Pediatric Exercise Science, 2015, 27, 30-33 http://dx.doi.org/10.1123/pes.2015-0032 © 2015 Human Kinetics, Inc.
Endocrinology and Metabolism Alon Eliakim Tel Aviv University
Citation Vanheest JL1. Rodgers CD, Mahoney CE, De Souza MJ. Ovarian suppression impairs sport performance in junior elite female swimmers. Med Sci Sports Exerc. 2014; 46(1):156–166. PubMed doi:10.1249/MSS.0b013e3182a32b72
Introduction: Competitive female athletes restrict energy intake and increase exercise energy expenditure frequently resulting in ovarian suppression. The purpose of this study was to determine the impact of ovarian suppression and energy deficit on swimming performance (400-m swim velocity). Methods: Menstrual status was determined by circulating estradiol (E2) and progesterone (P4) in ten junior elite female swimmers (15–17 yr). The athletes were categorized as cyclic (CYC) or ovarian-suppressed (OVS). They were evaluated every 2 weeks for metabolic hormones, bioenergetic parameters, and sport performance during the 12-week season. Results: CYC and OVS athletes were similar (p > .05) in age (CYC = 16.2 ± 1.8 yr, OVS = 17 ± 1.7 yr), body mass index (CYC = 21 ± 0.4 kg·m, OVS = 25 ± 0.8 kg·m), and gynecological age (CYC = 2.6 ± 1.1 yr, OVS = 2.8 ± 1.5 yr). OVS had suppressed P4 (p < .001) and E2 (p = .002) across the season. Total triiodothyronine (TT3) and insulin-like growth factor (IGF-1) were lower in OVS (TT3: CYC = 1.6 ± 0.2 nmol·L, OVS = 1.4 ± 0.1 nmol·L, p < .001; IGF-1: CYC = 243 ± 1 μg·mL, OVS = 214 ± 3 μg·mL p < .001) than CYC at week 12. Energy intake (p < .001) and energy availability (p < .001) were significantly lower in OVS versus CYC. OVS exhibited a 9.8% decline in Δ400-m swim velocity compared with an 8.2% improvement in CYC at week 12. Conclusions: Ovarian steroids (P4 and E2), metabolic hormones (TT3 and IGF-1), and energy status markers (EA and EI) were highly correlated with sport performance. This study illustrates that when exercise training occurs in the presence of ovarian suppression with evidence for energy conservation (i.e., reduced TT3), it is associated with poor sport performance. These data from junior elite female athletes support the need for dietary periodization to help optimize energy intake for appropriate training adaptation and maximal sport performance
Commentary Strenuous physical activity may affect the female reproductive system and lead to athletic amenorrhea (3). The prevalence of amenorrhea among female athletes is up to 20 times higher than the general population and appears to be higher in young athletes who train intensively and in sports that emphasize leanness (e.g., long-distance runners, ballet dancers). A major concern of athlete amenorrhea is the low estrogen levels, which, despite a possible relative protection by the weight-bearing activity, may lead to reduced bone mass. This is particularly important in children and adolescent athletes since bone mineral density reaches about 90% of its peak by the end of the second decade (2) and because about one quarter The author is with the Sackler School of Medicine, Meir Medical Center, Tel Aviv University, Tel Aviv, Israel. Address author correspondence to Alon Eliakim at [email protected].
