We will need to regularly measure the body weight, circumferences, skinfolds, and body composition, as discussed in the composition chapter. These will be ideal for making sure we are getting the right changes. The ability to lose weight and gain muscle also depends on the person.

Losing as much as 1 pound of fat may be possible while building muscle, but it is a dynamic response and might not work for all. There are three main ways we lose weight. This is through dehydration, lean weight loss, and fat loss. Dehydration is not recommended, but it is used for making weight in last minute situations like making a weigh-in.

Lean body mass and muscle mass weight loss may result from knocking back the calorie intake, losing weight too fast, and not eating the right levels of macronutrients or exercising appropriately.

Athletes and other clients that have excess levels of body fat should plan to stop their gaining of weight first before losing fat begins. Athletes need to plan to change body composition in the off season times. The pre-season and the in season nutrition should focus on performance maximization.

One example would be reducing the total intake of daily calories by 3 — 4 calories per every pound of lean body mass. Fat contains 3, calories per pound. So, it should take around six days usually to lose one pound of fat.

Losing at a rate faster than that could result in more muscle mass being lost. In total, the fat loss is usually around 4 — 5 pounds per month. Ectomorphs are the ones that have the easiest time losing fat, but it is going to be harder for them to gain muscle.

Mesomorphs are also able to lose the fat easily, but they are also able to put on muscle mass the easiest. Endomorphs are the ones that carry the most body fat, they can lose fat quickly, and they likely need to stick to a low fat program for their nutrition. This is not the preferred time to lose weight.

It is going to be at a much slower rate than the off season. We do this by reducing by 2 calories for every pound of your lean body mass. Rule one: you should always eat a minimum of five meals per day.

This ensures muscles are not cannibalized for energy to survive. Rule two: the 1 — 2 — 3 rule is to be used. Rule three: you should ask yourself what you are doing the next three hours, and then if that involves a nap or some rest, you should eat a little less.

Rule four: the ZIGZAG calorie intake of reducing the body fat mass or increasing the lean body mass is used. We discussed that in previous chapters. Rule five: is the final rule of thumb for the most serious athletes. You should make use of supplements to fill in the gaps in nutrition that may occur.

J Acad Nutr Diet. info amystephensnutrition. com Book your Session. Amy Stephens MS, RDN, CSSD, CDCES. Licensed dietitian specializing in sports nutrition and eating disorders.

change body composition in a healthy way. By Amy Stephens RDN CSSD Edited by Amy Gregorek. Why important. Factors influencing body composition.

Off season. To convert pounds to kilograms, divide by 2. Focus on timing of meals. Increase protein to stay full. Aim for grams of protein per meal. Grilled chicken, sliced turkey, hard-boiled egg or edamame. Cut back on added sugars from sweets or processed foods.

Too much sugar can cause a sugar crash and leave you feeling lethargic and increase hunger. Avoid getting too hungry, as this can lead to overeating. Keep the refrigerator stocked with fruits, veggies, lean proteins like chicken, sliced turkey, low-fat cottage cheese, hummus, low-fat plain yogurt.

Snack on fruits, vegetables and small portions of nuts. Snack foods tend to be less nutritious and the calories can often add up to another meal. Add more food at meals to cut back on snacking. Veggies in dip such as hummus, peanut butter or tzatziki.

Rice cake with peanut butter or yogurt with fruit. Avoid weighing yourself daily. Your weight fluctuates daily from fluid shifts and seeing the scale increase and decrease can be discouraging. Aim for at least 8 hours of sleep each night because sleep allows your stress and hunger hormones to reset.

Hormones like ghrelin, insulin and cortisol increase during stress which affect metabolism. Increases in circulating thyroid hormones are associated with an increase in the metabolic rate, whereas lowered thyroid levels result in decreased thermogenesis and overall metabolic rate [ 20 ].

Leptin, synthesized primarily in adipocytes, functions as an indicator of both short and long-term energy availability; short-term energy restriction and lower body fat levels are associated with decreases in circulating leptin.

Additionally, higher concentrations of leptin are associated with increased satiety and energy expenditure [ 21 ]. Similar to leptin, high levels of insulin convey a message of energy availability and are associated with an anorexigenic effect.

Conversely, the orexigenic hormone ghrelin functions to stimulate appetite and food intake, and has been shown to increase with fasting, and decrease after feeding [ 24 ].

