| Description |
The purpose of this dissertation was to examine the development of neuromuscular fatigue during exercise and the excitability of the corticospinal motor pathway in healthy aging and in patients with heart failure and a preserved ejection fraction (HFpEF). In the first study, I examined the relationship between the degree of muscle activation and the excitability of the corticospinal pathway (i.e., the primary motor pathway in humans) during isometric knee extensor and cycling exercise. Briefly, I found that increasing levels of muscle activation progressively facilitates the corticospinal pathway via modulating the excitability of the spinal motoneuron pool and this relationship appears to be independent of contractile modality (i.e., isometric small muscle mass vs. dynamic large muscle mass exercise). Based on these findings, I concluded that it is critical to control for the level of muscle activation when examining corticospinal excitability during or after exercise. The second study sought to determine the influence of aging on the development of neuromuscular fatigue and exercise-induced corticospinal alterations during cycling (characterized by large cardiopulmonary stress) or rhythmic dynamic single-joint knee extension (characterized by minimal cardiopulmonary stress). Following cycling and single-joint exercise, older participants demonstrated an enhanced development of neuromuscular fatigue during exercise at a given absolute intensity. However, compared to their younger counterparts, the old developed less central fatigue during exercise performed at the same relative intensity. Active muscle mass had little influence on the discrepancy in the exercise-induced development of neuromuscular fatigue between young and old individuals, indicating the influence of age on the development of fatigue may be more dependent on exercise intensity (i.e., absolute vs. relative comparisons) rather than exercise involving different degrees of active muscle mass. Additionally, corticospinal excitability was unaltered by exercise in either condition or group, indicating aging does not alter the influence of exercise on corticospinal excitability and, consequently, its role in determining exercise-induced fatigue. The third study aimed to elucidate the impact of HFpEF on corticospinal excitability and the development of neuromuscular fatigue during exercise. During dynamic exercise performed at the same relative intensity, patients with HFpEF only completed approximately one-half of the work performed by healthy control participants, but developed a similar degree of end-exercise neuromuscular fatigue compared to their healthy counterpart. When examined following exercise at the same absolute intensity, HFpEF patients demonstrated a greater degree of both peripheral and central fatigue. The greater fatigue in the HFpEF was not related to an impaired motor pathway as corticospinal excitability was unchanged following exercise in both groups. Based on these findings, I concluded that patients with HFpEF are characterized by a substantially compromised fatigue resistance during physical activity. In summary, this dissertation characterizes the development of neuromuscular fatigue and alterations within the corticospinal pathway during exercise in health and disease. |
