Resistance Exercise Minimal Dose Strategies for Increasing Muscle Strength in the General Population: an Overview.

Many individuals do not participate in resistance exercise, with perceived lack of time being a key barrier. Minimal dose strategies, which generally reduce weekly exercise volumes to less than recommended guidelines, might improve muscle strength with minimal time investment. However, minimal dose strategies and their effects on muscle strength are still unclear. Here our aims are to define and characterize minimal dose resistance exercise strategies and summarize their effects on muscle strength in individuals who are not currently engaged in resistance exercise. The minimal dose strategies overviewed were: "Weekend Warrior," single-set resistance exercise, resistance exercise "snacking," practicing the strength test, and eccentric minimal doses. "Weekend Warrior," which minimizes training frequency, is resistance exercise performed in one weekly session. Single-set resistance exercise, which minimizes set number and session duration, is one set of multiple exercises performed multiple times per week. "Snacks," which minimize exercise number and session duration, are brief bouts (few minutes) of resistance exercise performed once or more daily. Practicing the strength test, which minimizes repetition number and session duration, is one maximal repetition performed in one or more sets, multiple days per week. Eccentric minimal doses, which eliminate or minimize concentric phase muscle actions, are low weekly volumes of submaximal or maximal eccentric-only repetitions. All approaches increase muscle strength, and some approaches improve other outcomes of health and fitness. "Weekend Warrior" and single-set resistance exercise are the approaches most strongly supported by current research, while snacking and eccentric minimal doses are emerging concepts with promising results. Public health programs can promote small volumes of resistance exercise as being better for muscle strength than no resistance exercise at all.

Plantar flexor muscle stretching depresses the soleus late response but not tendon tap reflexes.

The purpose of this study was to investigate changes in muscle spindle sensitivity with early and late soleus reflex responses via tendon taps and transcranial magnetic stimulation, respectively, after an acute bout of prolonged static plantar flexor muscle stretching. Seventeen healthy males were tested before and after 5 min (5 × 60-s stretches) of passive static stretching of the plantar flexor muscles. Maximal voluntary isometric torque and M wave-normalized triceps surae muscle surface electromyographic activity were recorded. Both soleus tendon reflexes, evoked by percussion of the Achilles tendon during rest and transcranial magnetic stimulation-evoked soleus late responses during submaximal isometric dorsiflexion were also quantified. Significant decreases in maximal voluntary isometric plantar flexion torque (-19.2 ± 13.6%, p = .002) and soleus electromyographic activity (-20.1 ± 11.4%, p < .001) were observed immediately after stretching, and these changes were highly correlated (r = 0.76, p < .001). No changes were observed in tendon reflex amplitude or latency or peak muscle twitch torque (p > .05). Significant reductions in soleus late response amplitudes (-46.9 ± 36.0%, p = .002) were detected, although these changes were not correlated with changes in maximal electromyographic activity, torque or tendon reflex amplitudes. No changes in soleus late response latency were detected. In conclusion, impaired neural drive was implicated in the stretch-induced force loss; however, no evidence was found that this loss was related to changes in muscle spindle sensitivity. We hypothesize that the decrease in soleus late response indicates a stretch-induced reduction in a polysynaptic postural reflex rather than spindle reflex sensitivity.

Lack of cortical or Ia-afferent spinal pathway involvement in muscle force loss after passive static stretching.

This study investigated whether modulation of corticospinal-motoneuronal excitability and/or synaptic transmission of the Ia afferent spinal reflex contributes to decreases in voluntary activation and muscular force after an acute bout of prolonged static muscle stretching. Fifteen men performed five 60-s constant-torque stretches (15-s rest intervals; total duration 5 min) of the plantar flexors on an isokinetic dynamometer and a nonstretching control condition in random order on 2 separate days. Maximum isometric plantar flexor torque and triceps surae muscle electromyographic activity (normalized to M wave; EMG/M) were simultaneously recorded immediately before and after each condition. Motor-evoked potentials (using transcranial magnetic stimulation) and H-reflexes were recorded from soleus during EMG-controlled submaximal contractions (23.4 ± 6.9% EMG maximum). No changes were detected in the control condition. After stretching, however, peak torque (mean ± SD; -14.3 ± 7.0%) and soleus EMG/M (-17.8 ± 6.2%) decreased, and these changes were highly correlated (r = 0.83). No changes were observed after stretching in soleus MEP or H-reflex amplitudes measured during submaximal contractions, and interindividual variability of changes was not correlated with changes in EMG activity or maximum torque. During EMG-controlled submaximal contractions, torque production was significantly decreased after stretching (-22.7 ± 15.0%), indicating a compromised muscular output. These data provide support that changes in the excitability of the corticospinal-motoneuronal and Ia afferent spinal reflex pathways do not contribute to poststretch neural impairment.NEW & NOTEWORTHY This study is the first to specifically examine potential sites underlying the decreases in neural activation of muscle and force production after a bout of muscle stretching. However, no changes were found in either the H-reflex or motor-evoked potential amplitude during submaximal contractions.

