5 MB 27/05/13 II Jornada Analítica

Transcrição

5 MB 27/05/13 II Jornada Analítica
Dr. Efraim Olszewer
Pituitary Gland and Hypothalamus
 Where nervous and
endocrine systems interact
 Hypothalamus regulates
secretions of anterior
pituitary
 Posterior pituitary is an
extension of the
hypothalamus
 Anterior pituitary produces
nine major hormones that
 Regulate body functions
 Regulate the secretions of
other endocrine glands
Pituitary Gland Structure
•
Posterior pituitary
(neurohypophysis): extension
of the nervous system via the
infundibulum
– Secretes neurohormones
•
Anterior pituitary
(adenohypophysis)
– Consists of three areas with
indistinct boundaries: pars
distalis, pars intermedia, pars
tuberalis
Hypothalamus, Anterior Pituitary, and Target Tissues
Releasing and Inhibiting Hormones
•
•
•
Tropins or tropic hormones: hormones that regulate the hormone secretions
of target endocrine tissues. All anterior pituitary hormones are tropins.
Releasing hormones secreted by the hypothalamus:
– GHRH. Growth hormone-releasing hormone. Causes the anterior
pituitary to release growth hormone.
– TRH. Thyroid-releasing hormone. Causes the anterior pituitary to release
thyroid-stimulating hormone (TSH).
– CRH. Corticotropin-releasing hormone. Causes anterior pituitary to
produce adrenocorticotropic hormone (ACTH)
– GnRH. Gonadotropin-releasing hormone. Causes anterior pituitary to
produce FSH (follicle stimulating hormone) and LH (luteinizing hormone).
– PRH. Prolactin-releasing hormone. Causes the anterior pituitary to
release prolactin.
Inhibiting hormones:
– GHIH. Growth hormone-inhibiting hormone, somatostatin. Causes the
anterior pituitary to decrease release of growth hormone.
– PIH. Prolactin-inhibiting hormone. Causes the anterior pituitary to
decrease release of prolactin.
Hypothalamus, Posterior Pituitary and Target Tissues
• Hypothalamic neurons
syntheisze ADH and oxytocin.
• Latter hormones travel to
post. pituitary via axons of
hypothalamic
neurons.
• ADH and oxytocin enter
circulation in post.
pituitary.
Hormones of Posterior Pituitary: ADH
Antidiuretic hormone (ADH). Also called vasopressin.
A. Osmoreceptors (specialized neurons of
hypothalamus monitor changes in
intercellular osmolality (relative
concentrations of electrolytes and water). If
the concentration of electrolytes increases or
if the concentration of water decreases, then
ADH secretion is stimulated.
B. Baroreceptors (specialized neurons found in
walls of atria of heart, large veins, carotid
arteries, aortic arch) sense changes in blood
pressure (BP). If BP decreases, then ADH
secretion is stimulated.
Control of ADH Secretion
Control of Oxytocin Secretion
Anterior Pituitary Hormones
•
•
•
•
•
•
•
•
•
Growth hormone (GH) or somatotropin
Thyroid-stimulating hormone (TSH)
Adrenocorticotropic hormone (ACTH)
Melanocyte-stimulating hormone (MSH)
Beta endorphins
Lipotropins
Luteinizing hormone (LH)
Follicle-stimulating hormone (FSH)
Prolactin
Growth Hormone (GH or somatotropin)
• Stimulates uptake of amino acids; protein
synthesis; growth in most tissues.
• Stimulates breakdown of fats to be used as
an energy source but stimulates synthesis
of glycogen: glucose sparing
• Promotes bone and cartilage growth
• Regulates blood levels of nutrients after a
meal and during periods of fasting
• Stimulates glucose synthesis by liver
Metabolic Action of Growth Hormone
Figure 16.6
Growth Hormone Stimulation: functions in
regulating growth, tissue maintenance, metabolism
GHRH from hypothalamus causes release of…
Growth hormone from anterior pituitary effects…
Target tissues: most tissues of the body
• Direct effect: GH binds to receptors on cells and causes changes
within the cells. Increased lipolysis and decreased use of
glucose for energy
• Indirect effect: causes liver and skeletal muscle to produce
somatomedins; e.g., insulinlike growth factors (IGF’s)
– Insulinlike growth factors: bind to receptors on
membranes of target cells. Stimulate growth in
cartilage, bone; increased synthesis of proteins in
skeletal muscle.
Regulation of GH Secretion
1. Stress and decreased glucose
levels increase release of GHRH
and decrease release of GHIH.
2. GHRH and GHIN travel via
thehypothalamohypophyseal
portal system to ant. pituitary
3. Increased GHRH and reduced
GHIH act on AP and result in
increased GH secretion.
4. GH acts on target tissues.
5. Increasing GH levels have neg
feedback effect on hypothala.
Growth Hormone: Inhibition
• Hypothalamus produces growth hormone inhibiting
hormone (GHIH = somatostatin)
• Inhibits production of GH by anterior pituitary.
• GHRH secretion in response to low blood glucose, stress,
increase in certain a.a.
• GHIH secretions in response to high blood glucose.
• Peak GH levels during deep sleep; levels lower at other
times of day.
• Hyposecretion of GH may result in dwarfism
• Hypersecretion may result in giantism or acromegaly depending on ossification of epiphyseal plates
TSH and Thyroid Hormones
• TRH from hypothalamus causes the release of
TSH from anterior pituitary which causes
secretion and storage of hormones T3 and T4
from and within the thyroid gland
• TSH increases activity of phospholipase that
opens Ca2+ channels, increasing Ca2+
concentration in cells of the thyroid gland
• T3 and T4 inhibit TRH and TSH secretion
Adrenocorticotrophic Hormone (ACTH)
•
CRH from hypothalamus causes release of
ACTH from anterior pituitary which
– Causes cortisol secretion from the adrenal
cortex (a glucocorticoid from the zona
fasciculata)
– Causes aldosterone secretion from the
adrenal cortex (a mineralocorticoid from the
zona glomerulosa)
– Binds directly to melanocytes of the skin;
causes increase in production of melanin.
Melanocyte Stimulating Hormone,
Endorphins, and Lipotropins
• ACTH, MSH, endorphins and lipotropins all derived from the
same large precursor molecule when stimulated by CRH
• MSH causes melanocytes to produce more melanin
• Endorphins act as an analgesic; produced during times of
stress.
• Lipotropins cause adipose cells to catabolize fat
LH, FSH, Prolactin
• Gonadotrophs: glycoprotein hormones that promote
growth and function of the gonads
• LH and FSH
– Both hormones regulate production of gametes
and reproductive hormones
• Testosterone in males
• Estrogen and progesterone in females
• GnRH from hypothalamus stimulates LH and FSH
secretion
• Prolactin: role in milk production
– Regulation of secretion: prolactin-releasing
hormone (PRH) and prolactin-inhibiting hormones
(PIH)
Thyroid
Gland
•
•
•
One of largest endocrine glands; Highly
vascular. Iodine enters follicular cells by active
transport. Only gland that stores hormone.
Histology
– Composed of follicles: follicular cells
surrounding thyroglobulin/thyroid
hormones
– Parafollicular cells: between follicles
Physiology
– Follicular cells secrete thyroglobulin into
lumen of follicle. Iodine and a.a. tyrosine
necessary for production of T3 and T4.
Hormones stored here attached to the
thyroglobulin then absorbed into follicular
cells; hormones disattached from
thyroglobulin and released into circulation.
