
























































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































ANNALES KINESIOLOGIAE • 6 • 2015 • 2

93

AN OVERVIEW OF TRAINING METHODS THAT PROMOTE 
THE HIGHEST LIPID OXIDATION DURING AND AFTER A 

SINGLE EXERCISE SESSION

Barbara PURKART1, Boštjan ŠIMUNIČ2, Mitja GERŽEVIČ2

1Physiotherapy Centre Barbara Purkart k.d., Ulica Gradnikove brigade 8, 1000 Ljubljana, 
Slovenia 

2University of Primorska, Science and Research Centre, Institute for Kinesiology Research, 
Garibaldijeva 1, 6000 Koper, Slovenia

Corresponding author:
Mitja GERŽEVIČ

University of Primorska, Science and Research Centre, Institute for Kinesiology Research, 
Garibaldijeva 1, 6000 Koper, Slovenia

Tel.: +386 5 663 58 05, +386 5 663 77 31
e-mail: mitja.gerzevic@zrs.upr.si

ABSTRACT

Given that physical activity is the most effective way to increase lipid oxidation, its 
effects are influenced by several factors. The goal of this review was to identify the most 
effective methods that facilitate the highest lipid oxidation during and after a single exer-
cise session. For this purpose, the available scientific literature was examined using Pu-
bMed, Web of Science, Google Scholar and Cochrane Library databases up to June 2013 
with the following keywords: excess post exercise oxygen consumption, exercise fatty 
acid, energy expenditure exercise and interval training. From the identified 48,583 poten-
tially relevant references, 172 of them met all the required criteria. It was found out that 
prolonged (> 30 min) moderate intensity (55 − 70 % VO2max) exercise such as walking, 
jogging or cycling is the most effective way to increase lipid oxidation during and after a 
single exercise session. Low-volume high-intensity interval exercise is supposed to be as 
effective as traditional exercise with continuous endurance, with the main effect on lipid 
oxidation after the session and similar long-term metabolic adaptations. However, more 
research is still needed to compare the effects of regular resistance exercise with traditio-
nal endurance and high-intensity interval exercise. Finally, nutrition is also a significant 
factor since food rich in fat and low in carbohydrates promotes greater lipid oxidation.

Keywords: endurance exercise, interval exercise, training, nutrition, fatty acid, tri-
acylglycerol.

review article                    UDC: 796.015:613.2
received: 2015-08-07

mailto:mitja.gerzevic@zrs.upr.si


94

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

PREGLED VADBENIH METOD, KI SPODBUDIJO NAJVEČJO 
OKSIDACIJO LIPIDOV MED IN PO POSAMEZNI VADBENI ENOTI

IZVLEČEK

Glede na to da je gibalna oz. telesna aktivnost najbolj učinkovit način povečanja 
oksidacije maščob, pa na njihovo porabo vpliva še vrsta drugih dejavnikov. Cilj tega 
preglednega članka je bil ugotoviti vplive in najbolj učinkovite metode za spodbujanje 
oksidacije maščobnih kislin med vadbeno enoto in po njej. Pregledali smo razpoložljive 
članke, ki so bili objavljeni do junija 2013 v sledečih bazah: PubMed, Web of Science, 
Google scholar in Cochrane Library. Pri iskanju smo uporabili naslednje ključne be-
sede: poraba kisika po vadbi, poraba maščobnih kislin med telesno aktivnostjo, poraba 
energije med telesno aktivnostjo in intervalni trening. Tako smo dobili 48.583 člankov, 
od katerih je našim kriterijem ustrezalo 172 člankov. Ugotovili smo, da je dolgotrajna 
telesna aktivnost srednje intenzivnosti, kot sta hoja in lahkoten tek, najbolj učinkovit 
način za povečevanje oksidacije maščobnih kislin. Visokointenzivna intervalna vadba 
je bolj učinkovita s stališča porabe energije, vendar pri enaki porabi maščobnih kislin. 
Potrebnih bo še nekaj nadaljnjih raziskav, ki bodo primerjale učinke redne vadbe za 
moč ter redne klasične aerobne in intervalne vadbe za razvoj vzdržljivosti. K večji oksi-
daciji maščobnih kislin pomembno vpliva tudi prehrana: hrana, bogata z maščobami in 
z nizko vsebnostjo ogljikovih hidratov, najbolj vzpodbuja oksidacijo maščobnih kislin. 

Ključne besede: vadba vzdržljivosti, intervalna vadba, trening, prehrana, maščob-
ne kisline, triglicerol

INTRODUCTION

Two of the greatest health threats in modern lifestyle are imbalanced nutrition and 
a sedentary lifestyle. Excessive diet and an increased sedentary lifestyle lead to obe-
sity and metabolic syndrome which are both associated with numerous comorbidities 
(Poirier et al., 2006). An excessive carbohydrate intake, especially fructose, leads to 
an increase in body weight, visceral adipose tissue, muscle fat, as well as liver fat; 
furthermore, sugar enhances lipogenesis and the production of uric acid including an 
increase in plasma triacylglycerols (TG) concentrations (Bray, 2013). Lipids are im-
plicated in the pathogenesis of several common human diseases, including: metabolic 
syndrome, cardiovascular disease and type 2 diabetes (Kiens, 2006). Enhanced lipid 
oxidation might be beneficial for counteracting lipid accumulation. Physical activity 
(PA) is the most effective way to increase lipid oxidation, due to the fact that it incre-
ases the metabolic rate (Kiens, Alsted, & Jeppesen, 2011). During PA the body has a 
higher energy demand. The body provides energy for PA converting chemical energy 



ANNALES KINESIOLOGIAE • 6 • 2015 • 2

95

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

to mechanical energy and heat. This chemical energy is derived from macronutrients 
(carbohydrates, proteins and lipids) in the body and converted to adenosine triphospha-
te (ATP) energy molecules, which are used for work. Depending on the intensity and 
the duration of PA, different metabolic pathways provide energy: ATP-phosphocreatine 
(PCr) system, anaerobic glycolysis and aerobic glycolysis with carbohydrate, protein 
and lipid oxidation (Frayn, 2010; McArdle, Katch, & Katch, 2010). Normally, during 
prolonged low- to moderate- PA intensities (33 − 65 % of maximal oxygen consumpti-
on − VO2max), lipids metabolised at the highest rate, reaching their maximum at ~64 ± 
4 % VO2max, whereas, at higher intensities, carbohydrates become the primary energy 
source (Achten, Gleeson, & Jeukendrup, 2002; Pérez-Martin et al., 2001). The type 
of energy source used depends on several factors, not just intensity, but also duration 
and the type of PA (Antonutto & di Prampero, 1995), gender, aerobic fitness, nutrition 
(Kiens, 2006), substrate availability within skeletal muscles (Jeppesen & Kiens, 2012; 
Kiens et al., 2011), amount of fatty tissue and the neuro-hormonal influence on the 
oxidation (Astrup et al., 1992; Mittendorfer, Fields, & Klein, 2004). However, during 
PA, the lipid used for energy turnover is derived from different sources (Kiens, 2006; 
Kiens et al., 2011): blood fatty acids bound to albumin, fatty acids liberated from the 
hydrolysis of circulating TG and fatty acids from lipolysis of TG located in lipid dro-
plets in skeletal muscles – muscle TG. 

Given that endurance PA is the most effective way to increase lipid oxidation (Kiens 
et al., 2011), its effects are influenced by several factors, and because different types of 
interval training and resistance exercise are used and promoted in sport and kinesiology 
practice, it will be the goal of this review to identify what are the influences and which 
are the most effective methods for facilitating the highest lipid oxidation during and 
after a single workout. 

METODHS

For the purposes of this review, the available articles in PubMed, Web of Science, 
Google Scholar and Cochrane Library were analysed up to June 2013. The following 
keywords were used for searching: excess post exercise oxygen consumption, exercise 
fatty acid, energy expenditure exercise and interval training. This search strategy iden-
tified 48,583 potentially relevant references, while only 172 articles met all the search 
topic requirements.

LIPID OXIDATION DURING ENDURANCE PHYSICAL ACTIVITY 

The factors influencing lipid oxidation during endurance physical activity are: in-
tensity, duration and type of PA, food intake, amount of fatty tissue, gender and physi-
cal fitness.



96

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

Effect of Intensity on Lipid Oxidation during Activity

PA can be divided into low-, moderate-, and high- intensity activities. In literature, 
boundaries between these levels are not strictly defined and they range from up to 55 % 
VO2max for low-intensity, from 55 % to 70 % VO2max for moderate-intensity, and excee-
ding 75 % VO2max for high-intensity PA. During low and moderate-intensity endurance 
PA, the predominant energy sources are lipids (Pillard et al., 2010). Lipid oxidation 
during high-intensity PA is lower than during moderate-intensity (Jeppesen & Kiens, 
2012). At the beginning of the previous century, it was discovered that by measuring the 
respiratory exchange ratio (RER), which is the ratio between eliminated CO2 and utili-
zed O2 during respiration, it is possible to determine also the type of energy source used 
(Scott, 2005). If RER is around 1, the body uses carbohydrates, while if it is between 
0.7 and 0.8, the body uses more lipids (Walsch, 2003) for energy transfer. By measuring 
RER, it was discovered that lipid oxidation increases from rest to an intensity level of 
65 % VO2max. Lipid oxidation during endurance PA that lasts from 60 to 90 min increases 
by 5 to 10 times (Krogh & Lindhard, 1920, in Jeppesen & Kiens, 2012; Cristensen & 
Hansen, 1939, in Jeppesen & Kiens, 2012). Further studies using RER measurements 
and monitoring of isotopes have confirmed the highest oxidation of lipids during mo-
derate-intensity endurance PA, namely, at the intensity level of 65 % VO2max, compared 
to low-intensity (25 % VO2max) and high-intensity (85 % VO2max) (Romijn et al., 1993). 
With the increased intensity of PA, lipid oxidation decreases. During 30 minutes of 
cycling, for example, at the intensity level of 75%, lipid oxidation is lower than at the 
intensity level of 55 % VO2max (van Loon et al., 2001). Even though, it has been known 
for almost a century that a total amount of oxidised fatty acids during high-intensity 
PA is lower than during moderate-intensity PA, the mechanisms behind this are still not 
clear. The limiting factor of fatty acid oxidation during the transition from rest to low or 
moderate-intensity PA is most probably the transport of fatty acid through the sarcolem-
ma (Bonen, Luiken, Arumugam, Glatz, & Tandon, 2000; Jepessen et al., 2011). When 
considering transition from moderate to high intensity PA, some earlier authors argue 
that oxidation of plasma fatty acids, lipoprotein derived TGs and muscular TGs proba-
bly decrease due to unavailability of free carnitine and / or decrease in the intracellular 
pH, but not as a consequence of a decrease in plasma free fatty acids availability (van 
Loon, Greenhaff, Constantin Teodosiu, Saris, & Wagenmakers, 2001). Modern studies 
prefer the notion that the availability of free carnitine in blood is the sole factor limiting 
the transport of fatty acids to the mitochondria in the muscle (Roepstorff et al., 2005; 
Kiens et al., 2011; Jeppensen & Kiens, 2012). When considering lipid oxidation during 
endurance PA, moderate intensity is shown as the most effective from the point of hig-
hest lipid oxidation during PA.



ANNALES KINESIOLOGIAE • 6 • 2015 • 2

97

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

Effects of Duration and Type of Activity on Lipid Oxidation during Activity

The type of energy source used during PA is not determined only by intensity level 
(as described above), but also by duration and type of PA. Phosphagens (adenosine 
triphosphate and creatine phosphate) are used during the first 5 to 10 seconds of maxi-
mum PA, followed by (rapid) anaerobic glycolysis, if maximum effort continues be-
yond 10 seconds (obviously the intensity decreases). At this stage, glycolysis maintains 
the energy transfer up to 2 or 3 minutes, with the glycogen in the muscle as the main 
energy source (McArdle et al., 2010). When intense exercise continues beyond several 
minutes, aerobic metabolism provides nearly all of the energy transfer. At this point, 
fat becomes the primary energy fuel and lipid oxidation the primary process of energy 
transfer for exercise and recovery when high-intensity, long-duration exercise depletes 
glycogen (McArdle et al., 2010) or when carbohydrates sparing and promotion of fat 
utilization occur as a training adaptation (Åstrand, Rodahl, Dahl, & Strømme, 2003; 
Fox & Mathews, 1981). 

