Key words
resistance exercise - lactate - anaerobic power - anaerobic metabolism - muscle adaption
Introduction
Resistance training represents a great strain for anaerobic energy metabolism. This
metabolic strain is an important prerequisite for muscle growth and adaption of
energy metabolism [1]. In various studies,
high-energy substrates, such as creatine phosphate (PCr) and adenylic acids (ATP,
ADP), were examined during strength exertion or strength training and significant
changes in concentration were observed during and immediately after exertion [2]
[3]. Other studies show the high burden on
anaerobic energy metabolism using lactate concentration [La+], which is
mostly considered post-load [4]
[5]
[6]
[7].
In the long term, regular strength training leads to the adaption of enzymes and
substrates of energy supply and muscle volume [7]
[8]
[9]
[10]
[11]. It has been shown, for example, that the
activity of anaerobic metabolism enzymes (lactate dehydrogenase (LDH), myokinase)
in
glycolytic muscle fibers is increased compared to oxidative fibers as a result of
chronic strength training. Takada et al. [2]
showed that the increases in inorganic phosphate (Pi) and adenosine
diphosphate (ADP) are associated with an increase in muscle volume following four
weeks of resistance training. Haun et al. [11]
determined increases in anaerobic energy metabolism enzymes (LDH,
phosphofructokinase (PFK)) through resistance training lasting several weeks.
Consequently, the energetic flow rate increases due to ATPs and an increased lactate
accumulation occurs with unchanged lactate elimination. Based on assumptions and
findings, metabolic stress is an important factor in muscle hypertrophy [1]
[7]
[11]. The studies suggest that increases in
muscle volume are associated with an adaption of the anaerobic energy
metabolism.
The rate of lactate accumulation (νLamax) (also known as the
glycolysis rate) can thus be regarded as an indirect measure of glycolysis activity
[12]
[13]. This rate can be determined based on the
acute increase in [La+] as a result of the load as a function of the load
time (tload). Thus, the activity of glycolysis can be estimated quite
simply on the basis of the change in [La+] as a function of the
tload and show the metabolic stress. This measure describes the
efficiency of the anaerobic energy metabolism, which increases significantly during
strength training and is dependent on movement speed [14]. Good reproducibility of
νLamax was shown during isokinetic force loading as well as
sprint loading [15]
[16]. The adaptation of the
νLamax has been examined in endurance studies. So far, only
one study is available that shows a reduction of νLamax following
endurance training that lasted several weeks [17]. This study compared sprint interval (SIT) training with continuous
endurance training (CET) and showed that after 6 weeks SIT, there was a significant
reduction in the νLamax. This remained unchanged at CET. The
adaptation of the νLamax through resistance training lasting
several weeks has not yet been investigated.
In resistance training, protocols are generally used that contain different exercise
volume load (volume load=set×reps×load; e. g.,
2500=5 sets×10 reps×50 kg; load based in% of 1RM)
[18]
[19]. The comparison of training protocols
showed that high-volume training causes significantly higher lactate concentrations
compared to low volume with high load after the exertion [20]
[21]. After an 8-week resistance exercise
period, Mangine et al. [20] did not observe a
change in [La+] immediately after the last exercise session in a high-volume
and a strength protocol. This [La+] is the result of the acute load and does
not show the efficiency of the anaerobic glycolysis.
With a focus on muscle volume, a few studies examined volume following resistance
training with different volume loads. For example, the impact of volume load in
resistance exercise was examined [22]. A
high-load protocol of 3 sets of 10 reps at 75% of 1 RM was compared with a
low load of 4 sets of reps until failure at 30% 1 RM on pectoralis major and
triceps brachii hypertrophy. The resistance training lasted 6 weeks with 3 training
days per week. The results showed that both resistance training protocols had
comparable muscle cross section increases. An another study by Schoenfeld et al.
[23] examined different training volumes
with a strength training protocol (7 sets, 3 reps at 3 RM) and a hypertrophy
training program (3 sets, 10 reps at 10 RM) over 8 weeks (3×weekly). The
results showed comparable increases in muscle thickness in the biceps brachii in
both groups. Both studies showed no significant impact on muscle hypertrophy at
different volume loads. However, adaptations of the energy metabolism based on
νLamax have hardly been considered in this context. If
metabolic stress is important for muscle hypertrophy, it would be helpful to know
how the metabolic measure νLamax adapts through resistance
training at different volume loads.
