International Journal of Sports and Exercise Medicine
A Recovery Based Intervention to Improve Retention in an Activity Centric Health and Fitness Program. An "outside-in" Approach
J. David Prologo*
Interventional Radiologist, Atlanta GA, USA
*Corresponding author: J. David Prologo, MD, Interventional Radiologist, Atlanta GA, USA, E-mail: jdprologo@hotmail.com
Int J Sports Exerc Med, IJSEM-1-026, (Volume 1, Issue 5), Hypothesis; ISSN: 2469-5718
Received: November 07, 2015 | Accepted: November 21, 2015 | Published: November 24, 2015
Citation: Prologo JD (2015) A Recovery Based Intervention to Improve Retention in an Activity Centric Health and Fitness Program. An "outside-in" Approach. Int J Sports Exerc Med 1:026. 10.23937/2469-5718/1510026
Copyright: © 2015 Prologo JD. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Introduction
One hundred eight million people were estimated to be on a diet in the United States in 2014 at any given time, with each of those making 4 to 5 attempts to lose weight each year - translating to approximately 2.5 billion dollars spent failing weight loss programs [1-3]. A variety of mechanisms have been studied and marketed in attempts to increase the length of time users will follow their diet and/or exercise programs, with largely disappointing results [2,4-6].
Temporal evaluation of clinical interventions to manage obesity have identified several points of potential exploitation. First, inverse correlates of success in this space have been defined, including - relevant to this proposal - degrees of calorie restriction or program structure [7,8]. Attempts to mediate these variables has also resulted in at least partial success, the most illustrative example being the Weight Watchers® program. Weight Watchers has enjoyed positive results based on the principles of less stringent dietary choices and dynamic scheduling with regard to intake [3,9]. Second, the neurophysiological response to diet and exercise responsible for so many repeat failures has been detailed [10-14]. These hormonal axes have been bypassed successfully via bariatric surgery, with subsequent real weight loss maintenance and disease control [15-17]. Third, the Obesity Medicine community has embraced an activity mediated transformative approach to health living - clearly stating that "exercise alters food preferences toward healthy foods... and healthy muscle trains the fat to burn more calories," and that lessons learned through the study of exercise biology point toward molecular modification through activity as the new frontier of healthy living [18,19]. Fourth, "something is better than nothing" [20-22]. Much of attrition is related to incomplete adherence and an "all or nothing" mentality from the user. Dieters realize they cannot maintain the entirety of a schedule and usually decide to quit the process altogether. Fifth, successful transformation is linked to exercise recovery [18,19,23-26].
Based on the principles delineated above (defined physiological responses to diet that limit progress, proven success using dynamic approaches with less stringent calorie requirements, activity mediated induction of long-term preference change, "something is better than nothing," and recovery importance), We propose a unique, dynamic, individualized, activity centric, adjustable program for weight loss and conversion to healthy living.
Nature of the Proposed Program
Overcoming the restrictive nature of commercial programs that result in diet failures
This is the epicenter of the proposal. There are no presently available all-inclusive diet and fitness (or even fitness alone) programs for patients or the public that address the clear relationship of structure with attrition [7,27,28]. As mentioned above, programs that do target this relationship on the diet/intake side of this equation have proven themselves effective over time [3]. Other facets of wellness that employ a dynamic structuring have also enjoyed consistent, objective, positive results. The most powerful example of these can be found in the phenomenon of Alcoholics Anonymous (AA). The AA system has been working for almost 80 years, had millions and millions of members, consistently reported success rates, has no leadership, and enjoys a worldwide presence [29,30]. It doesn't involve medication, doesn't cost money, doesn't implement a schedule, has no forced accountability (it's anonymous), and requires nothing of its members.
They AA program capitalizes on the inverse relationship between structure and success with regard to user effort - and by doing so integrate into the peaks and valleys of member's lives. They "stay with them" so to speak, as their lives oscillate, rather than superimposing a generalized schedule on to thousands of individuals with different emotions and domestic demands - which inevitably leads to failure.
This proposed program likewise adjusts to the individual user's biofeedback. So well-known are the changes that occur in between workouts that elite athletes and fitness professionals in the know purposefully capture this process as part of their training [23]. New set-points are established. Red blood cells are replenished, more efficient heart rates and blood pressures are established, stress hormones are decreased, calcium is put into bones, muscles change their structure, metabolic rates are increased, circulating fat and glucose are decreased, immune systems are strengthened, and overall wellbeing is improved. Each user will undergo the process of exercise recovery at a different rate, depending on their body habitus, basal metabolic rate, genetics, and exercise history [24-26].
Participants interested in a novel approach should be trained to recognize the body's feedback and to adjust their program accordingly. For example, an individual's personalized diet and fitness schedule may look like that in figure 1 on any given day. In this example, the user has progressed to Level 2 (upper right hand corner), and has 169.25 more points to earn in order to complete this level. The greyed out boxes represent completed days and the current day calls for "Level 2 Gym Workout Gamma." The innovation lies in the drop down option. The user has the option to change the current day to a different workout, recovery day, or off day - all of which are worth variable points depending on a multitude of factors included in the background algorithm (such as number of off days in a given span of time, involvement of the recovery intervention, and so on). When the user selects an alternate option, the program recalibrates according to a predetermined number of needed points to complete the level, which has been determined based on weighted calculations of the users initial input data. (Appendix) Each user will have an individualized goal - and their personal grid will recalibrate according to this goal when they switch a day, thereby truly "keeping them on track," in the face of dynamic scheduling. In this particular example (based on the programmers input), the user has switched to an off day and the program has rescheduled the workouts and recoveries in order to keep him/her on track toward the level 2 completion (notice remaining points and accumulated points are unchanged - the person has not lost ground by rescheduling). This response is in contradistinction to the negative feedback and negative connotation that accompanies "missing a day" of a predetermined rigid program schedule - an event that often leads to termination of the program as a whole, and restart some other day.