Testosterone, known primarily for its role in increasing muscle protein synthesis and muscle mass [ 22 ], may also play a role in regulating adiposity [ 25 ]. Changes in fat mass have been inversely correlated with testosterone levels, and it has been suggested that testosterone may repress adipogenesis [ 25 ].

More research is needed to delineate the exact mechanism s by which testosterone affects adiposity. Cortisol, a glucocorticoid that influences macronutrient metabolism, has been shown to induce muscle protein breakdown [ 22 ], and increased plasma cortisol within the physiologic range has increased proteolysis in healthy subjects [ 26 ].

Evidence also suggests that glucocorticoids may inhibit the action of leptin [ 27 ]. Results from a number of studies indicate a general endocrine response to hypocaloric diets that promotes increased hunger, reduces metabolic rate, and threatens the maintenance of lean mass.

Studies involving energy restriction, or very low adiposity, report decreases in leptin [ 1 , 10 , 28 ], insulin [ 1 , 2 ], testosterone [ 1 , 2 , 28 ], and thyroid hormones [ 1 , 29 ]. Subsequently, increases in ghrelin [ 1 , 10 ] and cortisol [ 1 , 30 , 31 ] have been reported with energy restriction.

Further, there is evidence to suggest that unfavorable changes in circulating hormone levels persist as subjects attempt to maintain a reduced body weight, even after the cessation of active weight loss [ 32 , 33 ].

Low energy intake and minimal body fat are perceived as indicators of energy unavailability, resulting in a homeostatic endocrine response aimed at conserving energy and promoting energy intake.

It should be noted that despite alterations in plasma levels of anabolic and catabolic hormones, losses of lean body mass LBM often fail to reach statistical significance in studies on bodybuilding preparation [ 1 , 2 ].

Although the lack of significance may relate to insufficient statistical power, these findings may indicate that unfavorable, hormone-mediated changes in LBM can potentially be attenuated by sound training and nutritional practices. Previous research has indicated that structured resistance training [ 34 ] and sufficient protein intake [ 35 — 37 ], both commonly employed in bodybuilding contest preparation, preserve LBM during energy restriction.

Further, Maestu et al. speculate that losses in LBM are dependent on the magnitude of weight loss and degree of adiposity, as the subjects who lost the greatest amount of weight and achieved the lowest final body fat percentage in the study saw the greatest losses of LBM [ 2 ].

The hormonal environment created by low adiposity and energy restriction appears to promote weight regain and threaten lean mass retention, but more research is needed to determine the chronic impact of these observed alterations in circulating anabolic and catabolic hormones.

The largest component, resting energy expenditure REE , refers to the basal metabolic rate BMR [ 8 ]. The other component, known as non-resting energy expenditure NREE , can be further divided into exercise activity thermogenesis EAT , non-exercise activity thermogenesis NEAT , and the thermic effect of food TEF [ 8 ].

Components of total daily energy expenditure TDEE. Adapted from Maclean et al. Metabolic rate is dynamic in nature, and previous literature has shown that energy restriction and weight loss affect numerous components of energy expenditure.

In weight loss, TDEE has been consistently shown to decrease [ 38 , 39 ]. Weight loss results in a loss of metabolically active tissue, and therefore decreases BMR [ 38 , 39 ]. Interestingly, the decline in TDEE often exceeds the magnitude predicted by the loss of body mass.

Previous literature refers to this excessive drop in TDEE as adaptive thermogenesis, and suggests that it functions to promote the restoration of baseline body weight [ 13 — 15 ]. Adaptive thermogenesis may help to partially explain the increasing difficulty experienced when weight loss plateaus despite low caloric intake, and the common propensity to regain weight after weight loss.

Exercise activity thermogenesis also drops in response to weight loss [ 40 — 42 ]. In activity that involves locomotion, it is clear that reduced body mass will reduce the energy needed to complete a given amount of activity. It has been speculated that this increase in skeletal muscle efficiency may be related to the persistent hypothyroidism and hypoleptinemia that accompany weight loss, resulting in a lower respiratory quotient and greater reliance on lipid metabolism [ 43 ].

The TEF encompasses the energy expended in the process of ingesting, absorbing, metabolizing, and storing nutrients from food [ 8 ].