30
of adult bone is accumulated during the 2 years that surrounds peak bone velocity. This osteopenia may expose the young female athlete to increased risk of skeletal fragility, fractures, vertebral instability and curvature, and may lead to excessive bone loss and increased fracture risk later in life (5). The association of eating disorders, amenorrhea, and osteoporosis was termed “the female athlete triad.” A major cause for athlete’s amenorrhea is suppression of the spontaneous hypothalamic pulsatile secretion of gonadotropin-releasing hormone (1). Several genetic, body composition (fat mass), hormonal, psychological and physiological mechanisms have been suggested to explain this suppression. However, it is now believed that the main cause for athletic amenorrhea is reduced energy availability (8). Energy availability is defined as energy intake minus expenditure. There seems to be an energy availability threshold of 30 kcal/kg/lean body mass/day, and menstrual disturbances occur only below this threshold. Therefore, individual nutritional differences may explain why despite similar training
Downloaded by Purdue Univ on 09/16/16, Volume 27, Article Number 1
Endocrinology and Metabolism 31
programs, some female athletes develop amenorrhea whereas others menstruate regularly. Low energy availability reduces luteinizing hormone (LH) pulsatility and estrogen levels and suppresses the secretion of other anabolic hormones such as triodothyronine (T3) and insulin-like growth hormone- I (IGF-I), both known to affect bone mineralization. It was shown that increased caloric intake (without changes in training intensity) can prevent this suppression (4). Recently, it was found that leptin administration to female athletes with reduced energy availability-associated amenorrhea resulted in increased LH pulsatility, estradiol levels and returns of menses, although the caloric intake and training load were unchanged (9). Similar to other energy-deficient states, the body conserves its energy sources to adapt to major stress (in this case, exercise) and will not lose energy on “luxurious” activities such as reproduction and growth. The linkage of athletic amenorrhea to energy balance suggests that this condition should be considered as a nutritional problem and therefore, prevented or reversed by dietary reforms. Only if nutritional changes will not renew menstruation, moderation of exercise intensity or capacity or both is warranted. Vanheest et al. (7) are among the first to study prospectively the influence of energy restriction associated ovarian suppression on athletic performance among elite adolescent swimmers (age 15–17 years). The authors have shown that reduced energy intake and availability that was associated with ovarian suppression (determined by reduced estradiol and progesterone levels) was also accompanied by lower T3 and IGF-I levels and by 9.8% decline in 400m swim velocity compared with 8.2% improvement among swimmers without ovarian suppression at the end of 12 weeks of training (in total, 18% difference!). This occurred despite similar training protocols and while the ovarian suppressed swimmers were still menstruating (although less regularly). Another manuscript that was published this year demonstrated a protective role of estradiol toward intense training-related increase of inflammatory cytokines (IL-6 leukocyte expression) in young female athletes (6).This suggests another important possible mechanism for the reduced training adaptation in ovarian suppressed female athletes. Transformation of this knowledge to athletes and coaches is essential because many of them promote
energy restrictive practices with the belief that it improves competitive performance. The results of the current study emphasize that athletes can maintain chronic energy deficit for varied periods with continued success in sport, however, prolonged negative energy balance results in training maladaptation. This may be particularly relevant for athletes during adolescence, a time with greater energy needs for growth and maturation.
References 1. Constantini NW. Clinical consequences of athletic amenorrhea. Sports Med. 1994; 17:213–223. PubMed doi:10.2165/00007256-199417040-00002 2. Glastre C, Braillon P, David L, et al. Measurement of bone mineral content ofthe lumbar spine by dual energy x-ray absorptiometry in normal children:correlations with growth parameters. J Clin Endocrinol Metab. 1990; 70:1330–1333. PubMed doi:10.1210/jcem-70-5-1330 3. Loucks AB, Horvath SM. Athletic amenorrhea: a review. Med Sci Sports Exerc. 1985; 17:56–72. PubMed 4. Loucks AB, Thuma JR. Luteinizing hormone pulsatility is disrupted at athreshold of energy availability in regularly menstruating women. J Clin Endocrinol Metab. 2003; 88:297–311. PubMed doi:10.1210/jc.2002-020369 5. Nemet D, Eliakim A. Pediatric sports nutrition: an update. Curr Opin Clin Nutr Metab Care. 2009; 12:304–309. PubMed doi:10.1097/MCO.0b013e32832a215b 6. Tringali C, Scala L, Silvestri I, et al. protective role of 17-b-estradiol towards IL-6 leukocyte expression induced by intense training in young female athletes. J Sport Sci 2014; 32: 452-461. > 7. Vanheest JL, Rodgers CD, Mahoney CE, De Souza MJ. Ovarian suppression impairs sport performance in junior elite female swimmers. Med Sci Sports Exerc. 2014; 46:156–166. PubMed doi:10.1249/ MSS.0b013e3182a32b72 8. Warren MP, Chua AT. Exercise-induced amenorrhea and bone health in theadolescent athlete. Ann N Y Acad Sci. 2008; 1135:244–252. PubMed doi:10.1196/ annals.1429.025 9. Welt CK, Chan JL, Bullen J, et al. Recombinant human leptin in women withhypothalamic amenorrhea. N Engl J Med. 2004; 351:987–997. PubMed doi:10.1056/ NEJMoa040388
