Nutritional Interventions to Stimulate Muscle Anabolism
897
sue remains in a catabolic state. Therefore, both
exercise and nutrition are required to allow muscle
to hypertrophy.
2. Nutrition and Muscle Protein Synthesis
Physical activity is the most powerful stimulus to
promote net muscle protein accretion. After a single
bout of resistance exercise, muscle protein synthesis
and degradation rates are elevated. As a result, net
muscle protein balance will remain negative in the
absence of food intake. Skeletal muscle hypertrophy
can only take place when food is ingested during the
early phases of post-exercise recovery.
[31]
Conse-
quently, carbohydrate and protein/amino acid inges-
tion during recovery from exercise forms an effec-
tive strategy to stimulate muscle protein synthesis,
inhibit protein degradation and, as such, to augment
net muscle protein accretion.
2.1 Carbohydrate
Pre-e
x
Post-e
x, pre-dr
ink
1st h post-dr
ink
2nd h post-dr
ink
3rd h post-dr
ink
PLA
CHO
*
40
20
0
20
40
Muscle phen
ylalanine balance
(nmol/min/100mL leg)
Fig. 1. Average net balance of phenylalanine (i) before exercise
(Pre-ex); (ii) after exercise, but before drink (Post-ex, pre-drink);
and (iii) during the first, second and third hour after ingestion of
drink (post-drink). Values are means
±
SE; n = 8 in each group
(reproduced from Borsheim et al.,
[36]
with permission). CHO = car-
bohydrate drink; PLA = placebo drink. *p < 0.05 vs placebo.
The ingestion of glucose during the post-exercise
recovery phase has been shown to significantly in-
covery does not stimulate translation initiation.
[41,42]
crease circulating plasma insulin levels.
[32-35]
The
Furthermore, ingestion of a complete meal (carbo-
latter has been shown to result in a decrease in
hydrate, protein and fat) has been reported to be
urinary 3-methylhistidine and urea excretion, sug-
more effective in stimulating post-exercise muscle
gesting that protein degradation is reduced.
[33]
How-
ever, muscle protein synthesis rates are not affected
protein synthesis when compared with feeding only
following carbohydrate ingestion.
[33,36]
Although
carbohydrate.
[42]
Recent human studies provide evi-
carbohydrate ingestion improves net leg amino acid
dence to suggest that insulin does not form a major
balance compared with water intake, the net balance
regulatory factor, and that amino acid availability
remains negative (figure 1).
[36]
represents the main stimulus for muscle protein syn-
The effects of carbohydrate supplementation on
thesis during resting conditions.
[43-45]
In a recent
protein metabolism have largely been attributed to
attempt to assess whether carbohydrate co-ingestion
the increase in circulating insulin concentrations. In
is required to maximise post-exercise muscle pro-
accordance, the elevation of plasma insulin levels
tein synthesis, we observed no surplus effect of
has been shown to increase net muscle protein an-
carbohydrate co-ingestion on post-exercise muscle
abolism in vivo in humans.
[16,37,38]
However, insulin
protein synthesis under conditions where ample
should not be regarded as a primary regulator of
amounts of protein are ingested.
[46]
Although carbo-
muscle protein synthesis as insulin exerts only a
hydrate co-ingestion does not seem to be required to
modest effect on muscle protein synthesis in the
maximise post-exercise muscle protein synthesis, it
absence of elevated amino acid concentrations.
[39]
is likely to assume that post-exercise carbohydrate
These observations are further supported by mea-
co-ingestion further inhibits muscle protein break-
surements in rodents (as reviewed by Kimball et
down rates, thereby improving net muscle protein
al.
[40]
), showing that merely an increase in circulat-
ing insulin concentration during post-exercise re-
balance.
[36]
©
2007 Adis Data Information BV. All rights reserved.
Sports Med 2007; 37 (10)
Study 