Chronic resistance training: is it time to rethink the time course of neural contributions to strength gain?

Resistance training enhances muscular force due to a combination of neural plasticity and muscle hypertrophy. It has been well documented that the increase in strength over the first few weeks of resistance training (i.e. acute) has a strong underlying neural component and further enhancement in strength with long-term (i.e. chronic) resistance training is due to muscle hypertrophy. For obvious reasons, collecting long-term data on how chronic-resistance training affects the nervous system not feasible. As a result, the effect of chronic-resistance training on neural plasticity is less understood and has not received systematic exploration. Thus, the aim of this review is to provide rationale for investigating neural plasticity beyond acute-resistance training. We use cross-sectional work to highlight neural plasticity that occurs with chronic-resistance training at sites from the brain to spinal cord. Specifically, intra-cortical circuitry and the spinal motoneuron seem to be key sites for this plasticity. We then urge the need to further investigate the differential effects of acute versus chronic-resistance training on neural plasticity, and the role of this plasticity in increased strength. Such investigations may help in providing a clearer definition of the continuum of acute and chronic-resistance training, how the nervous system is altered during this continuum and the causative role of neural plasticity in changes in strength over the continuum of resistance training.

Intensity matters: effects of cadence and power output on corticospinal excitability during arm cycling are phase and muscle dependent.

The present study investigated the effects of cadence and power output on corticospinal excitability to the biceps (BB) and triceps brachii (TB) during arm cycling. Supraspinal and spinal excitability were assessed using transcranial magnetic stimulation (TMS) of the motor cortex and transmastoid electrical stimulation (TMES) of the corticospinal tract, respectively. Motor-evoked potentials (MEPs) elicited by TMS and cervicomedullary motor-evoked potentials (CMEPs) elicited by TMES were recorded at two positions during arm cycling corresponding to mid-elbow flexion and mid-elbow extension (i.e., 6 and 12 o'clock made relative to a clock face, respectively). Arm cycling was performed at combinations of two cadences (60 and 90 rpm) at three relative power outputs (20, 40, and 60% peak power output). At the 6 o'clock position, BB MEPs increased ~11.5% as cadence increased and up to ~57.2% as power output increased ( P < 0.05). In the TB, MEPs increased ~15.2% with cadence ( P = 0.013) but were not affected by power output, while CMEPs increased with cadence (~16.3%) and power output (up to ~19.1%, P < 0.05). At the 12 o'clock position, BB MEPs increased ~26.8% as cadence increased and up to ~96.1% as power output increased ( P < 0.05), while CMEPs decreased ~29.7% with cadence ( P = 0.013) and did not change with power output ( P = 0.851). In contrast, TB MEPs were not different with cadence or power output, while CMEPs increased ~12.8% with cadence and up to ~23.1% with power output ( P < 0.05). These data suggest that the "type" of intensity differentially modulates supraspinal and spinal excitability in a manner that is phase- and muscle dependent. NEW & NOTEWORTHY There is currently little information available on how changes in locomotor intensity influence excitability within the corticospinal pathway. This study investigated the effects of arm cycling intensity (i.e., alterations in cadence and power output) on corticospinal excitability projecting to the biceps and triceps brachii during arm cycling. We demonstrate that corticospinal excitability is modulated differentially by cadence and power output and that these modulations are dependent on the phase and the muscle examined.

Extensor motoneurone properties are altered immediately before and during fictive locomotion in the adult decerebrate rat.

This study examined motoneurone properties during fictive locomotion in the adult rat for the first time. Fictive locomotion was induced via electrical stimulation of the mesencephalic locomotor region in decerebrate adult rats under neuromuscular blockade to compare basic and rhythmic motoneurone properties in antidromically identified extensor motoneurones during: (1) quiescence, before and after fictive locomotion; (2) the 'tonic' period immediately preceding locomotor-like activity, whereby the amplitude of peripheral flexor (peroneal) and extensor (tibial) nerves are increased but alternation has not yet occurred; and (3) locomotor-like episodes. Locomotion was identified by alternating flexor-extensor nerve activity, where the motoneurone either produced membrane oscillations consistent with a locomotor drive potential (LDP) or did not display membrane oscillation during alternating nerve activity. Cells producing LDPs were referred to as such, while those that did not were referred to as 'idle' motoneurones. LDP and idle motoneurones during locomotion had hyperpolarized spike threshold (Vth ; LDP: 3.8 mV; idle: 5.8 mV), decreased rheobase and an increased discharge rate (LDP: 64%; idle: 41%) during triangular ramp current injection even though the frequency-current slope was reduced by 70% and 55%, respectively. Modulation began in the tonic period immediately preceding locomotion, with a hyperpolarized Vth and reduced rheobase. Spike frequency adaptation did not occur in spiking LDPs or firing generated from sinusoidal current injection, but occurred during a sustained current pulse during locomotion. Input conductance showed no change. Results suggest motoneurone modulation occurs across the pool and is not restricted to motoneurones engaged in locomotion.