Citation Tran BD. Galassetti P. Exercise in pediatric type 1 diabetes. Pediatr Exerc Sci. 2014; 26(4):375–383. PubMed doi:10.1123/pes.20140066
The beneficial effects of exercise, including reduction of cardiovascular risk, are especially important in children with type 1 diabetes (T1DM), in whom incidence of lifetime cardiovascular complications remains elevated despite good glycemic control. Being able to exercise safely is therefore a paramount concern. Dysregulated metabolism in T1DM however, causes frequent occurrence of both hypo- and hyperglycemia, the former typically associated with prolonged, moderate exercise, the latter with higher intensity, if shorter, challenges. While very few absolute contraindications to exercising exist in these children, exercise should not be started with glycemia outside the 80–250 mg/dl range. Within this glycemic range, careful adjustments in insulin admin-
32 Eliakim
istration (reduction of infusion rate via insulin pumps, or overall reduction of dosage of multiple injections) should be combined with carbohydrate ingestion before/during exercise, based on prior, individual experience with specific exercise formats. Unfamiliar exercise should always be tackled with exceeding caution, based on known responses to other exercise formats. Finally, gaining a deep understanding of other complex exercise responses, such as the modulation of inflammatory status, which is a major determinant of the cardio-protective effects of exercise, can help determine which exercise formats and which individual metabolic conditions can lead to maximally beneficial health effects.
Downloaded by Purdue Univ on 09/16/16, Volume 27, Article Number 1
Commentary Type 1 diabetes mellitus (T1DM) is one of the most common chronic pediatric diseases. Physical exercise should be encouraged in children with T1DM since as in all children, physical activity may promote numerous essential health benefits. Moreover, physical activity plays an important role in the multidisciplinary treatment of T1DM. Despite that children with T1DM often avoid exercise participation because they are afraid from possible severe fluctuations in glycemic levels during exercise performance and the ensuing hours. Understanding of individual responses to particular exercise protocols should therefore be gained through personal experience, as well as careful precautions taken with regard to adjustments of insulin administration and carbohydrate supplements ingestion. Taking into account these precautions will allow children with T1DM to exercise freely, obtain all physical activity related health benefits and also may allow them to participate and excel in competitive sports, as documented by the many T1DM international-levels athletes and Olympic champions. This important review (3) summarizes the main current recommendations concerning exercise in T1DM and gives a detailed description of key issues related to the occurrence of both hyper- and hypoglycemia in association with exercise. More importantly, it gives practical
tools how to avoid these threatening conditions. The review highlights the very important concept of blunted exercise- associated counter-regulatory response following previous hypoglycemia, and possibly following previous exercise and psychological stress in particularly in males (1). Finally, it reviews the current relatively new concept of the possibly altered exercise-mediated cardiovascular protection, via modulations of acute and chronic inflammatory processes, in children with poorly controlled T1DM (2).
References 1. Galassetti PR, Tate D, Neill RA, Morrey S, Wasserman DH, Davis SN. Effect of sex on counter-regulatory responses to exercise after antecedent hypoglycemia in type 1 diabetes. Am J Physiol Endocrinol Metab. 2004; 287:E16–E24. PubMed doi:10.1152/ajpendo.00480.2002 2. Rosa JS, Flores RL, Oliver SR, Pontello AM, Zaldivar FP, Galassetti PR. Resting and exercise-induced IL-6 levels in children with type 1 diabetes reflects hyperglycemic profiles during the previous 3 days. J Appl Physiol. 2010; 108:334–342. PubMed doi:10.1152/japplphysiol.01083.2009 3. Tran BD, Galassetti PR. Exercise in pediatric type 1 diabetes. Pediatr Exerc Sci. 2014; 26:375–383. PubMed doi:10.1123/pes.2014-0066
Citation Fedewa MW, Gist NH, Evans EM, Dishman RK. Exercise and insulin resistance in youth: A meta-analysis. Pediatrics, 2014; 133:e163–e174.
