overall , glucose concentrations were 712% lower in all groups for 24  h after exercising , without significant differences between the modes of exercising . interestingly ,
glucose values exceeded 10  mmol / l for an average of about 2  h in glucose - intolerant persons and for more than 8  h in patients with type 2 diabetes .
this is in line with observations that even intravenous insulin infusion requires high insulin doses and tight manual control of infusions to restore normoglycaemia in type 2 diabetes   and that subcutaneous insulin infusion pumps fail to completely normalise postprandial hyperglycaemia in type 1 diabetes .
nevertheless , both modes of exercise similarly reduced the duration of excess glucose levels by more than 30% in patients with type 2 diabetes , with endurance - type training being gradually more efficient over the course of the first 6  h post exercise .
the duration of sensor glucose levels below 3.9  mmol / l was also not significantly different between control and exercise periods . of note , the average duration of 
( defined as blood glucose concentration < 3.9  mmol / l ) was generally prolonged in insulin - treated patients ( 3039  min ) and tended to be longer after endurance - type exercise ( 24  min ) compared with resistance - type exercise ( 12  min ) and control intervention ( 8  min ) in patients on oral agents .
in particular , between 6 and 12  h after endurance - type exercising , the duration of low glucose concentrations , albeit still short , was longer in insulin - treated patients .
while these data suggest an overall comparable efficacy of one bout of either endurance or resistance exercise on glycaemic profiles , they also point to differences in the time course of glucose lowering . for detailed analysis , one should consider the method employed to monitor glucose concentrations . although the authors converted the data obtained from the continuous glucose monitoring sensor into  blood glucose concentrations using the person s self - monitored capillary glucose data , these values reflect subcutaneous interstitial rather than blood glucose concentrations .
although the sensor device used by van dijk et al .   seems to provide a tight linear correlation between blood and sensor glucose values in patients with type 1 diabetes , sensor data underestimate glycaemia during high intensity exercise and overestimate glycaemia during low intensity exercise .
in addition , sensor data exhibit a delayed response compared with blood glucose during exercise recovery .
moreover , only 87% of the sensors from another provider gave adequate signals for 24  h in exercising adolescents with type 1 diabetes .
data on the accuracy of sensors in exercising patients with type 2 diabetes are still rare and the challenge to correctly assess hypoglycaemia has been mentioned by the senior author of the present paper before . of note ,
older patients with insulin resistance or long - standing type 2 diabetes may also have altered adipose tissue blood flow , which might differently affect blood and interstitial glucose levels . in any case , these limitations affect the absolute numbers rather than the overall conclusions of this paper .
other issues need to be considered when assessing the efficacy of resistance vs endurance training on glycaemic control in dysglycaemic states . in their study , van dijk et al .  
compared the glucose responses to only a single bout of each exercise protocol , which may be subject to considerable day - to - day variability . also , the short lag time of 4  days between the different interventions does not completely rule out carry - over effects of previous exercise on insulin sensitivity , which could last up to 6  days or more .
after acute endurance - type exercise , several cellular pathways ( fig .  1 ) , mainly amp - activated protein kinase , calcium signalling and p38 mitogen - activated protein kinase , stimulate myocellular glucose transport   and may also increase flux through atp synthase in vivo , even in relatives of patients with type 2 diabetes .
in addition , muscle insulin sensitivity improves in insulin - resistant humans following one bout of endurance exercising , as demonstrated by increased insulin - stimulated glucose transport / phosphorylation .
while no changes were found at the level of the insulin receptor , its substrates or phosphoinositide 3-kinase , and more distal components of insulin signalling , such as protein kinase c isoforms , rac1 and tbc1 domain family , member 4 may be more active   ( fig .  1 ) .
resistance exercise training activates the mammalian target of rapamycin / serine kinase 6 pathway , thereby increasing protein synthesis and muscle mass .
provide evidence for a glucose - lowering effect , obviously occurring independently of muscle mass .
