Endnu et skud på stammen omkring effekten af kombineret træning er dette studie fra K. Salins gruppe i Sverige (Wang 2011). Her har de undersøgt effekten af 1 times udholdenhedstræning efterfulgt af et styrketræningspas eller af en pause.
Træningsprotokol så således ud:
- Udholdenhed (E): 1t cykling ved ~65% of VO(2max)
- Udholdenhedstræning efterfulgt af styrketræning (ER): 1t cykling + 6 sets: Benpress ved 70-80% af 1 RM

Resultatet af studiet er ret overraskende. Det viser, at mRNA niveauet for markører involveret i mitokondriel biogenese og substratreguleringen, i højere grad er opreguleret ved udholdenheds træning (ER) efterfulgt af styrketræning end ved udholdenhedstræning (E) alene.
Det betyder, at du får mere ud af din træning, hvis du supplerer din udholdenhedstræning med lidt styrketræning. Altså, at du umiddelbart efter spinningstimen, sætter dig i Leg Press maskinen, og giver den gas en 10 min tid. Lidt i modstrid med, hvad man skulle forvente, – men fint i tråd med resultaterne fra studiet jeg omtalte tidligere her på bloggen (klik her for at læse det oplæg)
Husk det er DIN TRÆNING – kombiner den
Abstract
“Combining endurance and strength training (concurrent training) may change the adaptation compared with single mode training. However, the site of interaction and the mechanisms are unclear. We have investigated the hypothesis that molecular signaling of mitochondrial biogenesis after endurance exercise is impaired by resistance exercise. Ten healthy subjects performed either only endurance exercise (E: 1h cycling at ~65% of VO2max) or endurance exercise followed by resistance exercise (ER: 1h cycling + 6 sets of leg press at 70-80% of 1 RM) in a randomized cross-over design. Muscle biopsies were obtained before and after exercise (1 and 3h Post cycling). The mRNA of genes related to mitochondrial biogenesis (PGC-1α, PRC) and substrate regulation (PDK4) increased after both E and ER, but the mRNA levels were about 2-fold higher after ER (P<0.01). Phosphorylation of proteins involved in the signaling cascade of protein synthesis (mTOR, S6K1 and eEF2) was altered after ER but not after E. Moreover, ER induced a larger increase in mRNA of genes associated with positive mTOR signaling (cMyc and Rheb). Phosphorylation of AMPK, ACC and Akt increased similarly at 1h Post (P<0.01) after both types of exercise. Contrary to our hypothesis, the results demonstrate that resistance exercise, performed after endurance exercise, amplifies the adaptive signaling response of mitochondrial biogenesis compared with single-mode endurance exercise. The mechanism may relate to a crosstalk between signaling pathways mediated by mTOR. The results suggest that concurrent training may be beneficial for the adaptation of muscle oxidative capacity.”

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