Background and Objectives: The prevalence of obesity and diabetes is increasing among children, adolescents, and adults. Although estimates of the efficacy of exercise training on fasting insulin and insulin resistance have been provided, for adults similar estimates have not been provided for youth. This systematic review and meta-analysis provides a quantitative estimate of the effectiveness of exercise training on fasting insulin and insulin resistance in children and adolescents. Methods: Potential sources were limited to peer-reviewed articles published before June 25, 2013, and gathered from the PubMed, SPORTDiscus, Physical Education Index, and Web of Science online databases. Analysis was limited to randomized controlled trials by using combinations of the terms adolescent, child, pediatric, youth, exercise training, physical activity, diabetes, insulin, randomized trial, and randomized controlled trial. The authors assessed 546 sources, of which 4.4% (24 studies) were eligible for inclusion. Thirty-two effects were used to estimate the effect of exercise training on fasting insulin, with 15 effects measuring the effect on insulin resistance. Estimated effects were independently calculated by multiple authors, and conflicts were resolved before calculating the overall effect. Results: Based on the cumulative results from these studies, a small to moderate effect was found for exercise training on fasting insulin and improving insulin resistance in youth (Hedges’ d effect size = 0.48 [95% confidence interval: 0.22–0.74], p < .001 and 0.31 [95% confidence interval: 0.06–0.56], p < .05, respectively). Conclusions: These results support the use of exercise training in the prevention and treatment of type 2 diabetes.
Endocrinology and Metabolism 33
Downloaded by Purdue Univ on 09/16/16, Volume 27, Article Number 1
Commentary The global increase in childhood and adolescent obesity is associated with a parallel increase in type 2 diabetes mellitus (T2DM) (3). Previous meta-analytic reviews on the effect of exercise training on fasting insulin and insulin resistance have focused on adults (4) and children and adolescents with T1DM (2). Fedewa et al. in their recent important meta-analysis focused on the effect of exercise training on fasting insulin and insulin resistance in children and adolescents (1). Based on 24 studies that were eligible for inclusion in the meta-analysis from 1999 to 2013, a small to moderate beneficial effect was found for exercise training on reducing fasting insulin levels (11.4 U/ml; 95% CI: 5.2–17.5) and insulin resistance (2.0 HOMA-IR; 95% CI: 0.4–3.6). The effect of exercise training was more effective in children and adolescents with high BMI most probably due to the presence of greater insulin resistance in these individuals. The beneficial effect of exercise training on fasting insulin and insulin resistance was not influenced by gender, race, age and pubertal status suggesting that the estimated beneficial effect is similar for all youth aged 6–19 years. The relatively small amount of published scientific literature did not allow for thorough evaluation of the effect of different training protocols or the frequency, duration,
intensity, volume and mode of exercise training on fasting insulin and insulin resistance. The authors concluded that “in the absence of a clear consensus on the most effective type of exercise for treating these outcomes, emphasis should be placed on ways to incorporate physical activity, in addition to exercise training, into the lives of children and adolescents, especially those at risk for developing obesity and diabetes.”