– Parafollicular cells. Secrete calcitonin
which reduces [Ca2+] in body fluids when
Ca levels are elevated.
Biosynthesis of Thyroid Hormones
Thyroid Hormones
• Produced by follicular cells
• Triiodothyronine or T3 -less produced
• Tetraiodothyronine or T4 or thyroxine-more
– 99.6% of thyroxine in the blood is bound to
thyroxine-binding globulin (TBG) from the liver.
Rest is free.
– TBG has a higher affinity for T4 than for T3; amt of
free unbound T3 in plasma is 10x’s greater than
free T4.
– Only free thyroxine and T3 can enter cells; boundthyroxine serves as a reservoir of this hormone
– 33-40% of T4 converted to T3 in cells: T3 more
potent
– Bind with intracellular receptor molecules and
initiate new protein synthesis
– Increase rate of glucose, fat, protein metabolism in
many tissues thus increasing body temperature
– Normal growth of many tissues dependent on
presence of thyroid hormones.
Effects of T3 and T4
1. Maintain normal rate of metabolism.
2. Increase the rate at which glucose, fat, and protein are metabolized.
3. Increase the activity of Na+-K+ pump which increases body temperature.
4. Can alter the number and activity of mitochondria resulting in greater ATP
synthesis and heat production.
5. Normal growth and maturation of bone, hair, teeth, c.t., and nervous tissue
require thyroid hormone.
6. Both T3 and T4 play a permissive role for GH and GH does not have its normal
effect on tissues if T3 and T4 are lacking.
7. See Table 18.4 for effects of hypo- and hypersecretion
Regulation of T3 and T4 Secretion
Regulation of Calcitonin Secretion
• Produced by parafollicular cells
• Secretion triggered by high Ca2+
concentration in blood; acts to decrease
Ca2+ concentration
• Primary target tissue: bone. Decreases
osteoclast activity, lengthens life span of
osteoblasts.
Parathyroid Glands
•
•
•
Embedded in thyroid
Two glands on each side
Secrete PTH: target tissues are
bone, kidneys and intestines.
– Increases blood calcium and
phosphate levels
– Stimulates osteoclasts
– Promotes calcium reabsorption by
kidneys and PO4 excretion
– Increases synthesis of vitamin D
which, in turn, increases
absorption of Ca and PO4 by
intestines. Net loss of PO4 under
influence of PTH.
•
Regulation depends on calcium
levels.
Effects of Parathyroid Hormone
Figure 16.11
Adrenal Glands
• Near superior poles of
kidneys; retroperitoneal
• Inner medulla; outer
cortex
• Medulla: formed from
neural crest; sympathetic.
Secretes epinephrine and
norepinephrine
• Cortex: three zones from
superficial to deep
– Zona glomerulosa
– Zona fasciculata
– Zona reticularis
Adrenal Medulla
•
•
•
•
•
•
•
Secretory products are neurohormones: epinephrine and norepinephrine
Combine with adrenergic membrane-bound receptors
All function through G protein mechanisms
Secretion of hormones prepares body for physical activity
Effects are short-lived; hormones rapidly metabolized
Epinephrine
– Increases blood levels of glucose
– Increases fat breakdown in adipose tissue
– Causes dilation of blood vessels in skeletal muscles and cardiac muscles.
Epinephrine and norepinephrine increase heart rate and force of
contraction; cause blood vessels to constrict in skin, kidneys, gastrointestinal
tract, and other viscera
Hormones of Adrenal Cortex
• Mineralocorticoids: Zona glomerulosa
– Aldosterone produced in greatest amounts.
Increases rate of sodium reabsorption by
kidneys increasing sodium blood levels
• Glucocorticoids: Zona fasciculata
– Cortisol is major hormone. Increases fat and
protein breakdown, increases glucose
synthesis, decreases inflammatory response
• Androgens: Zona reticularis
– Weak androgens secreted then converted to
testosterone by peripheral tissues. Stimulate
pubic and axillary hair growth and sexual drive
in females
Regulation of Cortisol Secretion
Glucocorticoids (Cortisol)
• Help the body resist stress by:
– Keeping blood sugar levels relatively constant
– Maintaining blood volume and preventing
water shift into tissue
• Cortisol provokes:
– Gluconeogenesis (formation of glucose from
noncarbohydrates)
– Rises in blood glucose, fatty acids, and amino
acids
Stress and the Adrenal Gland
Figure 16.15
Pancreas
•
•
Located along small intestine and
stomach; retroperitoneal
Exocrine gland
– Produces pancreatic digestive
juices
•
Endocrine gland
– Consists of pancreatic islets
– Composed of
• Alpha cells; secrete glucagon
• Beta cells; secrete insulin
• Delta cells; secrete somatostatin
Glucagon
• A 29-amino-acid polypeptide hormone that is a
potent hyperglycemic agent
• Its major target is the liver, where it promotes:
– Glycogenolysis – the breakdown of glycogen to
glucose
– Gluconeogenesis – synthesis of glucose from lactic
acid and noncarbohydrates
– Release of glucose to the blood from liver cells
Insulin
• Target tissue is the liver, adipose tissue, muscle,
and satiety center of hypothalamus
• A 51-amino-acid protein consisting of two amino
acid chains linked by disulfide bonds
• Synthesized as part of proinsulin and then excised
by enzymes, releasing functional insulin
• Insulin:
– Lowers blood glucose levels
– Enhances transport of glucose into body cells
– Counters metabolic activity that would
enhance blood glucose levels
Regulation of Blood Glucose Levels
• The
hyperglycemic
effects of
glucagon and
the
hypoglycemic
effects of
insulin
Figure 16.17
Diabetes Mellitus (DM)
• Results from hyposecretion or hypoactivity of insulin
• The three cardinal signs of DM are:
– Polyuria – huge urine output
– Polydipsia – excessive thirst
– Polyphagia – excessive hunger and food
consumption
• Hyperinsulinism – excessive insulin secretion,
resulting in hypoglycemia
Diabetes Mellitus (DM)
Figure 16.18
Regulation of Insulin Secretion
Regulation of Blood Nutrient Levels
Regulation of Blood Nutrient Levels During
Exercise
Hormones of the Reproductive System
Male: Testes
• Testosterone
– Regulates production of sperm
cells and development and
maintenance of male
reproductive organs and
secondary sex characteristics
•
Inhibin
– Inhibits FSH secretion
Female: Ovaries
• Estrogen and Progesterone
– Uterine and mammary gland
development and function,
external genitalia structure,
secondary sex characteristics,
menstrual cycle
•
Inhibin
– Inhibits FSH secretion
•
Relaxin
– Increases flexibility of
symphysis pubis
Pineal Body
• In epithalamus; produces melatonin and arginine
vasotocin
Thymus Gland, GI Tract, Kidneys
• Thymosin. Development of the immune
system.
• GI tract: several hormones regulate
digestion and enzyme secretion. Studied
with digestive system.
• Kidneys – secrete erythropoietin, which
signals the production of red blood cells
• Adipose tissue – releases leptin, which is
involved in the sensation of satiety, and
stimulates increased energy expenditure
Hormone-like Substances
• Autocrines: chemical signals released by a cell and the
substance affects that same cell.
– Chemical mediators of inflammation which are
modified fatty acids: eicosanoids such as
prostaglandins, thromboxanes, prostacyclins,
and leukotrienes
• Paracrines: chemical signals released into intercellular
fluid and affecting nearby cells.