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Figure 1A and 1B: Sample grids from the program demonstrating the functionality of a proposed program founded on dynamic scheduling
View Figure 1
Restructuring the neurophysiological response to diet and exercise
The body's response to diet and exercise has been well documented. These signals are real, survival based, and nearly impossible to overcome [14,15,31,32]. Bariatric surgery works because it changes the levels of these molecules [15-17,33]. The central theme underpinning this point is that the brain can be changed to respond differently to input - to respond differently to diet and exercise [34-36]. The key is resetting this system and reversing the signals such that new neural circuitry is recruited to send retrograde messages to the brain that result in restructuring. This process leads to new antegrade signaling in the face of these stressors [37-39].
The dynamic nature of the program, in combination with intentional exercise and select recovery interventions - results in a new period between workouts that allows for adaptation (Figure 2). By attending to the inter-exercise adaption, users create new patterns through neuroplasticity, thereby leading to new responses in this setting. Each "off" day allows for restructuring, and each "recovery" day contains evidence based, lifestyle interventions to accelerate the process of adaptation.
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Figure 2a: To be successful, users must time their workouts at the end of recovery, in order to allow time for the application of stress through exercise to induce change.
View Figure 2a
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Figure 2b: Traditional programs schedule workouts in a static grid, without considering individual recovery time, so the workouts come too soon, before recovery is complete - leading to a downward spiral, and cyclic failures.
View Figure 2b
Accelerating transformative change according to Obesity Medicine principles through intentional exercise and recovery
The specific descriptions for users to follow each day are prescribed with the intent of inducing change. Specifically, the exercise regimen is not intended to burn calories so that the user can "lose weight," but rather to induce adaptation and change internally, so that the signaling pattern can be changed through retrograde signaling.
The exercise regimen is divide into "Levels" in order to communicate to the user that he or she is progressing. Clearly the concept of progression toward a goal has proven effective toward behavior modification in the setting of obesity management [7]. Moreover, the levels are progressively more involved and difficult - thereby allowing the user to maintain their progress over time. (Figure 3)
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Figure 3a: The program is arranged in levels, so that the user may benefit from both progression toward define goals and positive feedback.
View Figure 3a
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Figure 3b: The schedule is arranged around changing biofeedback in order to stabilize each quantum of progress made by the user
View Figure 3b
The recovery interventions should be selected based on scientific evidence of disease control effect, exercise recovery, and appetite control. Briefly, we propose three categories:
Sleep:The benefits of sleep, as it relates to exercise, weight loss, and fitness, can be divided broadly into two categories: recovery and the homeostasis of energy metabolism in humans. The first, recovery, is mediated through direct stimulation of protein transcription, through the production of antioxidant molecules, and through adjustment of immunological mediator profiles [40-46].
That is, exercise results in a disruption of our molecular structure, a disruption that the body seeks to correct. The new structure will have the capacity to endure a greater amount of exercise, thereby ultimately tipping the caloric balance. These specific anabolic processes are mediated by growth hormone, (GH) via hepatic production of insulin growth like factors (IGFs). Downstream adjustments translate to increased metabolism, less injury, and improved exercise capacity [47-50].
Growth hormone reaches its peaks during sleep: When the body is sleep deprived, it switches to survival mode and foregoes optimization. In order to optimize physical exercise induced adaptation, subjects must access this reorganization strategy, mediated by GH during sleep.
Similarly, the autonomic "fight or flight" response is attenuated when adequately rested, and parasympathetic output maximized, which optimizes rebuilding and adaptation. Otherwise, this response exists at a low level which is counterproductive to the exercise cause. In this situation, hormones and proteins, appropriately named "stress proteins," or "the stress response" circulate in relatively higher levels, resulting in increased storage of fat and toxicity to recovering muscles [43,51-53]. Finally, in the absence of adequate sleep following exercise, the body exhibits a pro-inflammatory response, consisting of pro-inflammatory cytokines and characteristic immune cell presence [54-56], which causes direct damage to muscles, in addition to hindering recovery. Conversely, sleep is associated with decreased levels of all of these mediators and uninterrupted reorganization of our underlying structure following exercise. (Figure 4)
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Figure 4a: In the absence of adequate rest, the body mediates change after exercise through proinflammatory cytokines (PIC), sympathetic nervous system activation (SN), growth hormone deficiency (GHD), and stress response proteins (SRP).
View Figure 4a
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Figure 4b: In the presence of adequate rest, the body mediates change after exercise through growth hormone (GH), insulin like growth factors (IGFs), muscle protein transcription (PT), and parasympathetic nervous system (PSN) activation.
View Figure 4b
Secondly, sleep is intricately related to the energy cycle and homeostasis. As is well known, the body's responses and adaptations are often rooted in evolution and survival. Humans originally needed to sleep, eat, and reproduce in order for the species to survive. As a result a bi-directional hormonal system evolved such that satiety resulted in sleep. Sleep is required for humans to "protect brain cells from the damaging effect of reactive oxygen species, allow sufficient time for the repair or replacement of essential cellular components . . . and deal with other biochemical consequences of waking metabolic activity" [57,58]. Studies have shown that sleep deprivation results in decreased energy expenditure during the day. This is an attempt by the body to equalize the energy in - energy out balance disrupted by extensive waking hours. That is, the longer a person is awake, the more energy they are expending - such that the body then slows down metabolism and kicks out hunger hormones leading to increased intake in an attempt to compensate [58-62]. Worse, the body would rather consume energy itself during sleep as part of the rebuilding process [63].