References 1. Fedewa MW, Gist NH, Evans EM, Dishman RK. Exercise and insulin resistance in youth: A meta-analysis. Pediatrics. 2014; 133:e163–e174. PubMed doi:10.1542/ peds.2013-2718 2. Kennedy A, Nirantharakumar K, Chimen M, et al. Does exercise improve glycemic control in type 1 diabetes? A systematic review and meta-analysis. PLoS ONE. 2013; 8:e58861. PubMed doi:10.1371/journal.pone.0058861 3. Pinhas-hamiel O, Zeitler P. The global spread of type 2 diabetes mellitus in children and adolescents. J Pediatr. 2005; 146:693–700. PubMed doi:10.1016/j.jpeds.2004.12.042 4. Thomas DE, Elliot EJ, Naughton GA. Exercise for type 2 diabetes mellitus. Cochrane Database Syst Rev. 2006; 3:CD002968. PubMed
Endocrinology and Metabolism Alon Eliakim Tel Aviv University
Citation Vanheest JL1. Rodgers CD, Mahoney CE, De Souza MJ. Ovarian suppression impairs sport performance in junior elite female swimmers. Med Sci Sports Exerc. 2014; 46(1):156–166. PubMed doi:10.1249/MSS.0b013e3182a32b72
Introduction: Competitive female athletes restrict energy intake and increase exercise energy expenditure frequently resulting in ovarian suppression. The purpose of this study was to determine the impact of ovarian suppression and energy deficit on swimming performance (400-m swim velocity). Methods: Menstrual status was determined by circulating estradiol (E2) and progesterone (P4) in ten junior elite female swimmers (15–17 yr). The athletes were categorized as cyclic (CYC) or ovarian-suppressed (OVS). They were evaluated every 2 weeks for metabolic hormones, bioenergetic parameters, and sport performance during the 12-week season. Results: CYC and OVS athletes were similar (p > .05) in age (CYC = 16.2 ± 1.8 yr, OVS = 17 ± 1.7 yr), body mass index (CYC = 21 ± 0.4 kg·m, OVS = 25 ± 0.8 kg·m), and gynecological age (CYC = 2.6 ± 1.1 yr, OVS = 2.8 ± 1.5 yr). OVS had suppressed P4 (p < .001) and E2 (p = .002) across the season. Total triiodothyronine (TT3) and insulin-like growth factor (IGF-1) were lower in OVS (TT3: CYC = 1.6 ± 0.2 nmol·L, OVS = 1.4 ± 0.1 nmol·L, p < .001; IGF-1: CYC = 243 ± 1 μg·mL, OVS = 214 ± 3 μg·mL p < .001) than CYC at week 12. Energy intake (p < .001) and energy availability (p < .001) were significantly lower in OVS versus CYC. OVS exhibited a 9.8% decline in Δ400-m swim velocity compared with an 8.2% improvement in CYC at week 12. Conclusions: Ovarian steroids (P4 and E2), metabolic hormones (TT3 and IGF-1), and energy status markers (EA and EI) were highly correlated with sport performance. This study illustrates that when exercise training occurs in the presence of ovarian suppression with evidence for energy conservation (i.e., reduced TT3), it is associated with poor sport performance. These data from junior elite female athletes support the need for dietary periodization to help optimize energy intake for appropriate training adaptation and maximal sport performance
Commentary Strenuous physical activity may affect the female reproductive system and lead to athletic amenorrhea (3). The prevalence of amenorrhea among female athletes is up to 20 times higher than the general population and appears to be higher in young athletes who train intensively and in sports that emphasize leanness (e.g., long-distance runners, ballet dancers). A major concern of athlete amenorrhea is the low estrogen levels, which, despite a possible relative protection by the weight-bearing activity, may lead to reduced bone mass. This is particularly important in children and adolescent athletes since bone mineral density reaches about 90% of its peak by the end of the second decade (2) and because about one quarter The author is with the Sackler School of Medicine, Meir Medical Center, Tel Aviv University, Tel Aviv, Israel. Address author correspondence to Alon Eliakim at [email protected].
