Effects of exercise in a cold environment on transcriptional control of PGC-1α

Abstract

Peroxisome proliferator-activated receptor-α coactivator-1α (PGC-1α) mRNA is increased with both exercise and exposure to cold temperature. However, transcriptional control has yet to be examined during exercise in the cold. Additionally, the need for environmental cold exposure after exercise may not be a practical recovery modality. The purpose of this study was to determine mitochondrial-related gene expression and transcriptional control of PGC-1α following exercise in a cold compared with room temperature environment. Eleven recreationally trained males completed two 1-h cycling bouts in a cold (7°C) or room temperature (20°C) environment, followed by 3 h of supine recovery in standard room conditions. Muscle biopsies were taken from the vastus lateralis preexercise, postexercise, and after a 3-h recovery. Gene expression and transcription factor binding to the PGC-1α promoter were analyzed. PGC-1α mRNA increased from preexercise to 3 h of recovery, but there was no difference between trials. Estrogen-related receptor-α (ERRα), myocyte enhancer factor-2 (MEF2A), and nuclear respiratory factor-1 (NRF-1) mRNA were lower in cold than at room temperature. Forkhead box class-O (FOXO1) and cAMP response element-binding protein (CREB) binding to the PGC-1α promoter were increased postexercise and at 3 h of recovery. MEF2A binding increased postexercise, and activating transcription factor 2 (ATF2) binding increased at 3 h of recovery. These data indicate no difference in PGC-1α mRNA or transcriptional control after exercise in cold versus room temperature and 3 h of recovery. However, the observed reductions in the mRNA of select transcription factors downstream of PGC-1α indicate a potential influence of exercise in the cold on the transcriptional response related to mitochondrial biogenesis.

Skeletal muscle cold shock and heat shock protein mRNA response to aerobic exercise in different environmental temperatures

“…In this same manner, exercise increases heat production and may limit any cold related response. Indeed, our data indicate an increase in core temperature during exercise with only very minimal differences between environments, which is supported by previous literature [23,29]. This core temperature response could explain the limited effect of environmental temperatures observed in the current study on CIRP and RBM3 mRNA.…”

“…It is possible that thermos-reception from the skin may ultimately lead to a differential mRNA response and that skeletal muscle mRNA may be altered. Indeed, we have previously observed an altered mRNA response to exercise in different environmental temperatures when core temperature was unaltered [23].…”

“…Muscle biopsies were taken pre-and 3 hours postexercise during each experimental trial for the analysis of mRNA of selected heat and cold shock proteins. While little is known of the timecourse of activation of transcription of cold shock protein mRNA, the 3 hour timepoint was chosen based on the response of many early response genes associated with exercise and temperature under similar conditions [23].…”

Exercise- and Cold-Induced Human PGC-1α mRNA Isoform Specific Responses

“…More specifically, aerobic exercise paired with environmental cold exposure has been shown to upregulate the transcription of PGC-1α [ 5 , 6 ]. Some studies have not detected a statistically significant upregulation of PGC-1α in the cold compared to control conditions but did observe non-statistical effects [ 7 , 8 , 9 , 10 ]. Taken collectively, it appears that environmental cold interventions during aerobic exercise enhance the exercise-induced transcription of PGC-1α in humans.…”

FOXO1 inhibition prevents renal ischemia–reperfusion injury via cAMP‐response element binding protein/PPAR‐γ coactivator‐1α‐mediated mitochondrial biogenesis

“…However, the relation between FOXO1 and PGC‐1α remains unclear. It has been reported that FOXO1 could directly bind to the PGC‐1α promoter and trigger the transcription of PGC‐1α in liver and muscle tissues (Ropelle et al, ; Shute, Heesch, Zak, Kreiling, & Slivka, ). But up‐regulated FOXO1 was accompanied by a reduction of PGC‐1α, while PGC‐1α overexpression suppressed the activation of FOXO1 and FOXO3 in muscle (Kang & Ji, ).…”