Parts of an in-house training that I've done to review endocrine physiology and strength training.

2. How the Endocrine System
Works
 Endocrine glands are stimulated to
release hormones (neural stimulation or
chemical stimulation).
 Hormones are released into blood and
act upon target tissues or directly on the
DNA in the nucleus of the cell.

3. What Do Hormones Do?
 Alter the rate of intracellular protein
synthesis
 Change the rate of enzyme activity
 Modify the plasma membrane transport
 Induce secretory activity

4. Hormones and Enzymes
 Hormones increase enzyme activity in
one of several ways:
 Stimulate increased production of the
enzyme
 Combine with the enzyme to alter its shape
and ability to act (can increase or decrease
the enzyme’s effectiveness)
 Activate inactive forms of an enzyme,
increasing the total quantity of active
enzyme

5. Receptors and Hormonal
Changes
 Every cell has a receptor to mediate the
signal or message from a hormone.
These are found:
 Outside the cell (binding proteins)
 In the cell membrane
 On the regulatory elements of DNA

6. Lock-and-Key Theory
 From Essentials 2nd Edition
 Lock-and-Key Theory: Each receptor is highly
specific for a single hormone
 Cross-Reactivity

8. Steroid vs. Polypeptide
Hormones
 Steroid hormones are fat soluble and
passively diffuse across the
sarcolemma.
 Steroid crosses sarcolemma, binds with
hormone-receptor complex (H-RC).
 H-RC arrives at genetic material of cell,
“opens” it, then transcriptional units are
exposed to code for specific proteins.

9. More on Hormone-Receptor
Binding
 The extent of a target cell’s activation
depends upon:
 Blood hormone levels
 Relative number of target cell receptors for
that hormone
 Sensitivity or strength of the union between
the hormone and the receptor

10. Hormone-Receptor Binding
 Upregulation: target cells form more
receptors in response to increasing
hormonal levels
 Downregulation: caused by prolonged
exposure to high hormone
concentrations, causes a desensitizing
of target cells so that they respond less
vigorously to hormonal stimulation

11. Steroid vs. Polypeptide
Hormones
 Polypeptide hormones are made up of
amino acids.
 Are not fat soluble and cannot pass the
sarcolemma, thus requiring a secondary
messenger to get their message to the cell
nucleus.
 Examples include growth hormone, leptin,
lutenizing hormone, and insulin.

12. Secondary Messengers and Non-
steroidal Hormones
 Non-steroidal hormone binds with a
receptor imbedded in the plasma
membrane.
 This reacts with the enzyme adenylate
cyclase.
 Adenylate cyclase interacts with ATP and
forms cyclic AMP.
 cAMP activates a protein kinase which then
activates a target enzyme to produce
changes in cellular function.

14. Factors That Determine
Hormone Levels
 Hormonal Stimulation: many hormones
influence the secretion of other hormones
 Humoral Stimulation: changing levels of
ions and nutrients in blood, bile, and other
fluids can influence hormone release
(increase in blood sugar leads to an
increase in insulin)
 Neural Stimulation: hormone release is
also affected by neural activity

15. Feedback Control of Hormone
Levels
 Negative feedback
 Positive feedback
 Cyclical variations

16. Feedback Control of Hormone
Secretion
 Negative Feedback:
 Release of the hormone has a negative
effect on its own release, this prevents
oversecretion of the hormone.
 The controlled variable is often the activity of
the target tissue. As a result, negative
feedback kicks in only when the target tissue
displays an appropriate level of activity.

17. Feedback Control, cont.
 Positive feedback:
 Rare, but in some instances the biological
action of a hormone causes additional
secretion of the hormone.
 This occurs until an appropriate
concentration is reached, at which point
negative feedback is initiated.
 Estrogen stimulates secretion of luteinizing
hormone (LH), which acts on the ovaries to
stimulate more estrogen, etc.

18. Feedback Control, cont.
 Cyclical variations:
 Some hormones are influenced by seasonal
changes, stages of development and aging,
daily cycle, or sleep.
 For example, growth hormone secretion is
increased during sleep.

