The Impact of Human Skeletal Muscle Heating and Cooling on Mitochondrial Related Gene Expression

Advisor Information

Dustin Slivka

Location

Dr. C.C. and Mabel L. Criss Library

Presentation Type

Poster

Start Date

7-3-2014 9:00 AM

End Date

7-3-2014 12:00 PM

Abstract

Signals within skeletal muscle for the adaptation of mitochondria have been shown to be temperature sensitive. Specifically, these signals have been shown to be enhanced during recovery from exercise in a cold environment. However, the effect of direct cold application to the muscle after exercise is unknown. PURPOSE: To determine if direct cold application during recovery from an exercise bout, will impact the muscle signal (gene expression) for mitochondrial development. METHODS: Trained male cyclists (n = 8, age 25 ± 3 y, height 181 ± 6 cm, weight 79 ± 8 kg, 12.8 ± 3.6% body fat, VO2 peak 4.52 ± 0.88 L · min-1 ) completed a 90-minute interval cycling protocol. The exercise was followed by 4 hours of recovery. During recovery ice was applied to one leg (IL) while the other leg (CL) served as a control. Thigh muscle temperature was measured using a probe placed into the muscle. Muscle biopsies were taken at 4 h post exercise from the front of the thigh of both legs to determine the muscle signal for mitochondrial development in IL relative to CL. RESULTS: The IL was colder (27 ± 4 °C) than CL (36 ± 0 °C) throughout recovery (p < 0.001). There were no differences in our five muscle signals of interest for mitochondrial development (p>0.05). CONCLUSION: When this data is considered with previous research, it appears that the critical stimuli for cold induced mitochondrial development is a change in core body temperature as opposed to a change in local muscle temperature.

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Mar 7th, 9:00 AM Mar 7th, 12:00 PM

The Impact of Human Skeletal Muscle Heating and Cooling on Mitochondrial Related Gene Expression

Dr. C.C. and Mabel L. Criss Library

Signals within skeletal muscle for the adaptation of mitochondria have been shown to be temperature sensitive. Specifically, these signals have been shown to be enhanced during recovery from exercise in a cold environment. However, the effect of direct cold application to the muscle after exercise is unknown. PURPOSE: To determine if direct cold application during recovery from an exercise bout, will impact the muscle signal (gene expression) for mitochondrial development. METHODS: Trained male cyclists (n = 8, age 25 ± 3 y, height 181 ± 6 cm, weight 79 ± 8 kg, 12.8 ± 3.6% body fat, VO2 peak 4.52 ± 0.88 L · min-1 ) completed a 90-minute interval cycling protocol. The exercise was followed by 4 hours of recovery. During recovery ice was applied to one leg (IL) while the other leg (CL) served as a control. Thigh muscle temperature was measured using a probe placed into the muscle. Muscle biopsies were taken at 4 h post exercise from the front of the thigh of both legs to determine the muscle signal for mitochondrial development in IL relative to CL. RESULTS: The IL was colder (27 ± 4 °C) than CL (36 ± 0 °C) throughout recovery (p < 0.001). There were no differences in our five muscle signals of interest for mitochondrial development (p>0.05). CONCLUSION: When this data is considered with previous research, it appears that the critical stimuli for cold induced mitochondrial development is a change in core body temperature as opposed to a change in local muscle temperature.