There are various lipids sources. During moderate-intensity PA, less than a half of 
lipids is derived from upper-body subcutaneous adipose tissue, a quarter comes from 
muscular TGs, and the rest is distributed among fatty acids from lower-body subcutane-
ous adipose tissue, intra-abdominal adipose tissue, plasma TGs and other (Horowitz, 
2003). If PA is so intense or long that glycogen stores are exhausted, the energy de-
rived from glycogen breakdown is supplemented by the breakdown of proteins (Kis-
ner & Colby, 2007). Nonetheless, the total energy expenditure of jogging exceeds that 
of walking (Wilkin, Cheryl, & Haddock, 2012), fractional lipid oxidation remains at 
comparable levels, since the respiratory exchange ratio does not demonstrate a discern-
ible pattern between walking and running (Stamford, 1975), meaning that carbohydrate 
and lipid oxidation increase simultaneously. At same relative intensity, expressed in 
per cent of VO2max, lipid oxidation is significantly higher while running compared to 
cycling (Capostagno & Bosch, 2010), also, more energy is being utilised (Zeni, Hoff-
man, & Clifford, 1996; Kravitz, Robergs, Heyward, Wagner, & Powers, 1997). When 
considering lipid oxidation, moderate intensity activity has to last at least 20 minutes to 
begin utilising lipids. The upper limit is dependable on individual body’s glycogen stor-
age capacity, to avoid undesirable protein depletion. Jogging and walking are shown to 
be more effective at lipid oxidation than cycling. 

Effects of Food Ingestion on Lipid Oxidation during Activity

The ingested food has also an effect on lipid oxidation as muscles adjust the levels 
of muscle enzymes depending on the food ingested (Spriet, 2011). In addition, most 
liver enzymes, which regulate glycolysis and fatty acid oxidation, are also regulated by 
nutrient availability (Rui, 2014). A 7-week diet, rich in fats, increases muscles’ ability 
to metabolized lipids, by increasing activity of enzymes and binding proteins, invol-
ved in the process of fatty acid oxidation in the muscle (Helge & Kiens, 1997; Kiens, 



98

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

2006). When untrained men were consuming fat rich diet for three days leading up to 
a moderate-intensity PA (cycling at an intensity of 70 % VO2max), lipid oxidation was 
significantly higher, compared to when they consumed a diet rich in carbohydrates 
(Christensen & Hansen, 1939, in Kiens et al., 2011). In the study performed by Galbo, 
Holst, and Christensen (1979), seven untrained men ran on a treadmill at 70 % VO2max 
intensity until exhaustion. Four days prior to the PA they were consuming carbohydrate 
and fat rich diets respectively. When they consumed fats, their glucagon, epinephrine, 
cortisol and growth hormone levels rose significantly compared to the carbohydrate 
diet. Food consumption in the days leading up to the PA affected not only their bodies’ 
energy stores, but also their hormone reaction, directly affecting their oxidation during 
PA. Food rich in carbohydrates, on the other hand, promotes oxidation of glucose, pro-
duction of lactate and inhibits oxidation of lipids (Galbo et al., 1979). A more recent 
study by Helge found once again a significantly greater lipid oxidation in the group that 
consumed fat rich diet (Helge, Richter, & Kiens, 1996; Helge, Wulff, & Kiens, 1998). 
Measuring exhaustion time parameters at the same absolute workload showed that en-
durance performance was enhanced similarly after both two and four weeks of adap-
tation to training and a fat-rich or a carbohydrate-rich diet (Helge et al., 1998). Helge, 
Watt, Richter, Rennie, and Kiens (2001) also demonstrated that circulating TG made a 
significant contribution to fuel utilization during endurance training after adaptation to 
a fat-rich diet. The increased lipid oxidation observed after training (cycling 60 to 75 
minutes per session at 65 to 85 % VO2max, four times per week, seven weeks) and fat 
diet adaptation originated from both a higher plasma fatty acid oxidation and utilization 
of circulating TG. In contrast, the carbohydrate sparing observed after fat diet adaptati-
on was due to muscle glycogen sparing and not to a diminished plasma glucose uptake 
(Helge et al., 2001). A longer-term adaptation to a fat-rich diet also leads to measurable 
changes in the capacity to recruit, transport and oxidize lipids (Helge & Kiens, 1997). 

Another physiological process that increases lipid oxidation is starvation (Cahill, 
2006). In the fasted state, fatty acids are oxidized mainly in the mitochondria to ge-
nerate energy supply as well as ketone bodies (Rui, 2014). Free fatty acid levels were 
increased approximately 9-fold after 60 h of fasting in healthy male subjects, leading to 
elevated muscular TG levels and decreased muscular insulin sensitivity (Hoeks et al., 
2010). Despite an increase in whole-body lipid oxidation, Hoeks et al. (2010) observed 
a reduction in mitochondrial capacity. Van Proeyen, Szlufcik, Nielens, Ramaekers, and 
Hespel (2011) investigated the effect of endurance training in the fasted state vs. trai-
ning in the fed state on muscle oxidation and substrate utilization. They found out that 
moderate-intensity endurance training on an empty stomach significantly stimulates 
muscle cells to increase lipid oxidation and facilitate utilizing muscular TGs, compa-
red to the group that consumed carbohydrates prior to, and during PA (untrained men, 
cycling 60 to 90 minutes daily for 6 weeks at intensity level of 70 % VO2max) (Van Pro-
eyen et al., 2011). Availability of endogenous fuels in muscles affects lipid oxidation in 
muscles as well as on the level of entire body. The amount of muscular TGs in muscles 
before the activity also influences lipid oxidation, in addition to intensity, duration and 
type of activity as well as gender, fitness level and ingested food (Kiens, 2006). Mode-



ANNALES KINESIOLOGIAE • 6 • 2015 • 2

99

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

rately trained boys showed 2.5 times local lipid oxidation in their muscles when they 
consumed fat rich diet, compared to carbohydrate rich diet (which replenished glycogen 
stores in muscles), at same workload (60 minutes of cycling at 65 % VO2max intensity). 
Since it is spent for acetyl-carnitine formation, free carnitine availability significantly 
decreases, reducing lipid oxidation capability during endurance PA (Roepstorff et al., 
2005). When muscle glycogen stores are low, a two times higher concentration of fatty 
acids can be observed in the plasma, as well as a significantly increased concentration 
of enzymes and binding proteins that participate in lipid oxidation (Wojtaszewski et al., 
2003). It has been shown that glycogen stores are inversely proportional to the levels of 
free carnitine. When glycogen stores in muscles are high, there is very little free carni-
tine in the cells; this limits fatty acid transport into mitochondria, which consequently 
limits lipid oxidation in the muscles (Jeppesen & Kiens, 2012). The intake of carnitine 
dietary supplement increased ability to metabolise lipids during low-intensity enduran-
ce PA (untrained healthy men cycled for 30 minutes at 50 % VO2max intensity), a 44 % 
decrease in Lactate concentration in the blood during high-intensity PA (30 minutes 
of cycling at 80 % VO2max intensity) was also observed (Wall et al., 2011). This may 
indicate increased lipid oxidation while taking carnitine dietary supplement at higher 
intensities as well (Jeppesen & Kiens, 2012). When considering lipid oxidation, after 
adaptation to a high-fat diet due to an increased uptake of lipids originating from the 
bloodstream and only a minor extent to an increased muscle TG utilization, greater 
lipid oxidation is observed during PA. The intake of carnitine dietary supplement might 
also stimulate lipid oxidation. Training on an empty stomach stimulates muscle cells to 
increase lipid oxidation and facilitate utilizing muscular TGs.

Effects of Adipose Tissue Amounts on Lipid Oxidation during Activity

The amount of fat tissue also affects the capability of lipid oxidation. Chronic im-
balances between energy intake and oxidation ultimately result in excess intracellular 
lipid accumulation, both at the whole body level and in individual organs or tissues. 
Obese and overweight people have a higher concentration of plasma fatty acids, most 
likely due to increased fatty acid release from an expanded fat mass; providing a link 
between obesity and ectopic lipid accumulation (Savage, Petersen, & Schulman, 2007). 
“Sedentary overweight subjects, compared to controls at the same exercise intensities, 
exhibit an alteration of the balance of substrate oxidation, reflected by lower rates of 
lipid oxidation and a shift of quantitative parameters to lower intensities” (Pérez-Martin 
et al., 2001). The amount of fatty acids increases as a reaction to low-intensity PA (un-
trained men cycling for 90 minutes at 50 % VO2max intensity). The increase in fatty acids 
oxidation during exercise is ≈ 50 % lower in obese and ≈ 35 % lower in overweight 
people when compared to lean controls (Scheen, Pirnay, Luyckx, & Lefebvre, 1983; 
Mittendorfer et al., 2004). The obese have four times higher transport of fatty acids 
through sarcolemma (Bonen et al., 2004) and fatty acids penetrate into muscles, where 
they accumulate as muscular TGs (Goodpaster, Theriault, Watkins, & Kelley, 2000). 



100

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

The accumulation of muscular TGs in muscles may result in insulin resistance and the 
development of diabetes (Kelley & Goodpaster, 2001). The rate of total fat oxidation, 
assessed by indirect calorimetry during the last 30 minutes of exercise, was not signifi-
cantly different between groups: lean, overweight and obese (Mittendorfer et al., 2004). 
That is why comparable RER levels were measured in overweight and lean untrained 
men (30 minutes cycling at anaerobic threshold) (Wong & Harber, 2006). Fat oxidation 
provided ∼30 % of total energy requirements during the exercise in lean, overweight, 
and obese men. However, the source of fatty acids used as fuel during the exercise vari-
ed between groups. In lean subjects about one-half of the fatty acids oxidized during the 
exercise, having derived from systemic plasma fatty acids and the other half from non-
-systemic fatty acids. The relative contribution of systemic plasma fatty acids to total 
fat oxidation decreased and the relative contribution of non-systemic fatty acid to total 
fat oxidation increased with increasing adiposity. Presumably, the predominant source 
of non-systemic fatty acids was the fatty acids that were released during lipolysis of 
intramuscular TG (Mittendorfer et al., 2004).

“Lipid accumulation in skeletal muscle and liver may be a result of increased deli-
very / synthesis of fatty acids to / in these tissues in those conditions in which energy 
intake exceeds adipose tissue storage capacity (as seen in obesity and lipodystrophy), 
or a consequence of either acquired or inherited mitochondrial dysfunction” (Savage 
et al., 2007). Obese people have a lower expression of the adipose tissue hormone 
adiponectin (Civitarese et al., 2006), which is one of the hormones (along with leptin 
and FGF21) that enhance mitochondrial proliferation in white adipose tissue and who-
le-body energy expenditure associated with the lipid burning in beige adipocytes (Un-
ger, Scherer, & Holland, 2013). In addition to lower hormonal response to endurance 
PA, ineffective lipid oxidation can be observed with obese people. They have smaller 
mitochondria and / or impaired oxidation process within the mitochondria thus, being 
handicapped in their effort to lose fat (Colberg, Simoneau, Thaete, & Kelly, 1995; Bo-
rer, 2008). It is possible that “hyperinsulinemia” in overweight and obese compared 
with lean men contributed also to the blunted lipolytic response to exercise. Although 
the relative decrease in plasma insulin concentration was similar in lean, obese and 
overweight, the absolute plasma insulin concentrations were greater during exercise in 
overweight and obese than in lean subjects. It is also likely that the attenuated lipolytic 
response to exercise in overweight and obese men was caused by a blunted increase in 
epinephrine secretion and a concomitant reduction in adipose tissue lipolytic response 
to circulating catecholamines (Mittendorfer et al., 2004). “Adipocyte dysfunction due 
to either obesity or lipodystrophy is associated with excessive and untimely delivery 
of fatty acids to the liver and skeletal muscle and probably contributes to insulin resis-
tance in both organs by altering the balance between fatty acids uptake / synthesis and 
the disposal leading to increases in intracellular lipid content.” Also, an increasingly 
sedentary lifestyle and the associated relative increase in fat mass almost certainly con-
tribute to aging induced insulin resistance. Muscle insulin resistance and accumulation 
of muscular TG precede the development of hepatic insulin resistance and type 2 di-
abetes (Savage et al., 2007). Exercise (insulin resistant boys; 45 minutes on elliptical 



ANNALES KINESIOLOGIAE • 6 • 2015 • 2

101

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

trainer) resulted in a greater than threefold increase in postprandial net muscle glycogen 
synthesis, reflecting improved muscle insulin responsiveness, and a ≈ 40 % reduction in 
net hepatic TG synthesis. The changes in the whole body energy storage were accom-
panied by a ≈ 30 % decrease in hepatic lipogenesis and were independent of changes 
in fasting or postprandial plasma glucose and insulin concentrations (Rabol, Petersen, 
Dufour, Flannery, & Schulman, 2011). Exercise, as well as weight loss, reduced insulin 
resistance (Houmard et al., 2002). When considering lipid oxidation, it seems an inver-
se relationship between adiposity and the lipolytic response to exercise. The limited 
availability of systemic plasma fatty acids as a fuel in overweight and obese men was 
associated with a compensatory increase in the oxidation of non-systemic fatty acids.