– Endorphins and enkephalins modulate
sensation of pain
– Several growth factors
Effects of Aging on
Endocrine System
• Gradual decrease in secretory activity of some glands
–
–
–
–
GH as people age except in people who exercise regularly
Melatonin
Thyroid hormones
Kidneys secrete less renin
• Familial tendency to develop type II diabetes
EXERCICIO
DANO CELULAR
RECUPERAÇÃO
ÁPICE DA PERFORMANCE
HUMANA
ELEVADOS NÍVEIS DE
HORMÔNIOS ANABOLIZANTES
HGH
Testosterona (H)
DHEA
T3 e T4
Estrogênios (M)
Progesterona (M)
Melatonina
Pregnenolona
PREMISSAS
1. MECANISMOS DE AÇÃO HORMONAL
2. NUTRIÇÃO CELULAR ADEQUADA VOLTADA PARA
O BOM DESEMPENHO HORMONAL
3. RESPOSTAS ENDOCRINAS E IMUNES DO
EXERCICIO
NUTRIÇÃO
X
HORMÔNIOS
X
RENDIMENTO
POR QUE ESTUDAR?
TROCA/COMUNICAÇÃO INTERCELULAR
SÍNTESE DE MOLÉCULAS
VARIAÇÃO DA ENERGIA LIVRE
MINERAIS ENVOLVIDOS COM A MODULAÇÃO
HORMONAL
 ZINCO
 SELENIO
 IODO
 CROMO
 VANADIO
 BORO
 COMPLEXO B
Nutrição
• Recomendações específicas da
DIRETRIZ DA SOCIEDADE
BRASILEIRA DE MEDICINA
DO ESPORTE
• ACSM - Medicine & Science in Sports & Exercise:
March 2009 - Volume 41 - Issue 3 - pp 709-731
SPECIAL COMMUNICATIONS: Position Stands
Proteínas
Gorduras
Carboidratos
Vitaminas
Minerais
Nutracêuticos
Fitoquímicos
Água
Desbiose
Detoxificação
Administração
Tabletes
Cápsulas
Soft gels
Líquidos
Pós e barras
.
Carboidratos
CARBOIDRATOS - ANTES
3A6
HORAS
5 MINUTOS
30 A 60
MINUTOS
Décombaz J, et al. Fructose and galactose enhance postexercise human liver
glycogen synthesis. Med Sci Sports Exerc. 2011 Oct;43(10):1964-71.
CARBOIDRATOS - DURANTE
INTENSIDADE
DURAÇÃO
DIETA/
OFERTA
AMBIENTE
Atenua respostas imunossupressoras
de citocinas e hormônios
(Gleeson, Venkatraman, Pendergast, Nieman,
Pendersen: 1998-2012)
EQUILÍBRIO E PROPORÇÃO
• CHO de 40 a 70 %
do valor energético
total
• GORDURAS não
mais que 30 % do
VET
Planejamento
• Dia a dia do Atleta
– ELITE X AMADORES
• Dia da Competição
• Semana de Competição
• Erros mais comuns
PONTOS-CHAVE
* Ao longo do TREINAMENTO:
• Manter balanço energético
para :
– Evitar overreaching e
overtraining
– Evitar desequilíbrios
hormonais
– Infecções oportunistas
PONTOS-CHAVE
* COMPETIÇÃO:
• Iniciar a prova corretamente hidratado
– Evitar :
– Desidratação;
– Complicações Gastro-intestinais;
– Fadiga e Cãibras;
Hopkins M, et al. The relationship between
substrate metabolism, exercise and appetite
control: does glycogen availability influence the
motivation to eat, energy intake or food choice?
Sports Med. 2011 Jun 1;41(6):507-21.
Erros mais comuns:
• Entender a real necessidade do atleta
• Açúcares simples
• Ingestão de sódio
– De 800 a 1200 mg para 1600 a 2500
mg
• Ingestão de estimulantes como cafeína
– Náuseas, dores de cabeça e
desidratação
• Gorduras e fibras
CARBOIDRATOS
•
•
•
•
•
Reposição de glicogênio
Manutenção da glicemia
Retardo da fadiga
Relação Insulina/Cortisol
Constituem mais de 50% do
valor energético total da
alimentação
• Podem chegar até 75% da
ingestão diária
Desempenho
1) Carboidratos de alto índice glicêmico
2) Recomendação – Esforço – 0,7 gr de cho/kg PC/hr
3) 8 mg Na por gr/CHO
Oxidação exógena de CHO
Asker E. Jeukendrup (2011): Nutrition for endurance sports: Marathon, triathlon, and
road cycling, Journal of Sports Sciences, 29:sup1, S91-S99
Esvaziamento Gástrico e a Liberação
de Fluidos
• A combinação de glicose e frutose esvazia
mais rapidamente que apenas a glicose.
• Acúmulo no plasma ainda é mais rápido.
• Isto sugere que a hidratação e aporte
de fluidos seja facilitada.
Pfeiffer B, et al. Nutritional intake and
gastrointestinal problems during competitive
endurance events. Med Sci Sports Exerc. 2012
Feb;44(2):344-51.
Sintomas Gastrointestinais
• Comum em corredores de endurance
• Sintomas associados com a ingestão de fibras, proteínas,
gorduras e bebidas com alta concentração de carboidratos
• Glicose com frutose – melhor tolerabilidade em função da
maior taxa de esvaziamento, aparecimento no plasma e
oxidação
– Currell K, et al. Plasma deuterium oxide accumulation following ingestion of different
carbohydrate beverages. Appl Physiol Nutr Metab. 2008. Dec; 33(6):1067-72.
– Jeukendrup AE, et al. Effect of beverage glucose and sodium content on fluid delivery. Nutr
Metab (Lond). 2009 Feb 20;6:9.
Conclusão – Glicose + Frutose
• Juntos conferem maior oxidação que quando comparada a glicose
isoladamente
• Aumenta a eficiência oxidativa
• Aumenta a biodisponibilidade de fluidos
• Parece reduzir a fadiga em exercício de muito longa duração
• Melhora a performance quando comparada a glicose isoladamente
Burke LM, et al. Carbohydrates for training and
competition. J Sports Sci. 2011;29 Suppl 1:S17-27.
Gorduras
Gorduras
• Dieta normal: Triglicerídeos, Colesterol e
Fosfolipídios
• Ácidos Graxos: Saturados, Monoinsaturados,
Poliinsaturados
• Esvaziamento Gástrico Lento
• Dietas Hiperlipídicas demoram a digerir
Jeukendrup AE. Nutrition for endurance
sports: marathon, triathlon, and road cycling.
J Sports Sci. 2011;29 Suppl 1:S91-9.
Gorduras
FAT LOADING?
ESTRATEGIA PARA MELHORAR O DESEMPENHO
EM ATIVIDADES DE LONGA DURAÇÃO?
Jeukendrup AE, Randell R. Fat burners: nutrition supplements
that increase fat metabolism. Obes Rev. 2011 Oct;12(10):841-51.
Jeukendrup AE, Saris WH, Brouns F, Halliday D, Wagenmakers JM. Effects of carbohydrate (CHO)
and fat supplementation on CHO metabolism during prolonged exercise. Metabolism. 1996
Jul;45(7):915-21.
Jeukendrup AE, Saris WH, Schrauwen P, Brouns F, Wagenmakers
AJ. Metabolic availability of medium-chain triglycerides
coingested with carbohydrates during prolonged exercise. J
Appl Physiol. 1995 Sep;79(3):756-62.