Based on the available studies, it is assumed that resistance training over several
weeks leads to a change in glycolytic enzymes and [La+] in the afterload. No
statements can be made about the changes in the νLamax caused by
resistance training. The aim of this study was to investigate the effect of 6 weeks
of resistance training with different training volumes load on
νLamax. If changes in νLamax are
associated with changes in performance from strength training over several weeks,
the νLamax could be an important parameter of anaerobic
performance in resistance training. It may be possible to assess metabolic
adaptations with varying training volumes in strength training using
νLamax.
Materials and Methods
Experimental design and subjects
After receiving information and giving written consent to participate in the
study, 24 healthy male strength-trained subjects were assigned to one of two
groups (high-volume, low-load=HVLL, low-volume, high-load=LVHL)
with different training volume loads. HVLL (n=14; age 25.0±4.3
years; height 179.7±7.1 cm; body mass 83.6±11.0 kg; body mass
index 25.9±3.1 kg m-²) trained at 50% of the
1RM with 5 sets and reps up to muscle failure. The subjects in LVHL
(n=10; age 24.6±2.8 years; height 178.1±6.0 cm; body
mass 80.5±11.2 kg; body mass index 25.4±3.3 kg
m-²) trained at 70% of the 1RM with 5 sets of 10
reps. All test subjects were free of injuries and chronic diseases. Furthermore,
all subjects had more than 2 years of training experience and had a training
scope of 1 to 4 training units per week at the beginning of the study. The
training scope ranged from 1.5 up to 5.0 hours per week. The study meets the
ethical standards in sports and exercise science and was approved by the local
ethical committee (V-361-17-HSch-νlamax-12122019) [24].
Measurements
Before the intervention, anthropometric data and the one repetition maximum (1RM)
were recorded. A maximum isokinetic strength test (Con-Trex® Multi Joint
System, Physiomed, Schnaittach, Germany) was performed before and after the
intervention to determine anaerobic performance and capacity. A concentric
isokinetic strength test was carried out with an ankle velocity of
180°s−1 and 10 reps (15 s load time). The maximum
(Pmax) and mean maximum power (meanPmax, mean of ten
reps) of the thigh extensors and flexors were evaluated. Pmax was
standardized to body mass.
To determine the lactate concentration [La+], capillary blood samples
(20µl) were taken from the earlobe before [La+]pre,
immediately after exercise, and up to the ninth minute post-exercise (up to the
third minute at 30-second intervals, from the third to the ninth minute at
60-second intervals). The calculation of the maximum glycolysis rate
(νLamax) was based on the pre-load lactate concentration
[La+]pre, maximum lactate concentration in the post-load
[La+]max, the loading time (tload), and the
alactic time interval of 3 seconds [13]
[25]. The reproducibility of the maximum
glycolysis rate by an isokinetic strength test showed a high correlation of
r>0.67 [15].
Intervention
Two to five days before the training intervention, the 1RM was recorded to
calculate the training load for each exercise [26]. Both groups trained their lower extremities 3 times a week for 6
weeks. The strength training program was carried out on sequential machines
(Gym80, Gelsenkirchen, Germany). The exercises consisted of leg press (LP), leg
extension (LE) and leg flexor (LC, in the prone position) sets and were
performed bilaterally in random order. Both training groups performed 5 sets
each with a break of 90 seconds between series. HVLL completed the maximum
possible number of repetitions until local muscle failure at 50% of the
1RM. LVHL completed 5 sets of 10 repetitions each at 70% of the 1RM.
There was a regeneration period of 24 to 48 hours between each training day. The
exercise sessions were observed by a practiced coach.
The absolute exercise volume load (EV) was calculated from the product of the
training weight (load) and the number of repetitions (rep), which was then
summed up over all sets and training sessions (TS) [19]. At relative EV (per TS), the total EV
was relativized to TS.