Effects of Gender and Fitness Level on Lipid Oxidation during Activity

Women utilise more of lipids than men at the same relative activity intensity level 
(Kiens, 2006), Lipid oxidation remains the same during luteal and follicular phase of 
the menstrual cycle (Matsuo, Saitoh, & Suzuki, 1999). Due to adaptation mechanisms, 
regular endurance PA increases lipid utilisation during PA (Costill, Fink, Getchell, Ivy, 
& Witzmann, 1979; Koivisto, Hendler, Nadel, & Felig, 1982; Gollnick, 1977; Short & 
Sedlock, 1997; Jeppesen & Kiens, 2012). An increased lipid oxidation occurs due to 
increased capillary density (Kiens, Essen-Gustavsson, Christensen, & Saltin, 1993), 
increased lipid binding protein activity, an increase of fatty acid oxidation controlling 
enzymes (Kiens & Lithell, 1993; Alsted et al., 2009; Jeppesen et al., 2012), reduced 
insulin secretion and increased activation of adiponectin hormone in the adipose tissue 
(Civitarese et al., 2006). These adaptations to regular endurance PA increase the ability 
of mobilisation, transportation and oxidation of lipids in people with aerobic stamina 
(Henriksson, 1977; Kiens et al., 1993; Jeppesen et al., 2012). When considering lipid 
oxidation, women utilise more lipids than men, and after adaptation to training, greater 
lipid oxidation (recruit, transport and oxidize lipids) is observed during PA.

LIPID OXIDATION AFTER CONTINUOUS ACTIVITIY

Following PA, body immediately requires oxygen to regenerate its oxygen energy 
supplies (in myoglobin and haemoglobin), synthesis of phosphagens, removal of lac-
tate from blood, increased need for oxygen in tissues due to increased temperature, an 
increase in catecholamine concentration and increased heart and respiratory muscles 
activity (Børsheim & Bahr, 2003). The period following the PA is known as the “excess 
post-exercise oxygen consumption” phase (EPOC) (Scott, 1997). Increased lipid oxi-
dation and decreased carbohydrate oxidation can be observed during most of the EPOC 
period (Maehlum, Grandmontagne, Newsholme, & Sejersted, 1986; Bahr, Ingnes, Vaa-
ge, Sejersted, & Newsholme, 1987; Bahr, Hansson, & Sejersted, 1990; Chad & Quigley, 
1991; Short & Sedlock, 1997), thus, it was imperative to further study the literature on 



102

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

how it describes the EPOC amount and duration, and how lipids are utilised after PA. 
Amount and duration of EPOC are influenced by intensity and duration of PA (Sedlock, 
Fissinger, & Melby, 1989), the method of carrying out the PA (Almuzaini, Potteiger, & 
Green, 1998), the menstrual cycle (Matsuo et al., 1999), aerobic fitness level (Sedlock, 
Lee, Flynn, Park, & Kamimori, 2010) and amount of fatty tissue (Wong & Harber, 
2006). Gender per se (Lamont, Romito, & Rossi, 2010), the amount of active muscles 
(Sedlock, 1991b) and nutrition (Bahr & Sejersted, 1991b) show no effect on EPOC. 

Effect of Intensity and Duration of Activity on Lipid Oxidation after Activity

Intensity of PA is exponentially related to the EPOC level (Brehm & Gutin, 1986; 
Sedlock et al., 1989; Gore & Withers, 1990; Bahr & Sejersted, 1991a; Frey, Byrnes, & 
Mazzeo, 1993; Smith and Naughton, 1993; Hardman, 2001; Børsheim & Bahr, 2003), 
the duration of PA on the other hand is in linear relation to the EPOC level (Bahr et al., 
1987; Chad & Wenger, 1988; Sedlock et al., 1989; Gore & Withers, 1990; Smith & 
Mc Naughton, 1993). Lipid oxidation following low-intensity long-term PA can be 
more than three times higher than during resting state (within three hours following 
120 minutes of PA at 51 % VO2max intensity) (Bahr et al., 1990), low-intensity and / 
or short-term PA, however, does not lead to longer EPOC (Børsheim & Bahr, 2003). 
When EPOC length was studied at constant intensity level and various durations 
of moderate-intensity PA (cycling at 70 % VO2max intensity), it was discovered that 
EPOC after 30, 45 and 60 minutes of moderate-intensity PA lasted ≈ 2 hours, ≈ 3 ho-
urs and ≈ 7 hours, respectively (Chad & Wenger, 1988), after 80 minutes of cycling up 
to 12 hours (Maehlum et al., 1986; Bahr et al., 1987). When EPOC length was studied 
at constant duration (80 minutes of cycling) and various intensity levels of moderate-in-
tensity PA (29 %, 50 % and 75 % VO2max), it was discovered that EPOC lasted respec-
tively for ≈ 20 minutes, ≈ 3 hours and ≈ 10 hours after the activity; respective EPOC 
amounts were ≈ 10 kcal, ≈ 30 kcal and ≈ 150 kcal (Bahr & Sejersted, 1991b). EPOC 
amount studies on trained participants, 8 hours after a 20-, 50-, and 80-minute run at of 
70% VO2max intensity, showed the values of ≈ 25 kcal, ≈ 50 kcal and ≈ 75 kcal, respec-
tively (Gore & Withers, 1990). Studying effect of intensity and duration on amount and 
duration of EPOC in trained men, showed that short term high-intensity PA brought 
about significantly higher EPOC (≈ 30 kcal) than a low-intensity PA, regardless of its 
duration (≈ 15 kcal). A short-term low-intensity PA resulted in significantly shorter 
EPOC (≈ 20 minutes), compared to a long-term low-intensity PA (≈ 30 minutes) and a 
short-term high-intensity PA (≈ 35 minutes) (Sedlock et al., 1989). 



ANNALES KINESIOLOGIAE • 6 • 2015 • 2

103

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

Effect of Dividing Activity into Sets and Amount of Working Muscles on Lipid 
Oxidation after Activity

Studying whether dividing PA into sets has any effect, it was found that the EPOC 
amount after 2 sets separated by 6 hours of rest (15 minutes of cycling at 70 % VO2max 
intensity) was significantly greater than if same PA was done in a single set (30 minutes 
of cycling at 70 % VO2max intensity) (Almuzaini et al., 1998). Similar findings were re-
ached in an earlier study where the EPOC amount after two sets (25 minutes of running 
at 70 % VO2max intensity) was significantly greater than if the PA was done in a single 
set (50 minutes of running at 70 % VO2max intensity) (Kaminsky, Padjen, & LaHam-
-Saeger, 1990). 

EPOC amount and duration following PA for upper limbs (20 minutes, at 60 % 
VO2max intensity on upper limb cycle ergometer) and PA for lower limbs (20 minutes, 
60 % VO2max intensity on lower limb cycle ergometer) are virtually the same (23 minu-
tes and ≈ 9 kcal for the upper limbs and 24 minutes and ≈ 10 kcal for the lower limbs). 
It can be concluded that the amount of active muscles as well as absolute VO2max value 
do not affect the amount and the duration of EPOC (Sedlock, 1991b). 

Effects of Gender on Lipid Oxidation after Activity

When comparing low-intensity PA (50 % VO2max, 500 kcal) and high-intensity PA 
(75 % VO2max, 500kcal) in women, three hours after a high-intensity PA (≈ 40 kcal) 
EPOC amount was greater than after low-intensity PA (≈ 20 kcal). During and after a 
low-intensity PA, more lipids were used (≈ 37 g) than during and after a high-inten-
sity PA (≈ 28 g). This difference, however, was not statistically significant (p = 0.07) 
(Phelain, Reinke, Harris, & Melby, 1997). The study has two obvious shortcomings: 
lipid oxidation following a high-intensity PA was still increased, indicating EPOC after 
high-intensity PA lasts longer than three hours, which in turn indicates that the EPOC 
period was not measured in its entirety, and, secondly, the effect of menstrual cycle was 
not taken into account. EPOC and lipid oxidation after PA (60 minutes of cycling at 
60 % VO2max intensity) are significantly greater in luteal than in follicular phase of the 
menstrual cycle (Matsuo et al., 1999). Not controlling the menstrual cycle could be the 
reason why no statistically significant differences were found in the amount and duration 
of EPOC (women cycling at various intensities) (Sedlock, 1991a). Normalising absolute 
EPOC value to lean mass results in disappearing gender differences (Tahara et al., 2008; 
Lamont et al., 2010).



104

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

Effects of Amount of Fatty Tissue, Food Ingestion and Fitness Level on Lipid 
Oxidation after Activity

EPOC in lean people lasts longer and is greater by one third than in overweight 
and obese people. Overweight and obese people have significantly higher RER value, 
which indicates that during the regeneration phase they use less lipids and that PA has a 
reduced effect on lipid oxidation increase during rest than in lean people (Wong & Har-
ber, 2006). Similar conclusions were drawn in an earlier study; it was found that during 
rest neither low-intensity PA (40 % VO2max) nor moderate-intensity PA (70 % VO2max) 
resulted in fatty acid oxidation increase in obese people (van Baak, 1999). Ingesting 
food prior to moderate-intensity PA had no effect on the EPOC amount and duration 
(Bahr & Sejersted, 1991b). 

Regular PA results in increased recovery effectiveness following PA (Hagberg, 
Hickson, Ehsani, & Holloszy, 1980): blood lactate level decreases, as does rectal tem-
perature and hormonal response (Sedlock et al., 2010), thus reducing the EPOC dura-
tion (Frey et al., 1993; Sedlock, 1994; Short & Sedlock, 1997). The amount of EPOC 
when comparing relative values is identical (Kaminsky et al., 1986; Sedlock, 1994; 
Short & Sedlock, 1997; Børsheim & Bahr, 2003; Sedlock et al., 2010). If we compare 
absolute values, EPOC amount following a regular PA is significantly reduced (Sedlock 
et al., 2010), while the ability to metabolise fatty acids increases (Kaminsky, Knowlton, 
Perkins, & Hetzler, 1986; Short & Sedlock, 1997; Børsheim & Bahr, 2003; Gill et al., 
2006; Ferreira et al. 2011). 

Energy expenditure was significantly higher during rest even up to 48 hours after 
moderate-intensity PA (60 minutes running at 70 to 75 % VO2max intensity) (Jamurtas et 
al., 2004). In spite of all this, we must be aware that EPOC represents only up to 10 % 
of energy expended during PA (LeCheminant et al., 2008) or, depending on PA dura-
tion (from 20 to 80 minutes) and intensity (30, 50 or 70 % VO2max) only 1 to 8.9 % of 
energy expended during PA (Gore & Withers, 1990). When considering lipid oxidation 
in recovery phase after PA, the increased lipid oxidation can be observed during most 
of the EPOC period. Intensity of PA is exponentially related to the EPOC level, the 
duration of PA on the other hand is in linear relation to the EPOC. Dividing PA into sets 
causes greater EPOC than if the PA is in a single set. EPOC in lean people lasts longer 
and is greater. Normalising absolute EPOC value to lean mass results in disappearing 
gender differences, however, lipid oxidation after PA is significantly greater in luteal 
than in follicular phase of the menstrual cycle. If we compare absolute values, EPOC 
amount following regular PA is significantly reduced when comparing relative values is 
identical, while the ability to metabolise lipids increases. The amount of active muscles 
as well as ingested food prior to PA has no effect on the amount and duration of EPOC. 