LIPÍDEOS: Ácidos Graxos N-3
“ A suplementação de ácidos graxos
poliinsaturados ômega 3
Influencia o equilíbrio das respostas
imunes no atleta por
influenciar a síntese de citocinas e
mediadores inflamatórios”
Andrade, PMM. Dietary Long Chain n-3 Fatty Acids and Anti-Inflammatory
Action:Potential Application in the field of Physical Exercise. Nutrition,
20:243,2004.
Metabolismo dos AGE
Ácidos Graxos N-6
Linoléico C 18:2
Enzima
Ácidos Graxos N-3
Alfa-linolênico C18:3
6-desaturase
Gama-linolênico C 18:3
C18:4
Elongase
Dihomo-Gama-linolênico
C 18:3
Prostaglandinas
Série 1
C 20:4
5-desaturase
Araquidônico C 20:4
Prostaglandinas
Série 2
Tromboxanos
Eicosapentanóico C 20:5
Leucotrienos
Série 4
Prostaglandinas
Série 3
Tromboxanos
Leucotrienos
Série 5
Elongase
Docosapentaenóico C 22:5
Elongase
6-desaturase
Beta-oxidação
Docosahexaenóico C 22:6
CONCENTRAÇÃO PLASMATICA
DE ACIDOS GRAXOS
RESPOSTA IMUNO-INFLAMATORIA
APÓS A SUPLEMENTAÇÃO DE AG N3
RESPOSTA HORMONAL
APÓS SUPLEMENTAÇÃO DE N3
Exposição Tóxica e Destoxificação em
atletas
• Inalaçao de toxinas ambientais
• Deposição e absorção cutânea de pesticidas nos
treinos ao ar livre (o que é potencializado pela
sudorese)
• Ingestão elevada de frutas e cereais cultivados
com agrotóxicos
• Suplementos com corantes, flavolizantes,
conservantes e outros ativos químicos
“O processo de detoxificação de
xenobioticos no organismo
pode representar significativa
utilização de nutrientes
essenciais, não somente para
a manutenção das funções
vitais como também para o
atendimento das exigencias
fisilógicas e metabolicas
associadas ao esforço físico.”
ÁGUA
Principal recurso ergogênico!!!!
– A taxa normal de transpiração nos atletas varia de
0.5 a 2.0 L/h !!!
– Depende da temperatura, humidade, intensidade do
esforço !!!
Maughan RJ, Noakes TD: Fluid replacement and exercise stress. A brief
review of studies on fluid replacement and some guidelines for the athlete. Sports Med 1991, 12(1):16-31.
REPOSIÇÃO HÍDRICA
• Antes do exercício - 600 a 800 ml de líquido 2 horas
antes da atividade
• Durante o exercício - 500 a 1000 ml/h (125 –250 ml
a cada 15 minutos)
• Após o exercício - 150% de líquidos considerando o
que foi perdido
• Água e Eletrólitos
Curr Sports Med Rep. 2004 Aug;3 (4):219-23.
GSSI,2002.
Água Alcalina
• Combate os radicais livres
– (ORP negativo)
• Equilíbrio funcional
• pH > 7
• Por que usar?
– Dietas modernas são ácidas;
– Suplementos esportivos são ácidos;
– Plástico aquecido libera xenoestrógenos;
Conclusão
• Adequar o balanço nitrogenado
• Adequar a ingestão de vitaminas do
metabolismo energético e do complexo B
• Compostos atioxidantes
• Proteínas de alto valor biológico
• Lipídios monoinsaturados
• Omega 3
AFINAL…..
“Não adianta ter uma Ferrari e
por gasolina de terceira no
tanque.”
Como o exercício de força altera o
metabolismo da fibra muscular?
Estrutura do Músculo Esquelético
Membrana celular: Sarcolema: retirada de cargas e produtos e condução de excitação elétrica para
fibra muscular.
Invaginação do Sarcolema: Tubulos T: transmissão do potencial para dentro do músculo
Retículo sarcoplasmático (RS): crescimento, reparo e substituição muscular
Miofibrilas: Milhares de filamento proteicos organizados – 2 tipos
•
Filamentos finos:
– Actina
– Tropomiosina
– Troponina
Banda I p/ A
•
Filamentos grossos:
– Miosina
Estende-se toda Banda A
•
Zona H: região na qual os
filamentos grossos não são
sobrepostos pelos finos
Suprimento sanguíneo do Músculo
esquelético
•
Vasos sanguíneos orientados em paralelo
•
N capilares - contraem e dilatam de acordo com controle
Nervoso, hormonal e local
Atividades aeróbias (corrida,natação,ciclismo):
 fluxo sanguíneo (até 100x) e superfície efetiva para
permuta de gases e nutrientes entre sangue e fibras
musculares (VASODILATAÇÃO)
Atividade de força muscular:
 fluxo sanguíneo durante contração (> pressão
intramuscular) – Fte energética p/ esforço muscular:
reações anaeróbias glicolíticas e Cr fosfato.
 fluxo sanguíneo e vasodilatação durante o
relaxamento
Óxido nítrico
•
 Neurotransmissores, estesse de cisalhamento e distensão dos vasos 
Liberação de NO pelas células do endotélio vascular
•
VASODILATADOR:
– > Fluxo sanguíneo
– > Aporte muscular de nutrientes, oxigênio e mensageiros químicos,
– Rápida eliminação das substâncias tóxicas acumuladas (ácido láctico, amónia,
etc)
– músculos conseguem produzir energia durante mais tempo, e, uma vez que
estão bem oxigenados, evitar o processo de anaerobiose provocado pela falta
de oxigénio.
•
Precursor: L-arginina
Distribuição das fibras musculares nas
diferentes categorias atléticas
Categoria atlética
% fibras vermelhas
% de fibras rápidas
Corredores de maratona
82
18
Nadadores
74
26
Atleta masculino nível médio
45
55
Halterofilistas
45
55
*Corredores de velocidade e
Saltadores
37
63
Guyton;1985.
Síntese Proteica
Após repetidas lesões das fibras musculares:
Miofibrilas das células
Aumentam número
Sofrem espessamento
 quantidade de proteínas contrateis nas fibras treinadas
 significativo ATP intramuscular, PCr e glicogênio muscular
 reserva de energia anaeróbica – Ritmo + rápido de
transferência de energia p/ treinamento de força
Hipertrofia do tec conjuntivo – Proteção p/ as articulações e
músculos de possíveis lesões.
Hormônios sinalizadores
• Insulina (Pâncreas)
• IGF (Fígado)
• GH ( Hipófise anterior)
• Testosterona
Hormônios são reconhecidos e captados por
receptor específico:
Membrana celular (tempo resposta: min ou seg)
Dentro do núcleo - Interage com DNA
(tempo resposta: min, hs ou dias)
Glicose
Aminoácidos
Arginina, Lisina
Insulina
Transporte glicose
(músculo e cels
adiposas
Estimula síntese
proteica
Inibe proteólise
 transporte de aa através
membrana plasmática
 níveis celulares de RNA
 formação de proteínas pelos
ribossomos
Substrato energético
(Glicose, AGL)
Jejum
Refeição rica em PTN
Exercício
Mistura de AA (arginina)
Stress
GH
Captação de
Glicose pelos
tecidos
Estimula produção
(fígado)
IGF (I e II)
Estágio IV sono
Estimula síntese
proteica
 Lipólise
 transporte de aa através
membrana plasmática
 níveis celulares de RNA
 formação de proteínas pelos
ribossomos
• Liberação: durante o sono
• Importante repouso e treinamento adequado
Testosterona
• Efeito direto sobre a síntese de tecido muscular
• Afeta indiretamente o conteúdo proteico das fibras –
promove liberação de GH
• Migra para nucleo celular (interage com receptores) que
iniciam a síntese proteica
• Mulheres: [ testosterona] 1/10 : aumenta com exercícío.