30
of adult bone is accumulated during the 2 years that surrounds peak bone velocity. This osteopenia may expose the young female athlete to increased risk of skeletal fragility, fractures, vertebral instability and curvature, and may lead to excessive bone loss and increased fracture risk later in life (5). The association of eating disorders, amenorrhea, and osteoporosis was termed “the female athlete triad.” A major cause for athlete’s amenorrhea is suppression of the spontaneous hypothalamic pulsatile secretion of gonadotropin-releasing hormone (1). Several genetic, body composition (fat mass), hormonal, psychological and physiological mechanisms have been suggested to explain this suppression. However, it is now believed that the main cause for athletic amenorrhea is reduced energy availability (8). Energy availability is defined as energy intake minus expenditure. There seems to be an energy availability threshold of 30 kcal/kg/lean body mass/day, and menstrual disturbances occur only below this threshold. Therefore, individual nutritional differences may explain why despite similar training
Downloaded by Purdue Univ on 09/16/16, Volume 27, Article Number 1
Endocrinology and Metabolism 31
programs, some female athletes develop amenorrhea whereas others menstruate regularly. Low energy availability reduces luteinizing hormone (LH) pulsatility and estrogen levels and suppresses the secretion of other anabolic hormones such as triodothyronine (T3) and insulin-like growth hormone- I (IGF-I), both known to affect bone mineralization. It was shown that increased caloric intake (without changes in training intensity) can prevent this suppression (4). Recently, it was found that leptin administration to female athletes with reduced energy availability-associated amenorrhea resulted in increased LH pulsatility, estradiol levels and returns of menses, although the caloric intake and training load were unchanged (9). Similar to other energy-deficient states, the body conserves its energy sources to adapt to major stress (in this case, exercise) and will not lose energy on “luxurious” activities such as reproduction and growth. The linkage of athletic amenorrhea to energy balance suggests that this condition should be considered as a nutritional problem and therefore, prevented or reversed by dietary reforms. Only if nutritional changes will not renew menstruation, moderation of exercise intensity or capacity or both is warranted. Vanheest et al. (7) are among the first to study prospectively the influence of energy restriction associated ovarian suppression on athletic performance among elite adolescent swimmers (age 15–17 years). The authors have shown that reduced energy intake and availability that was associated with ovarian suppression (determined by reduced estradiol and progesterone levels) was also accompanied by lower T3 and IGF-I levels and by 9.8% decline in 400m swim velocity compared with 8.2% improvement among swimmers without ovarian suppression at the end of 12 weeks of training (in total, 18% difference!). This occurred despite similar training protocols and while the ovarian suppressed swimmers were still menstruating (although less regularly). Another manuscript that was published this year demonstrated a protective role of estradiol toward intense training-related increase of inflammatory cytokines (IL-6 leukocyte expression) in young female athletes (6).This suggests another important possible mechanism for the reduced training adaptation in ovarian suppressed female athletes. Transformation of this knowledge to athletes and coaches is essential because many of them promote
energy restrictive practices with the belief that it improves competitive performance. The results of the current study emphasize that athletes can maintain chronic energy deficit for varied periods with continued success in sport, however, prolonged negative energy balance results in training maladaptation. This may be particularly relevant for athletes during adolescence, a time with greater energy needs for growth and maturation.
References 1. Constantini NW. Clinical consequences of athletic amenorrhea. Sports Med. 1994; 17:213–223. PubMed doi:10.2165/00007256-199417040-00002 2. Glastre C, Braillon P, David L, et al. Measurement of bone mineral content ofthe lumbar spine by dual energy x-ray absorptiometry in normal children:correlations with growth parameters. J Clin Endocrinol Metab. 1990; 70:1330–1333. PubMed doi:10.1210/jcem-70-5-1330 3. Loucks AB, Horvath SM. Athletic amenorrhea: a review. Med Sci Sports Exerc. 1985; 17:56–72. PubMed 4. Loucks AB, Thuma JR. Luteinizing hormone pulsatility is disrupted at athreshold of energy availability in regularly menstruating women. J Clin Endocrinol Metab. 2003; 88:297–311. PubMed doi:10.1210/jc.2002-020369 5. Nemet D, Eliakim A. Pediatric sports nutrition: an update. Curr Opin Clin Nutr Metab Care. 2009; 12:304–309. PubMed doi:10.1097/MCO.0b013e32832a215b 6. Tringali C, Scala L, Silvestri I, et al. protective role of 17-b-estradiol towards IL-6 leukocyte expression induced by intense training in young female athletes. J Sport Sci 2014; 32: 452-461. > 7. Vanheest JL, Rodgers CD, Mahoney CE, De Souza MJ. Ovarian suppression impairs sport performance in junior elite female swimmers. Med Sci Sports Exerc. 2014; 46:156–166. PubMed doi:10.1249/ MSS.0b013e3182a32b72 8. Warren MP, Chua AT. Exercise-induced amenorrhea and bone health in theadolescent athlete. Ann N Y Acad Sci. 2008; 1135:244–252. PubMed doi:10.1196/ annals.1429.025 9. Welt CK, Chan JL, Bullen J, et al. Recombinant human leptin in women withhypothalamic amenorrhea. N Engl J Med. 2004; 351:987–997. PubMed doi:10.1056/ NEJMoa040388