ANNALES KINESIOLOGIAE • 6 • 2015 • 2

105

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

INTERVAL TRAINING AND LIPID OXIDATION

During a high intensity PA, oxidation of plasma fatty acids, muscle and plasma 
TGs are lower than during a moderate intensity PA, despite greater energy expenditure 
(van Loon et al., 2001; Jeppesen & Kiens, 2012). Plasma glucose and muscle glycogen 
utilization is directly proportional to PA intensity (Romijn et al., 1993; van Loon et al., 
2001), while the mechanism balancing lipid oxidation has yet to be explained (Jeppe-
sen et al., 2011). “Carnitine could act as an acceptor of acetyl groups from acetyl-CoA, 
by forming acetylcarnitine, a reaction catalyzed by the mitochondrial enzyme carnitine 
acetyltransferase, when acetyl-CoA is generated faster than utilized by the Krebs cycle” 
(Jeppesen & Kiens, 2012). With increasing exercise intensities, muscle acetylcarnitine 
content is increased concomitantly with a decrease in the free carnitine content (Je-
ppesen & Kiens, 2012). On the other hand, a low muscle content of free carnitine is 
supposed to lead to a diminished supply of the long chain fatty acid CoA to β-oxidation, 
limiting long chain fatty acid oxidation during high intensity exercise. Thus, an incre-
ased availability of pyruvate, acetyl-CoA formation, and ‘binding’ of the free carnitine 
during high intensity exercise also provide a potential mechanism, whereby fatty acid 
oxidation is down-regulated” (Jeppesen & Kiens, 2012). A comparison was made bet-
ween lipid oxidation in untrained boys (aged 8 to 12), during and two hours after PA (30 
minutes of cycling at intensity that maximises lipid oxidation determined for individual 
boy) and during and two hours after PA to which high-intensity short-term burst was 
added (cycling at intensity that utilized maximum lipids and every two minutes four 
seconds of maximum intensity). It was found that the amount of lipids metabolised and 
the EPOC amount were the same, for the same work performed (Crisp, Fournier, Licari, 
Braham, & Guelfi, 2012). The same EPOC amount and the duration was found in adult 
men as well following interval PA (three minutes of cycling at 30 % VO2max intensity 
and two minutes at 90 % VO2max intensity, seven repetitions) and continuous modera-
te-intensity PA (≈ 30 minutes of cycling at 65 % VO2max intensity) for the same work 
performed. RER values were significantly lower in the 2-hour period following interval 
PA (McGarvey, Jones, & Petersen, 2005). Absolute values of metabolised fatty acids 
during and following the exercise were, unfortunately, not measured, so we still do not 
know whether lipid oxidation during and following a continuous PA is lower, equal or 
higher than during and after an interval PA for the same work performed. However, 
Hazell, Olver, Hamilton, and Lemon (2012) have recently demonstrated a similar total 
VO2 over 24 hours after sprint (high-intensity) interval exercise (four times 30-second 
maximal cycling at resistance of 10 % body mass with four-minutes rests) and conti-
nuous endurance exercise (30 minutes cycling at ~ 70 % VO2max) session (SIE = 498.0 
± 29.4 L; CEE = 500.2 ± 49.2 L; CTRL = 400.2 ± 44.6 L), indicating that the significant 
body-fat losses observed previously with sprint interval trainings are partially due to 
increases in oxidation post exercise.

Comparing the two hours following the high-intensity short-term burst of activ-
ity (four repetitions of 30-second intervals of sprinting on a cycle ergometer and 4.5 
minutes of rest) to resting, a 75 % lipid oxidation increase was found (Chan & Burns, 



106

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

2013). The EPOC duration and the amount following the interval PA depends on a 
number of high-intensity short-term burst (Bahr, Grønnerød, & Sejersted, 1992) and 
work to rest ratio (Gosselin, Kozlowski Devinney-Boymel, & Hambridge, 2012). After 
two minutes of cycling at 108 % VO2max intensity, EPOC amount is ≈ 30 kcal and lasts 
30 minutes; after 2 series with a 3-minute break, EPOC amount is ≈ 35 kcal and lasts 
60 minutes; after 3 sets with two 3-minute breaks EPOC amount is ≈ 80 kcal and lasts 
4 hours (Bahr et al., 1992). The highest energy expenditure and the lowest blood lactate 
values are found when using 30 seconds of moderate-intensity PA and 30 seconds of 
high-intensity short-term activity (Gosselin et al., 2012; Zuniga et al., 2011). In a recent 
study (Kelly, King, Goerlach, & Nimmo, 2013), two commonly used high-intensity 
short-term activity protocols (10 times 1 minute of high-intensity cycling followed by 
a one-minute rest and 10 times 4-minute high-intensity cycling followed by a 2-min-
ute rest), supposedly suitable for untrained people and people suffering from chronic 
diseases, were compared. It was discovered that during the 60 minutes after interval 
exercises, RER was lower in both protocols. But during the slow phase of EPOC period 
(from 1.25 to 9.25 hours) there were no significant differences between RER values or 
energy expenditure. They conclude that the effect on post-exercise metabolic rate was 
transient and relatively minor (Kelly et al., 2013).

Interval training causes both central (cardiovascular) and peripheral (skeletal mu-
scle) body adaptations (Gibala, Little, MacDonald, & Hawley, 2012). High-intensity 
short-term training (10 x 2 minutes 105 % VO2max with 2 minutes breaks) increased the 
anaerobic threshold significantly more than endurance training (50 % VO2max, 55 minu-
tes or 70 % VO2max 35 minutes) in the same time period (Poole & Gaesser, 1985). Mo-
dern studies have come to similar conclusions. Just two-week high-intensity intermit-
tent training (7 sessions every second day, each session consisted of 10 4-min cycling 
bouts at 90 % VO2max separated by 2 minutes of rest), increased post-training whole 
body lipid oxidation during the 60 minutes of cycling at 60 % VO2max in moderate trai-
ned women (menstrual cycle was not monitored) (Talanian, Galloway, Heigenhauser, 
Bonen, & Spriet, 2007). Studies show that low-volume high-intensity interval training 
increases a body’s capability of lipid oxidation just as effectively as higher-volume 
moderate-intensity endurance training (Gibala et al., 2006; Gibala & McGee, 2008). 
However, considering time, interval training is a more time efficient strategy than con-
tinuous training (Burgomaster et al., 2008). Interval training is safe for healthy people 
as well as people “at risk” (Shiraev & Barclay, 2012). Studies on obese and metabolic 
syndrome patients report a similar or a greater effect of high-intensity interval training 
compared to endurance training on life quality, cardio-metabolic risk factors, aerobic 
fitness and cardio-vascular function, as well as blood glucose reduction, insulin signal-
ling in adipose tissue and skeletal muscles, lowering the mean arterial blood pressure, 
and finally, on adipose tissue lipogenesis reduction, body weight and adipose tissue re-
duction (Earnest, 2008; Guiraud et al., 2012; Hansen, Dendale, van Loon, & Meeuseen, 
2010; Kessler, Sisson, & Short, 2012; Tjønna et al., 2008). In practice, this translates to 
similar or greater effect, for at least 60 % less time spent doing high-intensity interval 
training compared to endurance training. This is a very significant aspect considering 



ANNALES KINESIOLOGIAE • 6 • 2015 • 2

107

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

that “a lack of time” is the most commonly cited obstacle for participating in regular PA 
(Stutts, 2002; Kimm et al., 2006). When considering lipid oxidation, interval training 
is at least as effective as endurance training, with less time invested. Some people also 
find it more interesting.

RESISTANCE TRAINING AND LIPID OXIDATION

Muscles do not utilize lipids during resistance exercises (Melby, Scholl, Edwards, 
& Bullough, 1993). Resistance exercises are first ensued by anaerobic regeneration, 
the so-called “delayed glycolysis”, a glycolytic process at the start of regeneration. It is 
significantly faster and more effective at phosphagens re-synthesis than at aerobic pro-
cesses. It ensures re-synthesis of depleted phosphagens, up to the levels allowing oxida-
tive processes to allow sufficient regeneration (Margaria et al., 1933, in di Prampero & 
Feretti, 1999). An increase in lipid oxidation has been found during EPOC period 30 to 
120 minutes after finishing a resistance exercise (Binzen, Swan, & Manore, 2001). In-
tensity has been identified as a significant factor in EPOC amount following resistance 
exercise (Thornton & Potteiger, 2002) as well as the speed of execution (Scott, 2012) 
and the size of active muscle groups, a slight dependency on breaks between sets was 
also observed (Farinatti & Castinheiras, 2011; Haltom et al., 1999). No dependency 
was found towards the order in which the resistance exercise is carried out (Da Silva, 
Brentano, & Kruel, 2010), or the type of muscle contraction (Scott, 2012). During the 
first two hours following resistance exercise (2 sets, 8 repetitions at 85 % 8 RM), the 
EPOC amount was significantly higher than after the activities for strength endurance 
(2 sets, 15 repetitions 45 % 8 RM) at equal work carried out. No difference in RER 
was found following the resistance exercise or the activities for strength endurance 
(Thornton & Potteiger, 2002). Absolute lipid oxidation values were not measured, so 
we cannot conclude whether lipid oxidation after resistance exercise differs from those 
following activities for strength endurance. EPOC amount is dependent on execution 
speed of resistance exercises; it is significantly greater during slower execution (4s lift 
/ 1s release or 1s lift / 4s release) in comparison to faster execution (1.5 second lift / 1.5 
second release) (Scott, 2012). The EPOC amount following the resistance exercise of 
larger muscle groups is significantly greater than following resistance exercise of smal-
ler muscle groups at equal repetitions and unequal work performed. Duration of rest 
between sets (1 or 3 minutes) had no effect on EPOC in larger muscle groups (Farinatti 
& Castinheiras, 2011). A shorter break between sets (20 seconds; 2 circular exercises 
for the upper and lower part, 20 repetitions 75 % 20 RM) resulted in significantly grea-
ter EPOC amount compared to same resistance exercise with a 1-minute break (Haltom 
et al., 1999). EPOC amount during the first 2 hours following resistance exercise was 
≈ 30 kcal (Binzen et al., 2001). Part of these calories is used for delayed glycolysis and 
part for lipid oxidation.

Regular resistance training, however, increases muscle mass, therefore increasing 
oxidation rate during rest as well as absolute lipid utilisation (Dolezal, Potteiger, Jacob-



108

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

sen, & Benedict, 2000). Significantly, increased oxidation was found even 38 hours 
after the resistance training (31 minutes, 10 repetitions, maximum until exhaustion, 
for the entire body) (Schuenke, Mikat, & McBride, 2002), and 24 hours following 
the resistance training (60 minutes, 70 – 75 %, 1 repetition maximum, for the entire 
body) (Jamurtas et al., 2004). Heden (2011) found that in overweight people, there 
was a ≈ 5 % increase in oxidation rate up to 72 hours during rest after the resistance 
training, following the recommendations of the American Society for Sport Medicine 
(Haskell et al., 2007; Heden, 2011). 

Measuring local fatty acid oxidation during resistance exercise for the individual 
muscle groups (Dean et al., 2000) and (Helge, Stallknecht, Richter, Galbo, & Kiens, 
2007) concluded that resistance exercise caused no noticeable hormonal changes and 
enabled exceptionally good circulation and oxygen supply to active muscles. By mo-
nitoring isotopes, muscle biopsies, oxygen consumption and RER during unilateral 
extension of the knee against resistance intensity ranging from 25 % to 85 % of maxi-
mum power – Pmax), the total fatty acid oxidation in the thigh increased 15 times (at 
25 % Pmax intensity) compared to rest, and remained the same regardless of the inten-
sity. Free fatty acid oxidation in the thigh increased with resistance exercise intensity, 
reducing oxidation of plasma TG and muscular TG. At 100 % Pmax intensity fatty acid 
oxidation capability decreased by a third compared to 85 % Pmax intensity. These results 
contradict activities that incorporate the muscles of entire body, such as cycling, where 
maximum lipid utilisation is at 65 % VO2max. The reason may lie in significantly gre-
ater blood circulation in the active muscles, when we perform resistance exercise for 
individual muscle groups than when we perform PA that includes greater muscle mass. 
This “super fusion” creates muscle environment that retains free carnitine and promo-
tes lipid oxidation processes even at 80 % Pmax intensity. At intensities exceeding 80 % 
Pmax, the availability of free carnitine decreases, heavily diminishing the ability of lipid 
oxidation (Jeppeson & Kiens, 2012).

