Emma Z. Ross

Effects of dynamic and static stretching on vertical jump performance and electromyographic activity.

Hough, PA, Ross, EZ, and Howatson, G. Effects of dynamic and static stretching on vertical jump performance and electromyographic activity. J Strength Cond Res 23(2): 507-512, 2009-The results of previous research have demonstrated that static stretching (SS) can reduce muscular performance and that dynamic stretching (DS) can enhance muscular performance. The purpose of this study was to assess the effects of SS and DS on vertical jump (VJ) performance and electromyographic (EMG) activity of the m. vastus medialis. Eleven healthy men (age 21 ± 2 years) took part in 3 conditions (no stretching [NS], SS, and DS), on separate occasions in a randomized, crossover design. During each condition, measurements of VJ height and EMG activity during the VJ were recorded. A repeated-measures analysis of variance and post hoc analysis indicated that VJ height was significantly less (4.19 ± 4.47%) after SS than NS (p < 0.05) and significantly greater (9.44 ± 4.25%) in DS than SS (p < 0.05). There was significantly greater EMG amplitude in the DS compared with the SS (p < 0.05). The results demonstrated that SS has a negative influence on VJ performance, whereas DS has a positive impact. Increased VJ performance after DS may be attributed to postactivation potentiation, whereas the reduction in VJ performance after SS may be attributable to neurological impairment and a possible alteration in the viscoelastic properties of the muscular tendon unit (MTU). This investigation provides some physiological basis for the inclusion of DS and exclusion of SS in preparation for activities requiring jumping performance.

Supraspinal fatigue after normoxic and hypoxic exercise in humans

•  Processes leading to fatigue occur within the exercising muscle (peripheral fatigue) and the nervous system (central fatigue). •  We asked whether central processes of fatigue would be increased after strenuous exercise in environments where oxygen availability is reduced (hypoxia) compared to the same absolute exercise intensity at sea‐level. •  Our main finding was that the contribution of central processes to fatigue was increased after exercise in hypoxia (equivalent to ∼3800 m above sea‐level). •  The greater amount of central fatigue in hypoxia was due to suboptimal neural output from the brain and was associated with reductions in oxygen availability. •  The findings provide a plausible mechanism for why exercise performance is impaired at high altitude, and might help our understanding of exercise limitation in patients with reduced oxygen delivery to the brain.

Effect of graded hypoxia on supraspinal contributions to fatigue with unilateral knee-extensor contractions

Supraspinal fatigue, defined as an exercise-induced decline in force caused by suboptimal output from the motor cortex, accounts for over one-quarter of the force loss after fatiguing contractions of the knee extensors in normoxia. We tested the hypothesis that the relative contribution of supraspinal fatigue would be elevated with increasing severities of acute hypoxia. On separate days, 11 healthy men performed sets of intermittent, isometric, quadriceps contractions at 60% maximal voluntary contraction to task failure in normoxia (inspired O(2) fraction/arterial O(2) saturation = 0.21/98%), mild hypoxia (0.16/93%), moderate hypoxia (0.13/85%), and severe hypoxia (0.10/74%). Electrical stimulation of the femoral nerve was performed to assess neuromuscular transmission and contractile properties of muscle fibers. Transcranial magnetic stimulation was delivered to the motor cortex to quantify corticospinal excitability and voluntary activation. After 10 min of breathing the test gas, neuromuscular function and cortical voluntary activation prefatigue were unaffected in any condition. The fatigue protocol resulted in ∼ 30% declines in maximal voluntary contraction force in all conditions, despite differences in time-to-task failure (24.7 min in normoxia vs. 15.9 min in severe hypoxia, P < 0.05). Potentiated quadriceps twitch force declined in all conditions, but the decline in severe hypoxia was less than that in normoxia (P < 0.05). Cortical voluntary activation also declined in all conditions, but the deficit in severe hypoxia exceeded that in normoxia (P < 0.05). The additional central fatigue in severe hypoxia was not due to altered corticospinal excitability, as electromyographic responses to transcranial magnetic stimulation were unchanged. Results indicate that peripheral mechanisms of fatigue contribute relatively more to the reduction in force-generating capacity of the knee extensors following submaximal intermittent isometric contractions in normoxia and mild to moderate hypoxia, whereas supraspinal fatigue plays a greater role in severe hypoxia.

