Page 44 - 《运动与健康科学》(英文)2024年第2期

TaggedAPTARAEnd166 Y. Dai et al.
for 5-week saw increased Rin, decreased Vth for spike generation TaggedAPTARAH14. Exercise modulates ion channelsTaggedAPTARAEnd
and doublet threshold, as well as increased maximum steady-state TaggedAPTARAPIon channel activity is a significant regulator of the spinal
46
firing frequency and FI slope in their spinal motoneurons. In
motor system’s adaptability to acute or chronic exercise. Early
contrast, 2 weeks of hindlimb un-weighting resulted in decreased
modeling studies suggest that the transient sodium, persistent
excitability coinciding with increased rheobase, depolarized Vth,
sodium, and K(DR) channels play a dominant role in regu-
reduced AHP amplitude, and rightward-shifting of the FI lating Vth in cat lumbar motoneurons during fictive locomo-
47
curve. Altogether, these studies suggest chronic exercise, in its 30
tion. Indeed, numerous other studies have confirmed various
various forms, increases rodent spinal motoneuron excitability by
channels are involved in regulating neuronal plasticity and
modulating its RMP, Vth, rheobase, firing frequency, and AHP. 3,23,30
excitability during acute or after chronic exercise. These
Chronic exercise increases the gain of the FI relationship,
channels primarily include (a) transient sodium channels,
which physiologically translates into the motoneuron becoming
(b) persistent sodium channels, (c) L-type calcium channels,
more sensitive to its synaptic inputs, explaining their increased 23,6062
(d) K(DR) channels, and (e) K(Ca) channels. TaggedAPTARAEnd
firing frequencies and excitability. This adaptation allows moto-
neurons to maintain output more efficiently and optimize force
production for skeletal muscle movement. 3,48 Overall, these TaggedAPTARAH24.1. Transient sodium channelsTaggedAPTARAEnd
adaptive changes in electrophysiological properties observed in TaggedAPTARAPTransient sodium channels determine the threshold for AP
rodents indicate that spinal motoneurons become more excitable generation and make essential contributions to the regulation of
63,64
and fatigue resistant after chronic exercise. It is worth noting that neuronal output. Recent studies have found that 3 weeks of
while the majority of studies have demonstrated that chronic treadmill exercise increased neuronal excitability and caused
exercise increases motoneuron excitability, recent research has hyperpolarization of Vth in mouse spinal interneurons and
revealed that a 5-week endurance training program on a treadmill midbrain 5-HT neurons. 12,15,16 In fact, transient sodium channels
led to notable decreases in the Rin values and excitability of fast play a dominant role in modulating Vth and are one of the main
49 65,66
motoneurons. TaggedAPTARAEnd regulators in the recruitment order of MUs in mammals.
TaggedAPTARAPSpinal interneurons also undergo adaptive changes with Modeling studies suggest increasing transient sodium channel
chronic exercise. A recent study 12 in mice (postnatal 4250 conductance and/or hyperpolarizing channel state variables (acti-
days) reported that 3-week treadmill training increased neuronal vation m and inactivation h) hyperpolarize Vth in cat lumbar
excitability with hyperpolarization of Vth and reduction of rheo- moroneurons. 30 Furthermore, in vitro experiments in spinal
base in ventromedial and laminar X interneurons, accompanied neurons of neonatal rodents have shown that Vth can be hyperpo-
by a significant increase of AP amplitude in dorsal horn inter- larized by the voltage-gated sodium channel 1.1 (Nav1.1) agonist
neurons. These effects depended on the anatomic distribution of veratridine. 29 However, previous reports indicate that activation
67
the spinal interneurons. Furthermore, another study 16 demon- of protein kinase C depolarizes Vth. In addition, the a-subunit
strated that 3-week treadmill training hyperpolarized Vth, of sodium channels can be rapidly phosphorylated by protein
increased AP amplitude, and enhanced firing frequency in 5-HT kinase C at different membrane potentials, suggesting an element
neurons of the midbrain in mice (postnatal 4250 days). These of state-dependent regulation of transient sodium channels. 6870
findings suggest that exercise-induced plasticity of neuronal Furthermore, gene expression of the a-subunit of the transient
excitability is achieved not only in the spinal cord but also in the sodium channel Nav1.6 is significantly upregulated after just
3
midbrain, although there are a few examples where exercise does 5 days of treadmill training. Altogether, these results indicate
50
not alter the basic neuronal electrophysiological properties. TaggedAPTARAEnd that modulation of transient sodium channels could be a potential
TaggedAPTARAPSince direct recording of human motoneuron membrane prop- mechanism underlying Vth hyperpolarization during acute or
erties is not feasible, much of our understanding of how these chronic exercise. During fictive locomotion, the FI relationship
9,22,23
neurons adapt in response to exercise comes from indirect meas- of spinal motoneurons is highly varied, but the mechanisms
urements using surface or intramuscular electromyography. 51 underlying these variations are still unknown. Simulation results
Human models involving reduced or disused physical activity, suggest multi-channel modulations are involved in motor output
52
53
such as limb immobilization, bedrest, and spinal cord injury 54 during locomotion and further show that enhancement of tran-
are also utilized to investigate the plasticity of a motor unit (MU, sient sodium channel conductance and/or hyperpolarization of
a motoneuron with all of the skeletal muscle fibers it innervates). channel state variables (m and h) increase the FI slope and shift
Research on the impact of chronic exercise on MUs reveals that the curve to the left. These results are consistent with experi-
23
lifelong high-intensity physical activity may preserve motor unit mental observations and conclusively demonstrate that transient
function with advancing age. 4,55,56 Moreover, both strength sodium channels substantially contribute to neuronal plasticity
training and endurance training have been shown to enhance the and excitability in response to exercise.TaggedAPTARAEnd
output of the motoneuron pool, suggesting additional recruitment
of MUs during exercise. 57 In fact, a significant increase in the
TaggedAPTARAH24.2. Persistent sodium channelsTaggedAPTARAEnd
discharge rates of MUs is observed in the recording of a single
motor unit using intramuscular electromyography during TaggedAPTARAPPersistent sodium channels contribute to the generation of
maximal effort. 58,59 Collectively, these findings indicate that PICs 33,7175 and play an important role in the plasticity of spinal
exercise interventions increase the output of single MUs, which interneurons and brainstem 5-HT neurons. 15,16 Previous studies
have reported that persistent sodium channels regulate Vth and
in turn increases muscle strength.TaggedAPTARAEnd