When combining endurance PA with resistance exercise it was found that the order 
of PA and the resistance exercise execution had no effect on the size and the duration of 
EPOC (Drummond, Vehrs, Schaalje, & Parcell, 2005; Oliveira & Oliveira, 2011). The 
order, however, did have an effect on RER. Execution of endurance PA prior to resis-
tance exercise resulted in significantly lower RER, resulting in higher lipid oxidation, 
compared to the reverse order of endurance PA following resistance exercise (Oliveira 
& Oliveira, 2011). Resistance exercise (3 series at 70 % 1 repetition maximum, 10 repe-
titions, 105-second break between series or exercises, 7 exercises for upper and lower 
body), moderate-intensity PA (25 minutes of running at 70 % VO2max intensity), combi-
nation of moderate-intensity PA and resistance exercise (there was a 5-minute break in 
between) or resistance exercise and moderate-intensity PA, resulted in the same EPOC 
duration (≈ 40 minutes) following the session (Drummond et al., 2005). When conside-
ring lipid oxidation, the total amount of lipids utilized during and following resistance 
exercise is negligible compared to lipid oxidation during and following the endurance 
PA or interval training, but regular resistance training increases muscle mass, therefore 
increasing oxidation rate and lipid utilisation during rest.



ANNALES KINESIOLOGIAE • 6 • 2015 • 2

109

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

CONCLUSIONS

Prolonged (> 30 minutes) moderate intensity (55 – 70 % VO2max) PA, such as wal-
king, jogging or cycling, are the most effective way to increase lipid oxidation during 
and after a single exercise session. Studies also suggest no difference in lipid oxidation 
between periods following low-volume high-intensity interval exercise and traditional 
continuous endurance PA. However, time benefit of low-volume, high-intensity inter-
val exercise compared to traditional endurance PA is significant. Further research is 
required to confirm whether adding just a few seconds of sprints during moderate-in-
tensity endurance PA every so often would result in the same lipid oxidation as during 
a continuous PA without sprint intervals.

Regularity of PA seems most important. Regular continuous and regular interval 
exercise or activity triggers the same adaptation mechanisms, and increases one’s fatty 
acid mobility, transport and oxidation capability. Further research is necessary to com-
pare the effects of regular resistance, regular endurance and regular interval training 
on lipid oxidation effectiveness. Both regular endurance and regular interval training 
increase a certain amount of muscle mass, therefore increasing resting oxidation. It 
may also be of interest to compare the effects of Nordic walking, which additionally 
activates upper limb muscles in the movements and, thus, more muscle mass, as well as 
resistance exercise of the entire body on the effect of lipid oxidation.

Nutrition also significantly affects lipid oxidation. Food rich in fat and low in car-
bohydrates encourages lipid oxidation. It is essential not to exceed body’s daily energy 
requirements, which leads to increased body weight and obesity. Obese and overweight 
people are recommended to take part in regular endurance or interval training. Howe-
ver, from the standpoint of relieving lower limbs joints, it may be better to participate 
in cycling or swimming, despite lower lipid oxidation potential. 

REFERENCES

Achten, J., Gleeson, M., & Jeukendrup, A. E. (2002). Determination of the exercise in-
tensity that elicits maximal fat oxidation. Medicine & Science in Sports & Exercise, 
34(1), 92–97. VIEW ITEM

Almuzaini, K. S., Potteiger, J. A., & Green, S. B. (1998). Effects of split exercise sessions 
on excess postexercise oxygen consumption and resting metabolic rate. Canadian Jour-
nal of Applied Physiology, 23(5), 433–443. VIEW ITEM

Alsted, T. J., Nybe, L., Schweiger, M., Fledelius, C., Jacobsen, P., Zimmermann, R., 
et al. (2009). Adipose triglyceride lipase in human skeletal muscle is upregulated by 
exercise training. American Journal of Physiology, Endocrinology and Metabolism, 
296(3), 445–453. VIEW ITEM

Antonutto, G., & di Prampero, P. E. (1995). The concept of lactate threshold. The Journal 
of Sports Medicine and Physical Fitness, 35(1), 6–12. 

Åstrand, P. O., Rodahl, K., Dahl, H., & Strømme, S. B. (2003). Textbook of work physi-
ology – 4th edition. Champaign: Human Kinetics.

http://journals.lww.com/acsm-msse/Fulltext/2002/01000/Determination_of_the_exercise_intensity_that.15.aspx
http://www.nrcresearchpress.com/doi/pdf/10.1139/h98-026
http://ajpendo.physiology.org/content/296/3/E445.short


110

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

Astrup, A., Buemann, B., Christensen, N. J., Madsen, J., Gluud, C., Bennett, P., et al. 
(1992). The contribution of body composition, substrates and hormones to the variabili-
ty in energy expenditure and substrate utilization in premenopausal woman. The Journal 
of Clinical Endocrinology and Metabolism, 74(2), 279–286. VIEW ITEM

Bahr, R., Grønnerød, O., & Sejersted, O. M. (1992). Effect of supramaximal exercise 
on excess postexercise O2 consumption. Medicine and Science in Sports and Exercise, 
24(1), 66–71. VIEW ITEM

Bahr, R., Hansson, P., & Sejersted, O. M. (1990). Triglyceride/fatty acid cycling is incre-
ased after exercise. Metabolism, 39(9), 993–999. VIEW ITEM

Bahr, R., & Sejersted, O. M. (1991a). Effect of feeding and fasting on excess postexercise 
oxygen consumption. Journal of Applied Physiology, 71(6), 2088–2093. VIEW ITEM

Bahr, R., Ingnes, I., Vaage, O., Sejersted, O. M., & Newsholme, E. A. (1987). Effect of 
duration of exercise on excess postexercise O2 consumption. Journal of Applied Physi-
ology, 62(2), 485–490. VIEW ITEM

Bahr, R., & Sejersted, O. M. (1991b). Effect of intensity of exercise on excess postexerci-
se O2 consumption. Metabolism, 40(8), 836–841. VIEW ITEM

Binzen, C. A., Swan, P. D., & Manore, M. M. (2001). Postexercise oxygen consumption 
and substrate use after resistance exercise in women. Medicine and Science in Sports 
and Exercise, 33(6), 932–938. VIEW ITEM

Bonen, A., Luiken, J. J., Arumugam, Y., Glatz, J. F., & Tandon, N. N. (2000). Acute re-
gulation of fatty acid uptake involves the cellular redistribution of fatty acid translocase. 
Journal for Biology and Chemistry, 275, 14501–14508. VIEW ITEM

Bonen, A., Parolin, M. L., Steinberg, G. R., Calles-Escandon, J., Tandon, N. N., Glatz, 
J. F., et al. (2004). Triacylglycerol accumulation in human obesity and type 2 diabetes 
is associated with increased rates of skeletal muscle fatty acid transport and increased 
sarcolemmal FAT/CD36. FASEB Journal, 18, 1144–1146. VIEW ITEM

Borer, K. T. (2008). How effective is exercise in producing fat loss? Kinesiology, 40(2), 
126–137. VIEW ITEM

Børsheim, E., & Bahr, R. (2003). Effect of exercise intensity, duration, and mode on po-
stexercise oxygen consumption. Sports Medicine, 33(14), 1037–1060. VIEW ITEM

Bray, G. A. (2013). Energy and fructose from beverages sweetened with sugar or high-
-fructose corn syrup pose a health risk for some people. Advances in nutrition, 4(2), 
220–225. VIEW ITEM

Brehm, B. A., & Gutin, B. (1986). Recovery energy expenditure for steady state exerci-
se in runners and nonexercisers. Medicine and Science in Sports and Exercise, 18(2), 
205–210. VIEW ITEM

Burgomaster, K. A., Howarth, K. R., Phillips, S. M., Rakobowchuk, M., Macdonald, 
M. J., McGee, S. L., et al. (2008). Similar metabolic adaptations during exercise after 
low volume sprint interval and traditional endurance training in humans. The Journal of 
Physiology, 586(1), 151–160. VIEW ITEM

Cahill, G. F. Jr. (2006). Fuel metabolism in starvation. Annual review of Nutrition, 26, 
1–22. VIEW ITEM

Capostagno, B., & Bosch, A. (2010). Higher fat oxidation in running than cycling at the 
same exercise intensities. International Journal of Sport Nutrition and Exercise Metabo-
lism, 20(1), 44–45.

http://press.endocrine.org/doi/pdf/10.1210/jcem.74.2.1530952
http://journals.lww.com/acsm-msse/Abstract/1992/01000/Effect_of_supramaximal_exercise_on_excess.12.aspx
http://dx.doi.org/10.1016/0026-0495(90)90313-2
http://jap.physiology.org/content/71/6/2088
http://jap.physiology.org/content/62/2/485
http://dx.doi.org/10.1016/0026-0495(91)90012-L
http://journals.lww.com/acsm-msse/Fulltext/2001/06000/Postexercise_oxygen_consumption_and_substrate_use.12.aspx
http://www.jbc.org/content/275/19/14501.full
http://www.ncbi.nlm.nih.gov/pubmed?term=Calles-Escandon%20J%5BAuthor%5D&cauthor=true&cauthor_uid=15132977
http://www.ncbi.nlm.nih.gov/pubmed?term=Tandon%20NN%5BAuthor%5D&cauthor=true&cauthor_uid=15132977
http://www.ncbi.nlm.nih.gov/pubmed?term=Glatz%20JF%5BAuthor%5D&cauthor=true&cauthor_uid=15132977
http://www.ncbi.nlm.nih.gov/pubmed?term=Glatz%20JF%5BAuthor%5D&cauthor=true&cauthor_uid=15132977
http://www.fasebj.org/content/18/10/1144.full
http://hrcak.srce.hr/file/48758
http://link.springer.com/content/pdf/10.2165%2F00007256-200333140-00002.pdf
http://advances.nutrition.org/content/4/2/220.short
http://journals.lww.com/acsm-msse/Abstract/1986/04000/Recovery_energy_expenditure_for_steady_state.10.aspx
http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2007.142109/full
http://dx.doi.org/10.1146/annurev.nutr.26.061505.111258


ANNALES KINESIOLOGIAE • 6 • 2015 • 2

111

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

Chad, K. E., & Quingley, B. M. (1991). Exercise intensity: effect on postexercise O2 up-
take in trained and untrained women. Journal of Applied Physiology, 70(4), 1713–1719. 
VIEW ITEM

Chad, K. E., & Wenger, H. A. (1988). The effect of exercise duration on the exercise and 
post-exercise oxygen consumption. Canadian Journal of Sport Science, 13, 204–207.

