NEUOPHYSIOLOGICAL CHANGES AFTER UPPER AND LOWER LIMB GRADED EXERCISE TESTING.

Abstract

Aerobic exercise, including graded exercise testing (GXT), may cause neurophysiological changes of circuits in the primary motor cortex (M1) related to mechanisms of fatigue and/or plasticity. Investigating M1 inhibitory circuit changes over time in exercising compared to non-exercising muscles after GXT of the upper limbs (UL) and lower limbs (LL) may distinguish between different post-exercise mechanisms. PURPOSE: To evaluate M1 inhibitory circuit changes resulting from UL and LL GXT and determine their associations with fitness. METHODS: Six healthy subjects (30 ± 6 yrs) participated. Transcranial Magnetic Stimulation (TMS), Peripheral Nerve Stimulation (PNS), and Electromyography (EMG) were used for neurophysiological testing. Gas analysis was performed to evaluate VO2max (UL: 24.2 ± 4.8, LL: 35.1 ± 5.9 mL/kg/min) during GXTs. Surface electrodes were placed over the first dorsal interosseous (FDI) and tibialis anterior (TA) muscles. Measures of M1 and M1-related afferent inhibition included cortical silent period (CSP) and short-latency afferent inhibition (SAI), respectively. SAI inter-stimulus intervals (ISI) between PNS and TMS stimulations were 21-23ms (UL), and 32-35ms (LL). TMS coil orientation (CO) was altered between posterior-anterior (PA) and anterior-posterior (AP) for both measures of CSP and SAI. CSP and SAI were taken 0-45 min (POST1) and 45-90 min (POST2) post-exercise and compared to pre-exercise. Repeated measures ANOVAs were performed to evaluate effects of exercise type, CO, time, and ISI. RESULTS: CSP decreased at POST1 and increased at POST2 in FDI (97.9 ± 1.2% vs. 104.5 ± 2.5%, p < 0.05) with a trend toward significance in TA (99.3 ± 2.5% vs. 103.5 ± 4.9%, p = 0.19). Although SAI was found for the TA at 32ms (p<0.05) and FDI at 21-23ms (p < 0.05), the interaction of exercise type, CO, and ISI did not reach significance after Huynh-Feldt correction (FDI: p = 0.10, TA: p = 0.10). Univariate linear regression of VO2max and SAI revealed a potential relationship reliant on exercise type and CO (UL: R2 = 0.91, LL: R2 = 0.68). CONCLUSIONS: Changes in CSP suggest that exercise may cause early disinhibition followed by greater inhibition in M1 while changes in SAI may be influenced by fitness levels. Collectively, the results support UL and LL GXTs cause measurable M1 neurophysiological changes.