Abstract
PurposeThis study assessed the impact of normobaric hypoxia and acute nitrate ingestion on shivering thermogenesis, cutaneous vascular control, and thermometrics in response to cold stress.MethodEleven male volunteers underwent passive cooling at 10 °C air temperature across four conditions: (1) normoxia with placebo ingestion, (2) hypoxia (0.130 FiO2) with placebo ingestion, (3) normoxia with 13 mmol nitrate ingestion, and (4) hypoxia with nitrate ingestion. Physiological metrics were assessed as a rate of change over 45 min to determine heat loss, and at the point of shivering onset to determine the thermogenic thermoeffector threshold.ResultIndependently, hypoxia expedited shivering onset time (p = 0.05) due to a faster cooling rate as opposed to a change in central thermoeffector thresholds. Specifically, compared to normoxia, hypoxia increased skin blood flow (p = 0.02), leading to an increased core-cooling rate (p = 0.04) and delta change in rectal temperature (p = 0.03) over 45 min, yet the same rectal temperature at shivering onset (p = 0.9). Independently, nitrate ingestion delayed shivering onset time (p = 0.01), mediated by a change in central thermoeffector thresholds, independent of changes in peripheral heat exchange. Specifically, compared to placebo ingestion, no difference was observed in skin blood flow (p = 0.5), core-cooling rate (p = 0.5), or delta change in rectal temperature (p = 0.7) over 45 min, while nitrate reduced rectal temperature at shivering onset (p = 0.04). No interaction was observed between hypoxia and nitrate ingestion.ConclusionThese data improve our understanding of how hypoxia and nitric oxide modulate cold thermoregulation.
Highlights
Communicated by Narihiko Kondo.Across taxa, it is well documented that internal body temperature is positively associated with oxygen uptake (VO2) (Krogh 1914; Wood 1991)
As a rate of change over 45 min, serving as a proxy for peripheral heat exchange, and at the point of shivering onset, serving as a proxy for thermogenic thermoeffector thresholds: (1) over 45 min, hypoxia would blunt peripheral vasoconstriction, leading to an increase in skin blood flow and rate of heat loss compared to normoxia, with this response synergised following concomitant nitrate ingestion; (2) at shivering onset, no difference in skin or core temperature would be observed between hypoxia and normoxia, yet faster heat loss with hypoxia would result in a temporally earlier shivering onset, with this response further synergistically accelerated following concomitant nitrate ingestion
Experimental stressors were effective in their intended application; hypoxia elicited a significant reduction in peripheral oxygen saturation compared to normoxia [Estimated Marginal Means (EMM); normoxia, 99 (98–99) % vs. hypoxia, 88 (85–90) %, p < 0.001], while nitrate ingestion elicited a significant increase in plasma [ NO2−] compared to the placebo [EMM; placebo, 117 (82–151) nmol·L−1 vs. nitrate, 575 (394–757) nmol·L−1, p < 0.001]
Summary
It is well documented that internal body temperature is positively associated with oxygen uptake (VO2) (Krogh 1914; Wood 1991). In situations of systemic hypoxia, the thermoregulatory tendency is that of a reduction in body temperature (anapyrexia), with an accompanying reduction in VȮ 2, improving metabolic efficiency (Steiner and Branco 2002). A decline in skin and deep body temperature elicit robust thermogenic responses, the most effective of which is shivering (Stocks et al 2004). European Journal of Applied Physiology (2021) 121:1207–1218 this response might be considered metabolically costly under limited oxygen availability. It is conceivable that the competing demands of cold and hypoxia compromise the ability to maintain both thermal balance and adequate oxygenation when both stimuli are simultaneously encountered (Wood 1991)
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