What this means is that the body responds to less than optimal sleep duration by slowing metabolism, eating more, and foregoing rebuilding and strengthening activities - the latter of which would burn calories and energy itself. The same goes for poor sleep quality or interrupted sleep, which has also been shown to result in "increased hunger, uncontrolled and emotional eating, and cognitive restraint . . . as well as feelings of being less full," and lower resting metabolic rate [61,64]. The absence of adequate sleep creates a paradoxical scenario of unhealthy energy conservation and consumption for evolutionary survival, a principle demonstrated in studies examining fat retention in dieters who are sleep deprived, documenting worsened central obesity in women with decreased REM sleep, increased food intake and snacking during sleep deprived states, and food seeking behavior after partial sleep interruption [65,66]. Figure 5 demonstrates the disruption in equilibrium caused by sleep disturbance, which is worsened in the presence of exercise. The human body seeks to equalize the energy in - energy out balance for survival at baseline. The absence of sleep tips the balance toward energy conservation, which translates to weight gain, or in our case - the blocking of weight loss (Figure 5).
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Figure 5: In the absence of adequate sleep, energy balance is tipped toward conservation
View Figure 5
Diet: The proposed focus is categorically on structure and intake of the appropriate nutrients (Vs. Traditional calorie restriction protocols) [67,68]. If, while we are sleeping (above) the body sets out to build our scaffold, and there is no wood - there will be no change. The specific nutrients proposed for their roles in recovery are: Tryptophan, Tart Cherries, cottage cheese, and toast, Lunasin, Sweet Potato Proteins, and Polyphenols, Lysine, Glutamic Acid, and Heat Shock Proteins, Selenium and Molybdenum, Chinese Walnuts, Fish, Garlic, Protein simple carb mixes, Raw Vegetables, Water, Vinegar, and Chromium [40,67-108].
Active recovery: The term active recovery is meant to differentiate this change accelerant with the changes related to diet and sleep. Activities proposed under the heading Active Recovery are: Visualization, Yoga, meditation, and focused imagery, Mindfulness, Progressive Muscle Relaxation, Heat and cold immersions, Massage, Active Release, and/or Self-myofascial release, Compression Devices, and Mind-Body Approach [31,109-137].
Proposed Validation Strategy
In order to translate theory to guidelines, appropriate validation in necessary. The American Heart Association and The American College of Cardiology, in collaboration with the Centers for Disease Control here in Atlanta, GA - have published guidelines regarding the number of minutes of recommended physical activity for adults [138,139]. These minutes are reflected as "activity minutes" by the Fitbit (and other similar devices) through a combination of three dimensional accelerometry and heart rate recording. The data from these two inputs is correlated with user input regarding height, weight, and other physical characteristics so that metabolic equivalents of activity (METs [kcal/kg*hr]) can be determined for each user. MET data is then compared to existing data tables to determine activity intensity - and then converted to a digital output for the user labeled "activity minutes". This output has been validated and can be easily tracked via software linking to each study subject [140,141].
Secondly, retention rates are quantifiable. Using published absolute success rates (15% at month one, 10% at month 2, 5% at month 3, and 1% at month 6), the calculated sample size requirement to demonstrate a significant difference following implementation of this program is 54 subjects. Accounting for non-study related attrition over six months, a single arm of 75 subjects creates a cohort based on α < 0.001, power = 0.9, and an assumed population standard deviation of 8%. This translates to a 5% difference in "all or nothing" values, with the corresponding sample sizes for 3% and 2%, using the same parameters, at 149 and 335, respectively.
Using estimated activity minutes at the same temporal points (1, 2, 3, and 6 months), the required sample size is a bit less. Assuming the upper limit of the AHA/ACC/CDC guideline of 30 minutes 3-4 times/week to be 120 minutes, and a standard deviation of 40 minutes, to demonstrate a significant difference in activity minutes (designated as one activity day [30 minutes]), the sample size is 38. Any smaller designated difference would be difficult to for the public to interpret.
A multiple regression analysis should further be built in order to assess the impact of the following variables on outcome: age, race, sex, prior attempts to lose weight, prior number of pregnancies, starting BMI, and number of co-morbid conditions. Potential differences in the outcome variables of absolute attrition and activity minutes may be analyzed via analysis of covariance (ANCOVA) using baseline scores as covariates and a paired, two-sided t-test to evaluate least-squares mean changes, compared to baseline. The Bonferroni correction may be used to adjust for multiple comparisons.
Conclusion
At risk patients for obesity related complications primarily garner their information regarding health and fitness through marketing campaigns [142-145]. As a result, large companies are able to promulgate random information aimed to affect revenues, rather than long-term healthy adaptation. Medical and surgical management of bariatric patients in the 21st century has elucidated several principles of effectiveness with regard to obesity (Table 1). These principles may be incorporated into a new type of program to induce transformation and long term engagement, as above.
Table 1: Proposed, implementable principles of obesity medicine and bariatric intervention [3,7,10-19].
View Table 1
References
-
ABC News Staff (2012) 100 Million dieters, $20 Billion: The Weight Loss Industry by the Numbers ABC News.
