Human Muscle Contractility Research Articles

Acute normobaric hypoxia causes a rightward shift in the torque-frequency relationship but has no effect on postactivation potentiation.

Low fractions of inspired oxygen ([Formula: see text]; i.e., hypoxia) affect aspects of skeletal muscle contractility in humans, but it remains unclear if postactivation potentiation (PAP) and the torque-frequency (T-F) relationship are altered. We investigated the effects of 2 (H2) and 4 (H4) h of normobaric hypoxia ([Formula: see text] = 0.11 ± 0.47) on the magnitude of PAP of the knee extensors and the T-F relationship of the dorsiflexors in 13 and 12 healthy participants, respectively. To assess PAP, a resting twitch was evoked via femoral nerve stimulation before and 2-300 s after a 10-s maximal voluntary contraction (MVC). A T-F relationship was obtained by stimulating the common fibular nerve with a single pulse and 1-s trains between 5 and 100 Hz. During hypoxia, peripheral oxygen saturation decreased by ∼18% from 98.0 ± 0.8% at baseline (P < 0.001). MVC force and voluntary activation (VA) of the knee extensors were lower than baseline throughout hypoxia (e.g., ∼8% and ∼5%, respectively, at H2; P ≤ 0.027); however, the magnitude of PAP was not altered by hypoxia (P ≥ 0.711). Surprisingly, PAP did increase with time across the control day (P ≤ 0.012). MVC torque and VA of the dorsiflexors were unaffected by hypoxia (P ≥ 0.127), but the estimated frequency required to evoke 50% of 100 Hz torque increased by ∼1.2 Hz at H2 (P ≤ 0.021). These results imply that 2 h of normobaric hypoxia were sufficient to 1) impair neural drive to the knee extensors but not the mechanism(s) responsible for PAP and 2) lead to a rightward shift of the T-F relationship for the dorsiflexors.NEW & NOTEWORTHY Postactivation potentiation of the knee extensors was unaffected by 4 h of normobaric hypoxia exposure but may be confounded by hypoxia-related impairments to the conditioning contraction. In the dorsiflexors, contractile rates increased in hypoxia, which led to a rightward shift of the torque-frequency relationship, such that a higher frequency was required to obtain 50% of maximal torque. These results expand our understanding of the acute effects of hypoxia on skeletal muscle function.

Passive heat acclimation improves skeletal muscle contractility in humans.

The aim of this study was to investigate the effect of repeated passive heat exposure (i.e., acclimation) on muscle contractility in humans. Fourteen nonheat-acclimated males completed two trials including electrically evoked twitches and voluntary contractions in thermoneutral conditions [Cool: 24°C, 40% relative humidity (RH)] and hot ambient conditions in the hyperthermic state (Hot: 44-50°C, 50% RH) on consecutive days in a counterbalanced order. Rectal temperature was ~36.5°C in Cool and was maintained at ~39°C throughout Hot. Both trials were repeated after 11 days of passive heat acclimation (1 h per day, 48-50°C, 50% RH). Heat acclimation decreased core temperature in Cool (-0.2°C, P < 0.05), increased the time required to reach 39°C in Hot (+9 min, P < 0.05) and increased sweat rate in Hot (+0.7 liter/h, P < 0.05). Moreover, passive heat acclimation improved skeletal muscle contractility as evidenced by an increase in evoked peak twitch amplitude both in Cool (20.5 ± 3.6 vs. 22.0 ± 4.0 N·m) and Hot (20.5 ± 4.7 vs. 22.0 ± 4.0 N·m) (+9%, P < 0.05). Maximal voluntary torque production was also increased both in Cool (145 ± 42 vs. 161 ± 36 N·m) and Hot (125 ± 36 vs. 145 ± 30 N·m) (+17%, P < 0.05), despite voluntary activation remaining unchanged. Furthermore, the slope of the relative torque/electromyographic linear relationship was improved postacclimation (P < 0.05). These adjustments demonstrate that passive heat acclimation improves skeletal muscle contractile function during electrically evoked and voluntary muscle contractions of different intensities both in Cool and Hot. These results suggest that repeated heat exposure may have important implications to passively maintain or even improve muscle function in a variety of performance and clinical settings.