Citation Tran BD. Galassetti P. Exercise in pediatric type 1 diabetes. Pediatr Exerc Sci. 2014; 26(4):375–383. PubMed doi:10.1123/pes.20140066
The beneficial effects of exercise, including reduction of cardiovascular risk, are especially important in children with type 1 diabetes (T1DM), in whom incidence of lifetime cardiovascular complications remains elevated despite good glycemic control. Being able to exercise safely is therefore a paramount concern. Dysregulated metabolism in T1DM however, causes frequent occurrence of both hypo- and hyperglycemia, the former typically associated with prolonged, moderate exercise, the latter with higher intensity, if shorter, challenges. While very few absolute contraindications to exercising exist in these children, exercise should not be started with glycemia outside the 80–250 mg/dl range. Within this glycemic range, careful adjustments in insulin admin-
32 Eliakim
istration (reduction of infusion rate via insulin pumps, or overall reduction of dosage of multiple injections) should be combined with carbohydrate ingestion before/during exercise, based on prior, individual experience with specific exercise formats. Unfamiliar exercise should always be tackled with exceeding caution, based on known responses to other exercise formats. Finally, gaining a deep understanding of other complex exercise responses, such as the modulation of inflammatory status, which is a major determinant of the cardio-protective effects of exercise, can help determine which exercise formats and which individual metabolic conditions can lead to maximally beneficial health effects.
Downloaded by Purdue Univ on 09/16/16, Volume 27, Article Number 1
Commentary Type 1 diabetes mellitus (T1DM) is one of the most common chronic pediatric diseases. Physical exercise should be encouraged in children with T1DM since as in all children, physical activity may promote numerous essential health benefits. Moreover, physical activity plays an important role in the multidisciplinary treatment of T1DM. Despite that children with T1DM often avoid exercise participation because they are afraid from possible severe fluctuations in glycemic levels during exercise performance and the ensuing hours. Understanding of individual responses to particular exercise protocols should therefore be gained through personal experience, as well as careful precautions taken with regard to adjustments of insulin administration and carbohydrate supplements ingestion. Taking into account these precautions will allow children with T1DM to exercise freely, obtain all physical activity related health benefits and also may allow them to participate and excel in competitive sports, as documented by the many T1DM international-levels athletes and Olympic champions. This important review (3) summarizes the main current recommendations concerning exercise in T1DM and gives a detailed description of key issues related to the occurrence of both hyper- and hypoglycemia in association with exercise. More importantly, it gives practical
tools how to avoid these threatening conditions. The review highlights the very important concept of blunted exercise- associated counter-regulatory response following previous hypoglycemia, and possibly following previous exercise and psychological stress in particularly in males (1). Finally, it reviews the current relatively new concept of the possibly altered exercise-mediated cardiovascular protection, via modulations of acute and chronic inflammatory processes, in children with poorly controlled T1DM (2).
References 1. Galassetti PR, Tate D, Neill RA, Morrey S, Wasserman DH, Davis SN. Effect of sex on counter-regulatory responses to exercise after antecedent hypoglycemia in type 1 diabetes. Am J Physiol Endocrinol Metab. 2004; 287:E16–E24. PubMed doi:10.1152/ajpendo.00480.2002 2. Rosa JS, Flores RL, Oliver SR, Pontello AM, Zaldivar FP, Galassetti PR. Resting and exercise-induced IL-6 levels in children with type 1 diabetes reflects hyperglycemic profiles during the previous 3 days. J Appl Physiol. 2010; 108:334–342. PubMed doi:10.1152/japplphysiol.01083.2009 3. Tran BD, Galassetti PR. Exercise in pediatric type 1 diabetes. Pediatr Exerc Sci. 2014; 26:375–383. PubMed doi:10.1123/pes.2014-0066
Citation Fedewa MW, Gist NH, Evans EM, Dishman RK. Exercise and insulin resistance in youth: A meta-analysis. Pediatrics, 2014; 133:e163–e174.