-
Tsai AG, Wadden TA (2005) Systematic review: an evaluation of major commercial weight loss programs in the United States. Ann Intern Med 142: 56-66.
-
Gudzune KA, Doshi RS, Mehta AK, Chaudhry ZW, Jacobs DK, et al. (2015) Efficacy of commercial weight-loss programs: an updated systematic review. Ann Intern Med 162: 501-512.
-
Jeffery RW, Drewnowski A, Epstein LH, Stunkard AJ, Wilson GT, et al. (2000) Long-term maintenance of weight loss: current status. Health Psychol 19(1 Suppl): 5-16.
-
Looney SM, Raynor HA (2013) Behavioral lifestyle intervention in the treatment of obesity. Health Serv Insights 6: 15-31.
-
Hall KD (2015) Prescribing low-fat diets: useless for long-term weight loss? Lancet Diabetes Endocrinol .
-
Fabricatore AN (2007) Behavior therapy and cognitive-behavioral therapy of obesity: is there a difference? J Am Diet Assoc 107: 92-99.
-
(1998) Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults--The Evidence Report. National Institutes of Health. Obes Res 6 Suppl 2: 51S-209S.
-
Poston WS, Foreyt JP (2000) Successful management of the obese patient. Am Fam Physician 61: 3615-3622.
-
Berthoud HR (2006) Homeostatic and non-homeostatic pathways involved in the control of food intake and energy balance. Obesity (Silver Spring) 14 Suppl 5: 197S-200S.
-
Berthoud HR (2004) Neural control of appetite: cross-talk between homeostatic and non-homeostatic systems. Appetite 43: 315-317.
-
Howe SM, Hand TM, Manore MM (2014) Exercise-trained men and women: role of exercise and diet on appetite and energy intake. Nutrients 6: 4935-4960.
-
Gardiner JV, Jayasena CN, Bloom SR (2008) Gut hormones: a weight off your mind. J Neuroendocrinol 20: 834-841.
-
Kjaer M, Secher NH (1992) Neural influence on cardiovascular and endocrine responses to static exercise in humans. Sports Med 13: 303-319.
-
Weiss CR, Gunn AJ, Kim C, Paxton BE, Kraitchman DL, et al. (2015) Bariatric embolization of the gastric arteries for the treatment of obesity. J Vasc Interv Radiol 26: 613-624.
-
Chandarana K, Batterham RL (2012) Shedding pounds after going under the knife: metabolic insights from cutting the gut. Nat Med 18: 668-669.
-
Karra E, Yousseif A, Batterham RL (2010) Mechanisms facilitating weight loss and resolution of type 2 diabetes following bariatric surgery. Trends Endocrinol Metab 21: 337-344.
-
Kaplan L (2014) editor Obesity: A Panoptic Perspective. Overcoming Obesity. Phoenix, AZ: American Society of Bariatric Physicians.
-
Rowe GC, Safdar A, Arany Z (2014) Running forward: new frontiers in endurance exercise biology. Circulation 129: 798-810.
-
Association AH (2014) American Heart Association Recommendations for Physical Activity in Adults.
-
Searight R (2009) Realistic approaches to counseling in the office setting. Am Fam Physician 79: 277-284.
-
Jensen MD, Ryan DH, Apovian CM, Ard JD, Comuzzie AG, et al. (2014) 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society. Circulation. 129(25 Suppl 2): S102-S138.
-
Mujika I, Padilla S, Pyne D, Busso T (2004) Physiological changes associated with the pre-event taper in athletes. Sports Med 34: 891-927.
-
Janikowska G, Kochanska-Dziurowicz A, Zebrowska A, Bijak A, Kimsa M (2014) Adrenergic response to maximum exercise of trained road cyclists. J Hum Kinet 40: 103-111.
-
Pattyn N, Cornelissen VA, Eshghi SR, Vanhees L (2013) The effect of exercise on the cardiovascular risk factors constituting the metabolic syndrome: a meta-analysis of controlled trials. Sports Med 43: 121-133.
-
Menicucci D, Piarulli A, Mastorci F, Sebastiani L, Laurino M, et al. (2013) Interactions between immune, stress-related hormonal and cardiovascular systems following strenuous physical exercise. Arch Ital Biol 151: 126-136.
-
Dalle Grave R, Centis E, Marzocchi R, El Ghoch M, Marchesini G (2013) Major factors for facilitating change in behavioral strategies to reduce obesity. Psychol Res Behav Manag 6: 101-110.
-
Jakicic JM, Wing RR, Butler BA, Robertson RJ (1995) Prescribing exercise in multiple short bouts versus one continuous bout: effects on adherence, cardiorespiratory fitness, and weight loss in overweight women. Int J Obes Relat Metab Disord 19: 893-901.
-
Pagano ME, White WL, Kelly JF, Stout RL, Carter RR, et al. (2013) The 10-year course of Alcoholics Anonymous participation and long-term outcomes: a follow-up study of outpatient subjects in Project MATCH. Subst Abus 34: 51-59.
-
White W (1998) Slaying the Dragon The History of Addiction Treatment and Recovery in America. Bloomington, IL: The Chestnut Health Systems.
-
Minett GM, Duffield R (2014) Is recovery driven by central or peripheral factors? A role for the brain in recovery following intermittent-sprint exercise. Front Physiol 5: 24.
-
Peinado AB, Rojo JJ, Calderon FJ, Maffulli N (2014) Responses to increasing exercise upon reaching the anaerobic threshold, and their control by the central nervous system. BMC Sports Sci Med Rehabil 6: 17.