Statistical analysis
The arithmetic mean (mean), standard deviation (±SD), minimum (MIN), and
maximum (MAX) were calculated for all data (Microsoft Excel Version 16.0;
Microsoft, Redmond, WA, USA). The inferential statistical analysis was performed
using IBM SPSS Statistics Version 22 (IBM Corp., Armonk, NY, USA). The test for
normal distribution was performed using the Shapiro Wilk test. Homoscedasticity
was checked using Levene’s test. If the test requirements were met, the
training group and training time were checked for significant effects on the
dependent variables using two-way variance analysis. If the requirements for a
parametric test were not met, a Friedman test was used to check for significant
main effects. Comparisons between the two groups were then made using the
Mann-Whitney U test. Pre-post comparisons within the group were performed using
a dependent t-test and Wilcoxon’s test. The effect sizes were determined
for pre-post comparisons using Cohen’s d (d). η2 was
used as an effect measure in variance-analytical comparisons. The interpretation
of effect size’s based on [27].
The test power for νLamax was determined post-hoc
(G*Power, Version 3.1.9.2; Düsseldorf, Germany). Correlation
analyses using Spearman (no normal distribution) were used to check for changes
in performance associated with changes in νLamax. The level
of significance was set at p≤0.05.
Results
There were no significant differences in anthropometric data or performance between
the two training groups before the training intervention (p>0.05). The
training frequency (TF) after six weeks was 17.07±1.27 (94.9%) in
HVLL and 16.8±2.35 (93.3%) in LVHL (p=0.841). The relative
EV was 10868±2960 kg for HVLL and 4908±1989 kg for LVHL
(p=0.000; d=2.286). HVLL had an approximately 2.2 times higher EV
compared to LVHL. In HVLL, this resulted in 18.43±2.93 (13.91–25.92)
reps per set and exercise. The LVHL group always completed 10 reps per set and
exercise.
A significant time effect of νLamax was observed after 6 weeks of
strength training (p=0.032; d=0.974;
ηpart²=0.192). νLamax showed
an increase from 0.262±0.092 to 0.295±0.075
mmol·l−1·s−1 ([Fig. 1]). In HVLL, νLamax
increased significantly (p=0.022; d=0.406), but in LVHL the increase
of νLamax was not significant (p=0.233; d=0.384).
A significant group effect on νLamax could not be determined
(p=0.650; d=0.201;
ηpart²=0.010).
Figure 1 Pre-Post comparison of the mean values for
νLamax. left means of both groups, right means of
group HVLL and LVHL (error bars show the standard deviation)
The [La+]pre showed no significant differences between pre-test
and post-test in either group (p>0.05). [La+]max showed a
significant time effect (p=0.001; d=0.685;
ηpart²==0.376). The maximum lactate
concentration increased from 3.85±0.965 mmol l−1 to
4.45±0.771 mmol l−1. [La+]max
increased significantly in HVLL (p=0.012; d=0.410;
ηpart²=0.042) and in LVHL (p=0.039;
d=1.03; ηpart²=0.212). A significant
group effect was not observed for [La+]max (p=0.130;
d=0.652; ηpart²=0.096).
The isokinetic strength test showed significant time effects of mean Pmax
(p=0.000; d=2.268), relative mean Pmax (p=0.004;
d=1.436), Pmax (p=0.000; d=2.016), and rel
Pmax (p=0.004; d = 1.436). There was no
significant group effect (p>0.05; d<0.4). Significant increases in
the parameters of the isokinetic strength test were found within groups
(p<0.05) ([Table 1]). HVLL showed a
significant increase in mean Pmax (p=0.002; d=0.370),
relative mean Pmax (p=0.008; d=0.445), Pmax
(p=0.004; d=0.314) and relative Pmax (p=0.015;
d=0.335). LVHL also showed a significant increase in mean Pmax
(p=0.010; d=0.357), relative mean Pmax (p=0.008;
d=0.421), Pmax (p=0.027; d=0.361) and relative
Pmax (p=0.009; d=0.440).
