Matthew D. White

Adaptation of exercise ventilation during an actively-induced hyperthermia following passive heat acclimation

Hyperthermia-induced hyperventilation has been proposed to be a human thermolytic thermoregulatory response and to contribute to the disproportionate increase in exercise ventilation (VE) relative to metabolic needs during high-intensity exercise. In this study it was hypothesized that VE would adapt similar to human eccrine sweating (E(SW)) following a passive heat acclimation (HA). All participants performed an incremental exercise test on a cycle ergometer from rest to exhaustion before and after a 10-day passive exposure for 2 h/day to either 50 degrees C and 20% relative humidity (RH) (n = 8, Acclimation group) or 24 degrees C and 32% RH (n = 4, Control group). Attainment of HA was confirmed by a significant decrease (P = 0.025) of the esophageal temperature (T(es)) threshold for the onset of E(SW) and a significantly elevated E(SW) (P < or = 0.040) during the post-HA exercise tests. HA also gave a significant decrease in resting T(es) (P = 0.006) and a significant increase in plasma volume (P = 0.005). Ventilatory adaptations during exercise tests following HA included significantly decreased T(es) thresholds (P < or = 0.005) for the onset of increases in the ventilatory equivalents for O(2) (VE/VO(2)) and CO(2) (VE/VCO(2)) and a significantly increased VE (P < or = 0.017) at all levels of T(es). Elevated VE was a function of a significantly greater tidal volume (P = 0.003) at lower T(es) and of breathing frequency (P < or = 0.005) at higher T(es). Following HA, the ventilatory threshold was uninfluenced and the relationships between VO(2) and either VE/VO(2) or VE/VCO(2) did not explain the resulting hyperventilation. In conclusion, the results support that exercise VE following passive HA responds similarly to E(SW), and the mechanism accounting for this adaptation is independent of changes of the ventilatory threshold or relationships between VO(2) with each of VE/VO(2) and VE/VCO(2).

Human face‐only immersion in cold water reduces maximal apnoeic times and stimulates ventilation

In two studies, the cold shock and diving responses were investigated after human face immersion without prior hyperventilation to explore the mechanism(s) accounting for reductions in maximal apnoeic times (ATmax) at low water temperatures. In study 1, ATmax, heart rate (HR) and cutaneous blood cell velocity were measured in 13 non‐apnoea‐trained males during apnoeic face immersion in 0, 10, 20 and 33°C water and room air (AIR). In study 2, six males were measured during non‐apnoeic face immersion in 0, 10 and 33°C water for ventilation ( ), respiratory exchange ratio (RER), HR and oxygen consumption ( ), as well for end‐tidal partial pressures of oxygen ( ) and carbon dioxide ( ). Results indicated that the ATmax of 30.7 s (s.d. 7.1 s) at 0°C (P < 0.001) and 48.2 s (s.d. 16.0 s) at 10°C (P < 0.05) were significantly shorter than that of ∼58 s in AIR or 33°C. During apnoea at 0, 10, 20 and 33°C, both the deceleration of HR (P < 0.05) and peripheral vasoconstriction (P < 0.05), as well as the peak HR at 0°C (P= 0.002) were significantly greater than in AIR. At 0°C in comparison with 33°C, non‐apnoeic face immersions gave peaks in (P= 0.039), RER (P= 0.025), (P= 0.032) and HR (P= 0.011), as well as lower minimum values for (P= 0.033) and HR (P= 0.002). With as the covariate, ANCOVA showed that remained significantly greater (P= 0.003) at lower water temperatures. In conclusion, during face immersion at 10°C and below, there is a non‐metabolic, neurally mediated cold shock‐like response that shortens apnoea, stimulates ventilation and predominates over the oxygen conserving effects of the dive response.

Point: Humans do demonstrate selective brain cooling during hyperthermia

Selective brain cooling (SBC) is defined by the International Union of Physiological Sciences ([11][1]) as “a lowering of the brain temperature either locally or as a whole below arterial blood temperature.” Since the first observations of SBC in hyperthermic, nonhuman mammals ([1][2], [14][3

Reproducibility of relationships between human ventilation, its components and oesophageal temperature during incremental exercise

AbstractFor human exercise at intensities greater than ~70 to 85% of maximal levels of exertion, ventilation (VE) increases proportionately to core temperature (TC) following distinct TC thresholds. This suggested TC in humans could be a modulator of exercise-induced ventilation. This study tested the reproducibility of relationships between oesophageal temperature (Toes), ventilation and its components during incremental exercise. On two nonconsecutive days, at an ambient temperature of 22.1±0.3°C and RH of 45±5%, seven untrained adult males of normal physique pedaled on a seated cycle ergometer in an incremental exercise protocol from rest to the point of exhaustion. In each exercise session, ventilatory equivalents for oxygen consumption

High-level medium-chain triglyceride feeding and energy expenditure in normal-weight women

(V_{\text{E}} \cdot {V_{\text{O}_{\text{2}}}} ^{ - 1})

Human body temperature and new approaches to constructing temperature-sensitive bacterial vaccines

and carbon dioxide production

The effects of lower body positive and negative pressure on the hypoxic ventilatory decline

(V_{\text{E}} \cdot {V_{\text{CO}_{\text{2}}}} ^{ - 1})