-
Beckman LM, Beckman TR, Sibley SD, Thomas W, Ikramuddin S, et al. (2011) Changes in gastrointestinal hormones and leptin after Roux-en-Y gastric bypass surgery. JPEN J Parenter Enteral Nutr 35: 169-180.
-
Bezzola L, Mérillat S, Gaser C, Jäncke L (2011) Training-induced neural plasticity in golf novices. J Neurosci 31: 12444-12448.
-
Thomas C, Baker CI (2013) Teaching an adult brain new tricks: a critical review of evidence for training-dependent structural plasticity in humans. NeuroImage 73: 225-236.
-
Melzack R (2005) Evolution of the neuromatrix theory of pain. The Prithvi Raj Lecture: presented at the third World Congress of World Institute of Pain, Barcelona 2004. Pain Pract 5: 85-94.
-
Foell J, Bekrater-Bodmann R, Diers M, Flor H (2014) Mirror therapy for phantom limb pain: brain changes and the role of body representation. Eur J Pain 18: 729-739.
-
MacIver K, Lloyd DM, Kelly S, Roberts N, Nurmikko T (2008) Phantom limb pain, cortical reorganization and the therapeutic effect of mental imagery. Brain 131: 2181-2191.
-
Reilly KT, Sirigu A (2008) The motor cortex and its role in phantom limb phenomena. Neuroscientist 14: 195-202.
-
Halson SL (2014) Sleep in elite athletes and nutritional interventions to enhance sleep. Sports Med 44 Suppl 1: S13-23.
-
Nédélec M, McCall A, Carling C, Legall F, Berthoin S, et al. (2013) Recovery in soccer : part ii-recovery strategies. Sports Med 43: 9-22.
-
Dattilo M, Antunes HK, Medeiros A, Mônico Neto M, Souza HS, et al. (2011) Sleep and muscle recovery: endocrinological and molecular basis for a new and promising hypothesis. Med Hypotheses 77: 220-222.
-
Demarzo MM, Stein PK (2012) Mental Stress and Exercise Training Response: Stress-sleep Connection may be Involved. Front Physiol 3: 178.
-
Irwin MR, Carrillo C, Olmstead R (2010) Sleep loss activates cellular markers of inflammation: sex differences. Brain Behav Immun 24: 54-57.
-
Vgontzas AN, Pejovic S, Zoumakis E, Lin HM, Bixler EO, et al. Daytime napping after a night of sleep loss decreases sleepiness, improves performance, and causes beneficial changes in cortisol and interleukin-6 secretion. Am J Physiol Endocrinol Metab. 292: E253-E261.
-
Chaves VE, Júnior FM, Bertolini GL (2013) The metabolic effects of growth hormone in adipose tissue. Endocrine 44: 293-302.
-
Golbidi S, Laher I (2014) Exercise induced adipokine changes and the metabolic syndrome. J Diabetes Res 2014: 726861.
-
Yang J (2014) Enhanced skeletal muscle for effective glucose homeostasis. Prog Mol Biol Transl Sci 121: 133-163.
-
Kraemer WJ, Aguilera BA, Terada M, Newton RU, Lynch JM, et al. (1995) Responses of IGF-I to endogenous increases in growth hormone after heavy-resistance exercise. J Appl Physiol (1985) 79: 1310-1315.
-
Nishida Y, Matsubara T, Tobina T, Shindo M, Tokuyama K, et al. (2010) Effect of low-intensity aerobic exercise on insulin-like growth factor-I and insulin-like growth factor-binding proteins in healthy men. Int J Endocrinol 2010.
-
Meier-Ewert HK, Ridker PM, Rifai N, Regan MM, Price NJ, et al. (2004) Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk. J Am Coll Cardiol 43: 678-683.
-
Mullington JM, Haack M, Toth M, Serrador JM, Meier-Ewert HK (2009) Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Prog Cardiovasc Dis 51: 294-302.
-
Basta M, Chrousos GP, Vela-Bueno A, Vgontzas AN (2007) Chronic Insomnia and Stress System. Sleep Med Clin 2: 279-291.
-
Thomas KS, Motivala S, Olmstead R, Irwin MR (2011) Sleep depth and fatigue: role of cellular inflammatory activation. Brain Behav Immun 25: 53-58.
-
Vgontzas AN, Zoumakis E, Bixler EO, Lin HM, Follett H, et al. (2004) Adverse effects of modest sleep restriction on sleepiness, performance, and inflammatory cytokines. J Clin Endocrinol Metab 89: 2119-2126.
-
Liu L, Mills PJ, Rissling M, Fiorentino L, Natarajan L, et al. (2012) Fatigue and sleep quality are associated with changes in inflammatory markers in breast cancer patients undergoing chemotherapy. Brain Behav Immun. 26: 706-713.
-
Siegel JM (2005) Clues to the functions of mammalian sleep. Nature 437: 1264-1271.
-
Vanitallie TB (2006) Sleep and energy balance: Interactive homeostatic systems. Metabolism 55: S30-35.
-
Gallagher T, You YJ (2014) Falling asleep after a big meal: Neuronal regulation of satiety. Worm 3: e27938.
-
Nicolaidis S (2006) Metabolic mechanism of wakefulness (and hunger) and sleep (and satiety): Role of adenosine triphosphate and hypocretin and other peptides. Metabolism 55: S24-29.
-
St-Onge MP (2013) The role of sleep duration in the regulation of energy balance: effects on energy intakes and expenditure. J Clin Sleep Med 9: 73-80.