Nutrição - alternativa para “ativar” mecanismos
anabólicos?
Suplementos de aminoácidos – reforçam a
produção natural dos hormônios anabólicos?
•
•
•
•
•
•
Arginina
Ornitina
Lisina
Tirosina
Leucina
outros aminoácidos.
Doses muito elevadas e perigosas p/ aumentar liberação
GH
Leucina
• Qdo combinada com Insulina – efeitos anabólicos no músculo.
• Mecanismos ainda não esclarecidos.
• AA não serve apenas como substrato para síntese.
•  translação do mRNA  p70S6K
• Insulina e leucina ativam a p70S6K através de mecanismo
distintos no músculo esquelético humano.
• Evidência de que a leucina  degradação protéica
Mecanismos sinalizadores da insulina e de AA
Arginina
Estímulo para a liberação do GH
Lisina
Estímulo para a liberação do GH
Estímulo para liberação de Insulina
Arginina e Lisina
• Objetivo:
– Verificar efeito da ingestão dos AA arginina e Lisina na [GH]
• Protocolo:
– Placebo, 1,5mg de L-arginina e 1,5mg L-Lisina ,
Placebo sem exercício de força, AA sem exercícíos
de força.
• Resultados:
– [ ] GH > 30, 60 e 90 min com exercícío
– Ingestão dos aa não induziu mudanças [GH].
Metz e col, 1997.
Proteínas
• Não existe mecanismo de armazenamento
Excesso PTN é oxidado e N excretado
• Estão sempre sendo renavadas - Turnover
proteico
• Ritmo de renovação de 3 a 5g/kg/dia
• A maioria das PTN e enzimas estruturais são
sintetizadas e degradas a altas taxas (≠ meia vida)
• Ruptura das PTN em AA – enzimas hidrolíticas
(mecanismos influenciados pela insulina)
Proteínas
Gde parte dos AA liberados por proteólise são
reciclados p/ síntese PTN
~ 50g são degradados (0,8g/kg/dia)
– AA liberados - Renovação contínua PTN
– Catabolizados diretamente p/obtenção de
energia
– Transformados em gordura (PTN em
excesso)
– Transformados em carboidrato Neoglicogênese
Falta de PTN ou energia: aceleração do catabolismo proteico
AA podem entrar na rota da gliconeogênese
Catabolismo proteico
• PTN degradada em seus AA componentes
• Degradação dos AA
Liberação de Amônia
Incorporada às moléculas de Glutamina e Alanina
Transportadas para o Fígado
Detoxificação
Uréia (metabolicamente inerte)
Excreção
Rim
Taxa de conversão de aminoácidos derivados da amônia ate uréia é limitado
Contra- indicações – dieta rica em PTN
• Função renal  excreção de Nitrogênio 
sobrecarga renal  perda de água Desidratação
• Perda de Cálcio  Dietas ricas em PTN 
excreção urinária de Cálcio.
20 mg de Ca/1 g de PTN.
♀ EUA: 9/1.
• Aterogênese  Ptn de origem animal – ricas em
gordura.
Dietas hiperproteicas (< 2g/kg/dia)- Não associada ao
surgimento e/ou indução de patologias hepáticas e renais
Atenção: Indivíduos com histórico familiar de problemas renais
Balanço do Nitrogênio
INDIVÍDUO SAUDÁVEL +
Nitrogênio
ingerido
DIETA BALANCEADA
Nitrogênio
excretado
90 % urina
10 % fezes
EQUILÍBRIO
NITROGENADO
• Equilíbrio Nitrogenado
Ingesta = Excreção
• Balanço Nitrogenado Positivo
Ingesta > Excreção
- Crescimento (infância e adolescência)
- Gestação e lactação
- Treinamento resistido
Nitrogênio
ingerido
• Balanço Nitrogenado Negativo
Ingesta < Excreção
- Jejum prolongado
- Dietas pobres em proteína
- Infecções, queimaduras, cirurgias
-Ingestão adequada de PTN e CHO
(organismo cataboliza PTNenergia
(MM)
Nitrogênio
excretado
Nitrogênio
excretado
Nitrogênio
ingerido
Nitrogênio
ingerido
Nitrogênio
excretado
Digestão
Proteínas da dieta
Lúmen Intestinal
Aminoácidos
40%
Capilares
aa
+
Dipeptídios
Tripeptídios
60%
Enterócito
Aminoácidos
aa
Dipeptidases
Tripeptidase
•Somente fetos e recém-nascidos são capazes de captar algumas
PTN sem digestão prévia (Imunoglobulinas do colostro do leite).
•Velocidade de transporte dos peptídeos ultrapassa a velocidade de
transporte de aa.
•Após fracionamento das PTN pelas enzimas pancreáticas e
peptidases da borda em escova, os di e tripeptídeos produzidos são
transportados através da membrana da borda em escova
Dose de proteína ingerida
Como avaliar a ingestão de proteína?
• Consumo absoluto em gramas
• % de contribuição para o VCT
• Quantidade consumida por kg peso /dia
Níveis excessivos e perigosos
• Consumo absoluto por gramas: >165g/dia
• % de contribuição do VCT: > 35%
• Quantidade consumida por kg peso /dia:
>2,7g/kg/dia (em indivíduo de 80kg)
* hiperaminoacemia, hiperamonemia,
hyperinsulinemia, nausea, diarréia e até a morte
Recomendação prática
• Consumo absoluto por gramas: <118g/dia
• % de contribuição do VCT: < 25%
• Quantidade consumida por kg peso /dia: >1,5 2,0 g/kg/dia
• Aumento de ptn – Não deve ser alta em gordura
total e saturada
• Aumento de ptn – cuidado com deficiência
nutricional Bodybilders (200- 400g)
RDA
• Consumo absoluto por gramas: >118g/dia
• % de contribuição do VCT: > 15-20% de
• Quantidade consumida por kg peso /dia:
>0,8g/kg/dia
• Indivíduos que praticam atividade física
intensa - 1,2g a 1,7g/dia.
Recomendações
Situação
Recomendação
Atletas recreacionais (4x/sem por 0,8 a 1,0 g/Kg/dia
30 min)
Treinamento
de
resistência 1,2 a 1,6 g/Kg/dia
aeróbia
1,2 g/Kg/dia
Intensidade moderada
1,6 g/Kg/dia
Volume extremo (tour de
ciclismo)
Treinamento de força
Novatos
Regulares
1,2 a 1,7 g/Kg/dia
1,5 a 1,7 g/Kg/dia
1,0 a 1,2 g/Kg/dia
Atletas adolescentes durante o 1,5 g/Kg/dia
pico de crescimento
Maughan, 2004
Disponibilidade de CHO
• Fadiga precoce
• Diminuição da performance
• Catabolismo muscular
• Ingestão adequada de CHO previne:
– Gliconeogenese muscular
– Preservação da massa muscular
• Quantidade de CHO mínima: 120g/dia –150g/dia
Disponibilidade de CHO
•
> Secreção de Insulina: anabólico  captação de aa pelo
músculo.
•
Se 1g CHO/ Kg é ingerido na 1a hora após, há  quebra de
proteína muscular e um Balanço Positivo.
