The androgen hormone is responsible for the growth of secondary sex characteristics in humans, such as skeletal muscle. Upon an exercise stimulus, the androgen receptor (AR) plays a crucial role in transmitting the androgenic signal to the nucleus which upregulates transcription of target genes related to growth of skeletal muscle. AR content has been implicated in the hypertrophic response between high and low responders following resistance exercise training (RET) in males. Little is known of the impact of AR expression on acute skeletal muscle damage and whether AR may influence the adaptive response to RET in females. This study aimed to investigate acute changes to AR content following a single bout of muscle damage-inducing exercise as well as sex differences during skeletal muscle repair and hypertrophy. A skeletal muscle biopsy from the vastus lateralis was obtained from 26 healthy, young males (n=13) and females (n=13) at baseline and 48 hours following a single bout of 300 eccentric contractions of the quadriceps. Subsequently, participants performed whole-body RET 4 times a week for 10 weeks, followed by a final skeletal muscle biopsy under resting conditions. Females had greater AR mRNA than males at baseline (~53%) and post-damage (~126%; p<0.05) while AR protein content increased in both sexes similarly following a single bout of eccentric exercise (p<0.05). Damage- and RET-induced satellite cell response was associated with percent change in AR protein content in a sex-specific manner (p<0.05). RET-induced percent change in nuclear AR content was ~17% greater in males compared to females (p<0.05). Interestingly, following RET, males experiencing the highest percent change in myofibre cross sectional area (CSA) exhibited greater changes in nuclear-associated AR protein content compared to females with the highest percent change in CSA. Collectively, AR protein content is elevated following acute eccentric exercise and 10 weeks of RET. Findings from this study suggests that males are more reliant on AR-related mechanisms than females to induce skeletal muscle hypertrophy following RET. / Thesis / Master of Science in Kinesiology / Skeletal muscle is crucial for proper function and activities of daily living. Many factors can regulate the amount and quality of skeletal muscle such as the expression of a protein known as the androgen receptor (AR). The AR plays a role in many cellular pathways that can ultimately dictate the growth and size of a particular tissue like skeletal muscle. There is currently minimal research about AR during skeletal muscle damage and in female skeletal muscle. Understanding how exercise increases AR content in males and females could progress our knowledge of how muscle adapts differently to exercise between sexes. Therefore, the purpose of this study was to understand how the AR behaves in the muscle, in males and females, after a single session of exercise that damages the muscle or after long term resistance exercise (RE). We observed that the AR gene is more abundant in females than males at rest and following damaging exercise. Furthermore, we show that AR protein content increases in both sexes following a single session of damaging exercise and after chronic RE. Muscle stem cells are a component of the muscle that helps to heal muscle after exercise has been performed. In the current study, we demonstrate that AR has a closer relationship to muscle stem cells in males relative to females. Further, AR seems to be more closely linked to muscle growth in males than females. Altogether, AR is a component of the muscle that adapts to exercise differently in males and females. This study may, in part, explain how skeletal muscle responds differently between sexes after exercise.
| Identifer | oai:union.ndltd.org:mcmaster.ca/oai:macsphere.mcmaster.ca:11375/27888 |
| Date | January 2022 |
| Creators | Hatt, Aidan |
| Contributors | Parise, Gianni, Kinesiology |
| Source Sets | McMaster University |
| Language | English |
| Detected Language | English |
| Type | Thesis |
Page generated in 0.0017 seconds