-
Calvin AD, Carter RE, Adachi T, Macedo PG, Albuquerque FN, et al. (2013) Effects of experimental sleep restriction on caloric intake and activity energy expenditure. Chest 144: 79-86.
-
Wong-Riley M (2011) What is the meaning of the ATP surge during sleep? Sleep 34: 833-834.
-
Hursel R, Rutters F, Gonnissen HK, Martens EA, Westerterp-Plantenga MS (2011) Effects of sleep fragmentation in healthy men on energy expenditure, substrate oxidation, physical activity, and exhaustion measured over 48 h in a respiratory chamber. Am J Clin Nutr 94: 804-808.
-
Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD (2010) Insufficient sleep undermines dietary efforts to reduce adiposity. Ann Intern Med 153: 435-441.
-
Gonnissen HK, Hulshof T, Westerterp-Plantenga MS (2013) Chronobiology, endocrinology, and energy- and food-reward homeostasis. Obes Rev 14: 405-416.
-
Slattery K, Bentley D, Coutts AJ (2015) The role of oxidative, inflammatory and neuroendocrinological systems during exercise stress in athletes: implications of antioxidant supplementation on physiological adaptation during intensified physical training. Sports Med 45: 453-471.
-
Phillips SM (2014) A brief review of critical processes in exercise-induced muscular hypertrophy. Sports Med 44 Suppl 1: S71-77.
-
Hausswirth C, Le Meur Y (2011) Physiological and nutritional aspects of post-exercise recovery: specific recommendations for female athletes. Sports Med 41: 861-882.
-
Beelen M, Burke LM, Gibala MJ, van Loon L JC (2010) Nutritional strategies to promote postexercise recovery. Int J Sport Nutr Exerc Metab 20: 515-532.
-
Finger D, Goltz FR, Umpierre D, Meyer E, Rosa LH, et al. (2015) Effects of protein supplementation in older adults undergoing resistance training: a systematic review and meta-analysis. Sports Med 45: 245-255.
-
Trio PZ, You S, He X, He J, Sakao K, et al. (2014) Chemopreventive functions and molecular mechanisms of garlic organosulfur compounds. Food Funct 5: 833-844.
-
Mason S, Wadley GD (2014) Skeletal muscle reactive oxygen species: a target of good cop/bad cop for exercise and disease. Redox Rep 97-106.
-
Kono H, Rock KL (2008) How dying cells alert the immune system to danger. Nat Rev Immunol 8: 279-289.
-
Noble EG, Milne KJ, Melling CW (2008) Heat shock proteins and exercise: a primer. Appl Physiol Nutr Metab 33: 1050-1065.
-
Morton JP, Kayani AC, McArdle A, Drust B (2009) The exercise-induced stress response of skeletal muscle, with specific emphasis on humans. Sports Med 39: 643-662.
-
Bozaykut P, Ozer NK, Karademir B (2014) Regulation of protein turnover by heat shock proteins. Free Radic Biol Med 77: 195-209.
-
Lanneau D, Wettstein G, Bonniaud P, Garrido C (2010) Heat shock proteins: cell protection through protein triage. ScientificWorldJournal 10: 1543-1552.
-
Res PT, Groen B, Pennings B, Beelen M, Wallis GA, et al. (2012) Protein ingestion before sleep improves postexercise overnight recovery. Med Sci Sports Exerc 44:1560-1569.
-
Liu J, Jia SH, Kirberger M, Chen N (2014) Lunasin as a promising health-beneficial peptide. Eur Rev Med Pharmacol Sci 18: 2070-2075.
-
Ortiz-Martinez M, Winkler R, García-Lara S (2014) Preventive and therapeutic potential of peptides from cereals against cancer. J Proteomics 111: 165-183.
-
Jeong HJ, Lee JR, Jeong JB, Park JH, Cheong YK, et al. (2009) The cancer preventive seed peptide lunasin from rye is bioavailable and bioactive. Nutr Cancer 61: 680-686.
-
de Lumen BO (2005) Lunasin: a cancer-preventive soy peptide. Nutr Rev 63: 16-21.
-
Hsieh CC, Hernandez-Ledesma B, Jeong HJ, Park JH, de Lumen BO (2010) Complementary roles in cancer prevention: protease inhibitor makes the cancer preventive peptide lunasin bioavailable. PloS one 5: e8890.
-
Chen YY, Lai MH, Hung HY, Liu JF (2013) Sweet potato [Ipomoea batatas (L.) Lam. "Tainong 57"] starch improves insulin sensitivity in high-fructose diet-fed rats by ameliorating adipocytokine levels, pro-inflammatory status, and insulin signaling. J Nutr Sci Vitaminol (Tokyo) 59: 272-280.
-
Chang WH, Hu SP, Huang YF, Yeh TS, Liu JF (2010) Effect of purple sweet potato leaves consumption on exercise-induced oxidative stress and IL-6 and HSP72 levels. J Appl Physiol (1985) 109: 1710-1715.
-
Chao PY, Huang YP, Hsieh WB (2013) Inhibitive effect of purple sweet potato leaf extract and its components on cell adhesion and inflammatory response in human aortic endothelial cells. Cell Adh Migr 7: 237-245.
-
Slattery K, Bentley D, Coutts AJ (2014) The Role of Oxidative, Inflammatory and Neuroendocrinological Systems During Exercise Stress in Athletes: Implications of Antioxidant Supplementation on Physiological Adaptation During Intensified Physical Training. Sports Med 45: 453-471.
-
Knicker AJ, Renshaw I, Oldham AR, Cairns SP (2011) Interactive processes link the multiple symptoms of fatigue in sport competition. Sports Med 41: 307-328.