20. Hormone Types
 Anabolic
 Adrenal

21. Primary Anabolic Hormones
 Testosterone
 Growth Hormone
 Insulin-Like Growth Factors

22. Testosterone
 Primary hormone that interacts with
skeletal muscle tissue. Number of
effects:
 Promotes growth hormone response in
pituitary which influences protein synthesis
 Can effect nervous system (interact with
receptors on neurons and increase
neurotransmitters)
 Can bind to skeletal muscle fiber nuclei to
result in protein synthesis

23. Control of Testosterone
 Hypothalamus releases gonadotropin-
releasing hormone (GnRH)
 GnRH stimulates the anterior pituitary
gland to release lutenizing hormone
(LH)
 LH stimulates the testes to produce
testosterone
 Negative feedback (too much
testosterone negatively effects LH
secretion)

24. Increasing Testosterone
Through Training
 Large-muscle group exercises
 Heavy resistance (85-95% 1-RM)
 Moderate to high volume (multiple sets)
 Short rest intervals (30-90 seconds)

25. Growth Hormone
 Secreted by anterior pituitary, effects
many tissues in the body.
 Works off negative feedback.

26. Effects of Growth Hormone
 Increased amino acid
transport across cell
membranes
 Increased protein synthesis
 Increased utilization of fatty
acids
 Increased fat breakdown
 Increased availability of
glucose and amino acids
 Decreased glucose utilization
 Decreased glycogen
synthesis
 Increased collagen synthesis
 Stimulate cartilage growth
 Increased retention of Nitrogen,
Sodium, Potassium, and
Phosphorus
 Enhanced immune function
 Increases renal plasma flow,
filtration, and hypertrophy

27. What Stimulates Growth
Hormone Secretion?
 Decreased blood glucose
 Decreased blood free fatty acids
 Starvation, protein deficiency (very
potent)
 Trauma, stress, excitement
 Exercise
 Testosterone, estrogen
 Deep sleep

28. What Inhibits Growth Hormone
Secretion?
 Increased blood glucose
 Increased blood free fatty acids
 Aging
 Obesity
 Growth hormone

29. Training and Growth
Hormone
 Growth hormone seems to respond best
to moderate repetitions (10-RM) and
moderate rest (60 seconds) (for males
and females).
 In fact, total amount of work done seems
to be more important than intensity
when it comes to growth hormone
release.

30. Craig and Kang (1994)
 Looked at hGH
release after :
 75% 1-RM (15 second
set)
 90% 1-RM (15 second
set)
 75% & 90% sets (reps
to failure at 75%, rest
3 minutes, reps to
failure at 90%)

31. Insulin-Like Growth Factors
 Mediate some of the effects of Growth
Hormone.
 Are secreted by the liver after the liver is
stimulated by Growth Hormone, they may
be released or found in other types of cells.
 May help to promote tissue repair and
recovery.
 Thought to stimulate satellite cell
proliferation during hypertrophy.
 Role in hypertrophy is controversial.

32. IGFs and the Skeleton
 Help to regulate functions of bone cells.
 In genetically altered mice,
overexpressing IGFs leads to increased
growth and longer tails (Yakar and
Rosen, 2003)
 In genetically altered mice, knocking out
IGFs leads to short bones, low BMD
(Yakar and Rosen, 2003)

33. Adrenal Hormones
 Cortisol
 Catecholamines

34. Cortisol
 Catabolic hormone, related to glycogen
stores (when they are low, cortisol is
increased to gain energy from protein).
 Major effects:
 Converts amino acids to carbohydrates
 Increases enzymes that break down protein
 Inhibits protein synthesis
 Anti-inflammatory
 Role in training not clearly understood
yet

35. Cortisol
 Thought to be an indication of overtraining,
but this may be exaggerated…
 Crewther et al (2011):
 9 nationally ranked Olympic lifters
 Five week study; high volume weeks vs. low
volume weeks
 Real competitions on weeks 2 and 5
 Simulated competitions on weeks 1 and 4

36. Crewther et al (2011)
 No relation between training volume and
cortisol
 Cortisol higher during real competitions
than simulated ones
 Relationship between cortisol level and
performance on simulated competitions
 Cortisol may be really important for
performance…

37. Cortisol Control
 Physical or mental stress stimulates the
anterior pituitary to release ACTH
(adreno-corticotropic hormone).
 ACTH tells the adrenal glands to
produce cortisol.
 Works off negative feedback, I.e. when
cortisol levels too high then ACTH
production is reduced.

39. Training’s Effects
 Acute: Post-exercise
 Chronic: Long-term adaptations

40. How Exercise Effects
Hormones...
 During and after an exercise session
 After a month of intense training (and
how training level influences hormonal
results)
 After 12 weeks of training
 As a result of different exercise
protocols

41. McCall, et al. (1999).
 Effects of exercise on
hormonal
concentrations.
 Values taken before,
1/2 way through, and
10 minutes post a
strength training
workout.