Corticomotor excitability contributes to neuromuscular fatigue following marathon running in man

It is unknown whether changes in corticomotor excitability follow prolonged exercise in healthy humans. Furthermore, the role of supraspinal fatigue in decrements of force production and voluntary activation following prolonged exercise has not been established. This study investigated peripheral and central fatigue after a marathon (42.2 km) on a treadmill. Isometric ankle dorsiflexion force and electromyographic responses of the tibialis anterior in response to magnetic stimulation of the peroneal nerve (PNMS) and the motor cortex (TMS) were measured before, immediately after, 4 and 24 h post‐marathon (MAR) in nine volunteers (mean ±s.d. completion time, 208 ± 22 min). Maximal voluntary contraction decreased by 18 ± 7% immediately after MAR (P= 0.009) and remained significantly decreased after 4 h. The amplitude of the evoked response to TMS, but not to PNMS, was depressed immediately post‐MAR by 57 ± 25% (P= 0.04). Potentiated resting twitch force was reduced in response to both TMS and PNMS post‐MAR (71 ± 8 and 35 ± 2% decrease, P= 0.035 and 0.037, respectively), and voluntary activation was reduced to 61.9 ± 18% immediately post‐MAR (P < 0.05). All measures had returned to baseline values after 24 h. These results suggest that fatigue was attributable to both a disturbance of the contractile apparatus within the muscle and submaximal output from the motor cortex.

Voluntary activation of human knee extensors measured using transcranial magnetic stimulation

The aim of this study was to determine the applicability and reliability of a transcranial magnetic stimulation twitch interpolation technique for measuring voluntary activation of a lower limb muscle group. Cortical voluntary activation of the knee extensors was determined in nine healthy men on two separate visits by measuring superimposed twitch torques evoked by transcranial magnetic stimulation during isometric knee extensions of varying intensity. Superimposed twitch amplitude decreased linearly with increasing voluntary torque between 50 and 100% of mean maximal torque, allowing estimation of resting twitch amplitude and subsequent calculation of voluntary activation. There were no systematic differences for maximal voluntary activation within day (mean ±s.d. 90.9 ± 6.2 versus 90.7 ± 5.9%; P= 0.98) or between days (90.8 ± 6.0 versus 91.2 ± 5.7%; P= 0.92). Systematic bias and random error components of the 95% limits of agreement were 0.23 and 9.3% within day versus−0.38 and 7.5% between days. Voluntary activation was also determined immediately after a 2 min maximal voluntary isometric contraction; in four of these subjects, voluntary activation was determined 30 min after the sustained contraction. Immediately after the sustained isometric contraction, maximal voluntary activation was reduced from 91.2 ± 5.7 to 74.2 ± 12.0% (P < 0.001), indicating supraspinal fatigue. After 30 min, voluntary activation had recovered to 85.4 ± 8.8% (P= 0.39 versus baseline). These results demonstrate that transcranial magnetic stimulation enables reliable measurement of maximal voluntary activation and assessment of supraspinal fatigue of the knee extensors.

Time course of neuromuscular changes during running in well-trained subjects.

PURPOSE Prolonged exercise reduces the capacity of the neuromuscular system to produce force, which is known as fatigue. The purpose of this study was to examine the time course of neural and contractile processes during a 20-km running bout. METHODS Eight experienced runners (mean T SD: age = 31 T 6 yr, VO2max = 60.1 T 2.2 mL x kg(-1) x min(-1)) completed an all-out self-paced 20-km treadmill run. Isometric knee extensor torque and EMG responses of the vastus lateralis (VL) in response to percutaneous electrical stimulation and voluntary contraction were measured before and after 5, 10, 15, and 20 km of exercise. RESULTS Participants RPE, measured using the Borg 6-20 scale, increased steadily throughout the run to a value of 18 T 1 at exercise termination. Maximal voluntary contraction (MVC) of the knee extensors only decreased during the final 5 km of running, with a 15% +/- 12% (P = 0.02) decrease at 20 km. Vastus lateralis EMG during an MVC was reduced after 15 km (-18% +/- 21%, P = or <0.01) and 20 km (-20% +/- 22%, P = 0.03). A significant correlation (r = 0.71, P = 0.048) was observed between the final reduction in MVC and the maximal EMG. Voluntary activation, estimated by the twitch interpolation technique, decreased by 13% +/- 6% at 20 km (P = or < 0.01), and this was significantly correlated (r = 0.70, P = 0.049) with MVC loss. There were no significant changes in the amplitude of the electrically evoked muscle action potential (M-wave) or potentiated twitch during or after the 20-km run. CONCLUSIONS A reduction in knee extensor MVC only occurs during the final 5 km of a 20-km self-paced run. Impaired voluntary activation and neural drive but not contractile processes are responsible for this decreased strength.

Cerebrovascular and corticomotor function during progressive passive hyperthermia in humans