-
Diplock AT, Charleux JL, Crozier-Willi G, Kok FJ, Rice-Evans C, et al. (1998) Functional food science and defence against reactive oxidative species. Br J Nutr 80 Suppl 1: S77-112.
-
Fernandes AP, Gandin V2 (2015) Selenium compounds as therapeutic agents in cancer. Biochim Biophys Acta 1850: 1642-1660.
-
Berkoff F SJ (2013) Foods that Harm Foods that Heal. Digest R, edito, New York.
-
Wu H, Pan A, Yu Z, Qi Q, Lu L, et al. (2010) Lifestyle counseling and supplementation with flaxseed or walnuts influence the management of metabolic syndrome. J Nutr 140: 1937-1942.
-
Bao Y, Han J, Hu FB, Giovannucci EL, Stampfer MJ, et al. (2013) Association of nut consumption with total and cause-specific mortality. N Engl J Med 369: 2001-2011.
-
Falasca M, Casari I, Maffucci T (2014) Cancer chemoprevention with nuts. J Natl Cancer Inst 106.
-
Chen S, Zhang H, Pu H, Wang G, Li W, et al. (2014) n-3 PUFA supplementation benefits microglial responses to myelin pathology. Sci Rep 4: 7458.
-
Abedi E, Sahari MA (2014) Long-chain polyunsaturated fatty acid sources and evaluation of their nutritional and functional properties. Food Sci Nutr 2: 443-463.
-
De Caterina R, Zampolli A, Del Turco S, Madonna R, Massaro M (2006) Nutritional mechanisms that influence cardiovascular disease. Am J Clin Nutr 83: 421S-426S.
-
Burd NA, Tang JE, Moore DR, Phillips SM (2009) Exercise training and protein metabolism: influences of contraction, protein intake, and sex-based differences. J Appl Physiol (1985) 106: 1692-1701.
-
Koopman R, Wagenmakers AJ, Manders RJ, Zorenc AH, Senden JM, et al. (2005) Combined ingestion of protein and free leucine with carbohydrate increases postexercise muscle protein synthesis in vivo in male subjects. Am J Physiol Endocrinol Metab 288: E645-E653.
-
Keller U, Szinnai G, Bilz S, Berneis K (2003) Effects of changes in hydration on protein, glucose and lipid metabolism in man: impact on health. Eur J Clin Nutr 57 Suppl 2: S69-74.
-
Shahidi F, McDonald J, Chandrasekara A, Zhong Y (2008) Phytochemicals of foods, beverages and fruit vinegars: chemistry and health effects. Asia Pac J Clin Nutr 17 Suppl 1: 380-382.
-
Liljeberg H, Björck I (1998) Delayed gastric emptying rate may explain improved glycaemia in healthy subjects to a starchy meal with added vinegar. Eur J Clin Nutr 52: 368-371.
-
Ostman E, Granfeldt Y, Persson L, Bjorck I (2005) Vinegar supplementation lowers glucose and insulin responses and increases satiety after a bread meal in healthy subjects. Eur J Clin Nutr 59: 983-988.
-
O'Keefe JH, Gheewala NM, O'Keefe JO (2008) Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. J Am Coll Cardiol 51: 249-255.
-
Yu BL, Zhao SP, Hu JR (2010) Cholesterol imbalance in adipocytes: a possible mechanism of adipocytes dysfunction in obesity. Obes Rev 11: 560-567.
-
Wang ZQ, Zhang XH, Russell JC, Hulver M, Cefalu WT (2006) Chromium picolinate enhances skeletal muscle cellular insulin signaling in vivo in obese, insulin-resistant JCR:LA-cp rats. J Nutr 136: 415-420.
-
Lewicki S, Zdanowski R, Krzyzowska M, Lewicka A, Dä™bski B, et al. (2014) The role of Chromium III in the organism and its possible use in diabetes and obesity treatment. Ann Agric Environ Med 21: 331-335.
-
Debarnot U, Sperduti M, Di Rienzo F, Guillot A (2014) Experts bodies, experts minds: How physical and mental training shape the brain. Front Hum Neurosci 8: 280.
-
Knaepen K, Goekint M, Heyman EM, Meeusen R (2010) Neuroplasticity - exercise-induced response of peripheral brain-derived neurotrophic factor: a systematic review of experimental studies in human subjects. Sports Med 40: 765-801.
-
Skriver K, Roig M, Lundbye-Jensen J, Pingel J, Helge JW, et al. (2014) Acute exercise improves motor memory: exploring potential biomarkers. Neurobiol Learn Mem 116: 46-58.
-
Taylor AG, Goehler LE, Galper DI, Innes KE, Bourguignon C (2010) Top-down and bottom-up mechanisms in mind-body medicine: development of an integrative framework for psychophysiological research. Explore (NY) 6: 29-41.
-
Philips MF, Mattiasson G, Wieloch T, Bjorklund A, Johansson BB, et al. (2001) Neuroprotective and behavioral efficacy of nerve growth factor-transfected hippocampal progenitor cell transplants after experimental traumatic brain injury. J Neurosurg 94: 765-774.
-
Lewis NA, Howatson G, Morton K, Hill J, Pedlar CR (2015) Alterations in redox homeostasis in the elite endurance athlete. Sports Med 45: 379-409.
-
Pal R, Singh SN, Halder K, Tomer OS, Mishra AB, et al. (2015) Effects of Yogic Practice on Metabolism and Antioxidant-Redox Status of Physically Active Males. J Phys Act Health 12: 579-587.
