999 Nov;31(11):1558-63.

65.  Allison DB, Zannolli R, Faith MS, Heo M, Pietrobelli A, VanItallie TB, Pi-Sunyer FX, Heymsfield SB. Weight loss increases and fat loss decreases all-cause mortality rate: results from two independent cohort studies. Int J Obes Relat Metab Disord. 1999 Jun;23(6):603-11.

66.  Savard R, Despres JP, Marcotte M, Bouchard C. Endurance training and glucose conversion into triglycerides in human fat cells. J Appl Physiol. 1985 Jan;58(1):230-5.

67.  Viru A, Toode K, Eller A. Adipocyte responses to adrenaline and insulin in active and former sportsmen. Eur J Appl Physiol Occup Physiol. 1992;64(4):345-9.

68.  Hickner RC, Racette SB, Binder EF, Fisher JS, Kohrt WM. Effects of 10 days of endurance exercise training on the suppression of whole body and regional lipolysis by insulin. J Clin Endocrinol Metab. 2000 Apr;85(4):1498-504.

69.  Gommers A, Dehez-Delhaye M, Caucheteux D. Prolonged effects of training on adipose tissue glucose metabolism and insulin responsiveness in adult rats (author’s transl) Diabete Metab. 1981 Jun;7(2):121-6.

70.  Perreault L, Lavely JM, Kittelson JM, Horton TJ. Gender differences in lipoprotein lipase activity after acute exercise. Obes Res. 2004 Feb;12(2):241-9.

71.  Taskinen MR, Nikkila EA. Effect of acute vigorous exercise on lipoprotein lipase activity of adipose tissue and skeletal muscle in physically active men. Artery. 1980;6(6):471-83.

72.  Farese RV Jr, Yost TJ, Eckel RH. Tissue-specific regulation of lipoprotein lipase activity by insulin/glucose in normal-weight humans. Metabolism. 1991 Feb;40(2):214-6.

73.  Gregoire F, Genart C, Hauser N, Remacle C. Glucocorticoids induce a drastic inhibition of proliferation and stimulate differentiation of adult rat fat cell precursors. Exp Cell Res. 1991 Oct;196(2):270-8.

74.  Xu XF, Bjorntorp P. Effects of dexamethasone on multiplication and differentiation of rat adipose precursor cells. Exp Cell Res. 1990 Aug;189(2):247-52.

75.  Hentges EJ, Hausman GJ. Primary cultures of stromal-vascular cells from pig adipose tissue: the influence of glucocorticoids and insulin as inducers of adipocyte differentiation. Domest Anim Endocrinol. 1989 Jul;6(3):275-85.

76.  Hauner H, Entenmann G, Wabitsch M, Gaillard D, Ailhaud G, Negrel R, Pfeiffer EF. Promoting effect of glucocorticoids on the differentiation of human adipocyte precursor cells cultured in a chemically defined medium. J Clin Invest. 1989 Nov;84(5):1663-70.

77.  Hauner H, Schmid P, Pfeiffer EF. Glucocorticoids and insulin promote the differentiation of human adipocyte precursor cells into fat cells. J Clin Endocrinol Metab. 1987 Apr;64(4):832-5.

78.  Ramsay TG, White ME, Wolverton CK. Glucocorticoids and the differentiation of porcine preadipocytes. J Anim Sci. 1989 Sep;67(9):2222-9.

79.  Bujalska IJ, Kumar S, Hewison M, Stewart PM. Differentiation of adipose stromal cells: the roles of glucocorticoids and 11beta-hydroxysteroid dehydrogenase. Endocrinology. 1999 Jul;140(7):3188-96.

80.  Nougues J, Reyne Y, Barenton B, Chery T, Garandel V, Soriano J. Differentiation of adipocyte precursors in a serum-free medium is influenced by glucocorticoids and endogenously produced insulin-like growth factor-I. Int J Obes Relat Metab Disord. 1993 Mar;17(3):159-67.