Background and Objectives: The prevalence of obesity and diabetes is increasing among children, adolescents, and adults. Although estimates of the efficacy of exercise training on fasting insulin and insulin resistance have been provided, for adults similar estimates have not been provided for youth. This systematic review and meta-analysis provides a quantitative estimate of the effectiveness of exercise training on fasting insulin and insulin resistance in children and adolescents. Methods: Potential sources were limited to peer-reviewed articles published before June 25, 2013, and gathered from the PubMed, SPORTDiscus, Physical Education Index, and Web of Science online databases. Analysis was limited to randomized controlled trials by using combinations of the terms adolescent, child, pediatric, youth, exercise training, physical activity, diabetes, insulin, randomized trial, and randomized controlled trial. The authors assessed 546 sources, of which 4.4% (24 studies) were eligible for inclusion. Thirty-two effects were used to estimate the effect of exercise training on fasting insulin, with 15 effects measuring the effect on insulin resistance. Estimated effects were independently calculated by multiple authors, and conflicts were resolved before calculating the overall effect. Results: Based on the cumulative results from these studies, a small to moderate effect was found for exercise training on fasting insulin and improving insulin resistance in youth (Hedges’ d effect size = 0.48 [95% confidence interval: 0.22–0.74], p < .001 and 0.31 [95% confidence interval: 0.06–0.56], p < .05, respectively). Conclusions: These results support the use of exercise training in the prevention and treatment of type 2 diabetes.
Endocrinology and Metabolism 33
Downloaded by Purdue Univ on 09/16/16, Volume 27, Article Number 1
Commentary The global increase in childhood and adolescent obesity is associated with a parallel increase in type 2 diabetes mellitus (T2DM) (3). Previous meta-analytic reviews on the effect of exercise training on fasting insulin and insulin resistance have focused on adults (4) and children and adolescents with T1DM (2). Fedewa et al. in their recent important meta-analysis focused on the effect of exercise training on fasting insulin and insulin resistance in children and adolescents (1). Based on 24 studies that were eligible for inclusion in the meta-analysis from 1999 to 2013, a small to moderate beneficial effect was found for exercise training on reducing fasting insulin levels (11.4 U/ml; 95% CI: 5.2–17.5) and insulin resistance (2.0 HOMA-IR; 95% CI: 0.4–3.6). The effect of exercise training was more effective in children and adolescents with high BMI most probably due to the presence of greater insulin resistance in these individuals. The beneficial effect of exercise training on fasting insulin and insulin resistance was not influenced by gender, race, age and pubertal status suggesting that the estimated beneficial effect is similar for all youth aged 6–19 years. The relatively small amount of published scientific literature did not allow for thorough evaluation of the effect of different training protocols or the frequency, duration,
intensity, volume and mode of exercise training on fasting insulin and insulin resistance. The authors concluded that “in the absence of a clear consensus on the most effective type of exercise for treating these outcomes, emphasis should be placed on ways to incorporate physical activity, in addition to exercise training, into the lives of children and adolescents, especially those at risk for developing obesity and diabetes.”
References 1. Fedewa MW, Gist NH, Evans EM, Dishman RK. Exercise and insulin resistance in youth: A meta-analysis. Pediatrics. 2014; 133:e163–e174. PubMed doi:10.1542/ peds.2013-2718 2. Kennedy A, Nirantharakumar K, Chimen M, et al. Does exercise improve glycemic control in type 1 diabetes? A systematic review and meta-analysis. PLoS ONE. 2013; 8:e58861. PubMed doi:10.1371/journal.pone.0058861 3. Pinhas-hamiel O, Zeitler P. The global spread of type 2 diabetes mellitus in children and adolescents. J Pediatr. 2005; 146:693–700. PubMed doi:10.1016/j.jpeds.2004.12.042 4. Thomas DE, Elliot EJ, Naughton GA. Exercise for type 2 diabetes mellitus. Cochrane Database Syst Rev. 2006; 3:CD002968. PubMed