-
Mahagita C (2010) Roles of meditation on alleviation of oxidative stress and improvement of antioxidant system. J Med Assoc Thai 93 Suppl 6: S242-254.
-
Sharma H, Sen S, Singh A, Bhardwaj NK, Kochupillai V, et al. (2003) Sudarshan Kriya practitioners exhibit better antioxidant status and lower blood lactate levels. Biol Psychol 63: 281-291.
-
Sinha S, Singh SN, Monga YP, Ray US (2007) Improvement of glutathione and total antioxidant status with yoga. J Altern Complement Med 13: 1085-1090.
-
Horrigan BJ (2008) Mind-body medicine at the Mayo Clinic. Explore (NY) 4: 295-299.
-
Srinivasan T (2013) Bridging the mind-body divide. Int J Yoga 6: 85-86.
-
Nakata H, Sakamoto K, Kakigi R (2014) Meditation reduces pain-related neural activity in the anterior cingulate cortex, insula, secondary somatosensory cortex, and thalamus. Front Psychol 5: 1489.
-
Saatcioglu F (2013) Regulation of gene expression by yoga, meditation and related practices: a review of recent studies. Asian J Psychiatr 6: 74-77.
-
Pullen PR, Nagamia SH, Mehta PK, Thompson WR, Benardot D, et al. (2008) Effects of yoga on inflammation and exercise capacity in patients with chronic heart failure. J Card Fail 14: 407-413.
-
Anderson JG, Taylor AG (2011) The metabolic syndrome and mind-body therapies: a systematic review. J Nutr Metab 2011: 276419.
-
Felstead C (2014) Yoga for runners. Champaign, IL: Human Kinetics.
-
Hanh T (1975) The Miracle of Mindfulness. Boston, Mass: Beacon Press.
-
Younge JO, Gotink RA, Baena CP, Roos-Hesselink JW, Hunink MM (2015) Mind-body practices for patients with cardiac disease: a systematic review and meta-analysis. Eur J Prev Cardiol 22: 1385-1398.
-
Carlson CR, Hoyle RH (1993) Efficacy of abbreviated progressive muscle relaxation training: a quantitative review of behavioral medicine research. J Consult Clin Psychol 61: 1059-1067.
-
Häkkinen K, Alen M, Kallinen M, Newton RU, Kraemer WJ (2000) Neuromuscular adaptation during prolonged strength training, detraining and re-strength-training in middle-aged and elderly people. Eur J Appl Physiol 83: 51-62.
-
Rapaport MH, Schettler P, Bresee C (2012) A preliminary study of the effects of repeated massage on hypothalamic-pituitary-adrenal and immune function in healthy individuals: a study of mechanisms of action and dosage. J Altern Complement Med. 18: 789-797.
-
Wiest KL, Asphaug VJ, Carr KE, Gowen EA, Hartnett TT (2015) Massage Impact on Pain in Opioid-dependent Patients in Substance Use Treatment. Int J Ther Massage Bodywork 8: 12-24.
-
Lee SH, Kim JY, Yeo S, Kim SH, Lim S (2015) Meta-Analysis of Massage Therapy on Cancer Pain. Integr Cancer Ther 14: 297-304.
-
Ménétrier A, Mourot L, Degano B, Bouhaddi M, Walther G, et al. (2015) Effects of three postexercice recovery treatments on femoral artery blood flow kinetics. J Sports Med Phys Fitness 55: 258-266.
-
Born DP, Sperlich B, Holmberg HC (2013) Bringing light into the dark: effects of compression clothing on performance and recovery. Int J Sports Physiol Perform 8: 4-18.
-
Versey NG, Halson SL, Dawson BT (2013) Water immersion recovery for athletes: effect on exercise performance and practical recommendations. Sports Med 43: 1101-1130.
-
Bleakley CM, Davison GW (2010) What is the biochemical and physiological rationale for using cold-water immersion in sports recovery? A systematic review. Br J Sports Med 44: 179-187.
-
Vaile J, Halson S, Gill N, Dawson B (2008) Effect of hydrotherapy on the signs and symptoms of delayed onset muscle soreness. Eur J Appl Physiol 102: 447-455.
-
Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, et al. (2014) 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 129(25 Suppl 2):S1-S45.
-
Lim S, Wyker B, Bartley K, Eisenhower D (2015) Measurement error of self-reported physical activity levels in New York City: assessment and correction. American J Epidemiol 181: 648-655.
-
Corder K, Brage S, Ekelund U (2007) Accelerometers and pedometers: methodology and clinical application. Curr Opin Clin Nutr Metab Care 10: 597-603.
-
Ainsworth B, Cahalin L, Buman M, Ross R (2015) The current state of physical activity assessment tools. Prog Cardiovasc Dis 57: 387-395.
-
George KS, Roberts CB, Beasley S, Fox M, Rashied-Henry K; Brooklyn Partnership to Drive Down Diabetes (BP3D) (2015) Our Health Is in Our Hands: A Social Marketing Campaign to Combat Obesity and Diabetes. Am J Health Promot.
-
Peterson M, Chandlee M, Abraham A (2008) Cost-effectiveness analysis of a statewide media campaign to promote adolescent physical activity. Health Promot Pract 9: 426-433.
-
Finlay SJ, Faulkner G (2005) Physical activity promotion through the mass media: inception, production, transmission and consumption. Prev Med 40: 121-130.
-
Jensen MD, Ryan DH, Apovian CM, Ard JD, Comuzzie AG, et al. (2014) 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society. J Am Coll Cardiol 63: 2985-3023.