Chan, H. H., & Burns, S. F. (2013). Oxygen consumption, substrate oxidation, and blood 
pressure following sprint interval exercise. Applied Physiology, Nutrition and Metabo-
lism, 38(2), 182–187. VIEW ITEM

Civitarese, A. E., Ukropcova, B., Carling, S., Hulver, M., DeFrionzo, R. A., Mandari-
no, L., et al. (2006). Role of adiponectin in human skeletal muscle bioenergetics. Cell 
Metabolism, 4(1), 75–87. VIEW ITEM

Colberg, S. R., Simoneau, J. A., Thaete, F. L., & Kelly, D. E. (1995). Skeletal muscle 
utilization of free fatty acids in women with visceral obesity. The Journal of Clinical 
Investigation, 95(4), 1846–1853. VIEW ITEM

Costill, D. L., Fink, W. J., Getchell, L. H., Ivy, J. L., & Witzmann, F. A. (1979). Lip-
id metabolism in skeletal muscles of endurance trained males and females. Journal of 
Apllied Physiology, 47(4), 787–791. VIEW ITEM

Crisp, N. A., Fournier, P. A., Licari, M. K., Braham, R., & Guelfi. K. J. (2012). Adding 
sprints to continuous exercise at the intensity that maximises fat oxidation: Implications 
for acute energy balance and enjoyment. Metabolism, 61(9), 1280–1288. VIEW ITEM

Da Silva, R. L., Brentano, M. A., & Kruel, L. F. (2010). Effects of different strength train-
ing methods on postexercise energetic expenditure. Journal of Strength and Condition-
ing Research, 24(8), 2255–2260. VIEW ITEM

Dean, D., Daugaard, J. R., Young, M. E., Saha, A., Vavvas, D., Asp, S., et al. (2000). 
Exercise diminishes the activity of acetyl-CoA carboxylase in human muscle. Diabetes, 
49(8), 1295–1300. VIEW ITEM

di Prampero, P. E., & Ferretti, G. (1999). The energetics of anaerobic muscle metabolism: 
a reappraisal of older and recent concepts. Respiration Physiology, 118(2-3), 103–115. 
VIEW ITEM

Dolezal, B. A., Potteiger, J. A., Jacobsen, D. J., & Benedict, S. H. (2000). Muscle dam-
age and resting metabolic rate after acute resistance exercise with an eccentric overload. 
Medicine & Science in Sports & Exercise, 32(7), 1202–1207. VIEW ITEM

Drummond, M. J., Vehrs, P. R., Schaalje, G. B., & Parcell, A. C. (2005). Aerobic and 
resistance exercise sequence affects excess postexercise oxygen consumption. Journal 
of Strength and Conditioning Research, 19(2), 332–337. VIEW ITEM

Earnest, C. P. (2008). Exercise interval training: an improved stimulus for improving the 
physiology of pre-diabetes. Medical Hypothesis, 71(5), 752–761. VIEW ITEM

Farinatti, P. T., & Castinheiras Neto, A. G. (2011). The effect of between-set rest inter-
vals on the oxygen uptake during and after resistance exercise sessions performed with 
large- and small-muscle mass. Journal of Strength and Conditioning Research, 25(11), 
3181–3190. VIEW ITEM

Ferreira, A. P., Ferreira, C. B., de Souza, V. C., de Almeida Córdova, C. O., Branco 
Silva, G. C., Nóbrega, O. T., & de França, N. M. (2011). The influence of intense 
intermittent versus moderate continuous exercise on postprandial lipemia. Clinics (Sao 
Paulo), 66(4), 535–541. VIEW ITEM

Fox, E. L., & Mathews, D. K. (1981). The physiological basis of physical education and 
athletics. Philadelphia: Saunders College Pub.

http://jap.physiology.org/content/70/4/1713
http://www.nrcresearchpress.com/doi/pdf/10.1139/apnm-2012-0136
http://dx.doi.org/10.1016/j.cmet.2006.05.002
http://dx.doi.org/10.1172%2FJCI117864
http://jap.physiology.org/content/47/4/787
http://dx.doi.org/10.1016/j.metabol.2012.02.009
http://journals.lww.com/nsca-jscr/Abstract/2010/08000/Effects_of_Different_Strength_Training_Methods_on.38.aspx
http://diabetes.diabetesjournals.org/content/49/8/1295.short
http://dx.doi.org/10.1016/S0034-5687(99)00083-3
http://journals.lww.com/acsm-msse/Fulltext/2000/07000/Muscle_damage_and_resting_metabolic_rate_after.3.aspx
http://journals.lww.com/nsca-jscr/Abstract/2005/05000/AEROBIC_AND_RESISTANCE_EXERCISE_SEQUENCE_AFFECTS.16.aspx
http://dx.doi.org/10.1016/j.mehy.2008.06.024
http://journals.lww.com/nsca-jscr/Abstract/2011/11000/The_effect_of_Between_Set_Rest_Intervals_on_the.33.aspx
http://dx.doi.org/10.1590/S1807-59322011000400003


112

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

Frayn, K. (2010). Metabolic regulation. Oxford: John Wiley & Sons.
Frey, G. C., Byrnes, W. C., & Mazzeo, R. S. (1993). Factors influencing excess postexer-

cise oxygen consumption in trained and untrained women. Metabolism, 42(7), 822–828. 
VIEW ITEM

Galbo, H., Holst, J., & Christensen, N. J. (1979). The effect of different diets and of in-
sulin on the hormonal response to prolonged exercise. Acta Physiologica Scandinavica, 
107(1), 19-32. VIEW ITEM

Gibala, M. J., Little, J. P., MacDonald, M. J., & Hawley, J. A. (2012). Physiological 
adaptations to low-volume, high-intensity interval training in health and disease. The 
Journal of Physiology, 590(5), 1077–1084. VIEW ITEM

Gibala, M. J., Little, J. P., van Essen, M., Wilkin, G. P., Burgomaster, K. A., Safdar, 
A., et al. (2006). Short-term sprint interval versus traditional endurance training: similar 
initial adaptations in human skeletal muscle and exercise performance. The Journal of 
Physiology, 575(3), 901–911. VIEW ITEM

Gibala, M. J., & McGee, S. L. (2008). Metabolic adaptations to short-term high-intensity 
interval training: a little pain for a lot of gain? Exercise and Sport Sciences Reviews, 
36(2), 58–63. VIEW ITEM

Gill, J., Al-Mamari, A., Ferrell, W., Cleland, S., Sattar, N., Packard, C., et al. (2006). 
Effects of a moderate exercise session on postprandial lipoproteins, apolipoproteins and 
lipoprotein remnants in middle-aged men. Atherosclerosis, 185(1), 87–96. VIEW ITEM

Gollnick, P. D. (1977). Free fatty acid turnover and the availibility of substrates as a limi-
ting factor in prolonged exercise. Annals of the New York Academy of Science, 301, 
64–71. VIEW ITEM

Goodpaster, B. H., Theriault, R., Watkins, S. C., & Kelley, D. E. (2000). Intramuscular 
lipid content is increased in obesity and decreased by weight loss. Metabolism, 49(4), 
467–472. VIEW ITEM

Gore, C. J., & Withers, R. T. (1990). Effect of exercise intensity and duration on postexer-
cise metabolism. Journal of Applied Physiology, 68(6), 2362–2368. VIEW ITEM

Gosselin, L. E., Kozlowski, K. F., Devinney-Boymel, L., & Hambridge, C. (2012). Meta-
bolic Response of Different High Intensity Aerobic Interval Exercise Protocols. Journal 
of Strength and Conditioning Research, 26(10), 2866–2871. VIEW ITEM

Guiraud, T., Nigam, A., Gremeaux, V., Meyer, P., Juneau, M., & Bosquet L. (2012). Hi-
gh-intensity interval training in cardiac rehabilitation. Sports Medicine, 42(7), 587–605. 
VIEW ITEM

Hagberg, J. M., Hickson, R. C., Ehsani, A. A., & Holloszy, J. O. (1980). Faster adjust-
ment to and recovery from submaximal exercise in the trained state. Journal of Applied 
Physiology, 48(2), 218–224. VIEW ITEM

Haltom, R. W., Kraemer, R. R., Sloan, R. A., Hebert, E. P., Frank, K., & Tryniecki, J. 
L. (1999). Circuit weight training and its effects on excess postexercise oxygen con-
sumption. Medicine and Science in Sports and Exercise, 31(11), 1613–1618. VIEW 
ITEM

Hansen, D., Dendale, P., van Loon, L. J. C., & Meeuseen, R. (2010). The impact of 
training modalities on the clinical benefits of exercise intervention in patients with car-
diovascular disease risk or type 2 diabetes mellitus. Sports Medicine, 40(11), 921–940. 
VIEW ITEM

http://dx.doi.org/10.1016/0026-0495(93)90053-Q
http://onlinelibrary.wiley.com/doi/10.1111/j.1748-1716.1979.tb06438.x/epdf
http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2011.224725/full
http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2006.112094/full
http://journals.lww.com/acsm-essr/Abstract/2008/04000/Metabolic_Adaptations_to_Short_term_High_Intensity.3.aspx
http://dx.doi.org/10.1016/j.atherosclerosis.2005.06.009
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1977.tb38186.x/epdf
http://dx.doi.org/10.1016/S0026-0495(00)80010-4
http://jap.physiology.org/content/68/6/2362
http://journals.lww.com/nsca-jscr/Abstract/2012/10000/Metabolic_Response_of_Different_High_Intensity.34.aspx
http://link.springer.com/content/pdf/10.2165%2F11631910-000000000-00000.pdf
http://jap.physiology.org/content/48/2/218
http://journals.lww.com/acsm-msse/Fulltext/1999/11000/Circuit_weight_training_and_its_effects_on_excess.18.aspx
http://journals.lww.com/acsm-msse/Fulltext/1999/11000/Circuit_weight_training_and_its_effects_on_excess.18.aspx
http://link.springer.com/content/pdf/10.2165%2F11535930-000000000-00000.pdf


ANNALES KINESIOLOGIAE • 6 • 2015 • 2

113

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

Hardman, A. E. (2001). Issues of fractionization of exercise (short vs long bouts). Medici-
ne and Science in Sports and Exercise, 33(Supp. 6), 421–427. VIEW ITEM

Haskell, W. L., Lee, I. M., Pate, R. R., Powell, K. E., Blair, S. N., Franklin, B. A., et al. 
(2007). Physical activity and public health: updated recommendation for adults from the 
American College of Sports Medicine and the American Heart Association. Medicine 
and Science in Sports and Exercise, 39(8), 1423–1434. VIEW ITEM

Hazell, T. J., Olver, T. D., Hamilton, C. D., & Lemon, P. W. R. (2012). Two minutes of 
sprint-interval exercise elicits 24-hr oxygen consumption similar to that of 30 min of 
continuous endurance exercise. International Journal of Sport Nutrition and Exercise 
Metabolism, 22(4), 276–283. VIEW ITEM

Heden, T. (2011). One-set resistance training elevates energy expenditure for 72 h similar 
to three sets. European Journal of Applied Physiology, 111(3), 477–484. VIEW ITEM

Helge, J. W., & Kiens, B. (1997). Muscle enzyme activity in man: Role of substrate avai-
lability and training. The American Journal of Physiology, 272(5), 1620–1624. VIEW 
ITEM

Helge, J. W., Richter, E. A., & Kiens, B. (1996). Interaction of training and diet on me-
tabolism and endurance during exercise in man. The Journal of Physiology, 492(1), 
293–306. VIEW ITEM

Helge, J. W., Stallknecht, B., Richter, E. A., Galbo, H., & Kiens, B. (2007). Muscle me-
tabolism during graded quadriceps exercise in man. The Journal of Physiology, 581(3), 
1247–1258. VIEW ITEM

Helge, J. W., Wulff, B., & Kiens, B. (1998). Impact of a fat rich diet on endurance in man: 
role of dietary period. Medicine and Science in Sports and Exercise, 30(3), 456–461. 
VIEW ITEM

Helge, J. W., Watt, P. W., Richter, E. A., Rennie, M. J., & Kiens, B. (2001). Fat utilization 
during exercise: adaptation to a fat-rich diet increases utilization of plasma fatty acids 
and very low density lipoprotein-triacylglycerol in humans. The Journal of Physiology, 
537(3), 1009–1020. VIEW ITEM

Henriksson, J. (1977). Training induced adaptations of skeletal muscle and metabolism 
during submaximal exercise. The Journal of Physiology, 270(3), 661–675. VIEW ITEM

Hoeks, J., Van Herpen, N. A., Mensink, M., Moonen-Kornips, E., Van Beurden, D., 
Hesselink, M. K., et al. (2010). Prolonged fasting identifies skeletal muscle mitochon-
drial dysfunction as a consequence rather than cause of human insulin resistance. Dia-
betes, 59(9), 2117–2125. VIEW ITEM

Horowitz, J. F. (2003). Fatty acid mobilization from adipose tissue during exercise. Trends 
in Endocrinology and Metabolism, 14(8), 386–392. VIEW ITEM

Houmard, J. A., Tanner, C. Y., Cunningham, P. G., Pories, W. J., MacDonald, K. G., & 
Schulman, G. I. (2002). Effect of weight loss on insulin sensitivity and intramuscular 
long-chain fatty acyl-CoAs in morbidly obese subjects. Diabetes, 51(10), 2959–2963. 
VIEW ITEM

Jamurtas, A. Z., Koutedakis, Y., Paschalis, V., Tofas, T., Yfanti, C., Tsiokanos, A., et al. 
(2004). The effects of a single bout of exercise on resting energy expenditure and re-
spiratory exchange ratio. European Journal of Applied Physiology, 92(4–5), 393–398. 
VIEW ITEM