While the relative magnitude of TEF does not appear to change with energy restriction [ 46 ], such dietary restriction involves the consumption of fewer total calories, and therefore decreases the absolute magnitude of TEF [ 41 , 46 ]. There is evidence to suggest that spontaneous physical activity, a component of NEAT, is decreased in energy restricted subjects, and may remain suppressed for some time after subjects return to ad libitum feeding [ 29 ].

Persistent suppression of NEAT may contribute to weight regain in the post-diet period. In the context of weight loss or maintaining a reduced body weight, this process is complicated by the dynamic nature of energy expenditure.

In response to weight loss, reductions in TDEE, BMR, EAT, NEAT, and TEF are observed. Due to adaptive thermogenesis, TDEE is lowered to an extent that exceeds the magnitude predicted by losses in body mass.

Further, research indicates that adaptive thermogenesis and decreased energy expenditure persist after the active weight loss period, even in subjects who have maintained a reduced body weight for over a year [ 14 , 48 ].

These changes serve to minimize the energy deficit, attenuate further loss of body mass, and promote weight regain in weight-reduced subjects.

A series of chemical reactions must take place to derive ATP from stored and ingested energy substrates. In aerobic metabolism, this process involves the movement of protons across the inner mitochondrial membrane.

When protons are transported by ATP synthase, ATP is produced. Protons may also leak across the inner membrane by way of uncoupling proteins UCPs [ 49 ]. In the condition of calorie restriction, proton leak is reduced [ 16 — 19 ]. Uncoupling protein-1 and UCP-3, the primary UCPs of brown adipose tissue BAT and skeletal muscle [ 53 ], are of particular interest due to their potentially significant roles in energy expenditure and uncoupled thermogenesis.

Decreased UCP-3 expression could potentially play a role in decreasing energy expenditure, and UCP-3 expression has been negatively correlated with body mass index and positively correlated with metabolic rate during sleep [ 57 ]. Despite these correlations, more research is needed to determine the function and physiological relevance of UCP-3 [ 58 ], as contradictory findings regarding UCP-3 and weight loss have been reported [ 18 ].

Uncoupling Protein-1 appears to play a pivotal role in the uncoupled thermogenic activity of BAT [ 59 ]. Energy restriction has been shown to decrease BAT activation [ 60 ] and UCP-1 expression [ 61 ], indicating an increase in metabolic efficiency.

Along with UCP-1 expression, thyroid hormone and leptin affect the magnitude of uncoupled respiration in BAT. Thyroid hormone TH and leptin are associated with increased BAT activation, whereas glucocorticoids oppose the BAT-activating function of leptin [ 59 ]. Evidence indicates that TH plays a prominent role in modulating the magnitude of proton leak [ 53 ], with low TH levels associated with decreased proton leak [ 62 ].

The endocrine response to energy restriction, including increased cortisol and decreased TH and leptin [ 1 , 10 , 28 — 31 ], could potentially play a regulatory role in uncoupled respiration in BAT. It is not clear if decreases in proton leak and UCP expression persist until weight reverts to baseline, but there is evidence to suggest a persistent adaptation [ 19 , 55 , 56 ], which mirrors the persistent downregulation of TH and leptin [ 32 , 33 ].

Changes observed in proton leak, UCP expression, and circulating hormones appear to influence metabolic efficiency and energy expenditure. In the context of energy restriction, the observed changes are likely to make weight loss increasingly challenging and promote weight regain.

It has been reported that females have more BAT than males [ 63 ], and that energy-restricted female rats see greater decreases in BAT mass and UCP-1 than males [ 64 ], indicating a potential sex-related difference in uncoupled respiration during weight loss.

While future research may improve our understanding of the magnitude and relative importance of mitochondrial adaptations to energy restriction, current evidence suggests that increased mitochondrial efficiency, and a decline in uncoupled respiration, might serve to decrease the energy deficit in hypocaloric conditions, making weight maintenance and further weight reduction more challenging.

Hypocaloric diets induce a number of adaptations that serve to prevent further weight loss and conserve energy.

It is likely that the magnitude of these adaptations are proportional to the size of the energy deficit, so it is recommended to utilize the smallest possible deficit that yields appreciable weight loss.

This may decrease the rate of weight loss, but attenuate unfavorable adaptations that challenge successful reduction of fat mass.

