ABSTRACT
High intensity training (HIT) has been shown to improve maximal aerobic capacity and muscle protein synthesis but has not yet been investigated in senescent rats. We hypothesized that the change of speed (acceleration) during each bout of HIT acts as a stimulus responsible for the adaptations of the organism to exercise. Twenty two month-old (mo) rats (n=13) were subjected to a short acceleration protocol (20-30min) of exercise, comprising 3 independent bouts of acceleration and compared to an age-matched sedentary group (n=14). The protocol was repeated twice a week for two months. Following the protocol, performance, cardiac function, muscle mechanics, and the cellular and molecular pathways that are implicated in exercise adaptations were investigated. This new training, comprising only 16 sessions, improved maximal oxygen uptake (â©O2peak; +6.6%, p<0.05), running distance (+95.2%; p<0.001), speed (+29.7%; p<0.01) and muscle function of 24mo rats in only 8weeks. This new training protocol induced cardiac hypertrophy and improved fractional shortening (47.3% vs. 41.1% in the control group, p<0.01) and ejection fraction. Moreover, it also improved the mechanics of skeletal muscle by increasing developed force (+31% vs. the control group, p<0.05) and maximal mechanical efficiency, activated the IGF1/mTOR/Akt pathway, and reduced the Smad2/3 pathway. Our results clearly show that the change in speed is a stimulus to control cardiac and skeletal muscle mass. This acceleration-based training is not time-consuming and may be adaptable for athletes, the elderly or chronic disease patients in order to improve strength, oxidative capacity, and quality of life.
Subject(s)
Cellular Senescence , High-Intensity Interval Training/methods , Muscle Contraction , Muscle, Skeletal/physiology , Physical Conditioning, Animal/methods , Ventricular Function, Left , Acceleration , Adaptation, Physiological , Age Factors , Animals , Biomechanical Phenomena , Cardiomegaly, Exercise-Induced , Insulin-Like Growth Factor I/metabolism , Male , Muscle, Skeletal/metabolism , Myocardial Contraction , Oxygen Consumption , Phosphorylation , Proto-Oncogene Proteins c-akt/metabolism , Rats, Wistar , Signal Transduction , Smad2 Protein/metabolism , Smad3 Protein/metabolism , Stroke Volume , TOR Serine-Threonine Kinases/metabolism , Time FactorsABSTRACT
In the field of comparative physiology, it remains to be established whether the concept of VO2max is valid in the mouse and, if so, how this value can be accurately determined. In humans, VO2max is generally considered to correspond to the plateau observed when VO2 no longer rises with an increase in workload. In contrast, the concept of VO2peak tends to be used in murine studies. The objectives of the present study were to determine whether (i) a continuous ramp protocol yielded a higher VO2peak than a stepwise, incremental protocol, and (ii) the VO2peak measured in the ramp protocol corresponded to VO2max. The three protocols (based on intensity-controlled treadmill running until exhaustion with eight female FVB/N mice) were performed in random order: (a) an incremental protocol that begins at 10 m.min(-1) speed and increases by 3 m.min(-1) every 3 min. (b) a ramp protocol with slow acceleration (3 m.min(-2)), and (c) a ramp protocol with fast acceleration (12 m.min(-2)). Each protocol was performed with two slopes (0 and 25°). Hence, each mouse performed six exercise tests. We found that the value of VO2peak was protocol-dependent (p < 0.05) and was highest (59.0 ml.kg (0.75).min(-1)) for the 3 m.min(-2) 0° ramp protocol. In the latter, the presence of a VO2max plateau was associated with the fulfillment of two secondary criteria (a blood lactate concentration >8 mmol.l(-1) and a respiratory exchange ratio >1). The total duration of the 3 m.min(-2) 0° ramp protocol was shorter than that of the incremental protocol. Taken as a whole, our results suggest that VO2max in the mouse is best determined by applying a ramp exercise protocol with slow acceleration and no treadmill slope.