Table 1 Result of pre-test and post-test for all estimated
parameters. Data are presented as mean±standard deviation
(min-max).
|
HVLL
|
LVHL
|
|
Pre
|
Post
|
Pre
|
Post
|
|
meanPmax (W)
|
385.1±74.0
|
416.5±94.6*
|
378.8±169.5
|
434.5±141.5+#
|
|
(298.8–552.1)
|
(298.1–641.2)
|
(156.2–755.9)
|
(304.4–764.9)
|
|
relative mean Pmax (W·kg−1)
|
4.60±0.59
|
4.90±0.75*
|
4.68±1.77
|
5.35±1.39*#
|
|
(3.73–5.54)
|
(3.86–6.00)
|
(3.73–5.54)
|
(1.80–3.71)
|
|
Pmax (W)
|
424.3±80.2
|
452.3±97.5*
|
405.6±173.2
|
462.2±138.7+~
|
|
(342.3–584.8)
|
(329.2–686.6)
|
(190.7–797.2)
|
(330.7–780.0)
|
|
relative Pmax (W·kg−1)
|
5.08±0.69
|
5.33±0.80*
|
5.01±1.77
|
5.70±1.34*#
|
|
(4.04–6.26)
|
(4.26–6.43)
|
(2.20–8.17)
|
(4.02–8.03)
|
|
[La+]pre
(mmol·l−1)
|
0.59±0.17
|
0.68±0.18
|
0.96±0.22
|
0.94±0.34
|
|
(0.50–1.90)
|
(0.55–1.53)
|
(0.60–1.33)
|
(0.50–1.51)
|
|
νLamax
(mmol·l−1·s−1)
|
0.271±0.067
|
0.298±0.067*
|
0.249±0.122
|
0.291±0.089~
|
|
(0.133–0.371)
|
(0.196–0.421)
|
(0.034–0.465)
|
(0.104–0.402)
|
|
[La+]max
(mmol·l−1)
|
4.03±0.859
|
4.4±0.887*
|
3.61±1.09
|
4.53±0.611*~
|
|
(2.21–5.16)
|
(2.95–6.05)
|
(1.54–5.33)
|
(3.7–6.09)
|
*pre vs. post: p<0.05 by
t-test; + pre vs. post p<0.05
by Wilcoxon test; ~ time effect for both groups by ANOVA; # time
effect for both groups by Friedman test.
A correlation analysis showed that there was a significant correlation between
Pmax and νLamax prior to the training intervention
in LVHL (r=0.716; p=0.02). This was not found in HVLL
(r=0.189; p=0.521). In addition, a significant correlation between
ΔνLamax and ΔPmax was found across
all subjects (r=0.502; p=0.012).
Discussion
The aim of this study was to investigate the effect of 6 weeks of resistance training
with different training volume loads on νLamax. The
νLamax showed a significant time effect, but a significant
group effect was not found. The increases in performance were in a mean linear
relationship to the adaptation of the anaerobic energy metabolism using the
νLamax. Thus, νLamax as a physiological
measure of anaerobic energy metabolism seems to be a significant performance
parameter.
We presume that the significant performance increases in the isokinetic strength test
are the result of more activated muscle fibers [28]. The higher number of active muscle fibers results in greater
anaerobic activity, as shown by the post-test increases in [La+]. Hommel et
al. [17] found a significant reduction of
νLamax after 2 weeks in sprint interval training, which was
stabilized up to sixth week with increased maximal performance; oxygen uptake
(VO2max) was unchanged. The extent to which the resistance training
changed the VO2max cannot be answered, because the maximal oxygen uptake
was not measured here. Ozaki et al. showed in an overview that changes in
VO2max due to resistance exercise lasting several weeks were only
available for untrained subjects [29]. There
were inconsistent results in relation to the training volume. In part, no changes
but also slight increases in VO2max were found. Furthermore, no
significant change in mitochondria enzyme activity (e. g., citrate synthase
and succinate dehydrogenase) was reported following RT, which has the potential to
increase VO2max [[30]
[31]. Due to the design of our study, it is
not clear which temporal dynamics the adjustment of the maximum glycolysis rate has
during the training period. This would have required measurements of anaerobic
performance at intervals of one or two weeks.
In a six-week study with resistance training, muscle biopsy analyses showed
adaptations of the anaerobic energy metabolism and hypertrophy of the muscle fibers.