While many of us wonder just how much exercise we really need in order to gain health and fitness, a group of scientists in Canada are turning that issue on its head and asking, how little exercise do we need?

The emerging and engaging answer appears to be, a lot less than most of us think — provided we’re willing to work a bit.

In proof of that idea, researchers at McMaster University in Hamilton, Ontario, recently gathered several groups of volunteers. One consisted of sedentary but generally healthy middle-aged men and women. Another was composed of middle-aged and older patients who’d been diagnosed with cardiovascular disease.

The researchers tested each volunteer’s maximum heart rate and peak power output on a stationary bicycle. In both groups, the peaks were not, frankly, very high; all of the volunteers were out of shape and, in the case of the cardiac patients, unwell. But they gamely agreed to undertake a newly devised program of cycling intervals.

Most of us have heard of intervals, or repeated, short, sharp bursts of strenuous activity, interspersed with rest periods. Almost all competitive athletes strategically employ a session or two of interval training every week to improve their speed and endurance.

But the Canadian researchers were not asking their volunteers to sprinkle a few interval sessions into exercise routines. Instead, the researchers wanted the groups to exercise exclusively with intervals.

For years, the American Heart Association and other organizations have recommended that people complete 30 minutes or more of continuous, moderate-intensity exercise, such as a brisk walk, five times a week, for overall good health.

But millions of Americans don’t engage in that much moderate exercise, if they complete any at all. Asked why, a majority of respondents, in survey after survey, say, “I don’t have time.”

Intervals, however, require little time. They are, by definition, short. But whether most people can tolerate intervals, and whether, in turn, intervals provide the same health and fitness benefits as longer, more moderate endurance exercise are issues that haven’t been much investigated.

Several years ago, the McMasters scientists did test a punishing workout, known as high-intensity interval training, or HIIT, that involved 30 seconds of all-out effort at 100 percent of a person’s maximum heart rate. After six weeks, these lacerating HIIT sessions produced similar physiological changesin the leg muscles of young men as multiple, hour-long sessions per week of steady cycling, even though the HIIT workouts involved about 90 percent less exercise time.

Recognizing, however, that few of us willingly can or will practice such straining all-out effort, the researchers also developed a gentler but still chronologically abbreviated form of HIIT. This modified routine involved one minute of strenuous effort, at about 90 percent of a person’s maximum heart rate (which most of us can estimate, very roughly, by subtracting our age from 220), followed by one minute of easy recovery. The effort and recovery are repeated 10 times, for a total of 20 minutes.

Despite the small time commitment of this modified HIIT program, after several weeks of practicing it, both the unfit volunteers and the cardiac patients showed significant improvements in their health and fitness.

The results, published in a recent review of HIIT-related research, were especially remarkable in the cardiac patients. They showed “significant improvements” in the functioning of their blood vessels and heart, said Maureen MacDonald, an associate professor of kinesiology at McMaster who is leading the ongoing experiment.

It might seem counterintuitive that strenuous exercise would be productive or even wise for cardiac patients. But so far none have experienced heart problems related to the workouts, Dr. MacDonald said. “It appears that the heart is insulated from the intensity” of the intervals, she said, “because the effort is so brief.”

Almost as surprising, the cardiac patients have embraced the routine. Although their ratings of perceived exertion, or sense of the discomfort of each individual interval, are high and probably accurate, averaging a 7 or higher on a 10-point scale, they report enjoying the entire sessions more than longer, continuous moderate exercise, Dr. MacDonald said.

“The hard work is short,” she points out, “so it’s tolerable.” Members of a separate, exercise control group at the rehab center, assigned to complete standard 30-minute moderate-intensity workout sessions, have been watching wistfully as the interval trainers leave the lab before them. “They want to switch groups,” she said.

The scientists have noted other benefits in earlier studies. In unfit but otherwise healthy middle-aged adults, two weeks of modified HIIT training prompted the creation of far more cellular proteins involved in energy production and oxygen. The training also improved the volunteers’ insulin sensitivity and blood sugar regulation, lowering their risk of developing Type 2 diabetes, according to a study published last fall in Medicine & Science in Sports & Exercise.

