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Compensatory elevation of voluntary activity in mouse mutants with impaired mitochondrial energy metabolism.

Lapointe J, G Hughes B, Bigras E, Hekimi S - Physiol Rep (2014)

Bottom Line: We find that both Mclk1(+/-) and RISP(+/P224S) males are capable of restoring their defective metabolic rates by making significantly more voluntary use of a running wheel compared to wild type.However, this increase in voluntary activity does not reflect their exercise capacity, which we found to be impaired as revealed by a shorter treadmill distance run before exhaustion.In contrast to what is observed in Mclk1(+/-) and RISP(+/P224S) mutants, Sod2(+/-) mice with elevated oxidative stress and major mitochondrial dysfunction did not increase voluntary activity.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, McGill University, Montréal, Quebec, Canada Agriculture and Agri-Food Canada, 2000 College St., Sherbrooke, J1M 0C8, Quebec, Canada.

No MeSH data available.


Related in: MedlinePlus

Decreased exercise capacity in Mclk1+/− malemice. Assessment of forced exercise capacity was performed with 3‐month‐oldMclk1+/+ andMclk1+/− mice (n = 18) onthe Balb/C background. Total distance run on the treadmill by both genotypes (A). Bloodlevels of lactate (B) and glucose (C) from the tail vein before and after the endurance test. Barsrepresent means ± SEM and a value of P < 0.05 was consideredsignificant.
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fig05: Decreased exercise capacity in Mclk1+/− malemice. Assessment of forced exercise capacity was performed with 3‐month‐oldMclk1+/+ andMclk1+/− mice (n = 18) onthe Balb/C background. Total distance run on the treadmill by both genotypes (A). Bloodlevels of lactate (B) and glucose (C) from the tail vein before and after the endurance test. Barsrepresent means ± SEM and a value of P < 0.05 was consideredsignificant.

Mentions: The increased voluntary activity observed inMclk1+/− mutants, which may be a behavioraladaptation to their intrinsic mitochondrial dysfunction, did not provide any information about theirexercise capacity. For this we carried out a physical endurance task on a treadmill (see Methods).We scored the mean total distance that the mice were able to run before exhaustion in3‐month‐old Mclk1+/− males andsibling controls. The mutants exhibited significantly impaired exercise capacity (Fig. 5A). As expected, the treadmill endurance test significantlyincreased the animals' blood lactate levels, which were directly measured form the tail vein beforeand after the exercise (Fig. 5B). This is what is expectedif the level of blood lactate is a main reason for why the animals stop running. No significantdifference between genotypes was observed. We interpret these findings to indicate that animals ofboth genotypes stop running at the same level of blood lactate but thatMclk1+/− mice sustain a more rapidbuildup of lactate levels. Thus, it appears that insufficient aerobic capacity is likely the causeof the low exercise capacity in Mclk1+/− mutants.Analysis of blood glucose concentration revealed a trend for an increase after the treadmillexercise which did not differ between genotypes (Fig. 5C).


Compensatory elevation of voluntary activity in mouse mutants with impaired mitochondrial energy metabolism.

Lapointe J, G Hughes B, Bigras E, Hekimi S - Physiol Rep (2014)

Decreased exercise capacity in Mclk1+/− malemice. Assessment of forced exercise capacity was performed with 3‐month‐oldMclk1+/+ andMclk1+/− mice (n = 18) onthe Balb/C background. Total distance run on the treadmill by both genotypes (A). Bloodlevels of lactate (B) and glucose (C) from the tail vein before and after the endurance test. Barsrepresent means ± SEM and a value of P < 0.05 was consideredsignificant.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255820&req=5

fig05: Decreased exercise capacity in Mclk1+/− malemice. Assessment of forced exercise capacity was performed with 3‐month‐oldMclk1+/+ andMclk1+/− mice (n = 18) onthe Balb/C background. Total distance run on the treadmill by both genotypes (A). Bloodlevels of lactate (B) and glucose (C) from the tail vein before and after the endurance test. Barsrepresent means ± SEM and a value of P < 0.05 was consideredsignificant.
Mentions: The increased voluntary activity observed inMclk1+/− mutants, which may be a behavioraladaptation to their intrinsic mitochondrial dysfunction, did not provide any information about theirexercise capacity. For this we carried out a physical endurance task on a treadmill (see Methods).We scored the mean total distance that the mice were able to run before exhaustion in3‐month‐old Mclk1+/− males andsibling controls. The mutants exhibited significantly impaired exercise capacity (Fig. 5A). As expected, the treadmill endurance test significantlyincreased the animals' blood lactate levels, which were directly measured form the tail vein beforeand after the exercise (Fig. 5B). This is what is expectedif the level of blood lactate is a main reason for why the animals stop running. No significantdifference between genotypes was observed. We interpret these findings to indicate that animals ofboth genotypes stop running at the same level of blood lactate but thatMclk1+/− mice sustain a more rapidbuildup of lactate levels. Thus, it appears that insufficient aerobic capacity is likely the causeof the low exercise capacity in Mclk1+/− mutants.Analysis of blood glucose concentration revealed a trend for an increase after the treadmillexercise which did not differ between genotypes (Fig. 5C).

Bottom Line: We find that both Mclk1(+/-) and RISP(+/P224S) males are capable of restoring their defective metabolic rates by making significantly more voluntary use of a running wheel compared to wild type.However, this increase in voluntary activity does not reflect their exercise capacity, which we found to be impaired as revealed by a shorter treadmill distance run before exhaustion.In contrast to what is observed in Mclk1(+/-) and RISP(+/P224S) mutants, Sod2(+/-) mice with elevated oxidative stress and major mitochondrial dysfunction did not increase voluntary activity.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, McGill University, Montréal, Quebec, Canada Agriculture and Agri-Food Canada, 2000 College St., Sherbrooke, J1M 0C8, Quebec, Canada.

No MeSH data available.


Related in: MedlinePlus