Numerous enzymes of the lactacid energy metabolism (e. g., PFK, LDH)
increased their activities [11]. It is assumed
that the higher activity of anaerobic enzymes causes an increase in glycolysis
activity. This then results in a time-dependent increase in the maximum glycolysis
rate. For muscular work, this means more available ATP over the loading period. An
increase in glycolytic enzymes is a possible explanation for the increased maximum
glycolysis rate after the training intervention in both groups. However, the
increases in glycolytic enzymes, such as PFK, appear to be only marginally caused
by
chronic strength training [10]
[32]. Oxidative and therefore also metabolic
stress is considered relevant for hypertrophic muscle adaptation [33]. However, it is important to point out that
other factors are also of high importance for muscle hypertrophy. These include the
influence of amino acids intake, growth hormone concentrations, and mechanical
stress [34].
There was a high effect size (d=0.97) of resistance training on
νLamax for both groups (all subjects). Within both groups,
this was considered a medium effect (d=0.38 – 0.40). Statements
about which training protocol is more effective in increasing anaerobic performance
cannot be made at present. No significant differences between groups were found for
νLamax. The post hoc power analysis showed that a
variance-analytical comparison between the two groups would have required more than
500 subjects (for p-value of 0.05; d=0.2) to show significant differences.
The data show that there was a high dispersion of νLamax within
LVHL, which indicates a heterogeneous study cohort. A more homogeneous subject
cohort may also have resulted in a significant increase in group LVHL. Scott et al.
[19] pointed out that heterogeneous
subjects in a resistance exercise protocol are problematic. Subjects can certainly
be selected based on their training status; an assignment based on glycolysis
activity currently seems difficult to us.
There are currently no studies that directly examine the effects of resistance
training on νLamax. However, acute studies show that lower loads
with exhaustive reps lead to significantly higher metabolic stress (lactate
concentration) than higher loads with few reps [35]. It was also shown that higher reps (5 sets of 10 reps) compared to
lower reps (10 sets of 5 reps) at the same load also lead to increased metabolic
stress. This was reflected in a stronger reduction of ATP and PCr. The significantly
higher [La+] at 5 sets of 10 reps indicates the increased stress on
glycolytic enzymes [36]. A training experiment
at 70% of 1RM (with high volume) and 90% of 1RM (with low volume)
led to similar results [21]. In this training
study, the strong [La+] increases found in acute studies at high EV did not
lead to significantly different adjustments of νLamax between EV.
The variations in load and volume used here are not directly comparable with
existing studies. In order to clearly show the influence of the volume load, loads
above 70% of the 1RM and below 50% of the 1RM in the other group
should have been chosen.
The increases in Lamax due to training interventions are possibly the
result of increased glycolysis and have already been noted in previous studies [37]. If we presume that training-related
changes in anaerobic enzymes occur only to a small extent [10], it cannot be ruled out that untrained
volunteers would have shown more marked adjustments to νLamax.
Lactate as an intermediate product of glycolysis and its change in [La+]
over the tload is considered here in this highly intensive anaerobic test
(maximum one-legged strength test) as a measure of glycolysis activity. Adjustments
of the anaerobic enzyme activities that regulate [La+] can only be
speculated in this study. In the future, a 31phosphorus -magnetic
resonance spectroscopy (31P-MRS) may help show concentrations of energetic
substrates before and after several weeks of training. It should also be mentioned
that lactate concentrations determined from capillary blood are dependent on the
time constant of elimination. Furthermore, the lactate formed in the muscle is
transported through different compartments [38]. Thus, the lactate concentrations determined from capillary blood
will be lower than the acute reactions produced by the test in the muscle under
stress [39]. Furthermore, there was no control
of food intake in this study, there may be influences of increased or reduced
glucose intake on [La+] [40].
Conclusions
Based on the available data, six weeks of resistance training of the lower
extremities can increase anaerobic performance using the glycolysis rate. Effects
of
the volume load could not be determined. Thus, the effectiveness of training
protocols with high or low training-volume loads on νLamax cannot
yet be assessed.
Funding
This research received no external funding.