42. Fry, et al. (2000).
 Studied 22 participants in a
national junior-level
Olympic-style weightlifting
camp, 4 weeks in duration
 Each participant had placed
in the top three in their
weight class in national
competition

43. Fry, et al, cont.
 Training involved two phases:
 First week involved 3-4 sessions/day
 Weeks two through four involved 1-2
sessions/day
 Olympic-style lifting workouts, 70-100% of 1-
RM, sets of 1-5 reps
 Testing before and after week one, after
week four

44. Fry, et al, cont.
 Testing conducted around the following
session:
 15 vertical jumps (1/3 seconds)
 Snatch (1/15 seconds), add 5 kg each lift
until failure
 Snatch pulls, 3x10x65% 1-RM
 Blood drawn pre-exercise, 5 minutes post-
exercise, and 15 minutes post-exercise

45. Fry, et al, cont.
 Results:
 elite and non-elite
improved their total
(average of 1.6% for elite,
1% for non-elite)
 elite responded differently
hormonally to the high-
volume training than the
non-elite

46. Fry, et al, cont.
 Applications?
 Keep the limitations of this study in mind;
very small select sample size under very
specific conditions
 Indicates that the elite group tolerated the
high volume training better (smaller
hormonal response)
 Genetic, results of training, little bit of both?

47. McCall, et al. (1999).
 Studied 11 college-aged men.
 12 week strength training study,
3x/week, 8 exercises (4 for biceps
brachii) 3x10-RM, 1 minute rest.
 Took resting hormone measurements
before and after the 12 week study.

48. McCall, et al. (1999).
 Resting hormone concentrations don’t change
much after 12 weeks of strength training in this
study.
 Cortisol decreases, but little change on everything
else.

49. Smilios, I., et al. (2003).
 Studied 11 men with 2-8 years resistance training experience
 Looked into:
 How # of sets (2, 4, or 6) effects hormonal values after a
maximum strength, muscular hypertrophy, and strength
endurance protocol; and
 The hormonal response among the three protocols when
intensity, reps, and rest were kept constant

50. Smilios, et al. (2003)
 All 3 protocols used the following
exercises: bench press, lat pulldown,
squat, overhead press
Maximum Strength (MS) sets of 5 with 3’ rest; intensity
reduced on each set to allow 5 reps
to be completed (from 88% to
79.51% on 6th set)
Muscular Hypertrophy (MH) sets of 10 repetitions, 2’ rest;
intensity reduced from 75% to
58.94%
Strength Endurance (SE) sets of 15 repetitions, 1’ rest;
intensity reduced from 60% to 45.3%

51. Smilios, et al. (2003).
 Blood samples were drawn before, after,
after+15 minutes, and after+30 minutes
 Experimenters looked at lactate,
testosterone, growth hormone, and
cortisol

52. Lactate and Training
 Strength endurance produced the
highest lactate levels, followed by MH,
followed by MS.
 No real differences between 2, 4, or 6
sets on lactate production.

53. Lactate and Training, 4 sets
0
2
4
6
8
10
12
Lactate
SE
MH
MS

54. Testosterone and Training
 MS, MH, and SE did not differ on
testosterone concentrations.
 Concentrations were statistically no
different from control for MS, MH, SE for
2, 4, or 6 sets.

55. Growth Hormone and
Training
 Type of protocol effects growth
hormone:
 Higher for SE, followed by MH, followed by
MS
 4 sets seemed to yield the greatest release
of growth hormone

56. Type of Training and Growth
Hormone, 4 sets
0
2
4
6
8
10
12
14
16
18
20
hGH
SE
MH
MS

57. # of Sets and Growth Hormone,
MH Protocol
0
2
4
6
8
10
12
hGH
2 sets
4 sets
6 sets

58. Cortisol and Training
 Cortisol levels were highest for MH,
followed by SE, followed by MS for all
conditions except 2 sets (there
SE>MH>MS).
 Number of sets did not effect cortisol
levels

59. Applications?
 Reps/set and # of sets influences
hormonal response
 Training for MS will not have the same
type of hypertrophic response as
training with greater volume.

60. Acute vs. Chronic
Adaptations
 The body responds acutely.
 However:
 In as little as five weeks exercise stops
having an acute response.
 Suggests there is a need for variation.

61. Acute vs. Chronic
Adaptations
 There are no chronic changes in hormones in the
literature with the exception of a decrease in
resting cortisol levels.
 Reasons for this:
 Training may not be challenging enough.
Unlikely since subjects make gains.
 Training may not last long enough.
 There may not be changes to resting hormonal
levels from training. Suggest that acute training
drive’s the muscle’s response.