Velocidade de absorção de AA
Whey protein – Rápida Abs:
PTN soluvel – subito  AA, por curto período
Caseína - Lenta absorção
Fixa estômago - atrasa esvaziamento gástrico
Moderado  AA, por prolongado período
Síntese Proteica: Estimulada 68% após refeição WP e 31%
após refeição CAS
Catabolismo muscular: inibido 34% por 7h CAS
Será que uma rápida absorção resulta em uma
maior síntese protéica?
Ergogenic Aid - Defined
Substance or device that enhances energy
production, use, or recovery and provides an
athlete with a competitive advantage.
Ergogenic Aid - Examples
Mechanical (shoes)
Psychological (hypnosis)
Physiologic (blood doping)
Nutritional (creatine)
Pharmacologic (anabolic steroids)
Why do athletes use supplements?
•
•
•
•
Provide more convenient form of nutrient
Prevent a perceived deficiency
Provide direct ergogenic effect
Belief that every top athlete is taking it; they
can’t afford to lag behind
Many athletes will do whatever it takes to win…
• In 1995, 198 Olympic-level
power athletes were given
this scenario:
– You are offered a banned
substance with 2
guarantees:
• You will not be caught
• By taking the substance you
will win
Only 3 declined!
…at any cost
The same 198 athletes were
offered a banned substance
with 2 additional guarantees:
 You will win every event for the
next 5 years
 You will die at the end of those
5 years
50% still said they would use it!
Prevalence
1996-1999 10,449 boys and girls age
12-18 surveyed:
– 4.7% of boys and 1.6% of girls used
protein powder or shake, creatine, amino
acids/HMB, DHEA, growth hormone, or
anabolic steroids at least weekly to
improve appearance or strength
Placebo effect in athletes
Athletes are HIGHLY
suggestible
– 97% believe placebo
effect works
– 73% said they had
experienced it
– Beedie CJ. J Sports Sci
Med 2007
• “Expectancy Effect” is
significant
– Belief in efficacy 
performance
improvement
• Pill Colors
red/orange/yellow 
stimulant
• Injection > pill
• Expensive > cheap
Nocebo effect in athletes
Belief that a substance
negatively affects
performance
1.57% slower 3x30sec
sprints from nocebo
– Beedie et al.
Ergogenic Aid # 1
Anabolic Steroids
Analogs of testosterone
More than 100 types
Forms:
Oral
Injection
Topical (gels, creams)
Prevalence 2009
 Jr high: 2%
 12th grade: 5% (males 7%,
>females 2%)
Anabolic Steroids – Proven Effects
•
•
•
•
•
Increase in fat-free mass
Increase in body weight
Increase in arm girth
Increase in leg girth
Increase in bench press and
squat scores
• Increase in libido
Anabolic Steroids—Disproven Effects
• No effect on endurance exercise
– Males on treadmill
• Eur J Appl Physiol 2006
– VO2max in rats
• Med Sci Sports Exer 2004
Anabolic Steroids - Side Effects
Hepatocellular
damage
Cardiovascular disease
(stroke, MI)
Psychological
disturbance
Effects can sometimes
be permanent!
“Side effects of anabolic androgenic
steroids abuse”
Followed body builders for 2 years
•
•
•
•
Decr LH, FSH, SHBG
Decr sperm count and fertility index
Decr HDL (57  42)
No change liver/prostate US, hematological
indices
More side effects…
Men
–
–
–
–
–
–
–
–
Acne
Premature baldness
Prostatic hypertrophy
Prostatitis
*Injection complications
Testicular atrophy
*Impotence
*Gynecomastia
More side effects…
Adolescents
 Premature closure of physes
 Decreased libido
 Depression
More side effects…
Women
–
–
–
–
–
–
Clitoral enlargement
Menstrual dysfunction
Male-pattern baldness
*Masculinization
Deepening of voice
*Hirsutism
Side effects that can be PERMANENT
Premature growth plate closure
Testicular atrophy
Gynecomastia
Male pattern baldness
Female masculinization
Excessive hair growth
Deepening voice
Clitoral enlargement
Anabolic Steroid regulation
Illegal except by
prescription
Banned by the USADA,
NCAA, NFL, NBA, and
MLB
Prohormones
Precursors of testosterone
Androstenedione
Dehydroepiandrosterone
Androstenediol
Prohormones – the evidence
No improvement in
strength or lean body
mass
*Causes positive urine
test for steroids
Prohormones - Side Effects
• May be similar to anabolic
steroids, but probably less
frequent.
Prohormone regulation
• Anabolic Steroid
Control Act of 2004
– prohormones classified
as controlled substances
• Banned
– USADA, NCAA, NFL,
NHL, NBA, MLS
Stimulants
Stimulants
Caffeine
Amphetamines
Cocaine
Sympathomimetics
 Ephedrine
 Pseudoephedrine
 Phenylephrine
 Phenylpropanolamine (PPA)
Modafinil (Provigil)
Stimulant Use Prevalence
• Ephedrine:
– 3.5% in NCAA athletes
• Clin J Sports Med 2001
– 12% of HS boys/26% of girls have tried
• Med Sci Sports Exer 2002
• Caffeine
– 33% of British club track/field athletes
– 60% of British club cyclists
• Chester N, Int J Sports Med 2008
Caffeine’s Proven Effects
– Increased time to fatigue (”capacity”) in wide
range of lab protocols
• Prolonged submaximal (> 90 min)
• Sustained high-intensity (20-60 min)
• Short-duration supra-max (1-5 min)
– Likely beneficial in endurance and “stop-n-go”
sports
– No clear benefit in strength/power events
Caffeine in Endurance Running
•
•
•
•
•
•
4.2-sec faster 1.5-km
1-3% faster 5-km
24-sec faster 8-km
50-sec faster 10-km military pack
march
No change in 21-km race
Improved treadmill time-to-exhaustion in
marathoners
Caffeine in Other Sports
• Rowing: 1-3% faster 2000m
race
• Swimming: 24-sec faster
1500m race
– About 21 min
• Cycling: 3.5% higher mean
power in 40km race
Caffeine Dosing
• Doses 2-9 mg/kg in studies
• 2-5 mg/kg usually effective
• 250-500 mg
–
–
–
–
–
Cola: 40 mg
Coffee: 100 mg
Tea: 20-100 mg
Red Bull: 115 mg
Vivarin: 200 mg
• No difference in fx between “users” and “nonusers”
Caffeinated Sports Drinks
No proven performance benefit
– 18-km run times
– Pl vs carb drink vs carb+150mg
caffeine
– consumed 4x in race
– Int J Sports Med 2005
Ephedrine
78-sec faster 10-km run (with backpack &
helmet) vs placebo
– 30-sec faster than caffeine
-0.8 mg/kg
– No benefit when added to caffeine
Modafinil
Cycling at 85% VO2max
– 22% longer time to exhaustion vs Placebo
18.3 min vs 15.6
– Central mechanism: decreased RPE
– Dose 4 mg/kg
– No side-efx seen
Stimulant Mechanisms of Action
Not conclusively known
Likely: CNS-regulated decreased perceived
exertion
Stimulants - Side Effects
•
•
•
•
•
•
Anxiety*
Dysrhythmias*
Hypertension*
Hallucinations
Addiction
Death
Stimulant regulation
Many prohibited by WADA & NCAA
 Most ADHD meds
Some still allowed (cold meds)
 Pseudephedrine, PPA
Caffeine
 WADA: no longer monitored
 NCAA < 15 mcg/ml
 1 cup coffee = 100mg = 1.5
mcg/ml in urine
Blood Doping