Jeppesen. J., Albers, P. H., Rose, A. J., Birk, J. B., Schjerling, P., Dzamko, N., et al. 
(2011). Contraction induced skeletal muscle FAT/CD36 trafficking and fatty acid uptake 
is AMPK independent. Journal of Lipid Research, 52, 699–711. VIEW ITEM

http://journals.lww.com/acsm-msse/Fulltext/2001/06001/Issues_of_fractionization_of_exercise__short_vs.10.aspx
http://journals.lww.com/acsm-msse/Fulltext/2007/08000/Physical_Activity_and_Public_Health__Updated.27.aspx
https://www.researchgate.net/publication/227342497_Two_Minutes_of_Sprint-Interval_Exercise_Elicits_24-hr_Oxygen_Consumption_Similar_to_That_of_30_min_of_Continuous_Endurance_Exercise
http://link.springer.com/article/10.1007/s00421-010-1666-5/fulltext.html
http://ajpregu.physiology.org/content/272/5/R1620.full-text.pdf+html
http://ajpregu.physiology.org/content/272/5/R1620.full-text.pdf+html
http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.1996.sp021309/full
http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2007.128348/full
http://journals.lww.com/acsm-msse/Fulltext/1998/03000/Impact_of_a_fat_rich_diet_on_endurance_in_man_.18.aspx
http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7793.2001.01009.x/full
http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.1977.sp011974/full
http://diabetes.diabetesjournals.org/content/59/9/2117.full
http://dx.doi.org/10.1016/S1043-2760(03)00143-7
http://diabetes.diabetesjournals.org/content/51/10/2959.full
http://link.springer.com/article/10.1007/s00421-004-1156-8/fulltext.html
http://www.jlr.org/content/52/4/699.full


114

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

Jeppesen, J., & Kiens, B. (2012). Regulation and limitations to fatty acid oxidation during 
exercise. The Journal of Physiology, 590(5), 1059–1068. VIEW ITEM

Jeppesen, J., Jordy, A. B., Sjøberg, K. A., Füllekrug, J., Stahl, A., Nybo, L., et al. (2012). 
Enhanced Fatty Acid Oxidation and FATP4 Protein Expression after Endurance Exerci-
se Training in Human Skeletal Muscle. PLoS One, 7(1). VIEW ITEM

Kaminsky, L. A., Padjen, S., & LaHam-Saeger, J. (1990). Effect of split exercise sessions 
on excess postexercise oxygen consumption. British Journal of Sports Medicine, 24(2), 
95–98. VIEW ITEM

Kaminsky, L. A., Knowlton, R. G., Perkins, R. M., & Hetzler, R. K. (1986). Relation-
ships of aerobic capacity and percent body fat with plasma free fatty acid following 
walking. The American Journal of Clinical Nutrition, 44(5), 603–609. VIEW ITEM

Kelley, D. E., & Goodpaster, B. H. (2001). Skeletal muscle triglyceride: an aspect of re-
gional adiposity and insulin resistance. Diabetes Care, 24(5), 933–941. VIEW ITEM

Kelly, B., King, J. A., Goerlach, J., & Nimmo, M. A. (2013). The impact of high-intensity 
intermittent exercise on resting metabolic rate in healthy males. European Journal of 
Applied Physiology, 113(12), 3039–3047. VIEW ITEM

Kessler, H. S., Sisson, S. B., & Short, K. R. (2012). The potential for high-intensity inter-
val training to reduce cardiometabolic disease risk. Sports Medicine, 42(6), 489–509. 
VIEW ITEM

Kiens, B. (2006). Skeletal musle lipid metabolism in exercise and insulin resistance. Physi-
ological Reviews, 86(1), 205–243. VIEW ITEM

Kiens, B., Alsted, T. J., & Jeppesen, J. (2011). Factors regulating fat oxidation in human 
skeletal muscle. Obesity Reviews, 12(10), 852–858. VIEW ITEM

Kiens, B., Essen Gustavsson, B., Christensen, N. J., & Saltin, B. (1993). Skeletal muscle 
substrate utilization during submaximal exercise in man: Effect of endurance training. 
The Journal of Physiology, 469(1), 459–478. VIEW ITEM

Kiens, B., & Lithell, H. (1993). Lipoprotein metabolism influenced by training induced 
changes in human skeletal muscle. The Journal of Clinical Investigation, 83(2), 558–
564. VIEW ITEM

Kimm, S. Y., Glynn, N. W., McMahon, R. P., Voorhees, C. C., Striegel-Moore, R. H., 
& Daniels, S. R. (2006). Self-perceived barriers to activity participation among seden-
tary adolescent girls. Medicine & Science in Sports & Exercise, 38(3), 534–540. VIEW 
ITEM

Kisner, C., & Colby, L. A. (2007). Therapeutic exercise. F. A. Davis Company, Philade-
lphia.

Koivisto, V., Hendler, R., Nadel, E., & Felig, P. (1982). Influence of physical training 
on the fuel-hormone response to prolonged low-intensity exercise. Metabolism, 31(2), 
192–197. VIEW ITEM

Kravitz, L., Robergs, R. A., Heyward, V. H., Wagner, D. R., & Powers, K. (1997). Ex-
ercise mode and gender comparisons of energy expenditure at self-selected intensities. 
Medicine and Science in Sports and Exercise, 29(8), 1028–1035. VIEW ITEM

Lamont, L. S., Romito, R., & Rossi, K. (2010). Fat-free mass and gender influences the 
rapid-phase excess postexercise oxygen consumption. Applied Physiology, Nutrition 
and Metabolism, 35(1), 23–26. VIEW ITEM

LeCheminant, J. D., Jacobsen, D. J., Bailey, B. W., Mayo, M. S., Hill, J. O., Smith, B. 
K., et al. (2008). Effects of long-term aerobic exercise on EPOC. International Journal 
of Sports Medicine, 29(1), 53–58. VIEW ITEM

http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2011.225011/full
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0029391
http://bjsm.bmj.com/content/24/2/95.full.pdf+html
http://ajcn.nutrition.org/content/44/5/603.full.pdf+html
http://care.diabetesjournals.org/content/24/5/933.full.pdf+html?sid=751d0f05-7295-4c36-88fb-dc5b64316a0f
http://link.springer.com/article/10.1007/s00421-013-2741-5/fulltext.html
http://link.springer.com/content/pdf/10.2165%2F11630910-000000000-00000.pdf
http://physrev.physiology.org/content/86/1/205.full-text.pdf+html
http://onlinelibrary.wiley.com/doi/10.1111/j.1467-789X.2011.00898.x/full
http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.1993.sp019823/full
http://dx.doi.org/10.1172%2FJCI113918
http://journals.lww.com/acsm-msse/Fulltext/2006/03000/Self_Perceived_Barriers_to_Activity_Participation.19.aspx
http://journals.lww.com/acsm-msse/Fulltext/2006/03000/Self_Perceived_Barriers_to_Activity_Participation.19.aspx
http://dx.doi.org/10.1016/0026-0495(82)90135-4
http://journals.lww.com/acsm-msse/Fulltext/1997/08000/Exercise_mode_and_gender_comparisons_of_energy.7.aspx
http://www.nrcresearchpress.com/doi/pdf/10.1139/H09-120
https://www.researchgate.net/publication/5962990_Effects_of_long-term_aerobic_exercise_on_EPOC


ANNALES KINESIOLOGIAE • 6 • 2015 • 2

115

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

Maehlum, S., Grandmontagne, M., Newsholme, E. A., & Sejersted, O. M. (1986). Ma-
gnitude and duration of excess postexercise oxygen consumption in healthy young su-
bjects. Metabolism, 35(5), 425–429. VIEW ITEM

Matsuo, T., Saitoh, S., & Suzuki, M. (1999). Effects of the menstrual cycle on excess po-
stexercise oxygen consumption in healthy young women. Metabolism, 48(3), 275–277. 
VIEW ITEM

McArdle, W. D., Katch, F. I., & Katch, V. L. (2010). Exercise physiology: Nutrition, 
energy and human performance (7th ed.). Philadephia: Lippincott Wilkins & Wilkins.

McGarvey, W., Jones, R., & Petersen, S. (2005). Excess post-exercise oxygen consump-
tion following continuous and interval cycling exercise. International Journal of Sport 
Nutrition and Exercise Metabolism, 15(1), 28–37. VIEW ITEM

Melby, C., Scholl, C., Edwards, G., & Bullough, R. (1993). Effect of acute resistance 
exercise on postexercise energy expenditure and resting metabolic rate. Journal of Ap-
plied Physiology, 75(4), 1847–1853. VIEW ITEM

Melby, C. L., Tincknell, T., & Schmidt, W. D. (1992). Energy expenditure following a 
bout of non-steady state resistance exercise. The Journal of Sports Medicine and Physi-
cal Fitness, 32(2), 128–135. VIEW ITEM

Mittendorfer, B., Fields, D. A., & Klein, S. (2004). Excess body fat in man decreases pla-
sma fatty acid availability and oxidation during endurance exercise. American Journal 
of Physiology, Endocrinology and Metabolism, 286(3), 354–362. VIEW ITEM

Oliveira, N. L., & Oliveira, J. (2011). Excess postexercise oxygen consumption is unaf-
fected by the resistance and aerobic exercise order in an exercise session. Journal of 
Strength and Conditioning Research, 25(10), 2843–2850. VIEW ITEM

Pérez-Martin, A., Dumortier, M., Raynaud, E., Brun, J. F., Fédou, C., Bringer, J., et 
al. (2001). Balance of substrate oxidation during submaximal exercise in lean and obese 
people. Diabetes & Metabolism (Paris), 27(4), 466–474. VIEW ITEM

Phelain, J. F., Reinke, E., Harris, M. A., & Melby, C. L. (1997). Postexercise energy ex-
penditure and substrate oxidation in young women resulting from exercise bouts of dif-
ferent intensity. Journal of American College Nutrition, 16(2), 140–146. VIEW ITEM

Pillard, F., van Wymelbeke, V., Garrigue, E., Moro, C., Crampes, F., Guilland, J. C., 
Berlan, M., de Glisezinski, I., Harant, I., Rivière, D., & Brondel, L. (2010). Lipid 
oxidation in overweight men after exercise and food intake. Metabolism: clinical and 
experimental, 59(2), 267–274. VIEW ITEM

Poirier, P., Giles, T. D., Bray, G. A., Hong, Y., Stern, J. S., Pi-Sunyer, F. X., et al. (2006). 
Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight 
loss: an update of the 1997 American Heart Association Scientific Statement on Obesity 
and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical 
Activity, and Metabolism. Circulation, 113(6), 898–918. VIEW ITEM

Poole, D. C., & Gaesser, G. A. (1985). Response of ventilatory and lactate thresholds to 
continuous and interval training. Journal of Applied Physiology, 58(4), 1115–1121. 
VIEW ITEM

Rabol, R., Petersen, K. F., Dufour, S., Flannery, C., & Schulman, G. L. (2011). Reversal 
of muscle insulin resistance with exercise reduces postprandial hepatic de novo lipogen-
esis in insulin resistant individuals. Proceedings of National Academy of Science USA, 
108(33), 13705–13709. VIEW ITEM

Roepstorff, C., Halberg, N., Hillig, T., Saha, A. K., Ruderman, N. B., Wojtaszewski, 
J. F., et al. (2005). Malonyl-CoA and carnitine in regulation of fat oxidation in human 

http://dx.doi.org/10.1016/0026-0495(86)90132-0
http://dx.doi.org/10.1016/S0026-0495(99)90071-9
http://journals.humankinetics.com/ijsnem-back-issues/IJSNEMVolume15Issue1February/ExcessPostExerciseOxygenConsumptionFollowingContinuousandIntervalCyclingExercise
http://jap.physiology.org/content/75/4/1847
https://www.researchgate.net/publication/21720298_Energy_expenditure_following_a_bout_of_non-steady_state_resistance_exercise
http://ajpendo.physiology.org/content/286/3/E354.full-text.pdf+html
http://journals.lww.com/nsca-jscr/Abstract/2011/10000/Excess_Postexercise_Oxygen_Consumption_is.25.aspx
http://www.em-consulte.com/en/article/80029
http://www.tandfonline.com/doi/abs/10.1080/07315724.1997.10718664
http://dx.doi.org/10.1016/j.metabol.2009.07.023
http://circ.ahajournals.org/content/113/6/898.full
http://jap.physiology.org/content/58/4/1115
http://www.pnas.org/content/108/33/13705.full


116

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

skeletal muscle during exercise. American Journal of Physiology, Endocrinology and 
Metabolism, 288(1), 133–142. VIEW ITEM

Romijn, J. A., Coyle, E. F., Sidossis, L. S., Gastaldelli, A., Horowitz, J. F., Enderte, E., 
et al. (1993). Regulation of endogenous fat and carbohydrate metabolism in relation to 
exercise intensity and duration. American Journal of Physiology, Endocrinology and 
Metabolism, 265(3), 380–391. VIEW ITEM

Rui, L. (2014). Energy metabolism in the liver. Comprehensive physiology, 4(1), 177–197. 
VIEW ITEM

Savage, D. B., Petersen, K. F., & Schulman, G. L. (2007). Disordered Lipid Metaboli-
sm and the Pathogenesis of Insulin Resistance. Physiological reviews, 87(2), 507–520. 
VIEW ITEM

Scheen, A. J., Pirnay, F., Luyckx, A. S., & Lefebvre, P. J. (1983). Metabolic adaptation 
to prolonged exercise in severely obese subjects. International Journal of Obesity, 7(3), 
221–229. 

