excessive accumulation of fat in the liver , that is , intrahepatic triglyceride ( ihtg ) , is associated with increased prevalence rates of and risk for dyslipidemia , diabetes , and cardiovascular disease     [ 13 ] .  
data from epidemiological as well as metabolic studies indicate that increased ihtg content is accompanied by insulin resistance and dysregulation of lipid metabolism     [ 46 ] .
exercise is known to improve metabolic function     [ 7 , 8 ] ; however its effects on ihtg remain elusive     [ 9 , 10 ] .
data from studies in humans are scarce and not entirely consistent . in this paper ,
the results from a number of animal studies are briefly reviewed in an attempt to highlight putative factors that may modulate the effect of exercise on ihtg content .
many studies have evaluated the effect of aerobic exercise training on ihtg content in rodents ; their design varies in terms of sex , strain , background diet , training duration , the prandial status , and the time of assessment after the last bout of exercise ( table 1 )     [ 1237 ] .
results are largely heterogeneous , but a crude analysis of the data suggests that endurance training decreases ihtg ( median : 16% , range : 92% to + 97% , n = 50 studies ; table 1 ) .  
most frequently     [ 14 , 16 , 18 , 20 , 26 , 31 , 35 ] but not always     [ 15 , 17 , 34 , 37 ] , exercise has been shown to be more effective in reducing liver fat or attenuating its accretion in animals fed high - fat rather than standard , low - fat diets ( median decrease : 25% and 14% , resp .
this is consistent with data from human studies , in which exercise training appears to be more potent in reducing ihtg in subjects with increased baseline ihtg , for example , subjects with nafld , type ii diabetes , or the elderly .
the reasons why exercise is more effective in reducing ihtg on high - fat than low - fat diets are not entirely clear but are likely related to the hepatosteatotic effect of high - fat feeding .
fat is mainly stored as microvesicles ( < 1  m ) within hepatocytes , whereas the high - fat diet - induced hepatic steatosis occurs via accumulation of macrovesicles ( > 1  m )     [ 18 , 38 ] .
endurance training has been shown to completely prevent the high - fat diet - induced hepatic steatosis     [ 18 , 38 ] , that is , the hepatocyte surface area occupied by the lipid vacuoles , solely by reducing the number of lipid vacuoles in all sizes between 1 and 10  m ( i.e. , macrovesicles ) , without affecting the number of vacuoles of surface area < 1  m ( i.e. , microvesicles ) .  
hence exercise may have less of an effect when on low - fat diets , not only because of lower total ihtg content , but also because most of this fat ( 75% ) is stored in microvesicles , not macrovesicles .
a more pronounced ihtg - depleting effect of exercise has also been observed under other conditions that favor the development of fatty liver , such as overfeeding     , ovariectomy , ethanol ingestion , or tumor - bearing     .
apart from the fat content of the background diet , the type of dietary carbohydrate , protein     , and fat ( i.e. , saturated or unsaturated fatty acids ) , as well as the feeding pattern ( ad libitum or paired )   do not appear to affect , at least not in a major way , the exercise - induced change in ihtg content .   
the collective of available data in animals highlights a number of other putative factors that may modulate the effect of exercise on liver fat ; however , none of these factors has been formally tested using rigorous experimental designs .
concurrent weight loss or attenuated weight gain is not likely critical for the exercise - induced depletion of ihtg to manifest , albeit they may lead to greater reductions in liver fat when compared to no weight loss or similar weight gain ( median decrease : 27.5% and 14% , resp .
however , just like in humans , loss of visceral adipose tissue mass with exercise training is not necessarily coupled with a corresponding decrease in liver fat     [ 16 , 18 , 28 , 37 ] .  
likewise , human studies have shown that exercise - induced reductions in ihtg content can occur in the absence of changes in total body fat      or even visceral adipose tissue .   
exercise may be more effective in reducing ihtg content in males than in females ( median decrease : 25% and 14% , resp .
, figure 1(c ) ) , in fasted ( 6  h ) than in fed animals ( median decrease : 31% and 11% , resp .
, figure 1(d ) ) , and after longer ( 8  wk ) than shorter interventions      ( median decrease : 24% and 14% , resp . ; figure 1(e ) ) . the time elapsed from the last bout of exercise ( 24  h or 36  h )
may also mediate the observed changes in ihtg ( median decrease : 24% and 13.5% , resp .