Increasing the number of red blood
cells in the body to increase the
oxygen carried to muscle
 Administration of blood, red blood cells, or
related blood products
 Erythropoietin
Stimulates bone marrow to produce red blood cells
Blood Doping – proven effects
• Increased Endurance
– 7% increase in Hgb
– 5% increase in VO2 max
– 34% increase in time to
exhaustion at 95% VO2 max
– 44 second improvement in 5 mile
treadmill run time
(Williams and Branch summarized study findings)
Blood Doping - Side Effects
Infections with transfusions
Increased viscosity of blood
 Stroke, MI, PE
Blood Doping - regulation
Erythropoietin only by prescription
Doping prohibited by WADA, NCAA
Blood tested for antigens
Ceiling on allowable Hct level at 50
Beta-2-Agonists
Physiology
– Bronchodilation, tachycardia
– Examples: albuterol, terbutaline, salmeterol
Beta-2-Agonists – proven effects
Clear benefit in asthma and EIB
– No increase in ventilation of performance in
studies of NON-asthmatic athletes
Clenbuterol: anabolic (25% as effective as
anabolic steroids)
Side effects: tremor, tachycardia
Regulation
– WADA: most prohibited
– NCAA: inhalation permitted
Beta blockers
Physiology
– Decreased heart rate, reduced tremor, lower BP
Examples
– Atenolol
– Metoprolol
– Propranolol
Efficacy in sports
– Proven improved scores in shooting sports
Beta blockers
• Side effects
– Hypotension, bronchospasm, bradycardia
• Regulation
– NCAA: banned in Rifle sports
– WADA: banned in…
• Aeronautic, archery, autos, billiards, bobsled, boules,
bridge, curling, golf, gymnastics, motorcycling, modern
pentathlon, powerboating, bowling, sailing, shooting,
skiing, snowboarding, wrestling
– Alcohol banned for same reason
Creatine
Most popular nutritional
supplement
In 2000, >$300 million in sales in
the US
Creatine
Replenishes ATP in
anaerobic exercise
 Made in liver, kidneys, and
pancreas
 Dietary sources: meat, fish
 Stored in skeletal muscle
 Excreted as creatinine in
urine
Creatine – disproven effects
• Meta-analysis 2002:
– NO overall benefit on anaerobic performance
(weight lifting, sprint cycling, spring running,
sprint swimming, kayaking, arm cranking, or
jumping/kicking)
– 29 quality studies
• 35% were statistically significant between Cr and
Placebo
• 65% NON statistically significant
Creatine – disproven effects
• Meta-analysis 2003:
– No significant difference in field-based athletic
performance (e.g. running, swimming)
X
X X
Branch JD. Int J Sports Nutr Exerc Metab June 2003
Creatine – proven
effects
• 2003 meta-analysis of strength efx:
– 8% increase in 1RM strength vs placebo (20% vs
12%)
– 14% increase in # of reps
– Highly variable response
• Body Composition
– Increase in weight and lean body mass by 1-2
kg over short term
Rawson, Volek. J Strength Cond Res 2003.
Creatine Mechanisms of Action
Increases PCr energy availability
– ->Increased effort in resistance training
• Increased satellite cell and myonuclei
• Increased gene expression for contractile
proteins
– ? Due to more available energy
• Increased contractile protein synthesis
Creatine Mechanisms of Action
Creatine - Side Effects
Studies of 2-10 weeks: no side efx
Long term:
Creatine - regulation
Not banned anywhere
Surveys suggest ~ 50% of male college
athletes and 1/3 of all NFL players are on
creatine
β-Hydroxy-Methylbutyrate (HMB)
• Physiology
– A metabolite of the essential amino
acid leucine
– Produced in small amounts
endogenously
– Regulates protein metabolism
• Less catabolism, more anabolism
•  ? Increased muscle mass
HMB – proven effects
• Meta-analysis 2003:
– Small increase in lean mass and 25% greater
strength vs placebo
• Greater effect in untrained persons
– Less muscle breakdown
– Some utility in muscle wasting
• Side-efx: none reported in 3 studies
• Non-regulated
Nissen, Sharp. J Appl Physiol 2003
Buffering Agents: proven
• Mitigate metabolic acidosis after strenuous exercise
– Bicarbonate, citrate
• NaHCO3: Proven ergogenic efx in high-intensity exercise
–
–
–
–
–
–
100m & 200m swim
400 & 800 m run
Repeated sprints
Repeated judo throws
30 min high-intensity running
60 min max-effort cycle ergometry
• Citrate less effective in studies
Bicarbonate
Dose: 0.2 - 0.3 mg/kg
GI side effects common
β-Alanine
Supplementation results in higher skeletal
muscle CARNOSINE, an intracellular buffer
Proven effective in high-intensity anaerobic
performance
– >1 to <5 min duratio
n
Acidosis most prominent
– Delays onset of neuromusc fatigue
– Increased time to exhaustion
– (no change in VO2max or max strength)
β-Alanine
• Dose
– 3.2 – 6.4 gm/day
– Effective after 4 week supplementation
– 800 mg qid or 1600 mg slow-release qid
• Side-efx: paresthesias at doses higher than
above
– No others reported
• Not regulated or prohibited
Nitric Oxide-releasing agents
• Physiology
– Arginine is a precursor of NO
– NO regulates BP and blood flow to
organs
– Most supplements: Arginine αketoglutarate
• Claims
– Improves “pump” and blood flow to
muscles
– Increases strength and size
– Speeds recovery
Nitric Oxide-releasing agents: the evidence
Several studies in performance
– Endurance exercise:
No benefit in endurance athletes
Limited evidence of benefit in debilitated
pts
– Strength exercise: mixed results, no
benefit proven, more studies needed
Nitric Oxide-releasing agents
Side effects
– Diarrhea, nausea, migraines
Regulation: none
Peptide Hormones & Analogues
Adreno-corticotripon (ACTH)
Growth hormone (hGH)
Chorionic gonadotropin (hCG)
Insulin-like growth factor (ILGF-1)
Leutenizing hormine (LH)
Erythropoietin (EPO) etc.
Diuretics & Urine Manipulators
• Can be used to mask urine tests
• Examples
– Acetazolamide (altitude sickness)
– Furosemide (Lasix)
– Spironolactone (acne, HF)
– Hctz (Htn)
Anti-Estrogens
Often used to counteract
side-efx of anabolic
steroids
– Tamoxifen (breast cancer)
– clomiphene (infertility)
Other Substances
• NO proven ergogenic effects from:
–
–
–
–
–
–
–
–
–
–
Citrulline, Carnitine,
Coenzyme Q, Colostrum
Asparagine, Arginine, Pyruvate, Ribose
Choline, Chromium picolinate
Antioxidants, Bee pollen, Boron
Folate, Gamma-hydroxy-butyrate
Inosine, leucine
Yohimbine
Vitamins and Minerals
Branched chain amino acids
• Inconsistent effects in Overtraining Syndrome
Supplements, Herbals,
Energy Drinks
• ‘TAKE AT YOUR OWN RISK’
– Be VERY cautious to recommend any
• Not tested by the FDA
– Often contain traces of banned substances
– May not contain what label says
• No such thing as “side-effect free!”