Schuenke, M. D., Mikat, R. P., & McBride, J. M. (2002). Effect of an acute period of 
resistance exercise on excess post-exercise oxygen consumption: implications for body 
mass management. European Journal of Applied Physiology, 86(5), 411–417. VIEW 
ITEM

Scott, C. B. (1997). Interpreting energy expenditure for anaerobic exercise and recovery: 
an anaerobic hypothesis. The Journal of Sports Medicine and Physical Fitness, 37(1), 
18–23. VIEW ITEM

Scott, C. B. (2005). Contributions of anaerobic energy expenditure to whole-body thermo-
genesis. Nutrition & Metabolism, 2(1), 14. VIEW ITEM

Scott, C. B. (2012). The effect of time-under-tension and weight lifting cadence on aerobic, 
anaerobic, and recovery energy expenditures: 3 submaximal sets. Applied Physiology, 
Nutrition and Metabolism, 37(2), 252–256. VIEW ITEM

Scott, C. B., Leighton, B. H., Ahearn, K. J., & McManus, J. J. (2011a). Aerobic, ana-
erobic, and excess postexercise oxygen consumption energy expenditure of muscular 
endurance and strength: 1-set of bench presses to muscular fatigue. Journal of Strength 
and Conditioning Research, 25(4), 903–908. VIEW ITEM

Sedlock, D. A. (1991a) Effect of exercise intensity on postexercise energy expenditure in 
woman. British Journal of Sports Medicine, 25(1), 38–40. VIEW ITEM

Sedlock, D. A. (1991b). Postexercise energy expenditure following upper body exercise. 
Research Quarterly for Exercise and Sport, 62(2), 213–216. VIEW ITEM

Sedlock, D. A. (1994). Fitness level and postexercise energy expenditure. The Journal of 
Sports Medicine and Physical Fitness, 34(4), 336–342. VIEW ITEM

Sedlock, D. A., Fissinger, J. A., & Melby, C. L. (1989). Effect of exercise intensity and 
duration on postexercise energy expenditure. Medicine and Science in Sports and Exer-
cise, 21(6), 662–666. VIEW ITEM

Sedlock, D. A., Lee, M. G., Flynn, M. G., Park, K. S., & Kamimori, G. H. (2010). Excess 
postexercise oxygen consumption after aerobic exercise training. International Journal 
of Sport Nutrition and Exercise Metabolism, 20(4), 336–349. 

Shiraev, T., & Barclay, G. (2012). Evidence based exercise - clinical benefits of high inten-
sity interval training. Australian Family Physician, 41(12), 960–962.

Short, K. R., & Sedlock, D. A. (1997). Excess postexercise oxygen consumption and re-
covery rate in trained and untrained subjects. Journal of Applied Physiology, 83(1), 
153–159. VIEW ITEM

http://ajpendo.physiology.org/content/288/1/E133.full-text.pdf+html
http://ajpendo.physiology.org/content/265/3/E380.full-text.pdf+html
http://onlinelibrary.wiley.com/doi/10.1002/cphy.c130024/full
http://physrev.physiology.org/content/87/2/507.full-text.pdf+html
http://link.springer.com/content/pdf/10.1007%2Fs00421-001-0568-y.pdf
http://link.springer.com/content/pdf/10.1007%2Fs00421-001-0568-y.pdf
https://www.researchgate.net/publication/14029201_Interpreting_energy_expenditure_for_anaerobic_exercise_and_recovery_An_anaerobic_hypothesis
http://www.biomedcentral.com/content/pdf/1743-7075-2-14.pdf
http://www.nrcresearchpress.com/doi/pdf/10.1139/h11-158
http://journals.lww.com/nsca-jscr/Abstract/2011/04000/Aerobic,_Anaerobic,_and_Excess_Postexercise_Oxygen.4.aspx
http://bjsm.bmj.com/content/25/1/38.full.pdf+html?sid=51570019-4b6b-4fe0-9ff4-7228c198883b
https://www.researchgate.net/publication/15554733_Fitness_level_and_postexercise_energy_expenditure
http://journals.lww.com/acsm-msse/Abstract/1989/12000/Effect_of_exercise_intensity_and_duration_on.6.aspx
http://jap.physiology.org/content/83/1/153


ANNALES KINESIOLOGIAE • 6 • 2015 • 2

117

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ..., 93–118

Smith, J., & Mc Naughton, L. (1993). The effects of intensity of exercise on excess po-
stexercise oxygen consumption and energy expenditure in moderately trained men and 
women. European Journal of Applied Physiology and Occupational Physiology, 67(5), 
420–425. VIEW ITEM

Spriet, L. L. (2011). Metabolic regulation of fat use during exercise and in recovery. Nestle 
Nutrition Institute Workshop Series, 69, 39–53. VIEW ITEM

Stamford, B. A. (1975). Maximal oxygen uptake during treadmill walking and running at 
various speeds. Journal of Applied Physiology, 39(3), 386–389. VIEW ITEM

Stutts, W. C. (2002). Physical activity determinants in adults. Perceived benefits, barriers, 
and self-efficacy. American Association of Occupational Health Nurses, 50(11), 499–
507. VIEW ITEM

Tahara, Y., Moji, K., Honda, S., Nakao, R., Tsunawake, N., Fukuda, R., et al. (2008). 
Fat-free mass and excess post-exercise oxygen consumption in the 40 minutes after 
short-duration exhaustive exercise in young male Japanese athletes. The Journal of 
Physiological Anthropology, 27(3), 139–143. VIEW ITEM

Talanian, J. L., Galloway, S. D., Heigenhauser, G. J., Bonen, A., & Spriet, L. L. (2007). 
Two weeks of high-intensity aerobic interval training increases the capacity for fat oxi-
dation during exercise in women. Journal of Applied Physiology, 102(4), 1439–1447. 
VIEW ITEM

Thornton, M. K., & Potteiger, J. A. (2002). Effects of resistance exercise bouts of diffe-
rent intensities but equal work on EPOC. Medicine and Science in Sports and Exercise, 
34(4), 715–722. VIEW ITEM

Tjønna, A. E., Lee, S. J., Rognmo, Ø., Stølen, T. O., Bye, A., Haram, P. M., et al. (2008). 
Aerobic interval training versus continuous moderate exercise as a treatment for the 
metabolic syndrome: A pilot study. Circulation, 118(4), 346–354. VIEW ITEM

Unger, R. H., Scherer, P. E., & Holland, W. L. (2013). Dichotomous roles of leptin and 
adiponectin as enforcers against lipotoxicity during feast and famine. Molecular biology 
of the cell, 24(19), 3011–3015. VIEW ITEM

van Baak, M. A. (1999). Exercise training and substrate utilization in obesity. International 
Journal of Obesity, 23(Suppl. 3), 11–17. VIEW ITEM

van Loon, L. J., Greenhaff, P. L., Constantin Teodosiu, D., Saris, W. H., & Wagenma-
kers, A. J. (2001). The effects of increasing exercise intensity on muscle fuel utilisation 
in humans. The Journal of Physiology, 536(1), 295–304. VIEW ITEM

Van Proeyen, K., Szlufcik, K., Nielens, H., Ramaekers, M., & Hespel, P. (2011). Benefi-
cial metabolic adaptations due to endurance exercise training in the fasted state. Journal 
of Applied Physiology, 110(1), 236–245. VIEW ITEM

Wall, B. T., Stephens, F. B., Constantin Teodosiu, D., Marimuthu, K., Macdonald, I. 
A., & Greenhaff, P. L. (2011). Chronic oral ingestion of L-carnitine and carbohydrate 
increases muscle carnitine content and alters muscle fuel metabolism during exercise in 
humans. The Journal of Physiology, 589(4), 963–973. VIEW ITEM

Walsh, T. S. (2003). Recent advances in gas exchange measurement in intensive care pati-
ents. British journal of Anaesthesia, 91(1), 120–131. VIEW ITEM

Wilkin, L. D., Cheryl, A., & Haddock, B. L. (2012). Energy expenditure comparison 
between walking and running in average fitness individuals. Journal of Strength and 
Conditioning Research, 26(4), 1039–1044. VIEW ITEM

Wojtaszewski, J. F., MacDonald, C., Nielsen, J. N., Hellsten, Y., Hardie, D. G., Kemp, 
B. E., et al. (2003). Regulation of 5′AMP-activated protein kinase activity and substrate 

http://link.springer.com/article/10.1007/BF00376458
http://www.karger.com/Article/Abstract/329281
http://jap.physiology.org/content/39/3/386
http://search.proquest.com/docview/219321927/fulltext?accountid=31479
https://www.jstage.jst.go.jp/article/jpa2/27/3/27_3_139/_pdf
http://jap.physiology.org/content/102/4/1439
http://journals.lww.com/acsm-msse/Fulltext/2002/04000/Effects_of_resistance_exercise_bouts_of_different.24.aspx
http://circ.ahajournals.org/content/118/4/346.full?sid=fe311656-ce50-4274-bd9c-22efab414104
http://www.molbiolcell.org/content/24/19/3011.full
http://www.nature.com/ijo/journal/v23/n3s/pdf/0800879a.pdf
http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7793.2001.00295.x/full
http://jap.physiology.org/content/110/1/236
http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2010.201343/full
http://bja.oxfordjournals.org/content/91/1/120.full
http://journals.lww.com/nsca-jscr/Abstract/2012/04000/Energy_Expenditure_Comparison_Between_Walking_and.22.aspx


118

Barbara PURKART, Boštjan ŠIMUNIČ, Mitja GERŽEVIČ: AN OVERVIEW OF TRAINING METHODS THAT PROMOTE THE ...,  93–118

ANNALES KINESIOLOGIAE • 6 • 2015 • 2

utilization in exercising human skeletal muscle. American Journal of Physiology, En-
docrinology and Metabolism, 284(4), 813–822. VIEW ITEM

Wong, T., & Harber, V. (2006). Lower Excese Postexercise Oxygen Consumption and 
Altered Growth Hormone and Responses to Exercise in Obese Men. The Journal of 
Clinical Endocrinology and Metabolism, 91(2), 678–686. VIEW ITEM

Zeni, A. I., Hoffman, M. D., & Clifford, P. S. (1996). Energy expenditure with indoor 
exercise machines. The Journal of the American Medical Association, 275(18), 1424–
1427. VIEW ITEM

Zuniga, J. M., Berg, K., Noble, J., Harder, J., Chaffin, M. E., & Hanumanthu, V. S. 
(2011). Physiological responses during interval training with different intensities and 
durations of exercise. Journal of Strength and Conditioning Research, 25(5), 1279–
1284. VIEW ITEM

http://ajpendo.physiology.org/content/284/4/E813.full-text.pdf+html
http://dx.doi.org/10.1210/jc.2005-1148
http://jama.jamanetwork.com/article.aspx?articleid=402029
http://journals.lww.com/nsca-jscr/Abstract/2011/05000/Physiological_Responses_during_Interval_Training.13.aspx

	_GoBack
	_GoBack
	_GoBack
	_GoBack
	_GoBack
	_GoBack
	_GoBack