Since then, the scientists completed a small, follow-up experiment involving people with full-blown Type 2 diabetes. They found that even a single bout of the 1-minute hard, 1-minute easy HIIT training, repeated 10 times, improved blood sugar regulation throughout the following day, particularly after meals.

Of course, HIIT training is not ideal or necessary for everyone, said Martin Gibala, a professor of kinesiology at McMaster, who’s overseen the high-intensity studies. “If you have time” for regular 30-minute or longer endurance exercise training, “then by all means, keep it up,” he said. “There’s an impressive body of science showing” that such workouts “are very effective at improving health and fitness.”

But if time constraints keep you from lengthier exercise, he continues, consult your doctor for clearance, and then consider rapidly pedaling a stationary bicycle or sprinting uphill for one minute, aiming to raise your heart rate to about 90 percent of your maximum. Pedal or jog easily downhill for a minute and repeat nine times, perhaps twice a week. “It’s very potent exercise,” Dr. Gibala said. “And then, very quickly, it’s done.”

 

To view original article please visit www.nytimes.com

Athletes were studied a fortnight before their races, immediately afterwards and then about a week later

“My personal feeling is that extreme endurance exercise probably does cause damage to the heart in some athletes”

Professor Sanjay SharmaMedical director of the London Marathon

ScienceDaily (Jan. 16, 2012) — Using a sling or cast after injuring an arm may cause your brain to shift quickly to adjust, according to a study published in the January 17, 2012, print issue ofNeurology®, the medical journal of the American Academy of Neurology. The study found increases in the size of brain areas that were compensating for the injured side, and decreases in areas that were not being used due to the cast or sling.

“These results are especially interesting for rehabilitation therapy for people who’ve had strokes or other issues,” said study author Nicolas Langer, MSc, with the University of Zurich in Switzerland. “One type of therapy restrains the unaffected, or “good,” arm to strengthen the affected arm and help the brain learn new pathways. This study shows that there are both positive and negative effects of this type of treatment.”

For the study, researchers examined 10 right-handed people with an injury of the upper right arm that required a sling for at least 14 days. The entire right arm and hand were restricted to little or no movement during the study period. As a result, participants used their non-dominant left hand for daily activities such as washing, using a toothbrush, eating or writing. None of the people in the study had a brain injury, psychiatric disease or nerve injury.

The group underwent two MRI brain scans, the first within two days of the injury and the second within 16 days of wearing the cast or sling. The scans measured the amount of gray and white matter in the brain. Participants’ motor skills, including arm-hand movements and wrist-finger speed, were also tested.

The study found that amount of gray and white matter in the left side of the brain decreased up to ten percent, while the amount of gray and white matter in the right side of the brain increased in size.

“We also saw improved motor skills in the left, non-injured hand, which directly related to an increase in thickness in the right side of the brain,” said Langer. “These structural changes in the brain are associated with skill transfer from the right hand to the left hand.”

Langer noted that the study did not look at whether the decreases would be permanent.

“Further studies should examine whether using a restraint for stroke patients is really a necessity for improving arm and hand movement,” he said. “Our results also support the current trauma surgery guidelines stating that an injured arm or leg should be immobilized ‘as short as possible, as long as necessary.’”

The study was supported by the National Center of Competence in Research and the Swiss National Science Foundation.

 

To view Original article please visit www.sciencedaily.com

“There is a neuromuscular inhibitory response to static stretching,” says Malachy McHugh, the director of research at the Nicholas Institute of Sports Medicine and Athletic Trauma at Lenox Hill Hospital in New York City. The straining muscle becomes less responsive and stays weakened for up to 30 minutes after stretching, which is not how an athlete wants to begin a workout.”

PHYS ED

By GRETCHEN REYNOLDS

Published: October 31, 2008

WHEN DUANE KNUDSON, a professor of kinesiology at California State University, Chico, looks around campus at athletes warming up before practice, he sees one dangerous mistake after another. “They’re stretching, touching their toes. . . . ” He sighs. “It’s discouraging.”

