The influence of voice pitch on perceptions of trustworthiness across social contexts

Perceptions of trustworthiness are an important predictor of social outcomes, such as monetary exchanges, criminal sentencing, and the attainment of leadership roles. Higher testosterone levels predict both lower voice pitch and untrustworthy behavior, across economic and mating contexts. Here, we tested the influence of voice pitch on perceptions of trustworthiness across general, economic, and mating-related (mate poaching, infidelity) contexts. We found that the context of trust and the sex of the speaker both changed how voice pitch affected perceived trustworthiness. Listeners were more trusting of higher-pitched female voices in economic and mate poaching contexts, but trusted lower-pitched female voices more in general. Listeners were more trusting of higher-pitched male voices in economic and mating-related contexts, and also tended to perceive higher-pitched male voices as more trustworthy in general. Listeners' attributions of trustworthiness were generally unrelated to perceptions of attractiveness from similarly-pitched voices, indicating that trust-related attributions were independent of preferences for higher- or lower-pitched voices. Furthermore, perceptions of general trustworthiness were associated with perceptions of economic trust, but were not consistently associated with perceptions of mating-related trust. These findings provide evidence that voice pitch alone is sufficient to influence trust-related perceptions, and demonstrates that listeners use voice pitch as a cue to trustworthy behavior.     

Skeletal muscle lactate release and glycolytic intermediates during hypercapnia

The effects of respiratory acidosis on glycolysis in the autoperfused canine gastrocnemius-plantaris were studied using anesthetized dogs that were ventilated either with air (n = 30) or with 4% CO2-21% O2-75% N2 (n = 30). The left muscle group was stimulated at 3 Hz for up to 20 min, after which the active and the contralateral resting muscles were removed and frozen in liquid N2. Blood flow, VO2, Vco2, and tension development were unaffected by CO2. Glycogen catabolism was not affected, but lactate release (La) was lower (P less than 0.05) during activity with CO2; and greater fructose 6-phosphate, fructose 6-phosphate/fructose 1,6-diphosphate, and alpha-glycerophosphate/dihydroxyacetone phosphate ratios resulted (P less than 0.05). With respiratory acidosis, muscle lactate tended to accumulate early in contractions, but a net lactate uptake occurred during the last 10 min of contractions. Thus, respiratory acidosis reduced lactate efflux and there was a net uptake late in the contraction period. Glycogen phosphorylase did not appear to be affected by the respiratory acidosis, but there was evidence of inhibition at the phosphofructokinase step as well as a tendency for lactate to accumulate within the muscle. La often occurred in a direction contrary to the muscle-venous lactate concentration difference with either air or CO2 and La also decreased far more rapidly over time than did the arterial-venous H+.     

Effects of ischemic and hypoxic hypoxia on VO2 and lactic acid output during tetanic contractions

We measured O2 uptake (VO2), CO2 output (VCO2), and net lactic acid output (L) during a 30-min period of repetitive 1/s isotonic tetanic contractions of the dog gastrocnemius-plantaris muscle group. The conditions were modest ischemic hypoxia (ischemia), hypoxia hypoxia (hypoxia), and free-flow normoxia (control). The major goal was to assess the effects of these perturbations on L during contractions. Ischemia and hypoxia were initiated just before the start of the contractions and at minute 7 of contractions in separate groups of experiments. Whenever applied, both ischemia and hypoxia reduced VO2 compared with the control values. When ischemia was initiated at the start of contractions, L was reduced transiently compared with the controls. When ischemia began at minute 7, L was increased modestly but transiently compared with the controls. When hypoxia was initiated at the start of contractions, L was increased during the entire period of contractions. The L pattern was the same as in the controls, rising to a maximal value at 3 min and declining steadily to a lower value at 30 min. When hypoxia began at minute 7, L declined initially at a slower rate than it did in the controls and was thereby elevated above the controls from 9 to 30 min. Ischemia was associated with a more rapid reduction in mechanical performance than hypoxia. The data suggest that the mechanisms of the decreased mechanical performance and VO2 are different for ischemia and hypoxia.