The present study examined the integrative effects of passive heating on cerebral perfusion and alterations in central motor drive. Eight participants underwent passive hyperthermia [0.5°C increments in core temperature (Tc) from normothermia (37 ± 0.3°C) to their limit of thermal tolerance (T-LIM; 39.0 ± 0.4°C)]. Blood flow velocity in the middle cerebral artery (CBFv) and respiratory responses were measured continuously. Arterial blood gases and blood pressure were obtained intermittently. At baseline and each Tc level, supramaximal femoral nerve stimulation and transcranial magnetic stimulation (TMS) were performed to assess neuromuscular and cortical function, respectively. At T-LIM, measures were (in a randomized order) also made during a period of breathing 5% CO(2) gas to restore eucapnia (+5% CO(2)). Mean heating time was 179 ± 51 min, with each 0.5°C increment in Tc taking 40 ± 10 min. CBFv was reduced by ∼20% below baseline from +0.5°C until T-LIM. Maximal voluntary contraction (MVC) of the knee extensors was decreased at T-LIM (-9 ± 10%; P < 0.05), and cortical voluntary activation (VA), assessed by TMS, was decreased at +1.5°C and T-LIM by 11 ± 8 and 22 ± 23%, respectively (P < 0.05). Corticospinal excitability (measured as the EMG response produced by TMS) was unaltered. Reductions in cortical VA were related to changes in ventilation (Ve; R(2) = 0.76; P < 0.05) and partial pressure of end-tidal CO(2) (Pet(CO(2)); R(2) = 0.63; P < 0.05) and to changes in CBFv (R(2) = 0.61; P = 0.067). Interestingly, although CBFv was not fully restored, MVC and cortical VA were restored towards baseline values during inhalation of 5% CO(2). These results indicate that descending voluntary drive becomes progressively impaired as Tc is increased, presumably due, in part, to reductions in CBFv and to hyperthermia-induced hyperventilation and subsequent hypocapnia.

Transcranial magnetic stimulation in sport science: A commentary

Abstract The aim of this commentary is to provide a brief overview of transcranial magnetic stimulation (TMS) and highlight how this technique can be used to investigate the acute and chronic responses of the central nervous system to exercise. We characterise the neuromuscular responses to TMS and discuss how these measures can be used to investigate the mechanisms of fatigue in response to locomotor exercise. We also discuss how TMS might be used to study the corticospinal adaptations to resistance exercise training, with particular emphasis on the responses to shortening/lengthening contractions and contralateral training. The limited data to date suggest that TMS is a valuable technique for exploring the mechanisms of central fatigue and neural adaptation.

Changes in respiratory muscle and lung function following marathon running in man

Abstract Respiratory muscle fatigue has been reported following short bouts of high-intensity exercise, and prolonged, moderate-intensity exercise, as evidenced by decrements in inspiratory and expiratory mouth pressures. However, links to functionally relevant outcomes such as breathing effort have been lacking. The present study examined dyspnoea and leg fatigue during a treadmill marathon in nine experienced runners. Maximal inspiratory and expiratory pressure, peak inspiratory and expiratory flow, forced vital capacity, and forced expiratory volume in one second were assessed before, immediately after, and four and 24 hours after a marathon. During the run, leg effort was rated higher than respiratory effort from 18 through 42 km (P < 0.05). Immediately after the marathon, there were significant decreases in maximal inspiratory pressure and peak inspiratory flow (from 118 ± 20 cm H2O and 6.3 ± 1.4 litres · s−1 to 100 ± 22 cm H2O and 4.9 ± 1.5 litres · s−1 respectively; P < 0.01), while expiratory function remained unchanged. Leg maximum voluntary contraction force was significantly lower post-marathon. Breathing effort correlated significantly with leg fatigue (r = 0.69), but not inspiratory muscle fatigue. Our results confirm that prolonged moderate-intensity exercise induces inspiratory muscle fatigue. Furthermore, they suggest that the relative intensity of inspiratory muscle work during exercise makes some contribution to leg fatigue.

Muscle contractile function and neural control after repetitive endurance cycling.

PURPOSE To examine alterations in muscle contractile properties, cortical excitability, and voluntary activation as a consequence of 20 d of repetitive endurance cycling within a 22-d period. METHODS Eight well-trained male cyclists completed 20 prolonged cycling stages interspersed by two rest days (days 9 and 17), which replicated the 2007 Tour de France route and schedule. Isometric knee extensor torque and EMG responses of the vastus lateralis in response to percutaneous electrical stimulation and transcranial magnetic stimulation were measured before, on days 9 and 17, and 2 d after completion of Tour de France. Postexercise measurements on days 9 and 17 were taken >18 h after cessation of the previous exercise bout. RESULTS Maximal voluntary contraction of the knee extensors decreased by 20 +/- 10% (P < 0.01) during Tour de France but recovered after 2 d of rest. Peripherally evoked M-wave and potentiated twitch responses were also significantly decreased during Tour de France, up to 31 +/- 21% and 22 +/- 18%, respectively (P < 0.05), but returned to baseline values after 2 d of recovery. Voluntary activation was reduced to 75 +/- 8% (P < 0.05) during Tour de France and remained significantly depressed (79 +/- 7%, P < 0.05) after completion. The amplitude of motor evoked potentials was decreased by 44 +/- 28% (P < 0.01) on day 9 and remained significantly depressed during the remainder of, and after, Tour de France. CONCLUSIONS A reduction in knee extensor strength, which occurs after repetitive prolonged cycling exercise, is a result of both central and peripheral processes. Reduced sarcolemmal excitability and impairment of contractile mechanisms exists even after 18 h of recovery. An enduring reduction in corticomotor output persists even after 2 d of rest.