Effects of lengthening contraction on calcium kinetics and skeletal muscle contractility in humans

We have tested the hypothesis that the altered muscle contractility after lengthening contractions (LC) is caused by altered calcium (Ca2+) kinetics. Subjects (n = 8) performed 100 drop jumps and muscle contractility was measured pre- and post-exercise by maximal voluntary contraction (MVC) and transcutaneous electrical stimulation (1, 20 and 50 Hz). Muscle biopsies were analysed for muscle metabolites, rates of SR Ca(2+) uptake (CaU) and release (CaR) and myosin heavy chain (MHC) composition. The rates of torque relaxation and CaU were positively related to muscle fibre type composition (% MHC II). Muscle creatine (Cr) decreased and the ratio between phosphocreatine (PCr) and Cr increased 3 and 24 h post-exercise (P < 0.05 vs. pre-exercise). LC resulted in reduced MVC (-19%), twitch torque (-41%) and 20/50 Hz torque ratio (-30%) and a faster relaxation rate (P < 0.05). The contractile parameters recovered partially but remained altered 24 h post-exercise (P < 0.05). The average CaR was unchanged after LC (P > 0.05). However, the response varied between subjects and the relative post-exercise CaR was significantly related to the degree of LFF (post/pre 20/50 Hz force ratio) and to the decline in twitch force (post/pre twitch ratio). CaU was lower in seven of eight subjects after LC (P > 0.05). The decline in torque after LC could not be explained by metabolic factors since PCr/Cr ratio increased. The relation between CaR and fatigue suggests that the mechanism of fatigue in part may be attributed to intrinsic changes in the SR Ca2+ release channel. The faster torque relaxation after LC could not be explained by an increased rate of CaU.

In vivo quantification of muscle contractility in humans: healthy subjects and patients with myotonic muscular dystrophy.

The purpose of this study was to use direct in vivo contractility measurements to assess muscle function in patients with myotonic muscular dystrophy (MMD). The tetanic and twitch responses and several time parameters of muscle contraction were obtained from nine MMD subjects and nine able-bodied, age-matched controls. After a routine nerve conduction study, in vivo contractility measurements were obtained by stimulating the ulnar nerve at the wrist and recording the isometric flexor function of the intrinsic muscles at the metacarpophalangeal joint of the index finger. A series of single stimuli, paired stimuli, and fused tetanic stimulations were generated during a 20-minute experimental protocol. A stable tetanus was produced at 50Hz for 1.2 seconds. M-wave and contractile data were recorded at 1,000Hz by digitization of the analog signal and storage by the microcomputer. The MMD patients were weaker than controls (p less than .05), as shown by the 39% reduction in tetanic tension and 57% reduction in twitch tension. The MMD patients also had a significant impairment in relaxing their muscles as shown by the 1,100% increase in half-relaxation time after contraction, even though there was no evidence of repetitive firing after cessation of stimulus. These data show that MMD patients exhibit failure of sarcolemmal activation, altered excitation-contraction coupling mechanisms, and failure of the contractile machinery. The myotonia is due in part, to some defect in the contractile machinery; it is not solely due to failure of sarcolemmal activation.

Effect of acute hypercapnia on limb muscle contractility in humans

The effect of acute hypercapnia on skeletal muscle contractility and relaxation rate was investigated. The contractile force of fresh and fatigued quadriceps femoris (QF) and adductor pollicis (AP) was studied in normal humans by use of electrical stimulation. Maximum relaxation rate from stimulated contractions was measured for both muscles. Acute hypercapnia led to a rapid substantial reduction of contraction force. The respiratory acidosis after 9% CO2 was breathed for 20 min [mean venous blood pH 7.26 and end-tidal PCO2 (PETCO2) 65.1 Torr] reduced 20- and 100-Hz stimulated contractions of QF to 72.8 +/- 4.4 and 80.0 +/- 5.1% of control values, respectively. After 8 and 9% CO2 were breathed for 12 min, AP forces at 20- and 50-Hz stimulation were also reduced. Twitch tension of AP was reduced by a mean of 25.5% when subjects breathed 9% CO2 for 12 min [mean arterialized venous blood pH (pHav) 7.25 and PETCO2 66 Torr]. Over the range of 5% (pHav 7.38 and PETCO2 47 Torr) to 9% CO2, there was a linear relationship between twitch tension loss and pHav, arterialized venous blood PCO2, and PETCO2. Acute respiratory acidosis (mean PETCO2 61 Torr) increased the severity of low-frequency fatigue after intermittent voluntary contractions of AP. At 20 min of recovery, twitch tension was 63.2 +/- 13.4 and 46.8 +/- 16.4% of control value after exercise breathing air and 8% CO2, respectively. Acute hypercapnia (mean PETCO2 65.1 and 60.5 Torr) did not alter the maximum relaxation rate from tetanic contractions of fresh QF and from twitch tensions of AP.