The loss of muscle force production after muscle stretching is not accompanied by altered corticospinal excitability.

PURPOSE: The aim of the present study was to determine whether depression of maximal muscular force and neural drive subsequent to prolonged ( ≥ 60 s) passive muscle stretching is associated with altered corticospinal excitability or intracortical (GABAB-mediated) inhibition. METHODS: Fourteen healthy adult males were tested before and after 5 min (5 × 60-s stretches) of intense, passive static stretching of the plantar flexor muscles. Two protocols (A and B) were conducted in a randomized order. Transcranial magnetic stimulation was delivered to the contralateral motor cortex at rest (Protocol A) and during maximal voluntary contractions (Protocol B). Changes in maximal voluntary isometric torque, voluntary surface electromyographic activity of triceps surae muscles (normalized to M-wave; EMG/M), motor-evoked potentials (MEP), and cortical silent period (cSP; Protocol B) in soleus elicited by transcranial magnetic stimulation were examined 10 min after stretch. RESULTS: In both protocols A and B, significant decreases were observed immediately after stretching in maximal voluntary plantar flexion torque ( - 20.1 ± 15.9%, P = 0.004; and - 17.2 ± 13.5%, P = 0.006) and EMG/M ( - 18.0 ± 18.2%, P = 0.023; and - 13.0 ± 9.3%, P = 0.003). Decreases in torque and EMG/M were highly correlated (r = 0.67-0.85, P < 0.05). However, no changes were observed in MEP amplitudes during rest ( + 29.3 ± 50.0%) or maximum voluntary contraction ( + 1.9 ± 16.8%), or in cSP ( + 2.1 ± 15.1%). CONCLUSIONS: Impaired neural drive contributed to the stretch-induced force loss; however, changes in corticospinal excitability and intracortical inhibition could not explain the phenomenon.

Neuromuscular Factors Contributing to Reductions in Muscle Force After Repeated, High-Intensity Muscular Efforts.

Multiple neuromuscular processes contribute to the loss of force production following repeated, high-intensity muscular efforts; however, the relative contribution of each process is unclear. In Experiment 1, 16 resistance trained men performed six sets of unilateral isometric plantar flexor contractions of the right leg (3 s contraction/2 s rest; 85% maximal voluntary contraction torque; 90-s inter-set rest) until failure with and without caffeine ingestion (3 mg kg-1) on two separate days. Corticospinal excitability and cortical silent period (cSP) were assessed before and immediately, 10 and 20 min after the exercise. In Experiment 2, electrically evoked tetanic force and persistent inward current (PIC)-mediated facilitation of the motor neuron pool (estimated using neuromuscular electrical stimulation with tendon vibration) were assessed before and after the same exercise intervention in 17 resistance trained men. Results showed decreases in peak plantar flexion torque (Experiment 1: -12.2%, Experiment 2: -16.9%), electrically evoked torque (20 Hz -15.3%, 80 Hz -15.3%, variable-frequency train -17.9%), and cSP (-3.8%; i.e., reduced inhibition) post-exercise which did not recover by 20 min. Electromyographic activity (EMG; -6%), corticospinal excitability (-9%), and PIC facilitation (-24.8%) were also reduced post-exercise but recovered by 10 min. Caffeine ingestion increased torque and EMG but did not notably affect corticospinal excitability, PIC amplification, or electrically evoked torque. The data indicate that a decrease in muscle function largely underpins the loss of force after repeated, high-intensity muscular efforts, but that the loss is exacerbated immediately after the exercise by simultaneous decreases in corticospinal excitability and PIC amplitudes at the motor neurons.