• Some supplement ingredients are discussed on
USADA at http://www.usantidoping.org.dro/
Contamination facts
2001 IOC international study;
– 634 non-hormonal supplements,
– 15% contained undeclared steroids
2007 study of 58 USA supplements
– 25% contaminated w/ prohib steroids
– 11% contaminated w/ prohib stimulants
2008 UK study of 152 supplements
– 10% contaminated w/ steroids/stim
Drugs in Elite Athletes
2010-11 NCAA
Banned Drugs
The NCAA bans the following classes of drugs:
a. Stimulants
a. Phenylephrine and pseudoephedrine OK
b. Anabolic Agents
c. Alcohol and Beta Blockers (banned for rifle only)
d. Diuretics and Other Masking Agents
e. Street Drugs
f. Peptide Hormones and Analogues
g. Anti-estrogens
h. Beta-2 Agonists
Anti Doping in
Elite Amateur Competition
• WADA rules apply
– Testing will be done in accordance with
WADA/USADA
• Permitted/Prohibited?
http://www.usantidoping.org.dro
1-800-233-0393
2010 WADA
Prohibited Substances
Anabolic androgenic steroids
Other anabolic agents
– Clenbuterol, selective androgen receptor modulators
(SERM)
Erythropoiesis-stimulating agents
Growth hormone and growth factors
Chorionic gonadotropins, LH
Insulins
Platelet-rich plasma (IM injection)
– Other locations require Declaration
2010 WADA
Prohibited Substances
• Hormone antagonists and modulators
– DHT blockers (finasteride, dutasteride)
– They mask anabolic steroid use
• Diuretics and masking agents
– Acetazolamide, hctz, spironolactone
– Plasma expanders; glycerol, IV albumin, etc.
2010 WADA
Prohibited METHODS
• Enhancement of Oxygen Transfer
– Blood doping (transfusions, etc.)
• Gene doping
– Gene transfers
– Substances than alter gene expression
• Chemical or mechanical manipulation
– IV infusions, except if hospitalized
– Sample tampering
2010 WADA
Prohibited in COMPETITION
Stimulants, e.g. ADHD meds
– Exceptions:
Caffeine OK
Phenylephrine and PPA OK
Ephedrine < 10 mcg/ml
Pseudoephedrine < 150 mcg/ml
Narcotics
Cannabinoids
2010 WADA
Prohibited in COMPETITION
• Glucocorticoids by oral, IV, IM, rectal
– Declaration required for inhalation and other
injection sides
– Topicals OK
2010 WADA
Prohibited in PARTICULAR SPORTS
• Alcohol
– Aeronautic, archery, auto, karate, shooting,
motorcycle, bowling, powerboating
• Beta-blockers
– Aeronautic, archery, autos, billiards, bobsled,
boules, bridge, curling, golf, gymnastics,
motorcycling, modern pentathlon, powerboating,
bowling, sailing, shooting, skiing, snowboarding,
wrestling
What if prohibited med is required to
treat illness or injury?
Declarations and Therapeutic Use
Exemptions
Declaration required for:
– Non-systemic corticosteroid injections
– Inhaled albuterol, salmeterol, glucocorticoids
TUE required for
– All other prohibited substances
– Doc fills out, send to USADA, along with
supporting documents
– Process takes 1-2 months to approve
– Variable duration
Testing During Competition
• Commonly tested substances:
• Stimulants • Narcotics
• Cannabinoids
• Glucocorticosteroids
• Anabolic Agents
• Hormones and Related
Substances
• Diuretics and other Masking
Agents
• Beta-2 Agonists
• Anti-Estrogenics
• Prohibited methods, such as
blood doping
If a prohibited substance
or method is detected
in your sample – even
if it was unintentional –
it will result in a
doping violation.
Athletes’ Rights During Testing
Having an Athlete Representative and/or Language Specialist
present
Doping Control Officer (DCO) explain any part of the testing
process that you do not understand.
A copy of all forms used to document the
processing of your sample.
Providing feedback to improve testing policies or
procedures.
Note: If any portion of the test does not seem right to you,
document that on the doping control paperwork.
Athlete’s Responsibilities During Testing
• Comply with the doping control procedures.
• Bringing a photo ID to the Doping Control Station.
• Report to the Doping Control Station within 60
minutes of being notified for testing.
• Stay within view of the DCO (or Chaperone) from the
time you are notified until the sample collection procedures
are complete.
• Ensure that all paperwork is completely accurate
A2 Biology Topic 7
Performance enhancing drugs
Banned substances and practices
Anabolic steroids
Stimulants
Hormones and releasing factors
Beta-2 agonists
Narcotics
Beta blockers
Hormone agonists
Diuretics
Blood doping
Gene doping
Is it an infringement of athletes human rights to be required to give blood and urine samples?
Page reference: 178-179 Edexcel A2 Biology (concept) textbook
Steroid hormones
Pass through the plasma membrane and stimulate protein synthesis
Steroid
hormones
Other steroid
molecules
Mechanism of action of steroid hormones:
steroid hormone
cell surface membrane
Hormone enters
cell and binds with
receptor
Complex binds to DNA
and acts as a
transcription factor
receptor
nuclear
membrane
enters nucleus
hormone-receptor
complex
Switches on a gene for
synthesis of a protein
Testosterone
Stimulates protein synthesis
Results in bigger and stronger
muscles
Anabolic steroids
Natural testosterone is quickly
broken down.
testosterone
Testosterone is modified to
produce drugs that remain for
longer in the body
These synthetic anabolic
steroids are illegal.
nandrolone
Side-effects of using anabolic steroids
Infertility due to disruption of normal
hormone production:
- disrupted menstrual cycle
- reduced sperm production
-impotence
In addition:
- liver damage
- high blood pressure
- heart attacks
- increased aggression
21 year old body builder: A and B Severe
acne conglobata C After 8 weeks off
steroids and with antibiotics
Peptide hormones
Peptide hormones do not
enter the cell.
They bind to receptors on
the cell surface membrane.
They also act to switch
genes on or off.
Human erythropoietin
Mechanism of action of peptide hormones:
peptide hormone
receptor
cell surface membrane
Inactive secondary
messenger eg. cAMP
Secondary messenger
activated: initiates a
protein kinase cascade
acts as a transcription
factor which switches
on gene for a specific
protein
Erythropoietin
Erythropoietin is synthesised in the
kidneys
Causes the synthesis of enzymes
required for synthesis of red blood cells
(erythrocytes) in bone marrow.
Useful for treating anaemia.
Use of erythropoeitin
Increases number of blood cells and
therefore enhances oxygen supply to
muscles.
Improvement of 10% in aerobic
performance
Use is popular with endurance
athletes and cyclists
Side-effects of overuse of erythropoietin
Excess of red blood cells can lead
to strokes and heart attacks .
Attacks most common at night
due to low heart rate.
Thought to have caused the
unexpected deaths of 18
european cyclists between 1987 1991 .
Abuse difficult to prove as it is
naturally occurring.
Ethics of performance-enhancing drugs
Problems with deciding on what is illegal:
Ethical questions:
Creatine is not banned:
Classed as a nutritional supplement
Can cause kidney damage and high blood pressure
Is everything acceptable in
the pursuit of sporting
excellence?
Erythropoietin is banned:
Is a naturally occurring hormone
Can cause strokes and heart attacks
Isn´t it the choice of the
athlete to risk using drugs
or not?
Blood doping banned:
Donating, storing and transfusing own blood before
competition
Do use of performanceenhancing drugs improve
or ruin competition?
High altitude training not banned:
Increases number of red blood cells.
Caused by natural increase in erythropoietin production.
Are there circumstances
when drug use is
acceptable?
Essay
Read pages 182 – 183 (of concept approach textbook) and
answer question 2 on page 183:
Describe an absolutist and a relativist ethical position on the
proposal to set a maximum total red blood cell count for athlete
rather than measure erythropoietin levels.