, figure 1(f ) ) , suggesting that even acute exercise could affect liver fat . however , relevant information is scarce and inconclusive .
a single bout of aerobic exercise ( 3060  min ) did not affect ihtg content , measured immediately after exercise , in female rats      but caused a 30% decrease in male rats      of the same strain , under both standard and high - fat feeding conditions .
this is in line with data from exercise training studies in animals raising the possibility that males may be more sensitive to the ihtg - reducing effect of exercise than females ( figure 1(c ) ) , as well as with recent observations in humans .
studies in which male rats were exercised until exhaustion provide conflicting results , some observed a mild   or marked     [ 46 , 47 ] increase in hepatic steatosis whereas others found a decrease of 3060%   at the end of exercise .
if regular exercise reduces liver fat , cessation of exercise should lead to an increase in ihtg content .  
only a few animal studies have evaluated the effect of detraining on liver fat accumulation , and all have demonstrated that cessation of regular exercise ( after 616 weeks of training ) for a short ( 2 - 3 days ) or a long ( 6 weeks ) period of time is not associated with any significant changes in ihtg content compared with the trained state ( i.e. , before discontinuation of exercise ) when animals are fed a standard low - fat diet     [ 28 , 36 , 49 , 50 ] .
furthermore , detraining for 27 days does not alter the total number of hepatocyte lipid vacuoles and their size , even though it does activate precursors and processes in the liver known to initiate steatosis ( e.g. , decreased mitochondrial oxidative capacity , increased expression of de novo lipogenesis proteins , and increased malonyl coa levels ) .  
it is possible that this lack of an effect of detraining relates to the lesser potency of exercise in reducing liver fat content in animals fed standard low - fat diets ( figure 1 ) , so that changes after detraining are similarly less pronounced . for instance , two     [ 28 , 36 ] out of three studies that reported no effect of detraining on liver fat also failed to observe a training - induced decrease in ihtg content , suggesting that training and detraining have no effect on liver fat accumulation under low - fat feeding conditions .
whereas one study   did observe a training - induced decrease in liver fat in rats fed a low - fat diet but found no changes after detraining , implying that the ihtg - depleting effect of regular exercise is long - lived and is not readily reversed by detraining .
still , compared with sedentary , never - exercised counterparts , detrained animals appear to be relatively protected from mild hepatic steatosis induced by 2 weeks of high - fat feeding     , but not from the development of frank fatty liver 6 weeks after ovariectomy , even though cessation of exercise training in ovariectomized rats resulted in a nearly 40% increase in ihtg content compared with ovariectomized rats who did not stop exercising .
it is thus possible that the relevant molecular and biochemical adaptations to exercise are readily reversed when the exercise routine is interrupted ( < 1 week ) , however , changes in ihtg manifest later in time and only when strong triggering factors for liver fat accretion coexist , such as high - fat feeding or ovariectomy .
support for this notion is provided by an earlier study , where detraining resulted in a striking increase in ihtg content only when animals were subjected to starvation and refeeding .
the effect of exercise on ihtg content has recently attracted much scientific interest in light of the apparent detrimental metabolic effects of excessive liver fat accumulation .
although the results from a few studies in human subjects are promising , as exercise appears to reduce ihtg , the importance of the factors highlighted herein on the basis of studies in animals has never been evaluated in man .  
future studies should at least control for  in order to avoid confounding  or directly investigate the role of these factors in affecting the exercise - induced changes in liver fat content .
 an increase in intrahepatic triglyceride ( ihtg ) content is the hallmark of nonalcoholic fatty liver disease ( nafld ) and is strongly associated with insulin resistance and dyslipidemia . although regular aerobic exercise improves metabolic function , its role in regulating fat accumulation in the liver is incompletely understood , and human data are scarce . 
 results from exercise training studies in animals highlight a number of potential factors that could possibly mediate the effect of exercise on liver fat , but none of them has been formally tested in man . 
 the effect of exercise on ihtg content strongly depends on the background diet , so that exercise is more effective in reducing ihtg under conditions that favor liver fat accretion ( e.g. , when animals are fed high - fat diets ) . 
 concurrent loss of body weight or visceral fat does not appear to mediate the effect of exercise on ihtg , whereas sex ( males versus females ) , prandial status ( fasted versus fed ) , and duration of training , as well as the time elapsed from the last bout of exercise could all be affecting the observed exercise - induced changes in ihtg content . 
 the potential importance of these factors remains obscure , thus providing a wide array of opportunities for future research on the effects of exercise ( and diet ) on liver fat accumulation . 
1. Introduction
2. Exercise Training in Animals
3. Detraining after Regular Exercise
4. Conclusion