The New York Times

If you’re like most of us, you were taught the importance of warm-up exercises back in grade school, and you’ve likely continued with pretty much the same routine ever since. Science, however, has moved on. Researchers now believe that some of the more entrenched elements of many athletes’ warm-up regimens are not only a waste of time but actually bad for you. The old presumption that holding a stretch for 20 to 30 seconds — known as static stretching — primes muscles for a workout is dead wrong. It actually weakens them. In a recent study conducted at the University of Nevada, Las Vegas, athletes generated less force from their leg muscles after static stretching than they did after not stretching at all. Other studies have found that this stretching decreases muscle strength by as much as 30 percent. Also, stretching one leg’s muscles can reduce strength in the other leg as well, probably because the central nervous system rebels against the movements.

“There is a neuromuscular inhibitory response to static stretching,” says Malachy McHugh, the director of research at the Nicholas Institute of Sports Medicine and Athletic Trauma at Lenox Hill Hospital in New York City. The straining muscle becomes less responsive and stays weakened for up to 30 minutes after stretching, which is not how an athlete wants to begin a workout.

THE RIGHT WARM-UP should do two things: loosen muscles and tendons to increase the range of motion of various joints, and literally warm up the body. When you’re at rest, there’s less blood flow to muscles and tendons, and they stiffen. “You need to make tissues and tendons compliant before beginning exercise,” Knudson says.

A well-designed warm-up starts by increasing body heat and blood flow. Warm muscles and dilated blood vessels pull oxygen from the bloodstream more efficiently and use stored muscle fuel more effectively. They also withstand loads better. One significant if gruesome study found that the leg-muscle tissue of laboratory rabbits could be stretched farther before ripping if it had been electronically stimulated — that is, warmed up.

To raise the body’s temperature, a warm-up must begin with aerobic activity, usually light jogging. Most coaches and athletes have known this for years. That’s why tennis players run around the court four or five times before a match and marathoners stride in front of the starting line. But many athletes do this portion of their warm-up too intensely or too early. A 2002 study of collegiate volleyball players found that those who’d warmed up and then sat on the bench for 30 minutes had lower backs that were stiffer than they had been before the warm-up. And a number of recent studies have demonstrated that an overly vigorous aerobic warm-up simply makes you tired. Most experts advise starting your warm-up jog at about 40 percent of your maximum heart rate (a very easy pace) and progressing to about 60 percent. The aerobic warm-up should take only 5 to 10 minutes, with a 5-minute recovery. (Sprinters require longer warm-ups, because the loads exerted on their muscles are so extreme.) Then it’s time for the most important and unorthodox part of a proper warm-up regimen, the Spider-Man and its counterparts.

“TOWARDS THE end of my playing career, in about 2000, I started seeing some of the other guys out on the court doing these strange things before a match and thinking, What in the world is that?” says Mark Merklein, 36, once a highly ranked tennis player and now a national coach for the United States Tennis Association. The players were lunging, kicking and occasionally skittering, spider-like, along the sidelines. They were early adopters of a new approach to stretching.

While static stretching is still almost universally practiced among amateur athletes — watch your child’s soccer team next weekend — it doesn’t improve the muscles’ ability to perform with more power, physiologists now agree. “You may feel as if you’re able to stretch farther after holding a stretch for 30 seconds,” McHugh says, “so you think you’ve increased that muscle’s readiness.” But typically you’ve increased only your mental tolerance for the discomfort of the stretch. The muscle is actually weaker.

Stretching muscles while moving, on the other hand, a technique known as dynamic stretching or dynamic warm-ups, increases power, flexibility and range of motion. Muscles in motion don’t experience that insidious inhibitory response. They instead get what McHugh calls “an excitatory message” to perform.