Large caloric deficits are also likely to induce greater losses of LBM [ 66 , 67 ] and compromise athletic performance and recovery [ 68 , 69 ], which are of critical importance to athletes. Participation in a structured resistance training program [ 34 ] and sufficient protein intake [ 35 — 37 ] are also likely to attenuate losses in LBM.

A refeed consists of a brief overfeeding period in which caloric intake is raised slightly above maintenance levels, and the increase in caloric intake is predominantly achieved by increasing carbohydrate consumption.

While studies have utilized refeeding protocols that last three days [ 71 , 72 ], physique athletes such as bodybuilders and figure competitors often incorporate hour refeeds, once or twice per week.

The proposed goal of periodic refeeding is to temporarily increase circulating leptin and stimulate the metabolic rate.

There is evidence indicating that leptin is acutely responsive to short-term overfeeding [ 72 ], is highly correlated with carbohydrate intake [ 71 , 73 ], and that pharmacological administration of leptin reverses many unfavorable adaptations to energy restriction [ 33 ].

While interventions have shown acute increases in leptin from short-term carbohydrate overfeeding, the reported effect on metabolic rate has been modest [ 71 ]. Dirlewanger et al.

More research is needed to determine if acute bouts of refeeding are an efficacious strategy for improving weight loss success during prolonged hypocaloric states. A theoretical model of metabolic adaptation and potential strategies to attenuate adaptations is presented in Figure 2. A theoretical model of metabolic adaptation and potential strategies to attenuate adaptations.

Dotted lines represent inhibition. In the period shortly after cessation of a restrictive diet, body mass often reverts toward pre-diet values [ 29 , 74 , 75 ].

This body mass is preferentially gained as fat mass, in a phenomenon known as post-starvation obesity [ 29 ]. While many of the metabolic adaptations to weight loss persist, a dramatic increase in energy intake results in rapid accumulation of fat mass.

In such a situation, the individual may increase body fat beyond baseline levels, yet retain a metabolic rate that has yet to fully recover. There is evidence to suggest that adipocyte hyperplasia may occur early in the weight-regain process [ 76 ], and that repeated cycles of weight loss and regain by athletes in sports with weight classes are associated with long-term weight gain [ 77 ].

Therefore, athletes who aggressively diet for a competitive season and rapidly regain weight may find it more challenging to achieve optimal body composition in subsequent seasons.

Such a process involves slowly increasing caloric intake in a stepwise fashion. In theory, providing a small caloric surplus might help to restore circulating hormone levels and energy expenditure toward pre-diet values, while closely matching energy intake to the recovering metabolic rate in an effort to reduce fat accretion.

Ideally, such a process would eventually restore circulating hormones and metabolic rate to baseline levels while avoiding rapid fat gain. While anecdotal reports of successful reverse dieting have led to an increase in its popularity, research is needed to evaluate its efficacy.

Accordingly, the current article is limited by the need to apply this data to an athletic population. If the adaptations described in obese populations serve to conserve energy and attenuate weight loss as a survival mechanism, one might speculate that the adaptations may be further augmented in a leaner, more highly active population.

Another limitation is the lack of research on the efficacy of periodic refeeding or reverse dieting in prolonged weight reduction, or in the maintenance of a reduced bodyweight. Until such research is available, these anecdotal methods can only be evaluated from a mechanistic and theoretical viewpoint.

Weight loss is a common practice in a number of sports. Whether the goal is a higher strength-to-mass ratio, improved aesthetic presentation, or more efficient locomotion, optimizing body composition is advantageous to a wide variety of athletes.

As these athletes create an energy deficit and achieve lower body fat levels, their weight loss efforts will be counteracted by a number of metabolic adaptations that may persist throughout weight maintenance. Changes in energy expenditure, mitochondrial efficiency, and circulating hormone concentrations work in concert to attenuate further weight loss and promote the restoration of baseline body mass.

Athletes must aim to minimize the magnitude of these adaptations, preserve LBM, and adequately fuel performance and recovery during weight reduction. To accomplish these goals, it is recommended to approach weight loss in a stepwise, incremental fashion, utilizing small energy deficits to ensure a slow rate of weight loss.

Participation in a structured resistance training program and adequate protein intake are also imperative.

More research is needed to verify the efficacy of periodic refeeding and reverse dieting in supporting prolonged weight reduction and attenuating post-diet fat accretion.

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