this is in line with a previous report demonstrating that even a single session of resistance exercise can improve fasting glucose and insulin sensitivity as calculated by homa .
this paper further addressed the question of whether exercise intensity affects glycaemia and suggested a dose 
response relationship between programme variables of volume and intensity and 24 h post - exercise insulin sensitivity .
thus , the conclusions of the present paper are likely valid only for the intensity of the exercise prescription chosen.fig
. 1mechanisms of exercise - stimulated glucose uptake in skeletal muscle . upon acute endurance - type exercise ,
muscular contraction increases amp and amp - activated protein kinase ( ampk ) , calcium release from endoplasmic reticulum and ca / calmodulin - dependent protein kinase ii ( camkii ) as well as mitogen - activated protein kinase ( mapk ) .
post - exercise effects involve activation of peroxisome - proliferator activated receptor- coactivator 1 ( pgc1 ) , which by stimulating expression of nuclear respiratory factors ( nrf1 , nrf2 ) will increase atp synthesis and , later , mitochondrial biogenesis .
in addition , exercising improves insulin - dependent glucose transport and phosphorylation by hexokinase ii ( hkii ) , which includes more distal components of insulin signalling such as phosphoinositide - dependent kinase 1 ( pdk1 ) , tbc1 domain family , members 1 and 4 ( tbc1d1/4 ) , rac1 and protein kinase c ( pkc ) isoforms .
the effects of training on mitochondrial function and glucose metabolism may be modulated by variants in genes such as pparg or ndufb6 .
while the cellular mechanisms of acute resistance - type exercise are less clear , chronic resistance training activates the mammalian target of rapamycin ( mtor)/serine kinase 6 ( s6k ) pathway , ultimately leading to protein synthesis and increased muscle mass .
tca , tricarboxylic acid mechanisms of exercise - stimulated glucose uptake in skeletal muscle . upon acute endurance - type exercise ,
muscular contraction increases amp and amp - activated protein kinase ( ampk ) , calcium release from endoplasmic reticulum and ca / calmodulin - dependent protein kinase ii ( camkii ) as well as mitogen - activated protein kinase ( mapk ) .
post - exercise effects involve activation of peroxisome - proliferator activated receptor- coactivator 1 ( pgc1 ) , which by stimulating expression of nuclear respiratory factors ( nrf1 , nrf2 ) will increase atp synthesis and , later , mitochondrial biogenesis .
in addition , exercising improves insulin - dependent glucose transport and phosphorylation by hexokinase ii ( hkii ) , which includes more distal components of insulin signalling such as phosphoinositide - dependent kinase 1 ( pdk1 ) , tbc1 domain family , members 1 and 4 ( tbc1d1/4 ) , rac1 and protein kinase c ( pkc ) isoforms .
the effects of training on mitochondrial function and glucose metabolism may be modulated by variants in genes such as pparg or ndufb6 .
while the cellular mechanisms of acute resistance - type exercise are less clear , chronic resistance training activates the mammalian target of rapamycin ( mtor)/serine kinase 6 ( s6k ) pathway , ultimately leading to protein synthesis and increased muscle mass .
tca , tricarboxylic acid would individuals experience hyperglycaemia owing to the greater counter - regulatory hormone release associated with intense resistance exercise , or would those with impaired counter - regulation owing to long - standing well - controlled diabetes be at greater risk of hypoglycemia ? more data on metabolic and hormonal responses to acute exercising including plasma profiles of nefa , catecholamines , glucagon and growth hormone are needed to answer this question .
thus , the results apply only to middle - aged to elderly patients with insulin resistance and type 2 diabetes , but not to younger patients and those with type 1 diabetes with a lesser degree of insulin resistance and differences in hypoglycaemia counter - regulation .