Dynamic stretching is at its most effective when it’s relatively sports specific. “You need range-of-motion exercises that activate all of the joints and connective tissue that will be needed for the task ahead,” says Terrence Mahon, a coach with Team Running USA, home to the Olympic marathoners Ryan Hall and Deena Kastor. For runners, an ideal warm-up might include squats, lunges and “form drills” like kicking your buttocks with your heels. Athletes who need to move rapidly in different directions, like soccer, tennis or basketball players, should do dynamic stretches that involve many parts of the body. “Spider-Man” is a particularly good drill: drop onto all fours and crawl the width of the court, as if you were climbing a wall. (For other dynamic stretches, see the sidebar below.)

Even golfers, notoriously nonchalant about warming up (a recent survey of 304 recreational golfers found that two-thirds seldom or never bother), would benefit from exerting themselves a bit before teeing off. In one 2004 study, golfers who did dynamic warm- up exercises and practice swings increased their clubhead speed and were projected to have dropped their handicaps by seven strokes over seven weeks.

Controversy remains about the extent to which dynamic warm-ups prevent injury. But studies have been increasingly clear that static stretching alone before exercise does little or nothing to help. The largest study has been done on military recruits; results showed that an almost equal number of subjects developed lower-limb injuries (shin splints, stress fractures, etc.), regardless of whether they had performed static stretches before training sessions. A major study published earlier this year by the Centers for Disease Control, on the other hand, found that knee injuries were cut nearly in half among female collegiate soccer players who followed a warm-up program that included both dynamic warm-up exercises and static stretching. (For a sample routine, visitwww.aclprevent.com/pepprogram.htm.) And in golf, new research by Andrea Fradkin, an assistant professor of exercise science at Bloomsburg University of Pennsylvania, suggests that those who warm up are nine times less likely to be injured.

“It was eye-opening,” says Fradkin, formerly a feckless golfer herself. “I used to not really warm up. I do now.”

You’re Getting Warmer: The Best Dynamic Stretches

These exercises- as taught by the United States Tennis Association’s player-development program – are good for many athletes, even golfers. Do them immediately after your aerobic warm-up and as soon as possible before your workout.

STRAIGHT-LEG MARCH

(for the hamstrings and gluteus muscles)

Kick one leg straight out in front of you, with your toes flexed toward the sky. Reach your opposite arm to the upturned toes. Drop the leg and repeat with the opposite limbs. Continue the sequence for at least six or seven repetitions.

SCORPION

(for the lower back, hip flexors and gluteus muscles)

Lie on your stomach, with your arms outstretched and your feet flexed so that only your toes are touching the ground. Kick your right foot toward your left arm, then kick your leftfoot toward your right arm. Since this is an advanced exercise, begin slowly, and repeat up to 12 times.

HANDWALKS

(for the shoulders, core muscles, and hamstrings)

Stand straight, with your legs together. Bend over until both hands are flat on the ground. “Walk” with your hands forward until your back is almost extended. Keeping your legs straight, inch your feet toward your hands, then walk your hands forward again. Repeat five or six times. G.R.

 

 

More Articles in Sports »A version of this article appeared in print on November 2, 2008, on page MM20 of the New York edition.

 

To view original article please visit www.nytimes.com

Abstract

Recent research (Carney, Cuddy, & Yap, 2010) has shown that adopting a powerful pose changes people’s hormonal levels and increases their propensity to take risks in the same ways that possessing actual power does. In the current research, we explore whether adopting physical postures associated with power, or simply interacting with others who adopt these postures, can similarly influence sensitivity to pain. We conducted two experiments. In Experiment 1, participants who adopted dominant poses displayed higher pain thresholds than those who adopted submissive or neutral poses. These findings were not explained by semantic priming. In Experiment 2, we manipulated power poses via an interpersonal interaction and found that power posing engendered a complementary (Tiedens & Fragale, 2003) embodied power experience in interaction partners. Participants who interacted with a submissive confederate displayed higher pain thresholds and greater handgrip strength than participants who interacted with a dominant confederate.

Highlights

☆

The authors contributed equally and are listed alphabetically. We would like to thank Justin Fan and Kristin Jung for their considerable help in administering the experiments. We note that Justin illustrated the postures in Figure 3.

 

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