the study by van dijk et al .   was not designed to address the clinically relevant question of whether endurance- or resistance - type exercise training should be the first choice for recommendations on chronic physical activity in type 2 diabetes . in this context , a recent meta - analysis showed that structured aerobic , resistance or combined exercise training results in a decline in hba1c ranging from 0.51 to 0.73 percentage points in patients with type 2 diabetes , with an exercise duration of > 150  min / week being more efficient than a duration of 150  min / week ( reduction in hba1c of 0.89 vs 0.36 percentage points ) .
while the analysis suggests equal clinical efficacy of the various types of exercise in type 2 diabetes , the different numbers , sizes and designs of the studies included do not allow a final conclusion to be drawn .
it has been assumed that chronic endurance training might act primarily by improving insulin resistance , while resistance training would augment the capacity for glucose uptake by increasing skeletal muscle mass .
in addition , chronic exercise training can increase levels of pgc1 and , in turn , expression of genes encoding nuclear respiration factors to stimulate mitochondrial biogenesis and function ( fig .  1 ) , both of which are frequently impaired in insulin - resistant and diabetic states . endurance exercise training performed three times weekly markedly improved whole body insulin sensitivity and normalised muscular glucose transport / phosphorylation within 6  weeks in first - degree relatives of patients with type 2 diabetes .
combined endurance and resistance exercise for 12  weeks also normalised muscular mitochondrial density and capacity in individuals with type 2 diabetes , although insulin sensitivity remained reduced . on the other hand , both resistance and exercise training twice weekly improved atp synthase flux in vivo but failed to increase insulin sensitivity in first - degree relatives .
interestingly , the response of mitochondrial function was modified in part by a single nucleotide polymorphism ( snp ) in the ndufb6 gene , which encodes a subunit of complex 1 of the respiratory chain ( fig .  1 ) .
a snp in the pparg gene may further modulate the response of glucose metabolism to regular endurance exercise .
these recent reports underline the important roles of intensity and frequency of exercise training regardless of the mode of exercise and also point to individual , inherited predisposition defining the success of interventions aiming to increase physical activity . taken together
, the findings of van dijk et al   provide evidence for the comparable efficacy of one bout of a specific protocol of endurance or resistance exercise on post - exercise glycaemic control in insulin - resistant humans with or without type 2 diabetes .
but it remains to be determined who will benefit most from specific exercise protocols with regard to long - term glycaemic control and insulin sensitivity .
not only cellular mechanisms , but also long - term acceptability by patients , can differ between endurance and resistance training .
consequently , long - term adherence to exercise advice rather than specific modes of exercise might ultimately determine efficacy to improve glycaemia and , importantly , morbidity and mortality . as a result
, studies are now needed to determine whether we should resist or endure when exercising in the long run in real life .
 there is now evidence that a single bout of endurance ( aerobic ) or resistance exercise reduces 24  h post - exercise subcutaneous glucose profiles to the same extent in insulin - resistant humans with or without type 2 diabetes . 
 however , it remains to be determined which group would benefit most from specific exercise protocols , particularly with regard to long - term glycaemic control . 
 acute aerobic exercise first accelerates translocation of myocellular glucose transporters via amp - activated protein kinase , calcium release and mitogen - activated protein kinase , but also improves insulin - dependent glucose transport / phosphorylation via distal components of insulin signalling ( phosphoinositide - dependent kinase 1 , tbc1 domain family , members 1 and 4 , rac1 , protein kinase c ) . 
 post - exercise effects involve peroxisome - proliferator activated receptor- coactivator 1 and lead to atp synthesis , which may be modulated by variants in genes such as ndufb6 . 
 while mechanisms of acute resistance - type exercise are less clear , chronic resistance training activates the mammalian target of rapamycin / serine kinase 6 pathway , ultimately increasing protein synthesis and muscle mass . over the long term , adherence to rather than differences in metabolic variables between specific modes of regular exercise 
 might ultimately determine their efficacy . 
 taken together , studies are now needed to address the variability of individual responses to long - term resistance and endurance training in real life . 
Endurance and resistance training equally reduce 24h glucose post exercising
Continuous subcutaneous glucose monitoring
Acute exercise
Chronic exercise